Praise

‘I commend Reena for writing this complete guide to periodontics, made

possible by her knowledge of the area and, most importantly for advice on
such a practical subject, her detailed experience of clinical practice. As a
keystone of oral health, the periodontium is of increasing importance in our
complex world, with the developing knowledge of the relationships
between oral and general health. I am confident that this book will empower
readers to reach professional and personal heights of excellence in the care
of their patients and themselves.’
— Dr Stephen Hancocks OBE, former Editor-in-Chief, BDJ

‘This is not just another book on periodontology, of which there are many.
Reena has expertly captured the practical essence of the subject, and her
book is packed full of down-to-earth, practical advice, analogies, hints, and
tips to improve your care and communication with patients, and systems
that will make delivering periodontal care rewarding, successful and always
interesting.’
— Dr Len D’Cruz, Head of BDA Indemnity, General Dentist and
Practice Owner

‘Reena has dedicated her career to learning and becoming an expert in

periodontics, and this handbook will be extremely useful to anyone that
wants to take their perio knowledge to the next level.’
— Dr Yewande Oduwole, General Dentist
‘Finally! A concise, modern, and up-to-date step-by-step handbook for
clinicians managing periodontics at any stage of their career.’
— Anna Middleton, Dental Hygienist/Therapist

‘As a dental student, I found this book to be an excellent resource for

understanding periodontics. It’s clear and easy to navigate, making it
perfect for both quick reference as well as in-depth study. Covering
everything from foundational knowledge to advanced surgical
interventions, this book is a must-have textbook for any student looking to
strengthen their knowledge in perio.’
— Leena Soltan, Co-President, British Dental Student Association
DR REENA WADIA

THE

PERIO
HANDBOOK
THE COMPLETE GUIDE TO
MODERN PERIODONTICS
First published in Great Britain in 2024
by Rethink Press (www.rethinkpress.com)

© Copyright Reena Wadia

All rights reserved. No part of this publication may be reproduced, stored in or introduced
into a retrieval system, or transmitted, in any form, or by any means (electronic,
mechanical, photocopying, recording or otherwise) without the prior written permission of
the publisher.

The right of Reena Wadia to be identified as the author of this work has been asserted by
her in accordance with the Copyright, Designs and Patents Act 1988.

This book is sold subject to the condition that it shall not, by way of trade or otherwise, be
lent, resold, hired out, or otherwise circulated without the publisher’s prior consent in any
form of binding or cover other than that in which it is published and without a similar
condition including this condition being imposed on the subsequent purchaser.

Illustrations by Gemma Bull

 To my dedicated students, whose curiosity and passion inspire me every
day.

To the incredible team at RW Perio, for your unwavering commitment and

excellence.

To my talented referrers, for your trust and collaboration in advancing

periodontal care.

To my beloved daughter, for bringing endless joy and perspective to my life.

To my wonderful husband, for your unwavering support, encouragement,

and love.

To my parents, for their endless sacrifices and wisdom that have shaped
who I am today.

And to my Guru, Pujya Mahant Swami Maharaj, whose guidance and faith
light my path.

This book is for you all.

Contents
Foreword

Introduction

PART ONE The Foundations

1 The Periodontium And Beyond

1.1 Anatomy of the periodontium
1.2 Periodontitis – epidemiology and pathogenesis
1.3 Periodontitis and systemic disease

2 Think Like A Detective

2.1 History taking – asking the right questions
2.2 Systemic risk factors
2.3 Local risk factors

PART TWO Assessment And Diagnosis

3 Clinical Examination
3.1 Appearance of the gingivae
3.2 Assessment of biofilm
3.3 Making probing comfortable
3.4 The BPE
3.5 The six-point pocket chart
3.6 Assessment of dental implants

4 Special Investigations
 4.1 Radiographs
4.2 Sensibility testing

5 Diagnosis
5.1 Background
5.2 Periodontal health and gingival diseases
5.3 Periodontitis
5.4 Other conditions affecting the periodontium
5.5 Peri-implant diseases and conditions

6 Prognosis
6.1 Importance and details
6.2 Prognostic systems

PART THREE The Management

7 Treatment Planning
7.1 The stepwise approach
7.2 A typical treatment plan
7.3 Working as a team
7.4 Referral

8 Educating And Empowering Patients

8.1 Translating the clinical findings and treatment plan
8.2 Essential steps for effective home care
8.3 Behavioural change
8.4 Key recommendations
8.5 Oral hygiene analogies
8.6 Biofilm-retentive factors

9 Non-Surgical Periodontal Therapy

9.1 Consent
9.2 Local anaesthesia
 9.3 Full/half/quadrant approach
9.4 Adjuncts
9.5 MINST
9.6 Ultrasonics, hand instrumentation, and other devices
9.7 RSI and back/neck pain

10 Periodontal Challenges
10.1 Occlusal trauma and splinting
10.2 Furcations
10.3 Dentine hypersensitivity
10.4 Halitosis

11 Periodontal Emergencies And Their Management

11.1 Gingival abscess
11.2 Periodontal abscess
11.3 Pericoronitis/peri-coronal abscess
11.4 Necrotising gingivitis and periodontitis
11.5 Acute herpetic gingivostomatitis
11.6 Acute physical/chemical/thermal injury
11.7 Subgingival root fractures

12 Supportive Periodontal Care

12.1 Recall interval
12.2 Palliative periodontal care
12.3 Appointment structure

13 Dental Implants
13.1 Dental implants in periodontitis patients
13.2 Key recommendations
13.3 Management of peri-implant disease

14 Multidisciplinary Care
14.1 The perio–endo interface
 14.2 The perio–ortho interface

15 Pocket Reduction Surgery

15.1 Key aims and considerations
15.2 Surgical details

16 Gingival Recession And Surgery

16.1 Aetiology
16.2 Classification
16.3 Pathogenesis
16.4 Treatment

17 Crown-Lengthening Surgery
17.1 Definition and indications
17.2 Ideal ‘pink’ aesthetics
17.3 Causes of gingival excess
17.4 Treatment sequence

Conclusion

References

The Author
Foreword

The Perio Handbook, by Reena Wadia, is a refreshingly practical textbook.

It delivers the complexities of periodontal and peri-implant diseases in 16
bite-sized chapters mapped into 3 parts and includes key references to
ensure the contemporary evidence base is represented throughout.

Part One covers the key applied anatomy, epidemiology, pathogenesis, and
risk factors across two introductory chapters.

Part Two moves onto the clinical examination process, and as well as
discussing indices, looks at the initial and detailed examination process
alongside clinical investigations. It covers the important area of human
psychology, which is critical to gaining patient engagement, before
explaining the diagnostic process by employing the British Society of
Periodontology (BSP) implementation of the 2018 classification system. It
finishes with concisely written sections on prognostication and peri-implant
diseases.

Part Three has 10 chapters that take the reader through clinical management
of periodontal and peri-implant diseases, both non-surgically and surgically.
The approach employs the steps of care from the BSP’s adolopment of the
S3-level clinical guideline on Stages I–III periodontitis and also moves into
multidisciplinary care for oral rehabilitation via orthodontic treatment,
furcation management, perio–endo lesions, and periodontal emergencies. It
deals with the tricky issue of palliative periodontal treatment and the
importance of supportive care, focusing on real issues for patients such as
recession, hypersensitivity, and halitosis. The final chapters discuss basic
periodontal surgery for pocket reduction, tissue regeneration, and graft
surgery.
The book successfully distils the huge evidence base of this rapidly
expanding discipline into a practical guide designed for the whole dental
team. It is ideal for students and new graduates, and clearly focuses on key
periodontal topics for general practice.

Enjoy reading!

Professor Iain Chapple MBE

Past President of the British Society of Periodontology

Former Dean/Head of the School of Dentistry and current Director of

Research for the Institute of Clinical Sciences at the University of
Birmingham

European Federation of Periodontology past Treasurer, Secretary General,

Founding Chair of the Scientific Affairs Committee and recipient of the
2022 Eminence Award
Introduction

Welcome to your ultimate guide to modern periodontics. This book

provides a succinct yet thorough overview of the key topics that underpin
the daily practice of all dental professionals. Its structure is designed to
facilitate easy navigation and quick reference. The goal is to empower you
with the essential knowledge and tools required to ensure the best outcomes
for your patients and your practice. By following the guidelines and best
practices outlined in this book, clinicians will not only enhance patient care
but significantly reduce their medicolegal risk. This is particularly
important given that periodontal issues are among the most common causes
of dental litigation.

Part One covers the foundations, delving into the aetiology and
epidemiology of periodontal diseases and providing an overview of good
history taking and risk factors. Part Two looks at assessment, diagnosis, and
effective patient communication strategies. Part Three explores treatment
planning, providing effective oral hygiene advice in the limited time
available, non-surgical periodontal therapy, and the management of specific
conditions like occlusal trauma, furcations, dentine hypersensitivity, and
halitosis. This section also includes protocols for managing periodontal
emergencies and provides guidelines for supportive periodontal care. The
final part addresses advanced topics, including the integration of dental
implants in periodontitis patients, the perio–endo and perio–ortho
interfaces, and various surgical interventions such as pocket reduction,
gingival recession treatment, and crown-lengthening surgery. These
chapters are designed to equip clinicians with the knowledge needed to
handle complex cases and provide optimal patient care.
Each chapter is written with a focus on practical application, ensuring that
you can easily incorporate the latest evidence-based practices into your
daily routine. The book is structured to be a reliable reference, enabling you
to quickly find the information you need, whether you are preparing for a
procedure, educating a patient, or simply brushing up on a particular topic.
 PART ONE
THE FOUNDATIONS
1
The Periodontium And Beyond

We begin this book by introducing its core subject matter: the periodontium.
It’s super important to understand the anatomy of the periodontium in order
to recognise both health and disease. We will then outline the epidemiology
and pathogenesis of periodontitis before exploring the links between
periodontitis and the rest of the body.

1.1 Anatomy of the periodontium

The periodontium’s main purpose is to secure the tooth to the jawbone and
preserve the integrity of the surface of the masticatory mucosa. Lang and
Lindhe (2015) have extensively described the anatomy of the periodontium
in their book Clinical and Periodontology and Implant Dentistry, but in this
section we will highlight the key points.
 The anatomy of the periodontium in cross section

The gingiva – macroscopic

The gingivae form part of the masticatory mucosa. In the coronal direction,
the gingiva terminates in the free gingival margin. In the apical direction,
the gingiva is continuous with the lining mucosa, from which the gingiva is
separated by the mucogingival junction. In the palate there is no
mucogingival line present as the hard palate and the maxillary alveolar
process are covered by the same type of masticatory mucosa.
 The gingiva and supporting structures in cross section

The gingiva can be divided into two regions: the free gingiva and the
attached gingiva. The free gingiva, which is coral pink with a dull surface
and firm consistency, includes the gingival tissue on the buccal and
lingual/palatal sides of the teeth as well as the interdental papillae. It
stretches from the gingival margin down to the free gingival groove,
aligning with the tooth’s cementoenamel junction. The attached gingiva,
marked by the mucogingival junction in the apical direction, is also firm
and coral pink, often exhibiting small surface indentations called
‘stippling’. This part is securely attached to the underlying alveolar bone
and cementum through connective tissue fibres. In contrast, the darker red
alveolar mucosa below the mucogingival junction is loosely connected to
the bone underneath, making it more mobile relative to the underlying
tissue.

The contact points between teeth, the width of the surfaces where teeth
meet, and the cementoenamel junction shape the interdental gingiva, or
papilla. In the front of the mouth, the interdental papilla tends to be
pyramidal, whereas in the molar regions, the papillae are more flattened in
the buccolingual direction. This shape of the interdental papilla aligns with
the contour of the contact surfaces between teeth, forming a concave area
known as a col in the premolar and molar regions.

The gingiva – microscopic

The oral epithelium is a keratinised, stratified, squamous epithelium with
distinct cell layers: the basal layer, prickle cell layer, granular cell layer, and
keratinised cell layer. Besides the keratin-producing cells, which make up
about 90% of the cell population, it also includes melanocytes, Langerhans
cells, Merkel cells, and inflammatory cells.

The junctional epithelium has a free surface at the base of the gingival
sulcus. Similar to the oral sulcular and oral epithelium, it undergoes
continuous renewal via cell division in the basal layer. It narrows in the
apical direction, with a thickness ranging from fifteen to thirty cells at the
base of the gingival sulcus to one to three cells at its most apical end.
Lacking keratinisation on its free surface, it cannot serve as a physical
barrier. Hemidesmosomes and basal lamina allow the junctional epithelium
cells next to the tooth to attach to its surface, while on the opposite side,
these cells connect with the lamina propria of the gingiva.

The projections of connective tissue into the epithelium are known as

connective tissue papillae, and are separated by epithelial ridges or rete
pegs. The main tissue component of the gingiva is the connective tissue, or
lamina propria. The primary components of this connective tissue are
collagen fibres (60% of its volume), fibroblasts (5%), and vessels and
nerves (35%), all embedded in an amorphous ground substance, or matrix.
The different types of cells present in the connective tissue include
fibroblasts, mast cells, macrophages, and inflammatory cells. The
fibroblasts produce the connective tissue fibres, which can be classified into
collagen fibres, reticulin fibres, oxytalan fibres, and elastic fibres.
The matrix of the connective tissue is primarily produced by fibroblasts,
though some components are produced by mast cells, and others are derived
from the blood. This matrix serves as the medium in which the connective
tissue cells are embedded and is crucial for maintaining the normal function
of the connective tissue. The transport of water, electrolytes, nutrients, and
metabolites to and from the individual connective tissue cells takes place
within this matrix. The main components of the connective tissue matrix are
protein–carbohydrate macromolecules, which are typically classified into
proteoglycans and glycoproteins.

Periodontal ligament
The periodontal ligament is a soft, highly vascular and cellular connective
tissue that encases the roots of the teeth, linking the root cementum to the
socket wall. This periodontal ligament has an hourglass shape, being
narrowest at the mid-root level, and its width is about 0.25 mm (ranging
from 0.2 to 0.4 mm).

The key functions of the periodontal ligament include:

Flexible support for the teeth in their sockets (cushion)

Sensory receptor necessary for proper positioning of the jaws
Cell reservoir for tissue homeostasis and repair

The principal fibres of the periodontal ligament are the alveolar crest fibres,
horizontal fibres, oblique fibres, and apical fibres. Sharpey’s fibres are the
ends of these principal fibres that are embedded in the cementum or bone,
providing anchorage. The cells found in the periodontal ligament include
fibroblasts (the most common cell type), osteoblasts, cementoblasts,
osteoclasts, epithelial cells, and nerve fibres. As collagen matures, its fibrils
contract, and there is a constant and high turnover of collagen in the
periodontal ligament. This continuous process creates a permanent force
that keeps the tissues firmly connected.
Root cementum
Root cementum is a specialised mineralised tissue that covers the surface of
the tooth root. It connects the periodontal ligament fibres to the root and is
involved in repairing any damage to the root surface.

Although root cementum shares several characteristics with bone tissue, it

differs in some key aspects. Cementum lacks blood and lymph vessels, has
no nerve supply, and does not undergo physiological resorption or
remodelling. Instead, it continuously deposits throughout life. Like other
mineralised tissues, it contains collagen fibres embedded in an organic
matrix. Its mineral content, predominantly hydroxyapatite, constitutes about
65% by weight, which is slightly higher than that of bone, which is around
60%.

Alveolar bone
The alveolar bone, also known as the alveolar process, refers to the parts of
the maxilla and the mandible that form and support the sockets of the teeth.
The walls of the sockets are lined with cortical bone, and the area between
the sockets and between the compact jawbone walls is occupied by
cancellous bone. The cortical and cancellous alveolar bone are constantly
undergoing remodelling (ie resorption followed by formation) with the help
of osteoblasts, osteocytes, and osteoclasts.

Blood, lymphatic, and nervous supply

The dental artery, which is a branch of the superior or inferior alveolar
artery, dismisses the intraseptal artery before it enters the tooth socket. The
terminal branches of the intraseptal artery extend into the alveolar bone
through canals at various levels within the socket. These branches form
connections in the periodontal ligament space with vessels from the apical
region of the periodontal ligament and other terminal branches of the
intraseptal artery. Before the dental artery reaches the root canal, it gives off
branches that supply the apical region of the periodontal ligament.

The gingiva’s blood supply primarily comes from supraperiosteal blood

vessels, which are terminal branches of the sublingual artery, mental artery,
buccal artery, facial artery, greater palatine artery, infraorbital artery, and
posterior superior dental artery. Lymph capillaries, which are the smallest
lymph vessels, create an extensive network within the connective tissue.
Like other body tissues, the periodontium contains receptors that detect
pain, touch, and pressure (nociceptors and mechanoreceptors). Nerves
innervate the blood vessels in the periodontium, with pain, touch, and
pressure sensations having their central processing in the semilunar
ganglion and travelling to the periodontium via the trigeminal nerve and its
branches. The receptors in the periodontal ligament allow the detection of
small forces applied to the teeth.

1.2 Periodontitis – epidemiology and

pathogenesis
Periodontitis is the most prevalent chronic inflammatory disease in humans,
with eight out of ten people over the age of thirty-five experiencing some
form of gum issue (Chapple, 2014). Milder forms of periodontitis could
affect up to 50% of individuals, while severe periodontitis impacts 11.2% of
the population, making it the sixth most common health condition globally
(Kassebaum et al, 2014). Despite its widespread occurrence, it remains one
of the least acknowledged conditions.

Epidemiology and impact – the facts and figures

Periodontitis has been classed as a major public health problem due to its
high prevalence and significant effect on quality of life. In terms of its
socio-economic impact, severe periodontitis, along with dental caries, is
responsible for more years lost to disability than any other human disease,
and globally periodontitis is estimated to cost $54 billion in direct treatment
costs and a further $25 billion in indirect costs (GBD 2017 Disease and
Injury Incidence and Prevalence Collaborators, 2018). Periodontitis may
also have a negative impact on general health, which will be discussed in
more detail later in this chapter.

Pathogenesis
Both gingivitis and periodontitis are inflammatory conditions that occur due
to the formation and persistence of microbial biofilms. Gingivitis is
confined to the gingiva, while periodontitis involves additional damage to
the periodontal ligament and alveolar bone. The likelihood of gingivitis
advancing to periodontitis is highest among individuals who are more
susceptible, accounting for approximately 5–15% of the population. In
contrast, around 10% of the population appears to be resistant to
periodontal damage, even with ongoing biofilm accumulation, making
disease progression in these individuals uncommon (Chapple, 2014).

WHAT IS A BIOFILM?

A dental biofilm describes microorganisms attached to the tooth surface

embedded in an extracellular matrix in contact with a fluid phase (Jakubovics
et al, 2021). Biofilms serve as interactive microbial communities. Saliva is the
primary source of nutrients for health-associated biofilms, whereas gingival
crevicular fluid is a main source of nutrients for microorganisms in biofilms
associated with periodontal disease.
Both the quantity and quality of bacteria that colonise the gingival sulcus can
contribute to disease. These can also lead to the release of specific enzymes,
toxins, and metabolic products, which have the potential for periodontal tissue
damage. The bacterial flora changes with disease where more gram-
negative, anaerobic, and motile bacteria, such as Porphyromonas gingivalis,
make an appearance.

Disease occurs when there is a change in balance between the microbial

biofilm and host inflammatory and immune responses. It’s the host response
(rather than the biofilm) that causes 80% of the tissue damage; this response
is modified by local and systemic risk factors (Grossi et al, 1994). So while
optimal oral hygiene remains an important factor in achieving periodontal
health, it should not be the sole focus of attention. We will be discussing
risk factors in more detail in Chapter 2.

Periodontitis is regarded as a condition that is seen in susceptible patients

who have an exaggerated inflammatory/immune response to biofilm and/or
reduced levels of defence. This leads to chronic collateral damage to the
periodontal tissues because the host response is unable to successfully
remove the biofilm, resulting in the propagation of the periodontal lesion.
There has been debate over whether the change to the pathogenic microbial
biofilm comes before or after the inflammatory response. A review by Van
Dyke et al (2020) proposed that the inflammatory response is the key factor
that modulates the change to the pathogenic biofilm, and it is only in the
latter stages that the microbial pathogenicity becomes important.

1.3 Periodontitis and systemic disease

The whole body is connected, and the mouth should not be considered in
isolation from the rest of the body. It’s important to be aware of the links
between periodontitis and other systemic diseases and be able to
confidently discuss these with our patients. Highlighting these links can
help to communicate the importance of this condition and its treatment.

The overall mechanisms linking the conditions are largely inflammatory

and bacterial based. When explaining these links to patients, it’s important
to use them as a motivational tool rather than scaring them. Provide a
positive spin on the message and use this as an opportunity to promote the
importance of periodontitis prevention and treatment. Treating periodontitis
and shared modifiable risk factors can only have a positive effect on related
systemic disease and we dental professionals are ideally situated as front-
line healthcare professionals to facilitate this.

The following are some of the systemic conditions that can be associated
with periodontitis.

Diabetes
Diabetic patients with uncontrolled serum glucose levels are more likely to
suffer from periodontitis compared with well-controlled diabetic or healthy
individuals (Preshaw and Bissett, 2019). Periodontitis impacts the
effectiveness of diabetes control and the risk of complications. Severe
periodontitis affects HbA1C in individuals with and without diabetes, and
moderate to severe periodontitis is associated with an increased risk of
developing diabetes (Chapple et al, 2013).

Improvement of clinical periodontal parameters following standard non-

surgical therapy with effective oral hygiene can be achieved even in people
with poorly controlled diabetes. Randomised controlled trials consistently
demonstrate that mechanical periodontal therapy is associated with a 0.4%
reduction in HbA1C at three months – this impact is equivalent to adding a
second drug to a pharmacological regime for diabetes (Simpson et al,
2010).

Cardiovascular disease

Periodontitis and atherosclerosis share several characteristics and

mechanisms, such as the inflammatory processes and shared risk factors
(age, smoking, metabolic factors, stress) as well as genetic predisposition.
However, periodontitis and cardiovascular disease have been proven to be
significantly associated with each other, independent of the effects of
cofounders (Hirschfeld and Chapple, 2021).

Inflammatory bowel disease

Inflammatory bowel disease and periodontitis have a similar pathogenesis,

characterised by a hyperactivity of the immune response to commensal
microbiota in susceptible individuals (Hirschfeld and Chapple, 2021).

A meta-analysis of nine observational studies from different populations

reported a 4.5-fold higher periodontitis risk in adult patients with
inflammatory bowel disease. The overall quality of evidence should be
considered weak-moderate; however, the existing studies report a
significant association (Hirschfeld and Chapple, 2021).

Rheumatoid arthritis

There appears to be a clear epidemiological relationship between

rheumatoid arthritis and periodontitis, although the directionality of this
relationship is not known. Based on the current evidence, a causal
relationship cannot be proven, and, if proven in the future, it may be an
association in a subset of susceptible rheumatoid arthritis patients only
(Hirschfeld and Chapple, 2021). Future research is needed to investigate
this.

Respiratory diseases

While there are plausible mechanisms explaining the potential associations

between periodontitis and several respiratory diseases, a lack of
epidemiological evidence means associations in general are inconclusive
(Hirschfeld and Chapple, 2021).

Adverse pregnancy outcomes and fertility

There appears to be a modest association between periodontitis and pre-

eclampsia and weak evidence of an association between periodontal
diseases and pre-term and low-birth weight. Both associations are hampered
by the heterogeneity of the data. Despite extensive research spanning over
twenty-five years, definitive conclusions about the relationships between
periodontal health and negative pregnancy outcomes remain elusive
(Hirschfeld and Chapple, 2021).

Pregnancy can impact periodontal health due to changes in sex hormone

levels, which may increase gingival inflammation. This effect is likely
linked to the presence of oral biofilms, increased blood flow and
vascularity, and cellular alterations. Additionally, these hormonal changes
can heighten the inflammatory response to the biofilm, potentially leading
to oedematous changes or the development of a localised area of highly
vascular granulation tissue, known as an epulis.

Regarding fertility, there is extremely limited and weak evidence that

periodontal disease is associated with infertility. Larger observational
studies that adjust for confounding factors need to be implemented
(Hirschfeld and Chapple, 2021).

Neurodegenerative diseases

Knowledge in this field is still in its infancy, but it is known that the
progression of cognitive decline has a marked effect on individual dental
biofilm control (Hirschfeld and Chapple, 2021).

There is an indication that for a proportion of those who develop the

common non-familial Alzheimer’s disease, periodontitis could be involved
in the progression, if not the initiation of their condition. There is clear
epidemiological evidence of an association between the two conditions of
periodontitis and Alzheimer’s disease, which are both pro-inflammatory.
Furthermore, there is evidence that the co-existence of periodontitis is
associated with more rapid rates of cognitive decline, suggesting that the
presence of periodontitis has an adverse effect on the progression of
Alzheimer’s disease (Hirschfeld and Chapple, 2021).

The evidence for a link between periodontitis and Parkinson’s disease is

largely circumstantial. However, this is likely to become clearer with more
studies. Overall, further evidence is required to determine whether any
causative association between periodontitis and neurodegenerative disease
exists.

Stress and depression

Both stress and depression dysregulate the immune response and produce
changes in the central and peripheral nervous and endocrine systems.
Psychological factors can change health-related behaviour, leading to
unhealthy habits including alcohol and substance abuse, cigarette smoking,
and neglect of oral hygiene. These factors contribute to a higher risk of
periodontitis (Hirschfeld and Chapple, 2021).
2
Think Like A Detective

When dealing with patients with periodontitis, it’s important to think like a
detective. Every patient sitting in your chair has a ‘causal pie’ above their
head and although biofilm/suboptimal oral hygiene will be a slice of that
pie, you need to find out what the rest of the slices are. These will be
different for every patient and, if they are not identified, the accuracy of the
diagnosis and success of the treatment plan will be affected.

You need to think like a detective when it comes to working out whether
and why the patient has periodontitis. In the first instance, identifying a
periodontitis patient requires thorough history taking, which relies on
asking the right questions. Then, when trying to figure out the cause, a
consideration of risk factors comes into play.

2.1 History taking – asking the right questions

There are four quick trigger questions to ask all patients. If they answer yes
to any of these, this is a clue that they may be a periodontitis patient:

1. Do your gums bleed on brushing? It’s important to include ‘on

brushing’ as often patients will think it’s normal that their gums
bleed on brushing so may answer no if you ask them only if their
gums bleed. If they say no to this, then you can question them
about bleeding when using floss or interdental brushes.
 2. Are any of your teeth loose? Loose teeth are a strong indicator of
periodontitis. You can also ask them if the looseness is affecting
their ability to eat comfortably.
3. Any gum swellings or gum boils? Often patients won’t
understand what an abscess is so using the term ‘gum boil’ is
helpful.
4. Do you suffer from bad breath or notice a bad taste?
Individuals might be embarrassed to admit to bad breath, but tend
to be happier to admit to a bad taste, so always lead with this.

As well as serving as diagnostic clues, the above trigger questions might

reveal the patient’s ‘pain point’ – the reason they are seeking treatment.
Being aware of this means we can discuss how we will address it through
treatment, increasing motivation for treatment uptake and aiding patient
compliance.

2.2 Systemic risk factors

A risk factor is an occurrence or characteristic associated with the increased
rate of a subsequently occurring disease (Van Dyke and Dave, 2005). The
presence of biofilm is like the key having been turned in a car’s ignition,
but all the other risk factors are pressing on the accelerator, driving the
disease forward. Systemic risk factors may be among the key determinants
of susceptibility. Risk factors may affect the periodontal tissues, host
response, or the oral environment. They may be modifiable or non-
modifiable. They might also influence the treatment approach, so you must
ensure you pick up the key risk factors for periodontitis during your history
taking.

When you take your patient’s history, go through this in a logical order,
addressing the medical history, social history, and dental history, all of
which are relevant to periodontal disease.
Medical history
When taking the patient’s medical history, there are several key risk factors
to watch out for, notably diabetes, pregnancy, immunodeficiency and any
medications the patient may be taking.

Diabetes

Diabetes is a group of metabolic disorders characterised by hyperglycaemia

resulting from the body’s inability to control blood glucose (lack of
insulin/responsiveness). According to the International Diabetes Federation,
diabetes is now a global epidemic with 50% of cases being undiagnosed
(IDF, 2021). There are three main types: type 1, type 2, and gestational.

Patients with hyperglycaemia are three times more likely to develop periodontitis
(Chapple and Genco, 2013).

Diabetes increases patients’ susceptibility to and the severity of

periodontitis. It is classed as a modifiable risk factor as, though it cannot be
cured, it can be controlled, and control is the most important factor related
to this condition.

Practical tips for dealing with periodontitis patients with diabetes:

Ensure your patient has eaten before any treatment appointments

to minimise risk of a hypoglycaemic episode.
Check the patient’s glycaemic control by asking for the results of
a recent HbA1C test or by completing one on-site. The HbA1C
level (which is a measure of three-month control) should ideally
be <6.5%/48 mmol/mol.
Poorly controlled diabetics will be at higher risk of periodontitis
so may require more frequent periodontal examinations.
 Poor glycaemic control reduces the benefits of periodontal
therapy. Ensure the patient is aware of this and make a note of the
fact you have emphasised the importance of good control.
Be a supporter when it comes to oral hygiene. Diabetics have
many other general health issues to worry about so try and see
how you can fit oral hygiene into their overall self-care regime.
Following successful periodontal treatment, HbA1C reductions of
0.4% have been shown – a clinical equivalent to adding a second
drug to a pharmacological regime for diabetes (Chapple et al,
2013). This can be hugely motivational for patients.

Pregnancy

Stimulation of prostaglandin synthesis can result in vascular changes.

Hormonal changes mean that the inflammatory effects are magnified if the
dental biofilm is not adequately controlled; this results in oedematous
and/or proliferative alterations. The classic proliferative change is a
pregnancy epulis.

Practical tips for working with pregnant patients, as suggested by the

European Federation of Periodontology:

Identify the stage of pregnancy and perform a comprehensive

periodontal examination.
Pregnant women with a healthy periodontium should be provided
with oral health education, including detailed oral hygiene
instructions.
Emphasise to patients with gingivitis or periodontitis that non-
surgical periodontal therapy during pregnancy is safe, effective,
and beneficial.
 Following treatment, reassess the periodontal status according to
normal practice.
Once treated, frequent monitoring of the periodontal condition
should be maintained throughout pregnancy and if there is a
recurrence, a similar intervention should be provided.
For a pregnancy epulis, surgical excision can be performed for
large lesions that are impacting upon function or aesthetics.
However, if lesions are small, excision can be delayed until
postpartum with supportive measures carried out during
pregnancy.
If possible, other forms of elective periodontal surgery should also
be avoided during pregnancy.

It’s also important to be aware of other hormonal changes, as they will

impact on periodontitis risk; this includes puberty and the menopause.

Immunodeficiency

Ensure you closely examine immunodeficient patients as they can present

with necrotising periodontal disease (necrotising gingivitis or periodontitis).
Signs of necrotising disease include a pseudomembrane, punched-out
papillae, and halitosis. Immunodeficiency can be the result of HIV/AIDS
but in this case the signs may be subtle, as medications can now control
HIV/AIDS very well.

Necrotising periodontal disease is also not uncommon in patients with high

stress levels, those who are run down, smokers, and those with suboptimal
oral hygiene. Treatment includes gentle professional mechanical plaque
removal, adjunctive use of a mouthwash, and metronidazole antibiotics.

Medications
The role of biofilm in the overall pathogenesis is now regarded as
important, with most studies indicating that biofilm is a prerequisite for
gingival enlargement to occur. The gingival enlargement then makes it
more difficult to maintain optimal plaque control (Zoheir and Hughes,
2020). There are certain medications that increase the risk of gingival
enlargement in certain individuals (Zoheir and Hughes, 2020). Look out for
phenytoin (anticonvulsant for epilepsy), cyclosporin (immunosuppressive
for transplant patients), and -dipine medications, for example amlodipine
(calcium-channel blocker for hypertension).

FACTS ABOUT DRUG-INFLUENCED GINGIVAL ENLARGEMENT

The first signs of change are reported to arise about one to three
months following the start of dosing.
There appears to be a minimum threshold for drug plasma levels,
below which drug-influenced gingival enlargement is unlikely to
occur.
Phenytoin causes a largely fibrotic and pink enlargement, whereas
calcium-channel blockers are associated with a more vascular
overgrowth.
Enlargement classically begins at the interdental papilla region.

Practical tips on managing patients with gingival enlargement as a result of

prescribed medication:

Ensure you have an up-to-date medical history.

Contact the patient’s general medical practitioner (GMP) to find
out if it would be feasible to replace the risk factor drug with an
alternative. This might occur following initial therapy or at the
start if the overgrowth is severe.
Oral hygiene reinforcement, with an emphasis on angulation into
the gingival sulcus area, is particularly helpful here. Single-tufted
brushes are a useful adjunct.
 Complete a Basic Periodontal Examination (BPE) and six-point
pocket chart if needed. Radiographic examination will be key to
work out if there are areas of false pocketing.
Carry out supragingival and subgingival professional mechanical
plaque removal as necessary. Ensure that any plaque-retentive
factors, such as overhanging restorations, have been corrected.
Surgery may be indicated following non-surgical therapy if the
enlarged tissues are significant and very fibrous.
Regular supportive periodontal therapy will be key to minimise
recurrence.

Below is an example letter to a GMP, which can be used to request the

exploration of an alternative drug if required.

Dear Dr [Name]

Re: [Name, address, DOB]

I recently saw this patient regarding his gum issues.

I understand he is a patient of yours who is hypertensive and

taking [insert drug and dose].

On examination today, there was significant gum

swelling/enlargement, and he has been diagnosed with [insert
detailed periodontitis diagnosis]. This condition is having a
significant impact on his daily quality of life.

As you will know, calcium channel blockers are well

recognised to sometimes have adverse effects on the gums,
and his condition is typical of calcium-channel blocker-
associated periodontal disease.
 I am writing to ask if you would be able to assess him to
consider whether it may be possible for you to change his
medication to a non-calcium channel blocker
antihypertensive drug?

Best wishes,

Dr [Name]

[You can also include photos to emphasise the impact]

Family history/genetics

Interestingly, 50% of periodontitis susceptibility is due to host genetic

factors (Michalowicz et al, 2000). Evidence for this association is stronger
for Grade C forms of periodontitis, where the attachment loss can be
inconsistent with local risk factors. It may be helpful in these cases to tell
patients that ‘periodontitis can be an unfair condition.’ Patients may often
mention a family history of periodontitis, but the reliability can vary; for
example, if a patient says that their thirty-two-year-old sibling is having
surgery for periodontitis, that is likely more reliable than someone
mentioning that their parents had weak gums and lost all their teeth early.

Social history
As well as medical and family history, it’s also important to look at the
patient’s social history, to identify further potential risk factors, including
the following.

Smoking

While the prevalence of smoking has decreased steadily across the globe, it
remains a common risk factor for periodontitis. In fact, 42% of periodontitis
may be attributable to smoking (Tomar and Asma, 2000). Smoking
increases susceptibility to and severity of periodontitis in a dose-dependent
manner. Smokers will have deeper pockets, more recession, greater bone
loss (especially in the upper anterior regions), and increased tooth loss
compared to non-smokers (Tomar and Asma, 2000). Smokers are likely to
also have less marginal bleeding, masking the early critical signs of
periodontitis (Bergstrom and Bostrom, 2001).

Local effects of smoking include reduced tissue vascularity, as well as

impaired polymorphonuclear leucocyte chemotaxis and function. Systemic
effects include decreased salivary IgA, decreased serum IgG, and decreased
helper T cells (Ryder et al, 1998).

For smokers, there will be poorer success rates in both non-surgical and
surgical therapy with a greater chance of disease recurrence (Ah et al, 1994;
Bostrom et al, 1998). During maintenance, smokers will be more likely to
lose teeth than non-smokers. This all needs to be discussed with the patient
and clearly noted in their records.

Some practical tips on facilitating smoking cessation:

Don’t underestimate the impact of your role, even if it’s a brief

intervention (Ramseier et al, 2020). Smoking cessation is
essential. Ask (them if they are interested in stopping), advise
(them on the benefits for both general and oral health), and refer
(to smoking cessation services, if they are keen).
Use of NHS stop-smoking services (nhs.uk/smokefree) almost
triples the likelihood of successfully quitting.
Focus on the advantages of quitting rather than the disadvantages
of not quitting.

Vaping
Research shows that 37% of current smokers vape, so it’s important to ask
them about this (ASH, 2023). Vaping is reportedly better for general health
and is an effective tool to help smokers quit. The effects of vaping on the
periodontal condition are unknown, but most professionals speculate that
nicotine will likely have some negative impact, so in the long-term, vaping
cessation should be a part of the treatment plan (Holliday et al, 2021).

Stress

Stress is a significant risk factor for periodontitis, especially when there is

evidence of poor coping strategies (Wimmer et al, 2002; Hugoson,
Ljungquist, and Breivik, 2002). Ask patients about their stress levels and
negative life events. The mechanisms underlying this association are not
well understood but include a mix of behavioural changes and impact on
the immune system.

Dental history
Of course, the patient’s dental history is relevant to a diagnosis and
assessment of periodontitis, and history taking in this regard should cover
the following.

Diet/nutrition

Nutrition will modify the severity and extent of the disease by affecting host
resistance and potential for repair, and some nutritional deficiencies may
exacerbate gingival response to plaque (Raindi, 2016). For example,
micronutrient deficiencies have been shown to be inversely related to
periodontal health. Specifically, there is good quality evidence for an
association with vitamin C, magnesium/calcium levels, antioxidants,
docosahexaenoic acid, and vitamin D (Woelber et al, 2017). At a
macronutrient level, emerging evidence indicates that a carbohydrate-rich
diet increases the risk of inflammation and, thus, gingival bleeding, whereas
a switch to a palaeolithic diet results in a decrease in gingival bleeding
(Raindi, 2016).

When talking to patients about diet and nutrition, ensure that you:

Explain the potential dietary impact on both systemic and oral

disease
Encourage a well-balanced diet
Explain that diet modification is preferred over the use of
supplements

2.3 Local risk factors

Successful treatment will be dependent on detailed history-taking to pick up
the above risk factors, as these require appropriate management. When
examining the patient, further local risk factors may also be noted. These
act as biofilm-retentive factors, increasing the risk of periodontitis.
Examples include:

Calculus
Root caries and severe abrasive tooth wear
Restorations – overhangs, open margins
Orthodontic appliances, dentures, and crown/bridge work if not of
a hygienic design
Anatomical, eg enamel pearls or root grooves
Crowded dentition
High frenal attachment
Mouth breathing/incompetent lip seal/xerostomia

During the treatment of periodontitis, we need to tackle systemic patient-

level, mouth-level, tooth-level, and, finally, site-level risk factors.
 PART TWO
ASSESSMENT AND DIAGNOSIS
3
Clinical Examination

Before a treatment plan can be designed, a thorough clinical examination

must take place. During the examination it’s important to assess the
appearance of the gingivae as well as the level of biofilm control. Probing is
imperative when assessing the periodontium and comfortable probing is a
must-have skill. As part of the clinical assessment, one should also be
confident in assessing dental implants.

3.1 Appearance of the gingivae

Before probing, there must be a visual assessment of the gingivae during
which the following three categories should be considered:

1. Colour: Healthy gingivae are typically described as ‘coral pink’

and will be paler in colour than inflamed gingivae, which may
appear redder in colour.
2. Contour: A healthy gingiva will have a scalloped shape, tightly
adapted to the underlying tissues, and a knife-edge margin where it
abuts the tooth.
3. Consistency: Inflamed gingivae will appear swollen and ‘spongy’
in texture.

Make a note of the gingival phenotype. It would be considered thin if you

can see the probe shining through the gingival sulcus when probing, and
thick if not. Teeth tend to be more triangular shaped in thin phenotypes and
squarer in thick.

3.2 Assessment of biofilm

A general subjective assessment of biofilm/plaque control is often
completed, but objective measurements through scores are more useful.
Several systems for scoring biofilm exist. Two common examples are the
Simplified Plaque Index by Ainamo and Bay (1975) and the Plaque Control
Record developed by O’Leary et al (1972).

The Simplified Plaque Index (Ainamo and Bay,

1975)
This index consists of two possible scores:

0 – no plaque detected
1 – visible plaque detected

This dichotomous system makes a note of whether there is plaque detected

or no plaque detected for each tooth. This can then be used to produce a
percentage score.

The Plaque Control Record (O’Leary et al, 1972)

This system was developed to provide a simple method of recording the
presence of biofilm/plaque on individual tooth surfaces – ie mesial, distal,
buccal, and lingual/palatal. The teeth are disclosed, and each surface of the
tooth is examined. Those with plaque are recorded. After all the teeth have
been examined, the index is calculated by dividing the number of plaque-
containing surfaces by the total number of available surfaces, and this is
expressed as a percentage.
One disadvantage of the plaque score is that it gives only a snapshot of the
patient’s oral hygiene compliance at that moment in time. Marginal
bleeding may be a more reliable measure of the patient’s ability to remove
accessible plaque and control marginal inflammation.

Marginal bleeding is different to bleeding on probing. For marginal bleeding the

probe is run only along the gingival margin and for bleeding on probing you probe
to the base of the pocket.

The Simplified Gingival Index (Ainamo and Bay,

1975)
As a supplement to plaque measurement instruments, the Simplified
Gingival Index from Ainamo and Bay (1975) is a commonly used gingival
index for marginal bleeding, with scores as follows:

0 – no bleeding from the gingival margin detected after a

periodontal probe is briefly run along the gingival margin
1 – bleeding from the gingival margin detected after a periodontal
probe is briefly run along the gingival margin

While assessing biofilm, it is helpful to also assess calculus. This can be

completed through a visual assessment with a note made of the presence or
absence of supragingival and/or subgingival calculus.

3.3 Making probing comfortable

Ensure your probing is as comfortable as possible for the patient. For them,
this will be a preview of your future care; if they have an unpleasant
experience, this may affect their acceptance of the treatment plan. There are
both communication and technique tips to help with this.

Communication tips for probing:

 1. Explain and prewarn: Prior to probing, explain to the patient that
you will be completing ‘gum measurements, which are the only
way to check the health of the gums.’ This ensures they fully
understand why you need to probe. They should also be aware that
if their gums are inflamed, the probing may be slightly
uncomfortable, but give them the option of raising their hand to
ask you to stop if they need a breather. If there is some discomfort,
rather than the patient thinking you are causing the pain, their main
concern should be the fact they may have gum disease. By
explaining and pre-warning there is a mindset shift from the start.
2. Praise: It is not the most pleasant experience for our patients so
praising them on how well they are doing as you are probing can
be helpful. Also let them know when you are more than halfway
through, especially when completing full pocket charts.
3. Conversation after: If specific areas were sore, use this to your
advantage and explain why they might have been more
uncomfortable. This will engage the patient and link in well when
explaining the aetiology and treatment of gum disease.

Technique tips for probing:

Sweep/drag the probe: Don’t keep taking the probe in and out of
the pocket, potentially ‘stabbing’ the patient 192 times.
Appropriate pressure: Let the probe drop into the pocket (no
additional pressure) – technically you are aiming for 25 g, the
amount of force necessary to just blanch your fingernail when
pushing on it.
Finger rest: Use a finger rest, as close as possible to the tooth
being probed, to ensure good pressure control.
Appropriate angulation: Angle the probe along the root surface.
 Topical anaesthesia: Oraqix (lidocaine and prilocaine gel) may
be helpful in certain cases.
Recheck probing once numbed up for treatment: If the patient
is extremely uncomfortable, recheck the probing depths once
anaesthetised for treatment and adjust if needed.
Good vision: Using loupes with a light will provide good vision
to ensure you’re not having to repeatedly probe to recheck
measurements.

3.4 The BPE

The Basic Periodontal Examination (BPE) (2019) is the primary and
minimum standard of care for periodontal assessment in the UK. It’s a rapid
screening tool that indicates when further examination is required and
suggests basic guidance on the treatment needed.

The BPE consists of three steps, as follows:

1. Ensure you are using a BPE (WHO) probe – this has a ‘ball end’
0.5 mm in diameter and a black band from 3.5–5.5 mm.
2. Divide the dentition into six sextants and record the highest score
for each sextant. For a sextant to qualify for recording, it must
contain at least two teeth.
3. Probe all teeth in each sextant (except for the third molars unless
the first and/or second molars are missing). Even if a Code 4 is
identified in a sextant, you should continue to examine all sites in
the sextant.
 Example BPE score

Probing showing a BPE score of 4

If the patient is under the age of eighteen, a simplified BPE should be

performed. This involves assessing six index teeth (UR6, UR1, UL6, LL6,
LL1, and LR6). BPE Codes 0–2 are used in seven to eleven-year-olds,
while the full range of codes (0, 1, 2, 3, 4, and *) can be used in twelve to
seventeen-year-olds.

3.5 The six-point pocket chart

Remember, the BPE cannot be used to monitor the response to periodontal
therapy because it does not provide information about how sites within a
sextant change after treatment; it is just a screening tool. To assess the
response to treatment, a six-point pocket chart should be completed pre-
and post-treatment.

A full pocket chart involves taking measurements at six sites per tooth –
mesial, mid, distal on both the buccal and palatal/lingual aspects.
Periodontal probing depths, associated bleeding on probing (BoP), and
gingival recession will be measured. Mobility and furcation involvement
will also be noted on a full pocket chart. This will allow a more detailed
assessment of the periodontal condition to aid treatment planning. For
patients who have undergone periodontal therapy and are receiving
supportive periodontal care, a full pocket chart is recommended at least
annually.

The probing depth is the distance from the gingival margin to the location
of the tip of the periodontal probe. This may or may not be the true
histological attachment loss and, hence, the term probing depth is more
appropriate than pocket depth. According to the British Society of
Periodontology’s (BSP) (2019) guidance, when a six-point pocket chart is
indicated it is only necessary to record sites of 4 mm and above (although
six sites per tooth should be measured).

BoP is the most important measure of current periodontal disease status and
should always be recorded. It refers to the presence or absence of bleeding
following probing to the base of the pocket, where BoP indicates the
presence of inflammation. If there is suppuration (pus), this can also be
noted.

Recession is the distance from the cementoenamel junction to the gingival

margin. Identifying the exact level of the cementoenamel junction can be
tricky and may often need to be estimated.

Probing depth + recession = clinical attachment loss

To measure mobility, use the other side of your probe and mirror handle and
apply light force, alternating first one way and then the other. Observe the
tooth for movement buccolingually/mesiodistally as well as vertically. The
most commonly used system to record mobility was created by Miller
(1950).

Miller’s (1950) measure of mobility

Furcation involvement is usually assessed with probing, but radiographs

can also help with interpretation. A curved Nabers probe can be used if
needed. Each furcation entrance must be classified separately. There are
several classification systems; a commonly used one is that by Hamp et al
(1975).

Hamp et al’s (1975) furcation classification system

3.6 Assessment of dental implants

Assess the colour, contour, and consistency of the peri-implant tissues as
well as the oral hygiene. The BPE should not be used around implants;
instead, complete a four- or six-point pocket chart. Routine gentle probing
using your standard (metal) probe is safe. Make a note of the absence or
presence of any bleeding or suppuration on probing.
4
Special Investigations

The next step in the assessment journey after the clinical examination and
prior to making any diagnoses, is the special investigation phase.

4.1 Radiographs
Radiographs are the key method to assess bone levels. The type of
radiograph required is a matter of clinical judgement and this decision
should also take into consideration the overall dental needs of the patient.
For periodontal assessment, ensure the crestal bone levels are visible in all
areas. For mild bone loss, this may be captured through standard horizontal
bitewing radiographs. For more extensive disease, many clinicians would
regard periapical radiographs as essential to allow accurate assessment of
bone loss as a percentage of root length and visualisation of periapical
tissues. Dental panoramic radiographs can be helpful if there are other
issues, for example impacted third molars, or if orthodontic assessment is
needed, but supplemental periapical radiographs may be required anteriorly,
as bone levels are often not shown as clearly here due to the
superimposition of the spine.

The clinical need will determine the frequency of radiographic exposure

required. Before taking updated radiographs, always ask yourself, ‘Will this
change how I treat the patient?’ If it will not, you should question why the
radiograph is being taken.
Once you have assessed whether the radiographs are diagnostic or not,
report on the following five features:

1. Amount of bone loss – in millimetres or, if you can see the root
apex, then percentage
2. Pattern of bone loss – horizontal or vertical
3. Local factors – check for any evidence of calculus, restorative
overhangs, or open margins
4. Anatomy – root length and morphology. Do not underestimate the
importance of assessing this, as it will have a significant impact on
the prognosis of a tooth
5. Widening of the periodontal ligament space and signs of any
periapical pathology

When reading radiographs, scan in the same direction every time – coronal
to apical, or apical to coronal – this ensures you do not miss any important
details.

4.2 Sensibility testing

Sensibility testing assesses sensory/nerve supply to the tooth. If this is
negative, it may highlight any endo–perio lesions in more extensive disease.

Sensibility testing can be completed via thermal tests, such as Endo-Frost,

or through electric tests – eg an electric pulp tester can be used to indirectly
determine the state of pulpal health by assessing the condition of the nerves
within the dental pulp. Although false positives and negatives may be
encountered, these tests can be helpful in identifying endo–perio lesions.
5
Diagnosis

It’s now time to bring all the information together to come up with a
periodontal diagnosis or diagnoses. Formulating a diagnosis is imperative
prior to prescribing a treatment plan for the patient. We will explore the
updated classification and discuss periodontal health, gingival diseases,
periodontitis, other conditions of the periodontium and peri-implant disease.

5.1 Background
The 2017 World Workshop introduced a new classification system for
periodontal and peri-implant diseases and conditions, reflecting significant
advancements in biological and clinical research since the 1999
International Classification of Periodontal Diseases (Caton et al, 2018).
This revised system now explicitly defines clinical health and differentiates
between an intact and a reduced periodontium. It has eliminated the terms
‘aggressive’ and ‘chronic’ periodontitis, replacing them with a staging and
grading framework for periodontitis. To facilitate the application of this
updated classification in UK clinical settings, the BSP established an
implementation group to provide relevant guidance (Dietrich et al, 2019).

5.2 Periodontal health and gingival diseases

The first part of the updated classification focuses on periodontal health and
gingival diseases.
Periodontal health
Pristine periodontal health is very rare. ‘Clinical health’ has been defined as
probing depths of 3 mm or below, as well as less than 10% bleeding on
probing (Chapple et al, 2018).

Clinical gingival health may occur on an intact periodontium – in other

words, in the absence of detectable attachment and/or bone loss – or on a
reduced periodontium, either in a stable periodontitis patient or non-
periodontitis patient (Chapple et al, 2018).

Gingivitis: Dental biofilm-induced

Gingivitis that is dental biofilm-induced is defined as an inflammatory
lesion resulting from interactions between the biofilm and the host’s
immune-inflammatory response. It remains confined to the gingiva and is
reversible. A diagnosis of gingivitis can be made if 10% or more of sites
exhibit bleeding on probing (Chapple et al, 2018).

Gingivitis can develop on an intact periodontium or on a reduced

periodontium in an individual who has not had periodontitis. Additionally,
gingival inflammation might occur on a reduced periodontium in a patient
who has been successfully treated for periodontitis.

Gingivitis: Non-dental biofilm-induced

This form of gingivitis is not triggered by biofilm and typically does not
improve after biofilm removal. Non-dental biofilm-induced gingivitis may
present as part of a systemic condition or be localised to the oral cavity. A
key distinction from dental biofilm-induced gingivitis is that the
inflammation here extends beyond the mucogingival junction, while in
biofilm-related gingivitis the inflammation will remain more localised.

These are categorised under: a) genetic/developmental; b) specific

infections; c) inflammatory/immune; d) reactive; e) neoplasms; f)
endocrine, nutritional and metabolic; g) traumatic; h) pigmentation
(Chapple et al, 2018).

5.3 Periodontitis
There are now only three types of periodontitis: necrotising periodontal
diseases, periodontitis, and periodontitis as a manifestation of systemic
disease (Dietrich et al, 2019). Let’s start off with periodontitis, as this is the
type that will be seen most often in practice and that clinicians need to be
super confident in diagnosing.

Periodontitis
The most efficient way of coming up with the diagnostic statement for
periodontitis patients is by following the below six steps:

1. Periodontitis: The first step is to determine if they are a

periodontitis patient by reviewing the available radiographs and
checking for any bone loss. If there is bone loss due to
periodontitis, then they will be labelled as a ‘periodontitis’ patient
regardless of their clinical status. This is key as, once a patient is
diagnosed as such, they are a periodontitis patient for life – they
need to know this to ensure they keep up supportive periodontal
care. Be aware that bone loss can happen due to other reasons,
such as surgical extractions, crown-lengthening procedures, or
other pathology.
2. Extent: Assess the radiographs to determine the extent of bone
loss. This can be divided into:

Localised: up to 30% of teeth with bone loss

Generalised: more than 30% of teeth with bone loss
 Molar–incisor pattern: first molars with/without incisors
affected

3. Stage: The stage refers to the severity of the disease and can be
assessed as a percentage of the root length on periapical/dental
panoramic radiographs, or estimated from bitewings. Pick the
tooth with the most interproximal bone loss and classify as
follows:

Stage I (early/mild) – less than 15% bone loss or less than

2 mm (measurement from cementoenamel junction (CEJ)
if only bitewings available)
Stage II (moderate) – coronal third of root
Stage III (severe) – mid-third of root
Stage IV (very severe) – apical third of root
Note: In situations where it is clear that a patient has lost teeth due
to advanced periodontal bone loss, likely within the apical third of
the root, you may, on a case-by-case basis, immediately classify
this as Stage IV.

4. Grade: The grading is designed to reflect the patient’s

susceptibility to periodontitis and provides a good predictor of
future disease experience in the absence of treatment. The quickest
way of grading a patient is to apply the following:
Grade A is assigned if the greatest amount of radiographic
bone loss, in percentage terms, is less than half the
patient’s age in years.
Grade C is assigned if the greatest amount of bone loss, in
percentage terms, exceeds the patient’s age in years.
Grade B is assigned otherwise.
 5. Current disease status: So far, the focus has been on bone levels.
This next step is about understanding what we will be
treating/maintaining by determining the patient’s disease status.
The patient may be:

Stable – healthy/successfully treated

Disease remission – bleeding on probing more than or
equal to 10% of sites, with probing depths of less than or
equal to 3 mm and no probing depths of greater than 4 mm
Unstable – bleeding sites in probing depths of 4 mm or
more or any probing depth of 5 mm and above
6. Risk factor profile: The final step includes making a note of
whether the patient is diabetic and/or a (previous) smoker. These
risk factors form part of the diagnostic statement as they can be
measured and controlled. Any other risk factors can be noted on a
separate line from the diagnostic statement, as these are still
important to acknowledge to ensure we have a full picture of the
patient’s ‘causal pie’.

Necrotising periodontal diseases

These diseases rank among the most severe inflammatory conditions
associated with dental biofilm. They include necrotising gingivitis and
necrotising periodontitis. Necrotising gingivitis is limited to the gum
tissues, and necrotising periodontitis is where the necrosis extends into the
periodontal ligament and alveolar bone, causing attachment loss
(Papapanou et al, 2018). The mandibular anterior teeth are the most
frequently affected.

Necrotising gingivitis is marked by necrosis and ulceration in the free

gingiva. These lesions typically begin at the interdental papilla and often
have the classic ‘punched-out’ appearance. Marginal erythema may be seen,
and the necrotic lesions can extend to the marginal gingiva. A pseudo-
membrane may cover the necrotic area; removing this ‘membrane’ exposes
the underlying connective tissue, which then bleeds. The level of pain
experienced by the patient varies depending on the severity and extent of
the lesions, typically intensifying during eating and oral hygiene activities.
Less common symptoms include halitosis, fever, and malaise.

Necrotising periodontitis shares the features of necrotising gingivitis but

additionally involves necrosis of the periodontal ligament and alveolar
bone, leading to attachment loss. As the disease advances, an interproximal
crater forms, separating the buccal and lingual/palatal portions of the
papilla. If these craters deepen, the interdental crestal bone can become
exposed. When interproximal necrotic areas extend laterally and merge,
they create a large zone of tissue destruction. In severe cases, bone
sequestration may occur. Risk factors include high stress levels, heavy
smoking, and poor nutrition. The condition may also be linked to untreated
HIV/AIDS or other diseases and/or medications that have an
immunosuppressive effect, such as chemotherapy or antirejection drugs
used in transplant patients.

Periodontitis as a manifestation of systemic

disease
The third and final type is where plaque-induced periodontitis is a key
feature of a systemic disease (Jepsen et al, 2018). Most of these involve
systemic syndromes that impact the immune system, making the patient
more susceptible to periodontitis. The management of this kind of
periodontitis is still driven by a dysbiotic biofilm, so the focus is on biofilm
control. An example of systemic periodontitis is Papillon–Lefèvre
syndrome, where the immune system is dysfunctional and the biofilm is not
kept in check. Most importantly for us, the dysfunctional immune system
rapidly destroys the periodontium.

5.4 Other conditions affecting the periodontium

There are five subcategories under the ‘other conditions of the
periodontium’ section of the classification.

Systemic diseases and conditions affecting the

periodontal supporting tissues
These are systemic diseases or conditions that have periodontal
manifestations; mostly, these are in the gingivae (eg for Crohn’s,
sarcoidosis, or herpes simplex) but some affect the periodontal tissues (eg
ameloblastoma or chondrosarcoma’s histiocytosis) (Jepsen et al, 2018).

Broadly, these disorders can be subdivided into:

Systemic disorders that have a major impact on the loss of

periodontal tissues by influencing periodontal inflammation.
These tend to be genetic disorders, acquired immunodeficiency
diseases, and inflammatory diseases.
Other systemic disorders that influence the pathogenesis of
periodontal diseases.
Systemic disorders that can result in loss of periodontal tissues
independent of periodontitis – for example, neoplasms, and other
disorders that may affect the periodontal tissues.

Periodontal abscesses and endo–perio lesions

A periodontal abscess is a localised collection of pus within the gingival
wall of the periodontal pocket or sulcus. It can lead to rapid tissue
destruction, jeopardise the prognosis of the affected tooth, and carries a risk
of spreading infection systemically. Periodontal abscesses can be
subclassified based on their underlying causes.

An endo–perio lesion is a pathological communication between the pulpal

and periodontal tissues, which can be either acute or chronic. The main
signs are a deep periodontal pocket reaching the root apex and a negative or
altered response to pulp sensibility tests. These lesions can be further
categorised based on their signs and symptoms, which directly affect their
prognosis and treatment (Papapanou et al, 2018).

Mucogingival deformities and conditions

Gingival recession falls under this category, and can be classified as below,
as described by Jepsen et al (2018). This will be discussed in more detail
later in the book.

‘Recession Type 1 (RT1): Gingival recession with no loss of

interproximal attachment. Interproximal cementoenamel junction
(CEJ) is clinically not detectable at both mesial and distal aspects
of the tooth.
Recession Type 2 (RT2): Gingival recession associated with loss
of interproximal attachment. The amount of interproximal
attachment loss (measured from the interproximal CEJ to the
depth of the interproximal sulcus/pocket) is less than or equal to
the buccal attachment loss (measured from the buccal CEJ to the
apical end of the buccal sulcus/pocket).
Recession Type 3 (RT3): Gingival recession associated with loss
of interproximal attachment. The amount of interproximal
attachment loss is higher than the buccal attachment loss.’

Traumatic occlusal forces

Traumatic occlusal forces can cause damage to the teeth and the
surrounding periodontal structures. Signs of trauma may include increased
tooth mobility, adaptive tooth movement (fremitus), an enlarged periodontal
ligament space seen on radiographs, tooth migration, pain or discomfort
while chewing, and root resorption.
Primary occlusal trauma refers to injury resulting from traumatic occlusal
forces exerted on teeth with normal periodontal support, leading to adaptive
mobility. By contrast, secondary occlusal trauma occurs when normal or
traumatic occlusal forces affect teeth with compromised support, resulting
in progressive mobility (Jepsen et al, 2018).

Tooth- and prosthesis-related factors

This subcategory covers tooth anatomical factors, root proximity,
abnormalities and fractures, and tooth relationships in the dental arch that
are related to dental plaque biofilm-induced gingival inflammation and loss
of periodontal supporting tissues (Jepsen et al, 2018).

Dental materials may be associated with hypersensitivity reactions.

Clinically these may appear as areas of localised inflammation, unaffected
by adequate measures of plaque control. Additional diagnostic measures are
usually needed to confirm hypersensitivity.

5.5 Peri-implant diseases and conditions

There are various conditions and diseases that can affect peri-implant tissue;
before discussing these though, it’s important to understand what optimal
peri-implant health looks like.

Peri-implant health
In a state of health, there are no visual differences between the gingivae
surrounding natural teeth and implants. However, the probing depths are
typically deeper around implant sites versus those of natural teeth
(Berglundh et al, 2018). Additionally, the interproximal papillae around
implants may be shorter than those found between adjacent teeth.

Clinical methods to detect the presence of inflammation include visual

inspection, probing, and digital palpation. It is essential to probe the tissues
around implants to evaluate bleeding on probing, and to track any changes
in probing depth and mucosal margin migration. There is evidence that
probing of the peri-implant tissue using a light probing force is safe and
important (Berglundh et al, 2018). While a specific range of probing depths
indicative of health cannot be established, the clinical indicators of
inflammation carry greater significance. Implants can maintain healthy peri-
implant tissues even when there is diminished bone support.

Peri-implant mucositis
Peri-implant mucositis is usually reversible. The key clinical feature of peri-
implant mucositis is bleeding on gentle probing, but additional signs may
include erythema, swelling, and/or suppuration. Clinical signs of
inflammation are required for a diagnosis of peri-implant mucositis. An
increase in probing depth is commonly seen in peri-implant mucositis, due
to swelling or a reduced resistance during probing. There is strong evidence
from both animal and human studies to support the notion that dental
plaque is the primary cause of peri-implant mucositis (Berglundh et al,
2018).

Peri-implantitis
Peri-implantitis is an infectious condition that leads to inflammation in the
peri-implant mucosa and impacts the surrounding bone (Berglundh et al,
2018). This disease often presents without symptoms, which can leave
patients unaware of its progression. If regular maintenance and monitoring
visits are not conducted, individuals may experience substantial bone loss
before seeking dental care.
Summary of peri-implant conditions
6
Prognosis

Prognostic setting should be the next step following your diagnosis (or
diagnoses). It is also a prerequisite for drawing up your treatment plan.

6.1 Importance and details

Establishing a prognosis involves predicting the trajectory and outcome of a
particular disease, as well as the likelihood of recovery. When a prognosis
is provided, the aim is to anticipate how a tooth or multiple teeth will react
to treatment over time, taking into account all factors that could influence
the results.

From a medico-legal perspective, it is crucial for patients to be informed

about prognoses. Often, claims arise from patients saying they were not told
that a particular tooth was at risk of being lost in the future. From a clinical
point of view, this prognostic awareness can facilitate better decision-
making during the treatment planning process for both short- and long-term
care.

Determining the prognosis of individual teeth can be difficult due to the

multiple factors that influence treatment outcomes, but a thorough history,
identification of risk factors, detailed examination, and appropriate
radiographs will be important here.

The factors that need to be considered when determining a tooth’s prognosis

can be divided into patient factors and local factors (Mordohai et al, 2007).
The patient factors include:

1. Risk factors – such as diabetes, smoking, stress, and nutrition

2. Compliance with oral hygiene and maintenance

While the local factors are:

1. Probing depth and the tooth position – for example, the prognosis
of an incisor with probing depths of 5 mm will be far better than
the prognosis of a molar with a 10 mm pocket.
2. Furcation involvement – less favourable outcomes have been
shown for furcation-involved teeth, especially when Grade 2 or 3.
Maxillary molars with furcation involvement usually have poorer
prognoses than mandibular molars with furcation involvement.
3. Amount of bone loss – advanced bone loss has been reported to be
associated with greater future bone loss and reduced survival rates
when bone loss is over 75%. The amount of bone loss will also
affect the crown-to-root ratio and, if it is unsatisfactory, this may
affect the prognosis.
4. Anatomical defects, such as cervical enamel projections, enamel
pearls, and root grooves, are all local factors that may negatively
affect the prognosis.
5. Other associated pathology.

6.2 Prognostic systems

Several attempts have been made to devise prognostic classification
schemes and criteria. Although there is no accepted system for determining
a prognosis, and it is recognised that a high level of subjective clinical
judgement is involved, some common terms or categories can be used
(Nibali et al, 2016).
A commonly used prognostic system is good, fair, guarded, and hopeless.
Sometimes, ‘questionable’ or ‘poor’ are used instead of ‘guarded’. A more
simplified approach could be to use favourable, uncertain, and
unfavourable. This can be broken down as follows:

Favourable is when there is no evidence of disease or mild

disease, and you are likely to get an optimal result from treatment.
There are no major risk factors or local factors. The patient’s oral
hygiene is optimal, and they appear to have a good level of
compliance.
Uncertain is when you are unsure how the tooth will respond to
treatment. The level of disease is moderate, and there may be risk
factors or local factors involved.
Unfavourable teeth are not likely to respond to treatment and will
need to be extracted now or in the future. If asymptomatic and not
causing damage to neighbouring teeth, patients may wish to hold
onto unfavourable teeth until they cause issues.

A tooth-by-tooth prognosis is common practice when seeing a periodontal

patient, especially those with more severe disease. But on occasion, for
speed, you might want to group teeth together; for example, you might
observe that, ‘all of the molars have uncertain prognoses.’ Strictly speaking,
there is also a difference between the periodontal prognosis and the overall
prognosis so, if needed, you can split these up.

Prognostic setting is completed at the initial stage, prior to treatment.

However, it may be adjusted after initial treatment once a full appreciation
of the individual’s healing potential, compliance, and susceptibility can be
gained. Risk factors might also change during initial treatment. Therefore,
you might want to add a statement after your prognoses explaining that they
‘may change at the reassessment stage.’
 PART THREE
THE MANAGEMENT
7
Treatment Planning

The European Federation of Periodontology has issued the latest (EFP S3)
guidelines on treatment planning and management. They are evidence and
consensus-based and cover the management of Stage I–III (Sanz et al,
2020) and Stage IV periodontitis (Herrera et al, 2022). The British Society
of Periodontology has released an implementation paper to guide the
application of these guidelines to UK practice (West et al, 2021).

In these guidelines, a sequence of treatments is discussed, commencing

with the basis of therapy – examination, assessment of risk factors, and
diagnosis. The advice is to inform the patient of their diagnosis, including
the causes of their condition, risk factors, treatment alternatives, and
expected risks and benefits, including the option of no treatment. This is a
crucial conversation that can easily be glossed over in a busy general
practice setting.

This should be followed by an agreement on a personalised care plan. The

emphasis here is that every patient requires a bespoke plan that suits their
needs. This plan may require adjustments throughout the treatment process
based on the patient’s preferences, clinical observations, and any changes in
their overall health.

7.1 The stepwise approach

Commonly, dental professionals will apply the stepwise approach to
treatment planning, which consists of four steps:

1. Supragingival PMPR and risk factor control

2. Subgingival PMPR
3. Repeat subgingival PMPR or surgery
4. Supportive periodontal care

Step 1
Step 1 focuses on establishing a solid foundation for effective treatment and
ongoing maintenance. This involves providing thorough oral hygiene
instructions and facilitating behavioural changes. Efforts are made to
manage modifiable risk factors as effectively as possible, and supragingival
PMPR is performed.

PMPR = professional mechanical plaque removal

The term PMPR refers to professional mechanical plaque removal, and this
replaces all other historic terminology (Sanz et al, 2020). PMPR can be
divided into supragingival PMPR (carried out in Steps 1 and 4) or
subgingival PMPR (Steps 2, 3, 4).

The key expert consensus-based recommendations from the guidelines

include (West et al, 2021):

The same oral hygiene guidance to control gingival inflammation

should be practised throughout Steps 1–4 of periodontal therapy.
Supragingival PMPR and control of biofilm/plaque-retentive
factors as part of the first step of therapy.
As part of the first step of therapy in periodontitis patients, risk
factor control interventions (eg for diabetes and smoking) should
 be completed.

Step 2
The second step focuses on cause-related therapy once the patient is
engaged. ‘Engagement’ has been defined as:

≥ 50% improvement in plaque and marginal bleeding scores, or

Plaque levels ≤ 20% and bleeding levels ≤ 30%, or
The patient has met targets outlined in their personal self-care
plan, as determined by their dentist

A detailed periodontal pocket and bleeding chart should be completed prior

to subgingival PMPR.

The key expert consensus-based recommendations for Step 2, taken from

the guidelines, include (West et al, 2021):

Subgingival PMPR should be employed to treat periodontitis in

order to reduce gingival inflammation, the number of diseased
sites, and probing pocket depths.
Subgingival PMPR should be performed with hand or powered
(sonic/ultrasonic) instruments, either alone or in combination.
Subgingival PMPR can be performed using a traditional quadrant-
wise approach or full-mouth delivery using a one- or two-stage
technique within a twenty-four-hour period.
It is suggested that lasers are not used as adjuncts to subgingival
instrumentation.
It is suggested that adjunctive antimicrobial photodynamic
therapy is not used in patients with periodontitis.
 Adjuncts to mechanical debridement may be considered in
specific cases, including antiseptics for a limited period, or
systemic antibiotics. Systemic antibiotics may be considered for
specific patient categories, for example, Grade C.

Step 3
After completing Step 2, the patient’s treatment response is assessed. If the
patient is still unstable, meaning the endpoints of therapy have not been
met, additional treatment will be initiated. Conversely, if the patient is
stable and the treatment goals have been successfully achieved, they will
transition to a supportive periodontal care programme.

For patients who are engaged, further treatment options may be available,
including both non-surgical and surgical procedures (such as access flap,
resective, or regenerative techniques). Typically, surgery is not
recommended following just one phase of non-surgical treatment. At this
point, a referral to a complexity level 2 or 3 clinician may be necessary. If a
referral isn’t feasible, options include repeating subgingival PMPR or
placing the patient on supportive periodontal care (likely palliative). Further
discussion regarding surgical options will be provided in Part Four of this
book.

Step 4
Supportive periodontal care (SPC) is essential for preserving periodontal
stability and is recommended for all patients who have undergone treatment
for periodontitis. Patients should be informed about SPC prior to
commencing their treatment plan, otherwise they are likely to assume that
once active treatment is complete, they are ‘cured’. This can lead to
unhappy patients and potential medico-legal complaints. SPC may
incorporate both preventive and therapeutic measures from Steps 1 and 2.
The frequency of SPC appointments will be customised to meet the
individual needs of each patient. If signs of recurrent disease are identified,
re-treatment will be necessary, and a new diagnosis and treatment plan
should be established.

The key expert consensus-based recommendations from the guidelines

include (West et al, 2021):

SPC visits should be scheduled for intervals of three months to a

maximum of twelve months, with the frequency determined by
the patient’s risk profile and periodontal status after active
therapy.
When selecting a toothbrush and design of interdental brush, the
patient’s abilities, needs, preferences, and manual dexterity must
be considered.
For patients receiving SPC, tooth brushing should be
supplemented by the use of interdental brushes (where
anatomically possible).
Flossing is not the first-choice method of interdental cleaning for
SPC patients.
The use of other interdental cleaning devices in interdental areas,
not reachable by interdental brushes, may be considered when
receiving SPC.
If an antiseptic mouth rinse formulation is to be considered for the
adjunctive control of gingival inflammation for patients under
SPC, use of products that contain chlorhexidine, essential oils, or
cetylpyridinium chloride are suggested.

7.2 A typical treatment plan

Below is a template for a typical treatment plan for a patient with
periodontitis:
 1. Discussion of the importance of optimal diabetes control (if
relevant).
2. Smoking or vaping cessation (if relevant).
3. Oral hygiene instructions – brushing technique using an electric
toothbrush, use of a single-tufted brush, and daily use of
appropriately sized interdental brushes.
4. Full six-point pocket chart.
5. Full-mouth supragingival PMPR.
6. Subgingival PMPR for probing depths of 4 mm or more with
bleeding, or more than 5 mm under local anaesthesia – quadrant by
quadrant/half-mouth/full-mouth approach.
7. Reassessment eight weeks later, and further treatment planning.
8. Lifelong supportive periodontal care on a three-monthly basis.

7.3 Working as a team

When treating patients with periodontitis in practice, it can be helpful to
devise a practice protocol and decide which team member will focus on
which treatment step. Everyone should be singing from the same hymn
book – for example, BPEs should not be drastically different between team
members. Inconsistencies can lead to patient confusion and medico-legal
issues.

Hygienists/therapists form an integral part of the team, and dentists should

be aware of any requirements when working with them. If the
hygienist/therapist will be completing the treatment and providing the
majority of the care, it’s preferred that the hygienist/therapist decide on the
number of visits required and set the recall interval as needed.

7.4 Referral
The British Society of Periodontology has provided guidelines on patient
referrals (BSP, 2020). Referral of patients with periodontal diseases to
specialists or other appropriately qualified dental professionals depends on
several factors:

The stage and grade of disease, as well as the complexity of

treatment required
The patient’s desire to see a specialist or undergo specialist
treatment
The knowledge, experience, and training of oral healthcare
professionals to manage patients with a range of periodontal
conditions
The presence of genetic and lifestyle/behavioural risk factors

The BSP (2020) has outlined guidance for complexity levels 2 and 3.

Level 2 complexity
Treatment for conditions at this level can typically be managed by oral
healthcare professionals within a general dental practice, although referrals
may sometimes be necessary. In certain cases, periodontal or peri-implant
treatments might need to be provided by a specialist as part of a more
intricate, integrated treatment plan. This category includes patients with
Stage II, III, or IV periodontitis who have residual true pocketing of 6 mm
or more following initial periodontal therapy; Grade C periodontitis
determined by a specialist; or complexities such as furcation defects and
challenging root morphologies, especially when these are strategically
important and delegated by a specialist.

For conditions such as gingival enlargement, non-surgical management in

collaboration with medical professionals may be necessary. Pocket
reduction surgery may be included in this category, especially when
delegated by a specialist. Furthermore, certain non-plaque-induced
periodontal diseases, such as those induced by viral infections, autoimmune
disorders, abnormal pigmentation, vesiculobullous disease, or periodontal
manifestations of gastrointestinal and other systemic conditions, should be
managed here under specialist guidance. Peri-implant mucositis also falls
within this complexity level.

Level 3 complexity
Patients at this level are usually referred after lifestyle or behavioural risk
factors have been addressed and appropriate non-surgical treatments have
been completed in a general practice setting. Conditions at this level include
Grade C or Stage IV periodontitis and true pocketing of 6 mm or more.
Cases requiring periodontal surgery will fall under this category. Furcation
defects and other complex root morphologies that are unsuitable for
delegation must also be managed by a specialist. Additionally, non-plaque-
induced periodontal diseases that are not suitable for management by a
practitioner with enhanced skills require specialist care.

Patients who need multidisciplinary care should be referred to a specialist.

Furthermore, if patients with level 2 complexity do not respond to
treatment, they may need to be re-evaluated and referred to this complexity.
For non-plaque-induced periodontal diseases, a differential diagnosis should
be established, and joint care pathways should be developed in
collaboration with relevant medical colleagues. In some cases, it may be
necessary to manage these conditions collaboratively with practitioners
with enhanced skills. Specialists may also provide advice and assist with
treatment planning for colleagues. Finally, cases involving peri-implantitis
require specialist attention.

Patients with modifying factors, particularly those for whom behaviour

change is difficult, may need to be escalated to a higher level of care. Those
diagnosed with Grade C periodontitis should be referred for further
treatment following initial preventive guidance on managing risk factors
and oral hygiene instruction.

The modifying factors that are outlined in the BSP (2020) guidance include:
 ‘Coordinated medical or dental multi-disciplinary care
Regular tobacco smoking and tobacco substitute products that
deliver nicotine, eg vaping
Dental special care for the acceptance or provision of treatment
Concurrent mucogingival disease, eg erosive lichen planus
Medical history that significantly affects clinical management, eg:

Patients with a history of head/neck radiotherapy or

intravenous bisphosphonate therapy
Patients who are significantly immunocompromised or
immunosuppressed
Patients with a significant bleeding dyscrasia/disorder
Patients with a potential drug interaction’

Not referring at an appropriate time is a common reason for litigation. It’s

also much easier for patients to allege, after the event (usually loss of a
tooth), that they would have preferred a referral for specialist care.
Therefore, it’s important to minimise any delay in referral.
8
Educating And Empowering
Patients

Achieving success in periodontal treatment is a team sport and the patient is

at the centre of this. Educating patients is imperative to ensure they
understand their condition and what the treatment will involve. Patients also
need to take on responsibility for their condition and understand that much
of the success in treatment will be down to what they do at home.

In this chapter, we will discuss how to communicate clinical findings to the

patient as well as the benefits of treatment. We will then explore the key
steps for effective home care and behaviour change.

8.1 Translating the clinical findings and treatment

plan
There are various clinical findings that will need to be communicated and
explained in a way that both makes sense to the patient and motivates them
to take responsibility for maintaining oral health at home. The main things
you will need to discuss with patients are pockets and bleeding, your
diagnoses, and the proposed treatment plan. It’s essential that patients
understand all these elements in order to maximise chances of successful
treatment.
Pockets and bleeding
A pocket can be explained as the space between the tooth and gum that
opens and deepens as the disease of periodontitis progresses. It’s helpful to
use the phrase ‘open pocket’ for any site that requires active treatment, ie
that has probing depths of 4 mm with bleeding or 5 mm and above. A
‘closed pocket’ does not require active treatment, ie probing depths of 4
mm and below without bleeding. If the patient wants more detail, you can
mention that probing depths of 1–3 mm is considered healthy, 4–5 mm is
moderate, and 6 mm and above indicates severe disease. Highlighting all
the ‘open pockets’ on your pocket chart can be a useful way to help the
patient visualise the disease extent. This can then be used as a comparison
following treatment.

When discussing bleeding, it is key to emphasise that bleeding is not

normal and is an alarm bell in the body. For example, you could say, ‘We
wouldn’t ignore bleeding from any other part of our body, so we shouldn’t
ignore bleeding from our gums.’ It is useful to separate gingival/marginal
bleeding (related to suboptimal home care) from bleeding on probing (a
sign of active disease). When you are explaining your findings from the
pocket chart, you can use simplistic terms like ‘outside bleeding’ if they
mention their gums are bleeding on brushing, ie gingival bleeding, and
‘inside bleeding’, ie bleeding on probing.

Radiographic findings
Always explain to the patients that radiographs are required to check the
bone levels around their teeth. If they are reluctant for you to take
radiographs, ask them, ‘Would you let a mechanic fix your car without
lifting the hood? The same applies here; we need to see under the gum to be
able to diagnose and fix the issue.’

Radiographs are an excellent way to evidence to patients the damage that

has occurred through periodontitis. Show the patient where their bone level
should be, where it is now, and the end of the root. Radiographs are also
helpful for showing calculus and other local factors, such as overhangs. If
appropriate, root anatomy can form a part of the conversation in terms of
anchorage. For example, for someone with short conical roots, the impact
of 50% bone loss may be more significant than if the roots were long and
tapered.

Diagnosis
Medico-legally, patients need to know their periodontal diagnosis. Gum
disease is easy to understand, but it is still useful to use the technically
correct phrase, so gingivitis or periodontitis. The severity also needs to be
discussed; you may want to mention mild/moderate/severe or the stage of
their condition. Their grading can be considered as a marker of the patient’s
susceptibility as well as the rate of future disease progression without
treatment. For example, with a patient who is Grade C, you can emphasise
that they are highly susceptible and that, without treatment, there is a high
risk of tooth loss.

As well as the diagnosis, it’s worth talking about why the patient has the
condition, ie the risk factors, and the consequences of not treating it, such as
tooth loss and a potential impact on general health.

Treatment plan
To ensure the best chances of treatment uptake and compliance, it’s
important to translate the treatment plan and focus on what matters to the
patient. For instance, explaining that the treatment will ‘improve probing
depths’ may not be relatable; these clinical outcomes are important to us but
not necessarily to the patient. On the other hand, mentioning that, with
treatment, they will keep their teeth for longer, may not have to wear
dentures, or wake up with blood on their pillow may be more impactful.
Focus on patient-related factors that impact quality of life – the patient may
have mentioned what is bothering them during their initial presenting
complaint, so link back to that. Even when the patient’s condition is severe,
keep as positive a spin as possible when communicating the plan and focus
on the good news: you can do something to help them (even if a few teeth
may need to be sacrificed in the process).

8.2 Essential steps for effective home care

As periodontitis is a multifactorial inflammatory disease associated with
dysbiotic dental plaque biofilms, optimal biofilm control through effective
home care is the cornerstone of the prevention and treatment of periodontal
diseases. It is the first and most powerful step of therapy, aimed at guiding
behaviour change by empowering and motivating the patient to successfully
remove or disrupt supragingival biofilm.

Time is often limited in practice, so it’s helpful to follow a structure or

framework to maximise efficiency and effectiveness when providing oral
hygiene instructions for patients to apply at home. I recommend a five-step
process: orientate, disclose, demonstrate, reinforce responsibility, and apply
the GPS model.

Step 1: Orientate
Patients are generally unfamiliar with their oral anatomy and have
an inadequate spatial sense, so begin by introducing the basic
anatomy of the oral tissues. The teeth and gingivae can be
visualised using a mirror or intraoral camera.
Pull the patient’s lower lip down and show them, using a probe,
where the tooth is, where the gumline is, and where the pocket is.
Explain that the pocket is where ‘bugs’ get trapped, and that’s
why the toothbrush needs to be angled in that direction, towards
the gums.
Radiographs can be helpful in showing areas of calculus and
spaces that need to be cleaned.
Step 2: Disclose
Use a disclosing tablet/sponge/liquid to highlight to the patient
areas they are missing during their brushing. This will allow you
to provide more tailored advice.
Disclosing allows you to gain an accurate, objective plaque score
as a percentage rather than a subjective statement such as ‘oral
hygiene is good/fair/poor.’
Inform the patient of their score, as this can be a great
motivational tool for improving compliance. Patients should be
aiming for low percentages of plaque. However, if the patient is a
child, it may be helpful to flip this to percentage plaque-free to
make it more motivational, as children strive to score high
numbers.
Taking a photo for the patient on their camera phone is a great
idea, as they can refer to it easily between visits.

Step 3: Demonstrate
Set up a reminder system to request that the patient bring their
oral hygiene aids to their appointments. Ask them first to
demonstrate what they are doing and then adapt as needed.
Allowing the patient to demonstrate what they’re doing at home
will allow you to pick up if they have any manual dexterity issues
due to medical conditions, including arthritis. If this is the case,
always advise an electric toothbrush with a decent-sized handle. If
using a manual toothbrush, you can suggest they use putty around
the handle to help with the grip.
Demonstrating correct technique in their mouth will be more
helpful than using models, as the feel component is important.
 Test drive electric toothbrushes from the key manufacturers
should be used.
Ask the patient to video you showing them brushing and
interdental cleaning techniques in their mouth, as this can be a
helpful reminder for those needing extra guidance. Tailored oral
hygiene leaflets can also help reinforce all instructions.
For those patients constantly missing areas, ask them to start there
first, as patients are more likely to have the most energy and do a
better job at the start of their oral hygiene regime.
Keep it simple and repeat/reinforce the advice at each visit.

Step 4: Reinforce the patient’s responsibility

Emphasise to the patient that the outcome of the treatment plan is
80% about what they do at home and 20% about what we do. A
shift in mindset where they take ownership of their condition is
key for both short- and long-term success.

Step 5: GPS
GPS is an evidence-based technique that can help achieve behavioural
change (Tonetti et al, 2015), where G stands for goal setting, P is for
planning, and S is for self-monitoring. Below is an example of how you can
apply it in your practice:

Goal: ‘Today we found your plaque score was 80%, let’s try and
reduce this to 40%.’
Planning: ‘We can do this by just focusing on the brushing
technique we went through today. We can then review how you’re
doing in two to three weeks.’
 Self-monitoring: ‘I’m going to give you some of these plaque-
disclosing tablets. I want you to use them every week. Carry out
your usual home care regime, then use the tablet. Wherever you
see the pink/purple staining, go back and clean those areas. You
should notice them decrease with time, which means you’re
getting better.’

The last step in particular is extremely powerful and crucial to treatment

success.

8.3 Behavioural change

To understand our role in guiding behavioural change and motivating
patients, it’s useful to compare the dental professional’s role to that of a
personal trainer. We are there to guide them, but the patient must ultimately
put in the work. A daily timetable with time carved out for oral care is key.
For our part, we need to appreciate that behavioural change is not easy but
should reassure the patient that it does get easier with practice, and their
enjoyment of it may increase when the benefits become clearer. We must
provide honest feedback during the patient’s journey while rewarding
positive performance.

Several behavioural change models have been proposed for the field of
dentistry. Oral Hygiene TIPPS from the Scottish Dental Effectiveness
Programme aims to make patients feel more confident in their ability to
perform effective biofilm removal and help them plan how and when they
will look after their teeth and gums. Key steps include:

Talk with the patient about the causes of periodontal disease and
discuss any barriers to effective biofilm removal.
Instruct the patient on the best ways to perform effective biofilm
removal.
Ask the patient to practise cleaning his/her teeth and to use the
interdental cleaning aids while in the dental surgery.
 Put in place a plan that specifies how the patient will incorporate
oral hygiene into their daily life.
Provide support to the patient by following up at subsequent
visits.

Alternatively the COM-B model of behaviour change model suggests that

capability (C), opportunity (O), and motivation (M) are essential for any
behaviour (B) to change (Michie et al, 2011).

When the patient lacks motivation, it’s important to focus on patient-

derived change to ensure realistic steps forward. The aim here is to connect
change with what the patient values and ask them to come up with practical
goals.

8.4 Key recommendations

Any specific recommendations you make should consider the patient’s
abilities, preferences, and needs (Sanz et al, 2020).

Brushes
Advise power brushes (specifically rechargeable oscillating-rotating) over
manual toothbrushes where possible, as these have been shown to be more
effective in reducing plaque levels (Yaacob et al, 2014). Focused gum
brushing is key, angling the brush 45 degrees to the axes of the teeth, with
the end of the filaments pointing into the gingival crevice. The timer and
pressure indicator on the rechargeable brushes are helpful prompts for the
patient. For the rechargeable brush, it’s important to ensure the patient is not
using this like a manual brush but rather holding it against the tooth/gum for
three seconds or so before moving on to the next tooth. Tell the patient the
brush ‘is doing the work for you.’ Brushing twice a day is important.

Interdental brushes are the first choice for interdental cleaning (Slot et al,
2020). The correct size is key, so it can be helpful to check these for
patients and emphasise the need for a snug fit. During the active treatment
phase, these sizes may change. Interdental cleaning should be carried out at
least once a day before toothbrushing, and interdental brushes usually need
replacing every few days.

If the interdental brushes don’t fit, floss is recommended. To be effective,

the floss needs to be correctly adapted to the tooth surface by gently
wrapping it around the tooth once past the contact site. Use of floss holders
can make flossing easier.

Single-tufted brushes are popular amongst patients with periodontitis to

help address hard to reach areas. This may include distal and lingually
around molars, crowded areas, localised recession defects and in those with
a sensitive gag reflex. The single-tufted brush is best used with a pen grip
using the push, splay, wiggle technique.

Other tools
Oral irrigators or water flossers may be helpful for those patients who are
struggling with the above, but the evidence for their clinical efficacy is
sparse comparatively. Some patients may be keen to use these in addition to
other interdental cleaning.

Tongue cleaning is recommended, especially if there is a tongue coating.

This would be the final step in someone’s oral hygiene regime, likely once a
day.

When a patient asks you to recommend specific products, it’s worth having
your key one in mind, depending on their symptoms, to prevent extensive
discussion and loss of time during appointments. Your chosen product may
be related to the current evidence base and your patient’s experience.
Having a product prescription table (like the below) to hand that you can
update regularly may be helpful.
Example product prescription table

Sustainability
Patients may mention that they don’t want to use certain brushes due to the
plastic wastage. It’s important to emphasise that they can still be eco-
friendly without compromising their health. Plastic-free options do exist for
interdental brushes, but these may not always be of the appropriate size.
Instead, encourage recycling. There are specific oral hygiene recycling
boxes, and these can be housed in the dental practice so that patients can
bring any items they’d like to recycle with them each time they visit.

8.5 Oral hygiene analogies

Analogies can be helpful ways to communicate the importance of oral
hygiene to patients that avoid off-putting technical or medical terminology
that they might not engage with. Below are some examples you could
consider using:

Toothpaste is like face cream. You pick your cream depending on

your skin type. It’s the same for teeth. For example, if you have
sensitive teeth, you might need a toothpaste that is targeted to
address sensitivity, or if you have no issues, you just need a
regular fluoride toothpaste.
 Regular mouthwash is like perfume after a shower. You don’t
usually need it and there are no added health benefits unless it’s
been specifically recommended by your dental professional.
If you don’t clean in between your teeth, it’s like only cleaning
one side of your plate and then eating from it again. All surfaces
need to be thoroughly cleaned.
If you had a life-threatening condition and you were told to take
an important medication daily, you would. Look at interdental
brushes the same way; they are super important and should just
become part of your routine.
Oral irrigators or water flossers are not replacements for
interdental brushes. They are adjuncts, if you want to use them. If
you had a dirty dish that needed washing, using these devices is
like just rinsing the dish, but what you would really need to do to
get the dish properly clean is scrub. That’s what the interdental
brushes do.
The tongue is like a carpet – if it’s not vacuumed, debris will build
up and it will smell. In the same way, the tongue needs to be
cleaned regularly.

8.6 Biofilm-retentive factors

Biofilm-retentive factors can be considered as local risk factors for disease
initiation and progression, as they increase the likelihood that oral hygiene
will be compromised and that biofilm will accumulate. These should be
assessed and addressed where possible. Examples include anatomical and
caries and iatrogenic factors.

Anatomical factors
 Tooth position (crowding, teeth out of alignment, teeth out of
function, loss of contact points)
Gingival anatomy (recession, high frenal attachments)
Tooth anatomy (bulbosity of teeth, marginal ridges, abnormalities
such as enamel pearls, and dens in dente)
Root anatomy (furcations, root fissures/fossas/grooves)

Caries and iatrogenic factors

Carious cavities
Poorly designed restorations (lack of contact points, poor margins,
rough finish, lack of marginal ridge, poor contour, poor design)
Removable prostheses and appliances
9
Non-Surgical Periodontal
Therapy

As discussed in Chapter 7, the patient must be engaged before commencing

non-surgical periodontal therapy. Active treatment is required in probing
depths of 4 mm with bleeding on probing or 5 mm and above. The aim is to
‘close’ the pocket – to achieve probing depths of 4 mm (without bleeding
on probing) or below. Pocket depth reduction will occur by a combination
of gingival recession, long-junctional epithelium formation, as well as
resolution of gingival inflammation and cuff tightening. The true endpoints
of non-surgical periodontal therapy are an improvement in tooth prognosis,
a reduction in systemic inflammation and a positive impact on the patient’s
quality of life.

It’s important to be aware of expected improvements so that if these are not

achieved, you can investigate the factors at play before considering further
active treatment.

These are the improvements we would expect to see from non-surgical

therapy (Suvan, 2020):

For shallow sites (probing depths of 5 mm or less) the mean

reduction is 1.5 mm after three months and 1.6 mm after six to
eight months.
For deep sites (probing depths of 7 mm or more) the mean
reduction is 2.6 mm after three months and 2.6 mm after six to
 eight months.

Tomasi et al (2022) highlight that pocket closure is most predictable around

anterior teeth and least likely around molar teeth. Furthermore, the higher
the initial probing depth, the lower the likelihood of pocket closure.

Do not underestimate the power of good-quality non-surgical periodontal

therapy; according to Suvan (2020), 74% of pockets can be treated non-
surgically.

9.1 Consent
Written consent for non-surgical periodontal therapy is not essential but
verbal consent following a discussion is. The patient must be aware of the
treatment proposed, what is involved, and the benefits. When exploring side
effects and risks, the four key areas to discuss include:

1. Pain: Explain that some soreness is not uncommon, but it can

usually be managed with the same analgesia they would take for a
headache.
2. Bleeding: Bleeding on toothbrushing or use of interdental brushes
may initially increase before it settles down. Ensure this doesn’t
put the patient off their self-care regime.
3. Sensitivity: While frequently occurring, sensitivity is most often
short-term. Advise the use of a toothpaste for sensitivity, ensuring
the patient spits and doesn’t rinse it out.
4. Gum recession: As healing occurs and swelling reduces, gingival
recession may occur. The patient needs to be aware that this is a
good sign, and long-term management options can be discussed
following stability if it bothers them.

9.2 Local anaesthesia

When completing subgingival PMPR, local anaesthesia can be helpful to
ensure maximum patient comfort and the most effective instrumentation.
Being able to provide local anaesthesia comfortably is an important skill to
develop. Here are a few tips and tricks to help:

Create a calming environment by avoiding phrases like, ‘This will

hurt a bit,’ or ‘This will feel uncomfortable,’ and try to use
positive language like ‘You’re doing great, we are more than
halfway through’ instead. Ensure the needle/syringe isn’t within
view of the patient.
Manage the patient’s psychological state by providing them with a
control signal, asking them to focus on their breathing, and using
tools like music as a distraction.
One of the most discomfort-inducing steps in delivering local
anaesthesia is the penetration of the needle through the most
superficial tissues. To reduce this, you can use topical anaesthesia
in the form of a concentrated solution, gel, or spray that is applied
to the mucosa. Ensure this is left on for at least one minute before
inserting the needle.
Pressure adjacent to the injection site using a firm but dull object
(eg a mirror or cotton bud) can be a helpful distraction. Gently
shaking the mirror in the sulcus can also be a useful way of
distracting the patient.
Blunt needles can cause pain, so only use sharp needles. If you are
completing more than one quadrant, perhaps have two needles
ready on the tray. Always direct the needle bevel towards the
bone.
Ensure the anaesthetic solution is at room temperature or above.
To prevent discomfort, it is wise to allow refrigerated cartridges to
warm to room temperature prior to use.
 Once the needle has penetrated the mucosa, the main sensation of
discomfort felt by the patient is due to the deposition of the
solution. Deposition over a longer period helps to prevent
discomfort, and patients tend to show fewer signs of pain.
If not using traditional blocks, try and inject where already numb
– once you’ve provided the first infiltration, the area around that
point will be anaesthetised. Try and make your next injection
point in that same area and the patient is unlikely to feel it. Then
keep working back or forward. A popular choice of anaesthetic
for periodontal procedures is 4% articaine + 1:100,000 adrenaline,
which can be used as infiltrations across the mouth.
Make the most of technology such as The Wand, which is a
computer-controlled local anaesthesia delivery device.

When providing local anaesthesia, the bevel of the needle should be

facing the bone to reduce discomfort
9.3 Full/half/quadrant approach
According to the latest treatment guidelines (Sanz et al, 2020), in terms of
clinical treatment outcomes, there would appear to be no significant
difference between quadrant or full-mouth approaches. How the
treatment/appointments are divided will usually depend on other factors,
including:

The severity and extent of the disease.

Time available per appointment as well as the available patient
time.
Use of local anaesthesia.
Anxiety – to be discussed with patient, as some anxious patients
prefer shorter, more frequent appointments and others prefer one
longer appointment.
Plaque/biofilm score – if not optimal, splitting the appointments
over several visits may be helpful to provide repeated
opportunities for reinforcement.
Medical – a full-mouth approach could produce a systemic acute-
phase inflammatory response that may have the potential to be
harmful to patients, especially those with vascular co-morbidities
(Graziani et al, 2015, 2023).

9.4 Adjuncts
As per the discussion in Chapter 7, according to the S3 clinical guidelines
(Sanz et al, 2020), there may be a place for specific adjuncts in conjunction
with active treatment.

CHX
Chlorhexidine (CHX) mouth rinse may be used for a limited time in
specific cases, such as a patient with significant marginal inflammation that
is preventing them from completing an adequate oral hygiene regime at
home (Da Costa et al, 2017). The guideline also confirms that locally
delivered sustained-release chlorhexidine could be considered in patients
with periodontitis, though the clinical benefits remain small, equivalent to a
pocket reduction effect of approximately 10% (Sanz et al, 2020).

KEY FACTS ABOUT CHX

It is a biguanide.
The most common formulation is as a mouthwash (0.2% or 0.12%
w/v).
It’s been shown to be the most efficacious mouthwash in clinical
trials – antibacterial, antiviral and antifungal. It has an anti-plaque
effect which produces a prolonged and profound reduction in
plaque sufficient to prevent the development of gingivitis.
The effectiveness of this drug relies on its ability to reach the cell
walls, a process aided by electrostatic interactions. CHX, which is
positively charged, binds to the negatively charged bacterial cell
walls, specifically targeting phosphate and carboxyl groups. This
binding disrupts the osmotic barrier and hampers membrane
transport. CHX also adheres well to tooth surfaces and the oral
mucosa.
Indications: unable to carry out mechanical plaque control,
before/following surgery, immunocompromised, recurrent aphthous
ulceration.
Unwanted effects: staining of teeth/restorations/tongue, taste
disturbances, mucosal desquamation, parotid enlargement, and
allergy.

Antibiotics
Use of systemic antibiotics should be limited, as there is a balance to be
found between the benefits and risk of antimicrobial resistance (Herrera et
al, 2020). Patients with Grade C periodontitis might benefit (Sanz et al,
2020), but in general practice this will only be for a limited number of
patients, as patients with Grade C disease are likely to be referred for
specialist care. Other examples include those with necrotising periodontitis.
Antibiotics should always be used as an adjunct (not alone) and following
the last session of subgingival PMPR. Options for periodontitis may
include:

Azithromycin 500 mg, once a day for three days

Metronidazole 400 mg and Amoxicillin 500 mg, three times a day
for five days
Doxycyline 200 mg (loading dose), 100 mg once a day for
fourteen days

Azithromycin is a popular choice, due to the high chance of patient

compliance as only one tablet is required per day over three days.

9.5 MINST
Non-surgical periodontal therapy has evolved over the last few decades,
moving towards a less invasive and more personalised approach. Minimally
invasive non-surgical therapy (MINST) is a novel approach to non-surgical
periodontal therapy focused on biofilm removal without intentional loss of
tooth structure alongside minimal soft tissue trauma to allow optimal clot
stabilisation for wound healing (Nibali et al, 2019).

MINST is used particularly for intrabony defects to optimise healing by

avoiding intentionally making the root surfaces smooth and minimising
trauma through use of magnification, slimline ultrasonic tips, and mini
curettes. This technique aims to stimulate the formation of a stable blood
clot, by natural filling of the intrabony defect with blood following
debridement, allowing for potential regeneration. As well as allowing for
both clinical and radiographic improvement, even in advanced cases,
benefits also include reduced patient morbidity, a decreased chance of
needing surgery, and saved expense/time (Mehta et al, 2024; Nibali et al,
2019). If site-specific MINST is completed, then reassessment probing
should be delayed until around six months.

9.6 Ultrasonics, hand instrumentation, and other

devices
In general, no significant difference has been shown between the use of
hand and powered instrumentation in terms of deposit removal and
improved clinical parameters (Badersten et al, 1981; Loos et al, 1987; Sanz,
2020), but in furcation Grade II or III lesions, powered instruments are
more effective due to the difference in tip size (Drisko, 1998). There are
specific benefits of both ultrasonic and hand scaling, and so the use of a
blended approach is ideal for non-surgical periodontal therapy (Cobb,
1996). A suggested order of use would be ultrasonic followed by hand
followed by ultrasonic.

Ultrasonics
Ultrasonics are a type of powered scaler that can be magnetostrictive or
piezoelectric. The two kinds work in different ways. In piezoelectric
scalers, electrical energy activates ceramic crystals in the handpiece. In
magnetostrictive scalers, electrical energy is applied to stacked metal strips
and the magnetic field causes metal stacks to elongate and return to normal
length, creating vibrations that travel from body to tip.

Ultrasonics have a few key mechanisms of action:

1. Mechanical: Vibratory action of the oscillating metal tip against

the deposit that ablates the deposit.
2. Irrigation: Lavage action of water flowing over the tip flushes
biofilm from the tooth’s surface.
 3. Cavitation: Disruption of biofilm by shock waves resulting from
implosion of bubbles.
4. Acoustic microstreaming: Disruption of biofilm by turbulent
currents of water surrounding the tip.

Some top tips on good ultrasonic technique:

Maintain a light, feather-like touch to maximise tactile sensation

Adapt 2–4 mm of the active tip area and maintain a 0–15-degree
angulation from the long axis of the tooth
Utilise short, overlapping strokes in a methodical pattern
Use the lowest effective power setting and increase as required
Pick the most appropriate tip for the tooth surface in question
Inserts should be activated prior to insertion into pockets
Strokes should initiate at the gingival margin
Piezoelectric – only use lateral surface
Magnetostrictive – can use all sides
 The position of the ultrasonic tip and the use of short overlapping
strokes in an erasing motion

One of the most common reasons for ineffective ultrasonic instrumentation

is worn-down tips. Wear guides are available from the manufacturers, so
regular auditing and replacement of instruments as required is key. If the tip
of the handpiece is overheating, check that the water levels have been
properly adjusted, ensure there is the appropriate water pressure, and check
for a blocked water port. If using a system such as Cavitron, the handpiece
needs to be filled with water and the O-ring lubricated with water prior to
placing the insert.

If a patient has a pacemaker, it is best to avoid use of magnetostrictive

devices unless cleared by a medical professional. Piezoelectric devices are
usually fine to use on a patient with a pacemaker. If you’re ever unsure,
always check with the patient’s cardiologist.

Hand instrumentation
Understanding the various parts of a hand instrument will help you to
determine where to use it and how.
 The various parts of the hand instrument tip

Angulation of the shank: If the shank is straight, then that

instrument should be used anteriorly; if the shank is more curved,
that means it’s for posterior teeth.
Tip of the blade: If it’s got a sharp end, it should be used
supragingivally; if there is a blunt-ended blade, it should be used
subgingivally.
Number of sharp edges: If the blade has only one sharp edge,
it’s a Gracey, and you should only use that sharp side against the
root surface. If both edges are sharp, then it is universal, and the
instrument can be used on both sides.
Size of the blade: If the blade is small, this is a mini curette,
which is great for tight interproximal spaces, furcations, and the
MINST approach. If it’s a regular-sized blade, then that’s a
normal scaler.

Top tips on hand instrumentation:

Be methodical and keep anatomy in mind, as it is a blind

procedure.
 The tip of the blade should always point interdentally, and the
terminal shank should be parallel to the root surface.
Always use a finger rest, push down to the base of the pocket and
scrape up with appropriate pressure against the root surface.
Use a cotton roll/thin aspirator tip to collect the deposits.

Hand instruments that do not require sharpening are ideal; otherwise, it’s
important to ensure instruments are regularly and correctly sharpened at the
practice or sent off to an external sharpening service.

Other
Other devices on the market can be very helpful in biofilm disruption as
well as stain removal. AIRFLOW® by EMS is a popular option. Patients
tend to accustom well to AIRFLOW and it can reduce the time required for
treatment or SPC. It can be used prior to and after ultrasonic/hand
instrumentation. The PLUS® powder can be used in all areas so would be
the powder of choice when managing periodontitis patients. The PLUS
powder is erythritol based (antibacterial component) and also contains
chlorhexidine. This powder is suitable for all patients, including diabetics
and vegans. Alternatively, the CLASSIC® powder would be limited to
heavy stain removal on enamel.

There are many benefits of using EMS AIRFLOW with the PLUS powder:

1. Use of AIRFLOW at the start of treatment makes the calculus

more visible.
2. At the end of treatment, it’s great for stain removal and can access
areas rubber cups will struggle to reach.
3. Excellent for orthodontic patients where access is difficult.
4. It’s comfortable for patients.
5. Minimally invasive so less risk of damaging the tooth/root surface.
 6. You can use it on soft tissue, for example the tongue if the patient
has a tongue coating.
7. It can be used safely around implants.

When using the AIRFLOW, ensure the saliva ejector is at the back of the
mouth and the high-volume suction is following the handpiece around the
mouth. The AIRFLOW handpiece should not be used perpendicular to the
tooth surface; keep it at a 3–5 mm distance and ensure continuous
movement.

Position of the AIRFLOW and high-volume suction

In terms of settings, always keep the water on 100% and adjust the power as
needed. There are a variety of other similar devices available.
9.7 RSI and back/neck pain
Non-surgical periodontal therapy can be taxing on the hands, wrists, and
fingers, as well as the back, neck, and shoulders. As such, repetitive strain
injury (RSI) is not uncommon among dentists. To reduce the chances of
this, build in short rest periods, stretch and exercise your fingers while
reaching for your next instrument, and build strength through the use of
hand/grip-strengthening devices.

Ensure you think about your positioning as well as the use of loupes to
reduce back/neck pain related to administering periodontal therapy.
10
Periodontal Challenges

There are a number of key challenges that we face when it comes to

periodontal management. Occlusion is relevant to all forms of dentistry
including periodontics, but is a topic of ongoing debate. Splinting is also a
common treatment modality that is considered by dentists, but it’s important
to be aware of the indications and best ways of splinting. Furcations can be
challenging to diagnose and manage. Then we have conditions such as
dentine hypersensitivity and halitosis that are common in our periodontal
patients yet may not always be straightforward to treat.

10.1 Occlusal trauma and splinting

Let’s first turn our attention to occlusal trauma and indications for splinting.

Occlusal trauma
Traumatic occlusal force can be defined as ‘any occlusal force resulting in
injury to the teeth and/or the periodontal attachment apparatus’ (Jepsen,
2018). Occlusal trauma is a term used to describe the injury to the
periodontal attachment apparatus. A diagnosis may be made in the presence
of one or more of the following: progressive tooth mobility, adaptive tooth
mobility (fremitus), radiographically widened periodontal ligament space,
tooth migration, discomfort/pain on chewing, and root resorption (Fan and
Caton, 2018).
Primary occlusal trauma refers to damage that causes changes in the tissue
due to excessive occlusal forces on a tooth or teeth that have healthy
periodontal support (Jepsen, 2018). This type of trauma is characterised by
adaptive mobility of the affected teeth and does not worsen over time. On
the other hand, secondary occlusal trauma occurs when normal or excessive
occlusal forces impact a tooth or teeth that have weakened periodontal
support, such as in individuals with periodontitis (Jepsen, 2018). In cases of
secondary trauma, teeth may show progressive mobility, migration, and
discomfort during use.

Occlusal trauma is a co-factor that might increase the rate of progression of

periodontitis (Passanezi and Sant’Ana, 2019). When treating patients with
secondary occlusal trauma, the treatment of the periodontitis itself should
remain the primary focus. In addition, if the patient has parafunctional
habits, the provision of an occlusal splint should be considered. If occlusal
adjustments are indicated to help correct occlusal disharmonies, these must
be carried out carefully to preserve centric stops.

Splinting
The list below gives the key indications for permanent splinting
(Hirschfield, 1937; Ferencz, 1987; Nyman and Lang, 1994):

To immobilise mobile teeth that are causing discomfort or

affecting function
To immobilise teeth where there is progressive increase in
mobility
To prevent further movement of teeth, including drifting,
overeruption, or relapse of orthodontically treated teeth

Temporary splinting is commonly used prior to completing treatment

including regenerative therapy, and there is evidence to show that this will
improve periodontal outcomes by reducing tooth mobility (Cortellini et al,
2001).
The periodontitis must be addressed prior to splinting, as a splint will make
biofilm control more difficult. A range of different materials have been
suggested and are used for splinting. One of the most common is a
composite resin. However, composite resin alone is weak and brittle, so will
fracture easily. Fibreglass-reinforced composite or archwire and composite
would be more appropriate options. The latter is preferable whenever
possible, as it allows some independent tooth movement, thus stimulating
the periodontal ligament and alveolar bone, preventing atrophy. The use of
fibre-reinforced composite resin produces a more rigid splint that can result
in alveolar bone atrophy and may ultimately lead to the need to extract the
tooth.

10.2 Furcations
A furcation defect can be defined as bone resorption and interradicular
attachment loss in multirooted teeth (AAP, 2001). The assessment and
classification of furcations was discussed in Chapter 3. Furcation
involvement is more likely to occur in moderate-advanced periodontitis. In
teeth with short root trunks, furcation involvement can occur earlier in
disease. Maxillary molars are the most difficult to assess and treat as they
have furcations with many entrances in the proximal areas. When assessing
molar teeth from first to third, keep in mind that as you move further down
the series:

The roots become progressively shorter

The roots divide more apically
Access becomes more difficult for both the patient and clinician
The space between the roots gets smaller
The buccal plate gets thicker
The prognosis gets poorer and the complexity of treatment
becomes greater
 The components of the root complex and furcation area

Management of furcations
Teeth with furcation involvement due to periodontitis usually show
progression if left untreated. The overall aims of treatment should be to
eliminate/disrupt biofilm from the exposed surfaces of the root complex and
to establish anatomy that facilitates self-performed biofilm control.
Summary of the treatment options available for furcations

Biofilm control by non-surgical management (oral hygiene instruction and

subgingival PMPR) is indicated when access is sufficient for brushes and
instruments to control biofilm and calculus and to resolve any
inflammation, for example Grade I FI buccal/lingual furca. If biofilm
control is not optimal, non-surgical management will become a permanent
maintenance routine. If the furcation has divergent roots and a short root
trunk, then non-surgical treatment may be enough. In a Grade II or III
furcation lesion it is almost impossible to render the lesion free of biofilm
via conservative means.

Surgery may be used with either a resective or regenerative approach. For

regenerative therapy, the procedures with the highest success for horizontal
bone level gain are bone replacement grafts, guided tissue regeneration with
resorbable membrane, plus bone replacement grafts and enamel matrix
derivative (Jepsen et al, 2020).

Furcation-plasty involves both:

Odontoplasty: Removal of tooth substance at the entrance of the

furcation to eliminate or reduce the horizontal component of the
defect. This aims to widen the entrance of the furcation and,
 therefore, improves the patient’s ability to keep it clean. This can
result in sensitivity, as the pulp is in close vicinity.
Osteoplasty: Recontouring of the alveolar bone crest at the level
of the furcation entrance. The aim is to reduce the buccolingual
dimension of the bone crest in the furcation area.

Furcation-plasty is mainly used in buccal and lingual furca, as proximal

sites are very difficult to access. However, if teeth are missing on either side
of the tooth being treated, then access may be easier.

Tunnel preparation is often used as an adjunct to flap surgery for deep

defects, and is more suitable for molars with short root trunks and wide
divergent roots. The flap is raised, granulation tissue removed, root surfaces
debrided, and interradicular bone removed. Odontoplasty and osteoplasty
may also be carried out. Flaps are then repositioned apically. The creation
of a tunnel should facilitate cleaning with an interdental brush or similar.
CHX and fluoride varnish might then be applied.

Root resection involves sectioning and removal of one or two of the roots of
a multirooted tooth. All of the crown is retained. This is a good option if a
couple of roots have suffered more bone loss, but the root to be retained has
sufficient support. The tooth requires endodontic treatment prior to
resection, and it is important not to leave behind a spur/projection following
resection. Repreparation of what’s left into a cleansable structure is often
the key to success. It is usually advisable to place a crown following root
resection.

Hemisection is the removal of a root and part of the crown that it supports.
Again, this will first require endodontic treatment and a crown after
treatment. This is often a good option for bruxists or if there is any type of
occlusal trauma.
 Hemisection vs root resection

Treatment may not always be possible, in which case extraction is an

option. This might be considered when attachment loss is so great that none
of the roots can be maintained; it could also be an option when treatment
does not result in tooth/gingival anatomy that allows adequate self-
performed oral hygiene. Extraction is also likely to be considered when a
tooth has poor restorative/endodontic status, or when there is increased
mobility; repeated periodontal abscesses; small, fused roots; and no
strategic or aesthetic value to the tooth.

When considering the above treatment options, there are a number of tooth-
and patient-related factors that need to be taken into account (Hughes,
2013).

Tooth-related factors:

Root trunk length: Generally, shorter root trunks are preferable.

Early furcation involvement in disease means remaining
periodontal tissues are more likely to support the roots. Longer
root trunks indicate advanced furcation involvement with reduced
support for stability.
Root cone divergence: Smaller divergence complicates access
and separation. Orthodontic treatment can increase the distance
between roots after separation, aiding in cleaning and restoration.
 Length and shape of root cones: Short and small roots are less
stable after separation. Thin roots with narrow canals pose
endodontic treatment challenges. Small roots are also inadequate
as abutments for prosthetic procedures.
Fusion of root cones: Separation is technically challenging.
Fusion can be identified through clinical assessment, radiographs,
and flap surgery.
Remaining support around individual roots: This is determined
by probing around the separated roots. Minimal remaining
support makes the root a poor candidate for restorative treatment
and less likely to be stable.
Stability of individual roots: Assess stability after separation.
Access for oral hygiene aids: Post-treatment, the tooth must
allow for effective oral hygiene. If not, long-term treatment
success is compromised.

Patient-related factors include:

Patient opinion
Smoker – one would likely avoid any surgical treatment
Cost
Predictability
General health and age
Functional and aesthetic demands
Level of biofilm control
Access

10.3 Dentine hypersensitivity

Dentine hypersensitivity (DH) is ‘characterised by a short, sharp pain
arising from exposed dentine in response to stimuli – typically thermal,
evaporative, tactile, osmotic, or chemical – that cannot be ascribed to any
other form of dental defect or pathology’ (Holland et al, 1997). A practice-
based study of 18–35-year-olds found an incidence rate for DH of 42%
(West et al, 2013).

The aetiology of DH can be attributed to Brannstrom’s hydrodynamic

theory, which describes the fluid movement within the dentinal tubules. For
DH to occur, there must be (West et al, 2015):

1. Dentine exposure (lesion localisation) – soft tissue loss (gingival

recession) or hard tissue loss (abrasion and erosion)
2. Tubule exposure (lesion initiation) – abrasion or erosion

Dentine hypersensitivity is not uncommon amongst periodontitis patients,

and it can also present following periodontal treatment. It is distressing and
can affect the patient’s quality of life.

Management of DH
The first steps in management are to modify or eliminate the aetiological
and predisposing factors. This might include:

Appropriate home care regime

Treatment of periodontitis
Dietary advice
Referral to the GP if there are any signs of reflux
Mouthguard if there are any signs of parafunction

The next step would be to recommend the use of proven, efficacious

products that are available over the counter, such as toothpaste or tooth
mousse. Professionally applied agents would be reserved for the more
severe or non-responding cases (West et al, 2015). In terms of the evidence
base, there is sound evidence for the use of products containing: stannous
fluoride, strontium acetate, arginine/calcium carbonate, and/or calcium
sodium phosphosilicate (West et al, 2015). If this doesn’t work, you can
move on to professionally applied products, including varnish and dentine
adhesive sealers. In terms of their mode of action, agents may cause nerve
desensitisation or tubule occlusion.

When treating patients with DH either during active treatment or SPC,

ensure they are as comfortable as possible by rubbing prophy polish onto
the tooth, using ultrasonics with warm water and, if needed, giving local
anaesthesia.

10.4 Halitosis
Halitosis (from the Latin for breath, halitus, and the Greek suffix osis,
meaning abnormal) is the presence of unpleasant or offensive breath odour
independent of its origin (Greenman et al, 2005). Halitosis can have
significant detrimental social implications for the sufferer and can have a
significant impact on their normal social interactions (Eli et al, 2001).

The exact prevalence of halitosis remains unclear. Many epidemiological

studies are challenging to assess since they often rely on subjective self-
reports of bad breath, which tend to lack accuracy and sensitivity.
Nevertheless, existing data indicates that halitosis is a widespread issue that
can impact individuals across various age groups. Most research suggests
that around 30% of the population experiences halitosis (van Dortsten and
Van der Weijden, 2007).

Intra-oral halitosis, often referred to as oral malodour, pertains to cases

where the cause of bad breath originates within the oral cavity. By contrast,
extra-oral halitosis arises from sources outside the mouth, which can be
categorised into blood-borne and non-blood-borne types. Additionally,
conditions such as pseudo-halitosis and halitophobia describe individuals
who believe they have halitosis despite professional evaluations indicating
otherwise. Other forms of halitosis include temporary or transient halitosis,
as well as ‘morning breath’.
Research indicates that approximately 85% of individuals with persistent
genuine halitosis have odours originating from inside the mouth (Scully et
al, 2001). The primary cause of intra-oral halitosis is often attributed to
tongue coating, while gingivitis and periodontitis can also contribute to the
condition. Various acute conditions, including peri-coronal infections, acute
herpetic gingivostomatitis, and necrotising gingivitis, can produce a notably
strong odour known as ‘foetor oris’. Additionally, factors such as
xerostomia (dry mouth), oral candidiasis, certain medications, poorly fitting
restorations, and dental caries may further exacerbate intra-oral halitosis
(Kumar et al, 2014).

Intra-oral halitosis is primarily caused by the release of volatile compounds

resulting from bacterial degradation of epithelial cells, salivary and serum
proteins, and food residues. Numerous molecular species can contribute to
the overall malodour, though key among those are volatile sulphur
compounds such as methyl mercaptan, hydrogen sulphide, and dimethyl
sulphide. The formation of these compounds occurs through the breakdown
of organic debris and protein substrates by various anaerobic bacteria,
particularly those with proteolytic capabilities (Miller and Dyer, 2011).

The dorsum of the tongue serves as an ideal habitat for anaerobic bacteria,
due to the favourable redox potential found in the deep crypts associated
with the structure of the tongue papillae. The tongue coating consists of
shed epithelial cells, food particles, bacteria, and salivary proteins, creating
an environment conducive to producing volatile sulphur compounds and
other odorous substances (Roldán et al, 2013). Anaerobic bacteria also play
a crucial role in the subgingival plaque associated with periodontitis, where
elevated levels of volatile sulphur compounds are often detected in
periodontal pockets and gingival crevicular fluid from individuals suffering
from gingivitis or periodontitis (Scully et al, 2001).

To diagnose halitosis, a comprehensive approach is necessary, including a

detailed medical history, examination of soft tissues for tongue coating,
periodontal assessment, and an organoleptic evaluation. During the
organoleptic assessment, the clinician evaluates the odour of exhaled air
from both the mouth and nose. At the most basic level, clinicians can use
their own judgement to determine the presence or absence of malodour in a
patient (Yoshida et al, 2014).

Management of halitosis
The treatment of halitosis is primarily determined by its underlying cause.
Once intra-oral halitosis has been diagnosed, you should sensitively let the
patient know about their diagnosis but keep the conversation focused on
how we can help them address this. For management, you should take the
following steps:

1. Provide personalised guidance on halitosis, discussing the specific

causes that are relevant to the patient. Highlight the importance of
self-care practices to improve the condition, and reassure the
patient that effective treatment can help reduce or eliminate bad
breath (Friedman et al, 2015).
2. Encourage the patient to refrain from smoking and limit the intake
of foods that may contribute to halitosis.
3. Advise the patient to maintain oral moisture by staying hydrated
and using sugar-free chewing gum to stimulate saliva production
(Scully et al, 2001).
4. Optimise the patient’s oral hygiene routine by recommending
brushing teeth twice daily and incorporating daily interdental
cleaning to remove biofilm and food particles (Sanz et al, 2015).
5. Instruct and motivate the patient to use a tongue scraper if tongue
coating is present, as tongue cleaning has been shown to be an
effective method for reducing intra-oral halitosis caused by
bacteria on the tongue (Roldán et al, 2013; Outhouse et al, 2006).
6. Suggest the use of chemical agents with proven efficacy if
necessary (Slot et al, 2015). Mouth rinses and toothpaste
containing active ingredients like chlorhexidine, cetylpyridinium
 chloride, and zinc compounds (such as CHX+CPC+Zn and
ZnCl+CPC) can help to significantly reduce halitosis (Rosenberg
et al, 2006).
7. Provide periodontal treatment if the patient exhibits signs of
gingivitis or periodontitis. Additionally, address any other oral
health issues that may contribute to halitosis.
8. Identify and rectify local dental factors such as overhanging
restorations and dental caries that may exacerbate the condition.
9. Review the patient’s halitosis status after appropriate therapy,
suggesting further measures if the issue persists.

It is crucial to recognise that a small percentage of patients, less than 10%,

may suffer from extra-oral halitosis or halitophobia and might need to be
referred to a medical specialist. This could include consultations with oral
medicine specialists, otorhinolaryngologists, to check for chronic tonsillitis
or sinusitis, or physicians to assess potential underlying conditions such as
gastrointestinal, hepatic, endocrine, pulmonary, or renal diseases. Referral
to a psychologist or psychiatrist may also be necessary for those
experiencing halitophobia (Yoshida et al, 2014).
11
Periodontal Emergencies And
Their Management

Patients might often present to us in pain or with acute problems that cause
them to seek urgent care. It’s important to be aware of these ‘periodontal
emergencies’ and be confident in solving them efficiently. In this chapter,
we will cover a range of conditions that may present as an emergency.

11.1 Gingival abscess

A gingival abscess is ‘a localised purulent infection affecting the marginal
gingiva or interdental papillae’ (AAP, 2000). Clinically, it is characterised
by a rapidly expanding localised swelling, which may present as either
shiny and smooth or pointed. The presence of suppuration is common, and
patients often experience significant pain and tenderness upon palpation of
the affected area.

Gingival abscesses frequently occur due to the impaction of subgingival

foreign objects and typically develop in previously healthy gingivae. The
literature implicates various foreign bodies, such as fragments of nails in
individuals with nail-biting habits. For abscesses caused by the impaction of
oral hygiene aids, the term ‘oral hygiene abscesses’ has been suggested
(Gillette, 1980).
Management of a gingival abscess involves incision, drainage, and
irrigation with saline to alleviate acute symptoms. Addressing the
underlying cause is crucial, and mechanical debridement may be beneficial
in this regard. The short-term use of chlorhexidine mouthwash or warm
saline rinses is commonly recommended, particularly when the area is too
tender for brushing. Follow-up appointments are necessary to ensure
resolution.

11.2 Periodontal abscess

A periodontal abscess is defined as a localised buildup of pus within the
gingival wall of a periodontal pocket, resulting in the destruction of
collagen fibre attachment and the loss of nearby alveolar bone. Clinically, it
often appears as an ovoid swelling on the lateral side of the tooth root. In
some cases, abscesses that are deeper within the periodontium may show up
as diffuse swelling or reddening, with the affected area typically being
sensitive to touch. This condition is usually associated with a deep
periodontal pocket and may cause bleeding and discomfort when probing.
Suppuration might occur through a fistula or an opening in the periodontal
pocket, which could be spontaneous or triggered by finger pressure (Herrera
et al, 2000).

Common signs of a periodontal abscess include increased tooth mobility

and tenderness on percussion, and the patient might report that the tooth
feels ‘high in their bite’. Radiographs often reveal some degree of bone loss
around the affected tooth, and sensibility testing should provide a positive
response.

A periodontal abscess is often a complication of existing periodontitis,

especially in cases with complex morphology, furcation involvement, or
vertical defects, where the closure of the pocket margins can lead to
infection spreading to adjacent periodontal tissues. Factors such as changes
in the subgingival microbiota, increased bacterial virulence, or reduced host
defences can impair the drainage of pus, leading to the development of an
abscess. This can occur in situations such as:
 Following subgingival PMPR, where calculus fragments may
become dislodged and pushed into the periodontal tissues (Dello
Russo, 1985).
After surgical therapy, associated with foreign bodies like
membranes or sutures (Garrett et al, 1997).
Acute exacerbation of periodontitis (Fine, 1994).
Systemic antimicrobial intake without subgingival debridement in
severe periodontitis, leading to overgrowth of opportunistic
bacteria (Helovuo et al, 1993).

Managing a periodontal abscess involves addressing the acute symptoms to

prevent further tissue damage. If the tooth can be saved, the first step is to
establish drainage either through the periodontal pocket or via an external
incision, followed by thorough cleaning of the area. Adjusting the occlusion
can offer immediate relief. Systemic antibiotics are only necessary if there
is systemic involvement or if the infection is spreading.

If the tooth is deemed unsalvageable, extraction may be the most

appropriate course of action. Since most periodontal abscesses occur in
areas with pre-existing periodontal issues, it is crucial to reassess
periodontal treatment once the acute phase has resolved. For patients who
have not previously received treatment, appropriate periodontal care should
be initiated. For those already undergoing treatment, it should continue after
addressing the acute abscess. For patients receiving supportive periodontal
therapy, any potential recurrence of the abscess should be carefully
evaluated, including assessing the extent of tissue damage and its effect on
the tooth’s long-term prognosis (Herrera, 2000).

11.3 Pericoronitis/peri-coronal abscess

Pericoronitis is the inflammation of the soft tissues surrounding the crown
of a partially erupted tooth, whereas a peri-coronal abscess refers to the
localised accumulation of pus within the gingival flap overlying an
incompletely erupted tooth. The condition most frequently affects the
partially erupted and impacted mandibular third molar, as the overlying
operculum provides a perfect environment for debris and bacteria
accumulation. Trauma from an opposing tooth often exacerbates the
condition.

Clinically, patients often present with a red, swollen, and potentially

suppurative lesion that is painful to touch. Common symptoms include
cheek swelling at the mandibular angle, trismus, and radiating pain to the
ear. Systemic complications such as lymphadenopathy, fever, and general
malaise may also occur.

In terms of management, after administering anaesthesia, the operculum

should be irrigated to remove debris. In some instances, you might need to
excise the operculum and carry out occlusal adjustment on the opposing
tooth to prevent further trauma. Antibiotics are recommended only if there
are systemic symptoms or evidence of spreading infection. Once the acute
infection phase has resolved, you must decide whether there is any need for
tooth extraction.

11.4 Necrotising gingivitis and periodontitis

Necrotising periodontal diseases are among the most severe inflammatory
lesions linked to the oral biofilm; they commonly affect the mandibular
anterior teeth. Necrotising gingivitis is marked by necrosis and ulcers in the
free gingiva, often starting at the interdental papilla and presenting a
‘punched-out’ appearance. Marginal erythema and progression to the
marginal gingiva may occur, with a pseudo-membrane forming over the
necrotic area. Removing this pseudo-membrane reveals underlying
connective tissue that bleeds. Pain severity correlates with the extent of the
lesion and typically increases with eating and oral hygiene activities.
Additional symptoms may include halitosis, fever, and malaise.

Necrotising periodontitis shares these features but also involves necrosis of

the periodontal ligament and alveolar bone, causing attachment loss.
Disease progression can result in an interproximal crater separating the
buccal and lingual/palatal parts of the papilla. Deep craters may denude the
interdental crestal bone, and lateral spread of interproximal necrosis can
create extensive destruction zones. Severe cases can involve bone
sequestration. Associated risk factors include high stress, heavy smoking,
and poor nutrition. Both necrotising gingivitis and periodontitis may be
linked to untreated HIV/AIDS, other immunocompromising conditions, or
immunosuppressive drugs.

Treatment of both conditions involves careful superficial debridement to

remove biofilm and calculus, preferably using ultrasonic instruments to
minimise pressure on ulcerated tissues. Debridement should be done daily
and progressively deeper as patient tolerance improves, typically over two
to four days during the acute phase. To reduce pain and aid healing,
mechanical oral hygiene should be limited, and patients should use
chemical plaque control agents like 0.2% chlorhexidine mouthwash twice
daily. Additional antibacterial effects against anaerobes can be achieved
with 3% hydrogen peroxide diluted 1:1 with warm water or other oxygen-
releasing agents. If periodontal condition does not improve with
debridement alone, systemic antimicrobials, such as metronidazole (400 mg
TDS for five days), should be considered due to their efficacy against strict
anaerobes (Loesche et al, 1982).

As symptoms and signs improve, strict oral hygiene should be enforced and
debridement completed as necessary. The post-acute phase of management
should address any pre-existing periodontal disease and systemic risk
factors, with close monitoring and support for affected patients.

11.5 Acute herpetic gingivostomatitis

Herpetic gingivostomatitis is a prevalent viral infection of the oral mucosa,
characterised by small ulcers with raised edges. These ulcers can appear
across various areas in the mouth, including both attached and unattached
mucosal surfaces. Caused by the herpes simplex virus, herpetic
gingivostomatitis is the initial manifestation of primary herpes simplex
infection, which is more severe than subsequent presentations such as
herpes labialis. Patients often experience generalised pain in the gingiva and
oral mucosa, along with systemic symptoms like lymphadenopathy, fever,
and malaise. The lesions typically persist for seven to ten days and heal
without leaving scars. This condition is most frequently observed in
children aged two to five years.

Given that the condition is self-limiting, treatment primarily focuses on

hydration and symptom management. Palliative care is important to relieve
pain and ensure the patient can eat and drink. Paracetamol is commonly
administered, with the recommended dosage for children aged two to four
years being 180 mg every four to six hours. In severe cases, especially in
immunocompromised patients, hospital referral is necessary for potential
intravenous antiviral treatment.

11.6 Acute physical/chemical/thermal injury

This category of acute periodontal lesions is not caused by the oral biofilm
but understanding these conditions is crucial for accurate diagnosis and
effective treatment.

Physical injuries may present as erosions or ulcers, sometimes accompanied

by gingival recession. Less commonly, they can manifest as hyperkeratosis,
vesicles, or bullae. Continuous mild trauma might lead to hyperkeratotic
lesions, while more aggressive trauma can cause superficial lacerations.
These injuries can be either asymptomatic or cause intense localised pain.

Physical injuries to the oral tissues can often stem from poor oral hygiene
practices, trauma, or parafunctional habits. For example, using a harsh
toothpaste and brushing too aggressively can lead to gingival ulcers or
erosions. Similarly, improper use of dental floss or other interdental tools
may cause gingival ulceration, inflammation, and recession. In children and
teenagers, self-inflicted injuries are common and can involve fingers, nails,
or objects like pencils (Creath et al, 1995; Krejci, 2000). Traumatic injuries
can also result from broken teeth, orthodontic appliances, or oral piercings.

Thermal injuries are typically painful, with gingival tissues appearing

erythematous and desquamated, sometimes accompanied by vesicles,
erosions, or ulcers. Such injuries are often caused by burns from hot food or
drinks.
Chemical lesions occur after direct contact with a chemical agent on the
mucosa, resulting in maculae, vesicles, erosions, or ulcers, depending on the
agent and duration of exposure (Herrera et al, 2014). Common sources
include oral bleaching agents, etchants, and certain dental products,
especially when used improperly or with ill-fitting trays (Sapir and
Bimstein, 2000; De Bruyne et al, 2000).

Treatment of the above depends on the diagnosis and the source of trauma,
so a thorough clinical examination and patient history are essential to
identify the cause. Management involves eliminating the initiating factor
and addressing pain symptoms. Generally, lesions heal without further
intervention, but additional treatment may sometimes be necessary. It is
important to differentiate these lesions from those associated with
mucocutaneous diseases, which may not have a clear initiating factor. In
such cases, mechanical oral hygiene may be paused, and chemical plaque
control can be used to help identify the cause.

11.7 Subgingival root fractures

When a tooth fracture extends from the supragingival area apically in a
subgingival direction, it can cause acute pain and lead to periodontal
infection. Patients may or may not recall a specific traumatic event during
chewing. Key risk factors include heavily restored teeth without cuspal
coverage and those with bruxism. Additionally, fractures are common in
patients with reduced periodontium due to an unfavourable crown-to-root
ratio.

Magnification and good lighting are essential for identifying fracture lines.
Diagnostic tools such as a ‘tooth sleuth’ can help by applying occlusal
pressure to individual cusps. Even if a fracture line is not visible, fractured
teeth often present with a localised deep pocket depth and potentially an
abscess. The affected tooth or fractured cusp might be highly sensitive to
percussion or may only cause pain upon release of biting pressure.
Fractures can be vertical along the root axis or angled, with varying degrees
of root involvement.
Management of tooth fractures depends on the vitality of the tooth and the
fracture’s location and extent. Initial steps might involve removing existing
restorations to thoroughly assess the tooth and confirm the diagnosis.
Treatment options typically include endodontic therapy followed by a full
coverage restoration if the tooth can be saved. A periodontal flap can be
helpful for better visualisation of the fracture, and crown lengthening might
be necessary to expose the most apical part of the fracture. If the tooth is
deemed untreatable, extraction will be required.
12
Supportive Periodontal Care

Supportive periodontal care (SPC) is an effective and integral component of

managing periodontitis patients. Its importance should be emphasised to
patients before commencing any active treatment. With supportive
periodontal therapy, periodontal health can be maintained in most patients,
even in advanced cases (Rosling et al, 2001).

The aims of SPC are to:

Monitor whether the condition is stable and provide an

opportunity to initiate treatment if progression is detected
Remove aetiological factors before the disease progresses
Reinforce smoking cessation and organise referral if appropriate

12.1 Recall interval

Recall intervals should be determined based on the patient’s risk profile.
The default is usually three months but can be up to twelve months. The
recall interval needs to be reviewed at every visit and if needed adjusted.
When considering risk and tailoring the recall interval, there are several
patient, treatment, and local factors to consider.

Patient factors
Patients with periodontitis who smoke are more prone to the disease and
generally experience less favourable treatment outcomes (Tomar and Asma,
2000). This necessitates more frequent dental appointments for monitoring
and management (Heasman et al, 2006). Similarly, systemic conditions like
uncontrolled diabetes significantly increase the likelihood of periodontitis
recurrence, thus requiring patients to have more regular check-ups (Löe,
1993). High stress levels in patients can also warrant more frequent
maintenance visits to manage periodontal health effectively (Genco et al,
1999).

Advancements in genetic research have identified markers that help

determine a patient’s susceptibility to periodontal diseases. Notably, studies
on interleukin-1 (IL-1) polymorphisms reveal that patients with IL-1
genotype positivity are more likely to suffer from advanced periodontitis
and see higher rates of tooth loss (Kornman et al, 1997). Additionally,
patients classified as high risk (Grade C) due to previous susceptibility to
severe periodontitis will also need more frequent reassessment and follow-
up appointments to manage their condition effectively.

Previous treatment
The interval is also dependent on previous treatment. For example, if there
has been recent surgery, the patient will have to be seen sooner than for
non-surgical treatment. The outcome of active treatment needs to be
considered too, as the limitations of active treatment are likely to continue
during maintenance, and this may warrant a shorter recall interval.

Local factors
Since biofilm is by far the most important aetiologic agent for the
occurrence of periodontal diseases, the full-mouth assessment of the
bacterial load is critical in the determination of the risk of disease
recurrence. In general, inadequate biofilm management will necessitate
more frequent dental visits. However, the amount of biofilm that can be
maintained without disease progression can differ from patient to patient.
For those facing challenges with biofilm control – whether due to
overcrowded or misaligned teeth, or physical limitations – more frequent
assistance may be essential.

The type of periodontal disease present, such as infrabony lesions, furcation

involvement, or gum recession, is also significant. Multi-rooted teeth are
particularly vulnerable to loss during the maintenance phase (Mavridis and
Mavridis, 2018). Additionally, the presence of root grooves and concavities
can further elevate the risk of recurrence, indicating a need for more regular
maintenance visits.

When considering the severity of past or existing periodontal disease,

factors such as age-related bone loss, tooth loss, BoP, and the depth of
pockets (5 mm or deeper) are important. The absence of BoP is a strong
indicator of periodontal stability, while a high prevalence of deep residual
pockets during SPC suggests an increased likelihood of disease progression
(Trombelli et al, 2015).

Patients with concurrent oral conditions, like erosive lichen planus or

mucous membrane pemphigoid, may also require more frequent
appointments, as their symptoms can make plaque control more
challenging.

Various tools are now available to assist in determining periodontal risk that
can help with the above considerations, and in general risk assessment for
our patients. For example, PreViser/DEPPA technology is an online
assessment tool that evaluates eleven factors: patient age, smoking,
diabetes, history of periodontal surgery, pocket depth, BoP, furcation
involvements, subgingival restorations, root calculus, radiographic bone
height, and the presence of vertical bone lesions (Meyer and Lewis, 2018).
A patient report is then produced as a biofeedback and communication tool.

The Periodontal Risk Assessment (PRA) is another online tool that has been
widely used in specialist teaching programmes (Cortellini and Tonetti,
2005). It is often referred to as the ‘spider diagram’, as it produces a
functional graphical representation of a patient’s risk based on six clinical,
systemic, and environmental factors: percentage bleeding on probing,
number of residual periodontal pockets ≥5 mm, number of lost teeth,
alveolar bone loss in relation to patient age, systemic and/or genetic
predispositions, and environmental factors (such as tobacco use). This then
guides the recall interval.

12.2 Palliative periodontal care

In the ideal scenario, there would be no (or very few) periodontal probing
depths of 4 mm with bleeding or 5 mm and above when a patient enters
SPC. However, in the case that a patient moves to supportive care with
acceptance of deep pockets, this is termed palliative periodontal care.

The aim here is to slow down the progression of the condition, though
active treatment is not occurring; in other words, the condition will not
improve. Palliative periodontal care may be needed when risk factors
remain unchanged. For example, if the patient is a smoker and not keen to
stop, then after two rounds of active treatment, you would not continue to
repeat this. Or if the patient’s biofilm self-care does not improve and you’ve
persisted with numerous efforts, you may wish to place them on palliative
care until this changes.

Patients can move back into the active treatment phase if these factors
change, for instance, if the patient stops smoking or the biofilm control
improves. Sometimes, pockets may be accepted when, for example, the
patient has declined a referral, and you do not feel you can achieve much
more improvement.

12.3 Appointment structure

The content of the SPC appointment depends on the type of treatment
completed and the outcome. A typical visit after successful non-surgical
treatment would involve:

1. Checking the patient’s medical history

2. Reviewing their oral hygiene regime and revising if necessary
 3. Reviewing and discussing control of any other risk factors
4. Probing all sites to check probing depth and bleeding after probing
– a full six-point pocket chart is required on a yearly basis
5. Supragingival PMPR as needed

Supportive periodontal care after partially successful non-surgical treatment

– ie some residual deep pockets and inflammation remain – will include all
of the above steps plus as much subgingival PMPR of residual deep pockets
as is practically possible.

There may be occasions where a significant relapse in the periodontal

condition gives rise to the need for the patient to enter the active treatment
phase. The patient may then require a few dedicated appointments for
subgingival PMPR to get them back on track; they will then enter SPC
again.
13
Dental Implants

Professor Brånemark is considered the pioneer of titanium endosseous

dental implants. He presented ten years of research at Cambridge University
showing that bone can grow intimately onto the surface of titanium
implants, in a process known as osseointegration (Brånemark et al, 1977).
This discovery paved the way for further development of dental
applications.

Dental implants have become a common solution for replacing missing

teeth. It’s important for patients to understand that restorations supported by
implants necessitate ongoing maintenance and can give rise to
complications, such as peri-implantitis, which may impact the implant’s
success and lifespan. Dental professionals are responsible for evaluating the
health of the tissues surrounding the implants and identifying any potential
peri-implant complications.

IMPLANTS: KEY TERMINOLOGY

Osseointegration: A direct structural and functional connection

between ordered, living bone, and the surface of a load-carrying
implant.
Endosseous dental implant: A device inserted into the jawbone
(endosseous) to support a dental prosthesis. It is the ‘tooth root’
analogue and is often referred to as a ‘fixture’.
Implant abutment: The component that attaches to the dental
implant and supports the prosthesis. A transmucosal abutment is
 one that passes through the mucosa overlying the implant. A
temporary or healing abutment may be used during the healing of
the peri-implant soft tissue before the definitive abutment is
chosen.
Abutment screw: A screw used to connect an abutment to the
implant.
Single-stage implant surgery: Involves surgically placing a
dental implant that is left exposed to the oral cavity following
insertion. This protocol is used in non-submerged implant systems.
Two-stage implant surgery: This involves the initial surgical
placement of a dental implant, which is buried beneath the mucosa
and then subsequently exposed with a second surgical procedure
some months later. It is used in submerged implant systems.

There are notable distinctions between natural teeth and dental implants.
The periodontal complex surrounding a tooth has evolved over millions of
years and is made up of highly specialised tissues, whereas the soft tissue
surrounding implants essentially consists of scar tissue. Osseointegration
occurs as a reaction to the foreign material, leading to direct contact
between bone and implant, accompanied by the formation of a soft-tissue
scar. Given these differences, it is reasonable to conclude that the tissues
around natural teeth and the peri-implant mucosa around implants will not
function in the same manner.

The table below outlines the histological comparison of the periodontium

versus peri-implant tissues (Jung and Ganeles, 2013):
Jung and Ganeles’ (2013) comparison of periodontium and peri-implant tissues

Compared to periodontal tissues, it is suggested that peri-implant tissues are

more susceptible to inflammatory reactions, a phenomenon also confirmed
immunohistochemically with an increase of inflammatory infiltrate in
comparison with natural teeth (Nishihara et al, 2015).

13.1 Dental implants in periodontitis patients

There are several important factors to be aware of when considering
periodontitis patients who have dental implants.

Risk of peri-implant disease

Patients with a history of periodontitis face an increased risk of developing
peri-implantitis (Schwarz et al, 2011). Long-term studies indicate that these
individuals tend to have greater probing depths and bone loss around
implants, along with a higher occurrence of peri-implantitis and elevated
overall failure rates (Roccuzzo et al, 2023). Research has shown that
implants placed in patients with periodontal susceptibility experience
significantly more bone loss than those placed in periodontally healthy
individuals, regardless of the type of implant used (Lang et al, 2011).
Therefore, it is crucial to address and manage periodontitis prior to implant
placement, ensuring that any deep probing depths are resolved (Sgolastra et
al, 2015). Additionally, individuals with a history of periodontitis should be
informed during the consent process about their increased risk of
complications associated with implant procedures.

Implant position
Implants should not be positioned too closely together, as this can hinder
effective biofilm management. Whenever feasible, it is recommended to
maintain a spacing of at least 3 mm between implants (Schwarz et al, 2015).
Any historical loss of hard or soft tissues may affect the ability to position
the implant correctly in three dimensions, so this must be considered prior
to placing. Improper buccolingual positioning can result in restorations that
have difficult-to-clean overhangs. Additionally, placing implants too deeply
can lead to increased probing depths and a significant subgingival
environment, which complicates optimal biofilm control. It’s essential to
consider these potential complications during the planning phase and to
evaluate the need for bone and/or soft-tissue grafting when necessary.

Screw versus cement

Whenever possible, screw-retained restorations are recommended. When
opting for cemented restorations, care must be taken to avoid excess cement
from being extruded into the peri-implant sulcus during the seating process.
Deeper crown margins typically lead to a higher volume of excess cement.
Any leftover cement can create a rough surface that facilitates microbial
colonisation, potentially resulting in peri-implant mucositis and even peri-
implantitis (Salgado et al, 2016). Excess cement can also act as a foreign
body, triggering an inflammatory response that may contribute to the
development of peri-implantitis.

Removable options
It may not always be necessary to provide a fixed restoration. Overdentures
are often a more easily cleaned and safer long-term solution for some
patients (Zitzmann and Marinello, 2001). A removable prosthesis can
replace both hard and soft tissue, which might provide a better aesthetic
outcome as well as allow better access to the peri-implant tissues for
ongoing plaque control.

The McGill consensus statement from 2002 (Feine et al, 2002) concludes
that: ‘patients are significantly more satisfied with implant supported
overdentures compared to conventional overdentures. Patients experience
more stable dentures, greater ease when chewing, greater comfort and can
speak more easily.’

Supportive peri-implant care

Longitudinal studies have shown that a lack of supportive therapy is
associated with a higher frequency of peri-implantitis (Sanz et al, 2015).
For this reason, supportive peri-implant care is integral to minimising risks.
Recall intervals should be tailored according to previous periodontal
therapy, the location of the soft tissues, the implant location, and the
prosthesis design (Pjetursson et al, 2012).
Extracting teeth to replace with implants
There is now a growing body of evidence to suggest that maintaining
periodontally involved teeth can provide better tooth survival outcomes and
can also be more cost-effective than placing implant-retained crowns
(Kumar et al, 2015; Misch et al, 2014; Pjetursson and Lang, 2008). Thus,
there has been a gradual move towards retaining periodontally involved
teeth for as long as possible before replacement with implants.

13.2 Key recommendations

Below are the key recommendations from the European Federation of
Periodontology (Herrera et al, 2022) with regard to dental implants:

Patients must be made aware of the potential risks of biological

complications, such as peri-implant diseases, and the importance
of preventive care.
A thorough and individual risk assessment should be conducted,
taking into account both systemic and local risk factors.
Modifiable risks, such as persistent probing pocket depth in the
remaining teeth and smoking habits, should be addressed. As
such, management of periodontal disease to eliminate residual
pockets that bleed upon probing, along with smoking cessation,
should occur before placing implants.
It is crucial to ensure that implant components and the
superstructure fit properly, in order to minimise areas where
biofilm can accumulate. If cemented implant restorations are
chosen, the margins of the restoration should align with the
mucosal margin to facilitate the effective removal of excess
cement.
Placing implants at a submucosal level to conceal crown margins
might increase the risk of peri-implant diseases.
 To enhance personal oral hygiene, clinicians should aim to have
keratinised, attached, and stable tissue surrounding the
transmucosal part of the implant during initial placement (for one-
stage procedures) or during abutment connection (for two-stage
procedures).
Infection control is critical in preventing peri-implant diseases;
therefore, patients should receive clear instructions regarding their
oral hygiene practices, along with regular monitoring and
reinforcement of these practices.
The placement of the implant and the design of the prosthesis
should allow for adequate access to facilitate regular diagnostic
probing and both personal and professional oral hygiene.
Professional supportive care for peri-implant health should be
tailored to the specific needs of each patient, with recall intervals
set at three, six, or twelve months, depending on their compliance.
During these visits, peri-implant tissues should be carefully
examined, including probing assessments, with a particular focus
on any bleeding upon probing.

13.3 Management of peri-implant disease

In a healthy state, it’s essential to reinforce self-care biofilm control through
personalised oral hygiene instructions. In addition to using a manual or
electric toothbrush, patients may be advised to incorporate interdental
brushes, superfloss, single-tufted brushes, and possibly irrigation devices
into their routine. Patients should also be enrolled in a supportive peri-
implant care programme.

For cases of peri-implant mucositis, the focus of intervention is on effective

biofilm control, which can be achieved through self-care or professional
treatment. Outcomes should be assessed after a period of two to three
months, and if peri-implant health has not been restored, re-treatment is
recommended. Addressing peri-implant mucositis is crucial for preventing
progression to peri-implantitis.

In instances of peri-implantitis, referral to a specialist or back to the original

dental professional who placed the implant may be necessary. Various
treatment strategies for peri-implantitis have been proposed, generally
based on protocols used for periodontal disease in natural teeth. A Cochrane
systematic review published in 2008 and updated in 2012 (Friedman, 2012),
which included nine randomised controlled trials, concluded that ‘there is
no evidence to suggest a superior protocol for the management of peri-
implantitis.’ Proposed treatments encompass both non-surgical and surgical
options, with or without adjunctive therapies. Typically, an initial non-
surgical treatment phase, including submarginal instrumentation, is carried
out. Following this, a re-evaluation of clinical outcomes will determine
whether the patient should enter a secondary preventive supportive peri-
implant care programme or proceed to surgical intervention, assuming the
affected implant is still considered treatable (Herrera et al, 2022).
14
Multidisciplinary Care

Successful periodontal care often involves interaction with other specialties.

In this chapter, we will focus on the perio–endo and the perio–ortho
interfaces.

14.1 The perio–endo interface

According to the updated classification (Papapanou et al, 2018), an endo–
perio lesion is a pathological communication between the pulpal and
periodontal tissues of a given tooth, which occurs in either an acute or
chronic form. These lesions can be further classified according to their
signs and symptoms, which have a direct impact on their prognosis and
treatment (eg presence or absence of fractures and perforations, and
presence or absence of periodontitis).

Endo–perio lesions can be triggered by a carious or traumatic lesion that

affects the pulp and, secondarily, the periodontium; by periodontal
destruction that secondarily affects the root canal; or by the concomitant
presence of both pathologies. There is no evidence for a distinct
pathophysiology between an endo–periodontal and a periodontal lesion
(Santos et al, 2017). Nonetheless, the communication between the pulp/root
canal system and the periodontium complicates the management of the
involved tooth.
 The perio–endo interface – the various routes of communication

Communication through dentin exposure can happen due to several factors,

such as developmental grooves, congenital lack of cementum resulting in
exposed tubules, gingival recession, or following post-periodontal mucosal
repositioning (PMPR). Communication also often occurs via lateral and
accessory canals. Radiographic indicators of these canals may include a
distinct lateral lesion, a notch on the lateral surface, and the extrusion of
filling material. The apical foramen serves as a further potential pathway
for communication.

Signs and symptoms

The primary signs of an endo–perio lesion will be a deep periodontal pocket
extending to the root apex and/or negative or altered response to pulp
vitality/sensibility tests (Kumar and Nisha, 2015).

Other signs/symptoms include radiographic evidence of bone loss in the

apical or furcation region, spontaneous pain or pain on
palpation/percussion, suppuration, tooth mobility, sinus tract/fistula, and
crown and/or gingival colour alterations. If the endo–perio lesion is
associated with traumatic and/or iatrogenic factors, further signs might
include root perforation, fracture/cracking, or external root resorption.
These can drastically impair the prognosis of the involved tooth.
A thorough history, probing, radiographic examination, and sensibility
testing are essential for establishing a diagnosis.

Treatment planning
Evaluating the prognosis of a tooth before treatment is crucial. In cases
where the pulp is the primary cause, the prognosis is usually predictable,
but if significant periodontal damage has subsequently impacted the root
canal, the prognosis becomes less certain.

Endo–perio lesions necessitate a thorough and collaborative approach to

treatment. Typically, endodontic treatment (or re-treatment) should be
performed first, followed by a reassessment of the periodontal condition
two to three months later to complete the necessary treatment (Friedman
and Stabholtz, 1999).

14.2 The perio–ortho interface

Orthodontics in patients with severe periodontitis can be challenging, and
evidence-based guidelines should be closely followed to ensure safe and
predictable results. The importance of achieving the periodontal outcomes
of shallow, maintainable pockets and control of inflammation before
considering orthodontic treatment is key. Orthodontic treatment should
involve careful risk assessment and treatment planning, as well as the use of
light and controlled force.

Orthodontics in Stage IV periodontitis

In terms of severity and complexity, Stage IV periodontitis shares
characteristics with Stage III, but also involves anatomical and functional
consequences due to tooth and periodontal attachment loss, such as tooth
flaring, drifting, and bite collapse. These issues necessitate further
interventions after active periodontal therapy has been completed.
The clinical practice guideline for managing Stage IV periodontitis offers
evidence-based recommendations (Herrera et al, 2022). It emphasises the
importance of interdisciplinary collaboration, including orthodontic
treatment, to rehabilitate the compromised dentition of these patients.

Cases of Stage IV periodontitis can exhibit significant phenotypic

differences due to varying patterns of periodontal breakdown, the number
of missing teeth, inter-maxillary relationships, and the condition of the
residual alveolar ridge. These factors contribute to different levels of
functional and aesthetic compromise, as well as distinct treatment
requirements. When discussing orthodontic management, the guidance
document highlights Case Type 2, which pertains to patients experiencing
pathological tooth migration characterised by elongation, drifting, and
flaring, all of which can be corrected orthodontically.

Orthodontic treatment can be planned during the second step of care and, in
some cases, during the third step. However, actual orthodontic interventions
should only be initiated once the goals of periodontal treatment – such as
achieving shallow, maintainable pockets and controlling periodontal
inflammation – have been met. Starting treatment too early may jeopardise
periodontal health.

Tooth movements
The advancement of periodontitis can lead to pathological tooth migration,
which is evident through symptoms like drifting, flaring, and elongation of
teeth. If this has occurred in individuals who have successfully undergone
treatment for Stage IV periodontitis, orthodontic therapy may be required to
enhance their dental aesthetics and functional occlusion. These patients
typically have a healthy yet diminished periodontal structure, so the
implications and requirements of orthodontic treatment may vary compared
to those without any attachment loss (Martín et al, 2021).

It is crucial to first achieve periodontal objectives, for example shallow,

maintainable pockets, and control of inflammation, before initiating
orthodontic treatment. The guidelines (Herrera et al, 2022) indicate that
orthodontic therapy does not significantly impact periodontal outcomes –
such as probing pocket depth and clinical attachment levels, gingival
inflammation, recession, or the risk of root resorption – provided the patient
maintains optimal periodontal health throughout the process.

Orthodontic movements often involve intrusion, retraction, and proper

alignment of teeth. The guidelines suggest that these movements are
unlikely to negatively affect periodontal conditions, gingival inflammation,
or gingival margin levels, and they do not significantly contribute to root
resorption (Papageorgiou et al, 2021). Benefits may include improvements
in the height of interdental papillae and a potential reduction in tooth
mobility. Yet it is stressed that orthodontic treatment should not start until
specific periodontal goals are met – specifically, no sites should have
probing depths of 5 mm or more with BoP, and none should exceed 6 mm
in probing depth (Sanz et al, 2020).

In patients with Stage IV periodontitis, tipped molars often result from

tooth loss and periodontal attachment loss, frequently accompanied by bite
collapse and reduced vertical dimension. In such cases, orthodontic
treatment can help upright the molars and support any necessary restorative
rehabilitation. The treatment guidelines (Herrera et al, 2022) examine
whether these movements could adversely affect the involved teeth in terms
of additional attachment and bone loss, but found insufficient evidence.
Thus, while orthodontic treatment is an option, the results may be
unpredictable.

As well as tilted and drifted teeth, patients with periodontitis may also have
intrabony defects. According to guidelines for treating Stages I–III
periodontitis, these defects should be addressed during step three of
periodontal therapy through surgical regenerative procedures. When
patients undergo orthodontic therapy, tooth movements may occur through
the regenerated tissues. The guidelines suggest that combined orthodontic
treatment can be safely administered to the affected teeth. In fact,
orthodontics is shown to significantly improve periodontal outcomes and
decrease gingival inflammation. There is strong evidence indicating that
both short (one month) and extended (six months) intervals between
periodontal regenerative treatment and orthodontic therapy yield
comparable results, suggesting that a long healing period after regenerative
procedures is unnecessary before starting orthodontics (Kloukos et al, 2021;
Papageorgiou et al, 2021). It is important to note, though, that in terms of
timing the grading is a B, indicating a recommendation rather than a strong
endorsement, due to limitations in the existing studies.

Biomechanics
The application of orthodontic forces leads to immediate changes in the
stress–strain distribution within the periodontal ligament (Kothiwale et al,
2020). This is accompanied by the bending of the alveolar bone, a
phenomenon known as the ‘cone effect’. The cone effect arises when a
force is resolved into horizontal and vertical components upon application
to an inclined plane. Specifically, horizontal forces induce an extrusive
component that, in healthy conditions, is regulated by the supracrestal fibres
(O’Leary et al, 2021). In teeth affected by periodontal disease, where bone
support is compromised, the distribution of stresses and strains occurs over
a reduced surface area. As a result, the resistance provided by the alveolar
crest diminishes, leading to a more pronounced extrusive component. For
patients with periodontitis, who may have already experienced tooth
extrusion, maintaining control over vertical movement is especially vital.

In individuals with diminished periodontal support, the centre of resistance

shifts further apically (Lindhe et al, 2015). This means that any force
applied at the crown level causing tooth movement has a significant
rotational component, making tipping movements easier to achieve. When
tipping occurs, the distribution of stress and strain becomes uneven, with
concentrations peaking at the coronal and apical regions. Elevated force
levels pose a risk of obstructing capillary vessels, leading to hyalinisation,
which is associated with indirect bone resorption and root resorption
(Kothiwale et al, 2020). As such, you should apply light, controlled forces
on these teeth to mitigate risks.

The bone support for periodontally affected teeth is not only reduced in the
vertical dimension but also often in the buccolingual dimension (Lindhe et
al, 2015). This reduction heightens the risk of hyalinisation, which can
cause indirect resorption from the periodontium, ultimately diminishing
vertical height and resulting in irreversible bone damage. For this reason,
you must consider carefully the force levels applied for specific tooth
movements.

Therefore, the biomechanical principles guiding orthodontic tooth

movement in patients with periodontitis, who maintain a healthy but
reduced periodontium, differ from those in healthy patients without
attachment loss. To the greatest extent possible, the activation of the
periodontal ligament must be limited in the teeth targeted for movement.
The force applied should be minimal, and loads should be evenly
distributed, focusing on root-controlled movements.

Fixed or removable?
Orthodontic tooth movements can be performed using either fixed
appliances (such as braces) or removable options (like removable plates and
thermoplastic aligners). In patients with advanced periodontitis who require
orthodontic treatment to improve or maintain periodontal stability, fixed
appliances are generally recommended over removable ones (Watanabe et
al, 2020).

Removable clear aligners are popular due to their aesthetic appeal and ease
of maintaining oral hygiene compared to fixed appliances (Miller et al,
2021). But traditional braces have long been accepted by adults, and there
are now more aesthetically pleasing options available for fixed appliances,
including ceramic brackets and lingual braces.

For patients with Stage IV periodontitis who have a healthy but reduced
periodontium, anchorage can often pose challenges. In these cases, you
could consider skeletal anchorage devices, such as implants or temporary
anchorage devices (TADs) like mini-screws or mini-plates, as potentially
valuable adjuncts to enhance the effectiveness of orthodontic therapy and
improve periodontal outcomes (Diem et al, 2019). While some patients may
experience discomfort with temporary anchorage devices, this has not been
thoroughly investigated in the literature.
Management of complications
Orthodontic appliances can lead to increased microbial colonisation and
biofilm retention, making it essential to implement a comprehensive oral
hygiene and supportive periodontal management protocol throughout the
course of orthodontic treatment. This approach is crucial for maintaining
periodontal health and preventing adverse effects, such as enamel
demineralisation, tooth discolouration, and additional loss of periodontal
support, including the formation of periodontal abscesses and subsequent
bone loss (Keller et al, 2021). Professional biofilm control and other SPC
should be tailored to the patient’s risk profile and clearly communicated
during the consent process (Kumar et al, 2020a).

During orthodontic therapy, you must closely monitor the patient’s

periodontal condition at each appointment. If there are any signs of
periodontal relapse or recurrence, active orthodontic treatment must be
paused. The affected teeth should be maintained passively while the
necessary periodontal treatment is provided and you reinforce a good oral
regime. Once periodontal health and stability have been restored, active
orthodontic therapy can resume (Hassan et al, 2019).

Gingival enlargement is more commonly associated with fixed orthodontic

appliances but can also occur with aligner systems. This enlargement may
impede the completion of orthodontic treatment. If it occurs, it is vital that
you communicate the importance of optimal oral hygiene; you can perform
a gingivectomy if necessary. Typically, if key periodontal parameters
remain stable, the procedure would be carried out after the completion of
orthodontic treatment (García et al, 2020).

As previously noted, orthodontic treatment doesn’t inherently increase the

risk of root resorption in patients with periodontitis. Apical root resorption
is thought to result from a combination of individual biological variability
and mechanical factors. This complication is more common with fixed
appliances compared to removable ones and tends to occur in cases with
longer treatment durations (Keller et al, 2021). Although periodontal factors
don’t seem to influence the likelihood of root resorption, its impact in
periodontitis patients with significant bone loss is an important
consideration from an anchorage perspective. If root resorption is detected
and progresses significantly, orthodontic treatment may need to be halted if
the risks outweigh the benefits. Generally, no specific treatment is required
unless the affected tooth or teeth lose vitality. If increased mobility is
observed, permanent retention through a fixed retainer may be necessary
(Hassan et al, 2019).

Maintenance and retention

Relapse after orthodontic treatment towards pre-treatment positions is
common, particularly in patients with compromised periodontal health. This
relapse can lead to both aesthetic and functional issues, undermining
treatment outcomes and patient satisfaction (Bishara et al, 2018). For this
reason, lifelong SPC and orthodontic retention are crucial after the
completion of orthodontic treatment. These protocols should be tailored
based on the individual patient’s needs and risk factors (Kumar et al,
2020a).

In summary, evidence supports the use of appropriately designed,

permanent fixed passive retainers, which may be used alone or in
conjunction with removable retainers. Even so, fixed retainers can be
susceptible to issues like retention failure, increased plaque accumulation,
and unintentional tooth movements due to distortion of the bonded wire
(Mason et al, 2019). As a result, lifelong supportive measures are crucial to
detect early retainer failures, such as partial debonds, to monitor any
undesired tooth movements, and to assess periodontal stability (Kumar et
al, 2020b). Additionally, consider the option of removable clear retainers
worn at night, for better retention and patient comfort.
15
Pocket Reduction Surgery

In the 1970s and 1980s, research established that non-surgical periodontal

therapy is effective at reducing inflammation in deep periodontal pockets
and improves clinical attachment levels (Caffesse et al, 1986). But even
with diligent efforts, residual biofilm and calculus often remain. As such,
surgical intervention might be necessary in cases where inflammation
persists even after non-surgical treatment (Haffajee and Socransky, 1994).

Historically, periodontal surgery aimed to remove diseased tissue, primarily

by excising diseased gingival tissue and what was thought to be necrotic
bone (Cobb, 1996). Understanding evolved with the recognition that
periodontal disease does not cause bone necrosis; rather, gingival
inflammation and bone loss are a defensive response to bacterial infection
(Nyman et al, 1982). As a result, the focus shifted towards pocket
elimination as the primary goal of periodontal therapy, leading to the
adoption of procedures such as gingivectomy and apically positioned flap
techniques to eliminate pockets and allow access for scaling and improved
oral hygiene (Löe, 1988).

By the 1980s, advancements in our understanding of periodontal biology,

disease pathogenesis, and wound-healing mechanisms led to a re-evaluation
of the need for pocket elimination. The focus shifted again, this time
towards obtaining access to the root surfaces for effective debridement and
creating gingival contours that facilitate effective self-performed biofilm
control (Karnik et al, 1999).
Access flaps, which include various techniques developed over nearly a
century – such as the original Widman flap (1918), the Neumann flap
(1920), the modified flap operation by Kirkland (1931), the apically
repositioned flap described by Friedman (1962), and the modified Widman
flap introduced by Ramfjord and Nissle (1974) – enabled thorough access
to root surfaces, root concavities, and furcations. The choice of surgical
technique in the 1970s and 1980s often reflected the philosophy of different
dental schools. Numerous clinical trials during this period showed that in
patients with excellent oral hygiene, the specific surgical technique
employed to access root surfaces had minimal impact on long-term
outcomes (Socransky et al, 1984). By contrast, patients with poor plaque
control continued to experience attachment loss, regardless of the surgical
method used (Cobb, 1996).

It became evident that successful post-operative plaque control is essential

for maintaining the periodontal environment after surgery. In addition,
patient-related factors, including compliance and smoking, were identified
as crucial influences on periodontal wound healing and overall treatment
outcomes (Tornes et al, 2005).

In recent years, advancements in periodontal surgical techniques have been

helped by the development of innovative instruments and the application of
illumination and magnification. Minimally invasive surgical approaches and
microsurgical techniques are currently under investigation, potentially
offering benefits in terms of wound healing, reduced recession, and
decreased patient morbidity (Sgolastra et al, 2016).

15.1 Key aims and considerations

The three main aims of pocket reduction surgery are to:

1. Allow access and visibility for adequate debridement

2. Establish a favourable dentogingival architecture to support oral
hygiene
 3. Reduce probing depths and possibly restore periodontal apparatus
when there has been attachment loss

Before proceeding with any surgical intervention, it is essential to have

completed at least one but ideally two sessions of non-surgical periodontal
therapy (subgingival PMPR). This initial treatment phase allows for the
elimination of local risk factors and provides an opportunity to evaluate the
patient’s oral hygiene practices and compliance. After non-surgical therapy,
the periodontal tissues typically exhibit reduced inflammation, which
allows better management of the surgical flap. Many periodontal cases can
be effectively managed non-surgically, and so this approach should always
be the first line of treatment (Garg, Ranjan, and Ranjan, 2022).

Engaging the patient in their care is crucial, as optimal biofilm control is

necessary to prevent deterioration of the periodontal condition post-surgery
(Nyman et al, 1977). As discussed earlier, healing outcomes can be
particularly poor in smokers; therefore, surgical interventions are often
postponed in these patients (Scabbia et al, 2001). It is also vital to consider
any systemic conditions or bleeding disorders that may affect surgical
outcomes. Adequate bone support is required for successful surgery, and the
pattern of bone loss will influence the choice of surgical technique, with
procedures typically focused on localised sites (Garg et al, 2022; Aapeng et
al, 2023).

The concept of critical probing depth can guide clinical decision-making in

periodontal therapy (Lindhe et al, 1982). This principle suggests a threshold
probing depth, above which surgical intervention may lead to attachment
gain, and below which the risk of attachment loss increases. Flap surgery is
generally indicated when probing depths exceed 5.4 mm, while non-
surgical options are preferred for depths ranging from 2.9 to 5.4 mm
(Wagner and Gmür, 1993; McGuire and Nunn, 1996). Clinicians often
round this number, commonly considering surgery for probing depths of 6
mm or more (Müller and Heine, 2019).

All surgical procedures typically result in a reduction of probing depths,

with the extent of this reduction being positively correlated with the initial
pocket depth. Although short-term results following surgery show greater
depth reduction compared to non-surgical treatment, long-term outcomes
(five to eight years) can vary significantly (Cortellini et al, 2017).

15.2 Surgical details

Persistence of large probing depths following active periodontal therapy is
associated with an increased probability of tooth loss, so surgery may be
used to address this. Pocket reduction surgery may be resective or
regenerative.

The overall steps in either type of pocket reduction surgery can be

summarised as follows:

1. Flap design/incisions
2. Removal of excised tissues (if resective surgery)
3. Raise flap
4. Debride root surfaces and bony defects
5. Management of bone
6. Check flap apposition and adjust if needed
7. Suturing

Probing after non-surgical treatment can be performed after two months.

For pocket reduction surgery, it’s important to wait three months for a
resective case and six months for a regenerative case. A radiograph should
also be taken for a regenerative case to assess evidence of bony infill.

Various resective surgical techniques exist, and are primarily employed

when there is horizontal bone loss. Once a flap is elevated, procedures such
as osteoplasty or ostectomy may be performed to enhance the bony
architecture, facilitating better tissue adaptation during suturing. In the
anterior regions, a papilla preservation flap (Cortellini and Tonetti, 2005) is
often used to maintain the interdental soft tissue and maximise coverage.
Typically, healing occurs through the formation of a long junctional
epithelium.

Regenerative therapies have been increasingly applied to enhance clinical

outcomes, particularly in areas with intrabony defects, which are associated
with a higher risk of disease progression. The guidelines from the EFP
(Sanz et al, 2020) recommend periodontal regenerative surgery for teeth
showing residual deep pockets of 3 mm or more, particularly where this is
in conjunction with intrabony defects. The benefits of a regenerative
approach include improved aesthetics, a more conservative treatment
strategy, enhanced clinical outcomes, long-term stability, and fewer
complications compared to traditional resective surgeries. However,
regenerative procedures may not be appropriate for every case and can be
sensitive to technique.

Periodontal breakdown results in three types of defects: suprabony

(horizontal), intrabony (vertical), and interradicular (furcation) defects.
Regenerative surgery is indicated for intrabony and interradicular defects,
when deemed suitable. Optimal outcomes are generally observed in deep,
narrow defects with three walls (Trombelli et al, 2013). Significant mobility
can hinder healing, necessitating splinting if mobility is considerable
(Aroca and Mombelli, 2015). Additionally, any compromised endodontic
status should be addressed before proceeding with surgery, as it may affect
outcomes (Vignoletti and Sanz, 2014). For furcation involvement, clinical
improvements can be anticipated in mandibular Grade 2 defects (Greenstein
and Cavallaro, 2006).

Successful regeneration relies on the coordinated development of new

alveolar bone, dental cementum, and a functionally oriented periodontal
ligament that interposes these two tissues. Key facilitators of this process
are site protection, maintenance of space, and stability of the blood clot
(Trombelli et al, 2014).

BONE GRAFTING DEFINITIONS

Osteogenic: New bone formation occurs as a result of bone-

forming cells contained in graft, eg enamel matrix derivative,
 autogenous bone
Osteoinductive: Bone formation induced in surrounding soft
tissue immediately adjacent to grafted material, eg demineralised
freeze-dried bone allograft (DFDBA)
Osteoconductive: Graft material does not directly contribute to
new bone formation but serves as a scaffold for bone formation by
adjacent host bone, eg freeze-dried bone allograft (FDBA), B-TCP
Autografts: Tissues transferred from one part of the body to
another part of the same person
Allogenic: Harvested from genetically distinct individuals within
the same species, eg freeze-dried undermineralised/demineralised
bone allograft
Xenogenic: Harvested from species genetically different from
humans, eg bovine anorganic cancellous bone, Bio-Oss
Alloplastic: Biologic materials that are synthesised or chemically
processed, eg beta tricalcium phosphate, porous hydroxyapatite,
non-porous hydroxyapatite, HTR polymer, bio-active glasses and
ceramics
Guided tissue regeneration (GTR): Attempt to control cells
repopulating site by placing a barrier membrane during wound
healing to prevent epithelial and connective tissue growth

Several materials have been proposed for use with regenerative therapy.
Below are key facts about the main ones used in practice.

Enamel matrix derivative

Product: Emdogain, Straumann.
Gel formation.
Enamel matrix proteins produced by Hertwig’s root sheath have
been shown to support regenerative processes. This purified
 fraction is obtained from the enamel layer of developing porcine
teeth (Stern et al, 2009).
The primary component of these proteins is amelogenin. This is a
hydrophobic protein that comprises over 90% of the total protein
content, along with other proteins such as enamelin and
ameloblastin. Amelogenin acts as a cell-adhesion matrix-bound
protein and is believed to function as an epithelial-mesenchymal
signalling molecule, effectively mimicking the biological events
that take place during root development and promoting
periodontal regeneration (Bartlett et al, 2013).
These proteins play a crucial role in wound healing, enhancing
soft tissue regeneration, and supporting angiogenic activity
(Bichara et al, 2017).
Enamel matrix derivatives significantly affect the behaviour of
various cell types by facilitating processes such as cell
attachment, spreading, proliferation, differentiation, and survival.
They also influence the expression of key transcription factors,
growth factors, cytokines, and other important molecules (Nanci
et al, 2019).

Bio-Oss®
Product produced by Geistlich.
Bovine-derived natural bone substitute.
The osteoconductive characteristics of Bio-Oss contribute to
effective and reliable bone regeneration. The particles of Bio-Oss
integrate seamlessly into the newly formed bone matrix, helping
to maintain volume over an extended period (Schlegel et al,
2015).
 Subsequent application of a Bio-Gide® collagen membrane
enables undisturbed regeneration in the augmented area
(Hämmerle and Trombelli, 2017).

Bio-Gide®
Product produced by Geistlich.
Porcine-derived collagen membrane that is resorbable.
Due to its bilayer structure, the membrane not only prevents the
ingrowth of soft tissue into the augmented site but also acts as a
guide for the appropriate cascade of bone, soft tissue and blood
vessel development (Buser et al, 2015).

Among the various materials employed today, there is currently evidence of

true periodontal regeneration (periodontal ligament, cementum, and bone)
for decalcified freeze-dried bone allograft, demineralised bovine bone
mineral (Bio-Oss), and enamel matrix derivative (Emdogain) (Sanz et al,
2020). By contrast, bioactive glass, hydroxyapatite, and tricalcium
phosphate, although efficient for improving clinical parameters, have
histologically shown limited evidence of regeneration. The regenerative
effect has been demonstrated for platelet-derived factors, but there is
currently no histologic evidence for periodontal regeneration for
autogenous platelet-rich plasma and platelet-rich fibrin.

According to the systematic review by Nibali et al (2019), enamel matrix

derivative in combination with papillary preservation flaps is the treatment
of choice for residual pockets with deep (≥3 mm) intra-bony defects. For
wider defects, consider the addition of demineralised bone matrix.

The surgical techniques used in regenerative therapy have evolved towards

more microsurgical and minimally invasive approaches. These less
traumatic methods enable careful flap preparation and suturing, resulting in
reduced tissue damage. Consequently, this facilitates quicker and more
effective integration of new capillary buds from the recipient site with the
severed vessels of the graft or flap. Employing papillary preservation flaps
has also been shown to improve clinical outcomes and should be seen as a
crucial prerequisite for any regenerative procedure (Huang et al, 2017;
Yamada et al, 2020).
16
Gingival Recession And
Surgery

As well as pocket reduction, there are surgical treatment options for

gingival recession.

Gingival recession refers to the apical displacement of the gingival margin,

which results in the exposure of the tooth root. This condition can adversely
affect aesthetic outcomes and is among the primary reasons patients seek
periodontal treatment. The severity and extent of recession can vary
significantly, and its impact on individuals is case-specific. The
development of gingival recession is not an inevitable consequence of age,
but it is, to a degree, a reflection of some pathological change (Khan et al,
2016).

16.1 Aetiology
The aetiology of gingival recession is multifaceted, often involving both
predisposing and precipitating factors. Predisposing factors heighten a
patient’s risk, while precipitating factors act as triggers for the onset of
recession.

A critical predisposing factor related to soft tissue is the presence of a thin

phenotype. When the probe can be seen shining through the gingival tissue
during probing, this indicates a thin phenotype. Individuals with a thin
phenotype typically have more delicate gingiva compared to those with a
thick phenotype, making them more susceptible to recession (Baker et al,
2018). Other soft-tissue factors include high frenal attachments and shallow
vestibular depths. Hard tissue factors contributing to recession include thin
buccal bone, as well as the presence of dehiscences or fenestrations. The
positioning of teeth within the arch, whether anatomical or because of
orthodontic treatment, along with a mismatch between root size and bone
width, can also influence the likelihood of developing gingival recession.
Finally, a loss of interproximal bone support is a significant contributor to
this condition (Trombelli, 2015).

The two main precipitating factors associated with gingival recession are
trauma and plaque accumulation. One of the most common forms of trauma
is aggressive brushing, typically resulting in buccal recession without loss
of interdental soft tissue. Other forms of trauma include flossing techniques
that may lead to Stillman’s clefts, as well as habits like nail biting or
picking at the gum line. Tongue and lip piercings can contribute to
recession in their respective areas. Trauma can also arise from
malocclusion, such as an overbite that causes injury to the palate or severe
Class II Division 2 malocclusions. Inadequate biofilm control may lead to
inflammation, further exacerbating gingival recession.

As clinicians, it is our responsibility to identify these contributing factors

and manage the modifiable ones, regardless of whether surgical
interventions are necessary. For instance, if aggressive brushing is not
recognised and corrected, any periodontal plastic surgery performed will
likely not yield long-term success (Zhang et al, 2021).

16.2 Classification
Previously, gingival recession was classified using Miller’s classification
(Miller, 1985). The latest classification system (Jepsen et al, 2018) divides
gingival recession into three different recession types (RT), as follows:

RT1: Gingival recession with no loss of interproximal

attachment. Interproximal CEJ is clinically not detectable in either
 mesial or distal aspects of the tooth.
RT2: Gingival recession associated with loss of interproximal
attachment. The amount of interproximal attachment loss is less
than or equal to the buccal attachment.
RT3: Gingival recession associated with loss of interproximal
attachment. The amount of interproximal attachment loss is
higher than the buccal attachment loss.

Further detail can be added on the depth of the recession, gingival

thickness, keratinised tissue width, presence of a detectable CEJ, and the
existence of a root surface concavity.

16.3 Pathogenesis
The mechanism behind trauma-induced gingival recession is fundamentally
different from that in gingival recession caused by bacterial factors. In cases
of trauma-induced recession, the causative agent affects the external
gingival surface, initially leading to gingival abrasion. With ongoing
trauma, the combined effect of direct tissue damage and secondary
inflammatory responses damages the gingival connective tissue, resulting in
the formation of a gingival ulcer. If the damage extends through the full
thickness of the gingival connective tissue, the root dehiscence becomes
exposed. This process, called centripetal, progresses from the exterior
towards the interior.

16.4 Treatment
In all instances, it is essential to address the modifiable aetiological factors.
For example, if excessive brushing is a primary contributing factor,
schedule an appointment specifically aimed at teaching gentle yet effective
home care practices. When surgical intervention is not clearly indicated, or
the patient is hesitant, careful monitoring of the gingival recession becomes
critical. This can be accomplished through regular six-point recession
measurements, along with photographic documentation and scanning,
typically every six to twelve months. Should there be signs of progression,
surgical intervention might then become necessary.

Surgery may be indicated for aesthetic purposes, to augment keratinised

tissue/tissue thickness and prevent progression of the gingival recession.
Decision-making should be based on: patient factors, aesthetic
requirements, need for gingival augmentation, single/multiple defects,
defect anatomy, and need for orthodontics. The following factors will
negatively affect the predictability of root coverage: reduction in level of
interdental support, short papillae height, tooth rotation, tooth extrusion,
large defects, convex root surfaces, flap tension and poor patient
compliance.

Several surgical techniques exist. Pedicle soft-tissue graft procedures

include:

Rotational flap procedures

Laterally sliding flap

Double papilla flap
Oblique rotational flap
Advanced flap procedures

Coronally advanced flap

Semilunar coronally repositioned flap
Regenerative procedures
Tunnelling

Free soft-tissue graft procedures include:

Epithelised graft
Subepithelial connective tissue graft
Free gingival graft
The free gingival graft is often employed to enhance the height of
keratinised tissue, thicken gingival tissue, and deepen the vestibule.
Although root coverage is not consistently achievable, the main aim of this
procedure is to promote periodontal health rather than improve aesthetics.
This results in a more resilient gum tissue (‘tough gum’) that protects the
tooth and makes cleaning more comfortable, thereby minimising the risk of
further recession. The graft material is harvested from the patient’s palate.

Coronally advanced flap

The coronally advanced flap is a pedicle soft-tissue graft procedure based
on a coronal shift of the soft tissues on the exposed root surface. It is the
treatment of choice for isolated recession defects. The most recent version
of this technique uses a trapezoidal flap design and a split–full–split-
thickness flap elevation approach (Cortellini and Bissada, 2018). The split
or partial thickness elevation at the level of the surgical papilla provides
anchorage and blood supply to the interproximal areas, as well as
improving blending in terms of colour and thickness (Cairo et al, 2018).
The full-thickness elevation of the soft tissue apical to the root exposure
confers the maximum flap thickness and, thus, creates a better opportunity
to achieve root coverage to the portion of the flap residing over the exposed
avascular root surface. The more apical split-thickness flap elevation
facilitates the coronal displacement of the flap (Tonetti and Jepsen, 2014).

There is extensive evidence supporting the use of root coverage procedures

in the treatment of localised gingival recession defects, but few studies
reporting the outcomes for the treatment of multiple gingival recessions.
The coronally advanced flap for multiple recession defects was introduced
by Zucchelli and De Sanctis (2000) as a novel approach to treat more than
two adjacent teeth with gingival recession. This technique comprises an
envelope type of flap (with no vertical releasing incisions) that anticipates
the rotational movement of the surgical papillae during the coronal
advancement of the flap (Cortellini and Bissada, 2018). When there are
multiple recession defects in one area, it is best to treat them all with one
procedure rather than focusing on the deepest defect alone. Coronally
advanced flaps are often used in conjunction with a connective tissue graft
sandwiched underneath. This is common when there is a lack of keratinised
tissue, or the flap is thin (Baldi et al, 1999). Covering the graft increases the
blood supply, and the aesthetic outcome is improved by hiding the white-
scar appearance of the grafted tissue.

Alternative materials to the palatal connective tissue graft are available but
these are likely to be less predictable (Tinti et al, 1992). Treatment of
multiple recession defects with coronally advanced flaps with or without
connective tissue grafts can have a considerable impact on periodontal and
overall smile aesthetics. Often, a combined restorative approach is required
in cases of abrasive tooth wear.

Other
In the ’90s, the tunnel procedure for root coverage was introduced (Allen,
1994). The unique feature of this procedure is that the interdental papillae
are left intact. A connective tissue graft is placed in the tunnel, and it does
not need to be completely covered if the dimension of the graft is sufficient
to ensure graft survival. The main proposed benefit of the technique is the
minimally invasive nature of the surgery. Recently, the tunnel technique
was modified to include coronal positioning of the marginal tissue, which
allows complete coverage of the graft.

Currently, there is a lack of good-quality evidence for other procedures,

such as the ‘pinhole’ surgical technique.

Healing
Tissue graft procedures are best suited to those with good bone levels and
interdental support. Healing for these types of surgery involves a mix of
repair and regeneration. Shallow probing depths occur. The surgical results
are likely to last sufficiently (enough to not have to repeat the surgery),
provided the aetiological factors have been addressed (Tonetti and Jepsen,
2014).
17
Crown-Lengthening Surgery

Another type of surgical treatment under the periodontal umbrella is crown

lengthening, commonly referred to by patients as a ‘gum lift’. This aims to
resolve gingival excess and might be offered for either aesthetic or
functional reasons.

17.1 Definition and indications

Crown lengthening has been described by Cohen et al (2007) as the surgical
removal of hard and soft periodontal tissue to gain supragingival tooth
length, allowing for longer clinical crowns and the re-establishment of the
biologic width. The term biologic width is no longer used, replaced by
‘supracrestal tissue attachment’ in the updated periodontal classification
(Jepsen et al, 2018). This encompasses the junctional epithelium and
supracrestal connective tissue. According to Garguilo, Wentz, and Orban
(1961), this should be approximately 2 mm. If the supracrestal tissue
attachment is not respected or recreated, this will result in the unwanted
consequences of gingival inflammation, pocketing recession, and/or bone
loss.
 The supracrestal tissue attachment is made up of the junctional
epithelium and supracrestal connective tissue

Crown-lengthening procedures are divided into two main categories:

aesthetic and restorative/functional. Aesthetic crown lengthening aims to
address issues such as excessive gingival display, short clinical crowns, and
uneven gingival contours. On the other hand, restorative or functional
crown lengthening is necessary when there is insufficient sound tooth
structure available for restoration, to gain access to subgingival fractures,
caries, or perforations, or to reposition crown margins that infringe upon the
supracrestal tissue attachment.

17.2 Ideal ‘pink’ aesthetics

A smile is generally described as ‘pleasant’ when it exposes all of the
maxillary teeth along with approximately 1 mm of facial gingiva. Gingival
exposure of up to 2–3 mm is normally found acceptable, whereas patients
are usually dissatisfied with any greater exposure (> 3 mm) (Garber and
Salama, 1996). Patients with a high smile line who expose a large band of
gingiva may be classified as having a ‘gummy’ smile.

The ideal gingival architecture consists of several features:

Gingival zenith position: The gingival zenith refers to the lowest

point of the gingival contour. According to Chu et al (2009), the
gingival zeniths for maxillary central incisors should ideally be
positioned about 1 mm distal to the crown’s midline. For lateral
incisors, the zenith should be approximately 0.4 mm distal, while
the zenith for canines is typically aligned centrally along the long
axis.
Relative gingival margins: In terms of apico-coronal positioning,
the zeniths of the lateral incisors should be positioned 1 mm
coronal to those of the central incisors and canines.
The gingival aesthetic line: This is the line connecting the
tangents of the zeniths of the central incisors and canines. The
angle formed at the intersection of this line with the maxillary
dental midline is referred to as the gingival aesthetic line angle,
with the ideal angle ranging between 45 to 90 degrees. Achieving
gingival symmetry between the right and left sides of the mouth is
also a key aesthetic consideration.

Lastly, it is important to take into account the ideal height-to-width ratios

for teeth: the central incisor should be at 80%, the lateral incisor at 70%,
and the canine at 75% (Gargiulo et al, 2006).

17.3 Causes of gingival excess

Before considering crown lengthening, a proper diagnosis is essential. The
latest classification scheme categorises gingival excess under mucogingival
deformities and conditions, encompassing various anatomical factors (Cairo
et al, 2018). Several causes can contribute to this condition, either
individually or in combination. The most prevalent factors include altered
passive eruption, dentoalveolar extrusion due to tooth wear, vertical
maxillary excess, and a short or hypermobile upper lip (Cortellini and
Bissada, 2018).

Identifying the specific cause(s) is crucial since not all cases are appropriate
for aesthetic crown-lengthening procedures. For instance, vertical maxillary
excess may necessitate maxillofacial surgery for resolution, while a
hypermobile lip could benefit from interventions such as botulinum toxin
injections or lip-repositioning surgery (Cairo et al, 2018).

Altered passive eruption is one of the conditions most frequently addressed

through aesthetic crown lengthening. This condition is relatively common,
affecting approximately 35% of the population (Cairo et al, 2018). The
process begins after the complete eruption of the tooth’s anatomical crown
and is characterised by the apical migration of the dentogingival junction.
As the epithelial attachment moves apically, the length of the clinical crown
increases until the junction reaches a physiological distance of 0.5–2.0 mm
coronal to the cementoenamel junction (CEJ). If the dentogingival junction
does not retract adequately during this passive phase, it results in altered or
delayed passive eruption (Goldman and Cohen, 1971).

Coslet, Vanarsdall, and Weisgold (1977) proposed a classification system

based on the relationship between the gingiva and the underlying alveolar
bone. Evaluating the position of the gingival margin in relation to the CEJ
and buccal bone crest, along with the relationships between the crown, root,
and alveolar crest, is essential to determine whether the observed gingival
excess, or ‘gummy’ smile, is due to altered passive eruption.

17.4 Treatment sequence

With crown lengthening, the planning phase is the most important.
Understanding key factors, such as where the reference point is and the
amount of bone removal required, is critical. The surgery itself may include
both soft and hard tissue adjustment. It’s also imperative that you
understand the restorative phase in terms of when and where you can
provisionalise and definitively restore, if required.

The treatment sequence for crown lengthening typically consists of three

stages:

1. Planning
2. The surgery itself
3. Further restorative treatment

Planning
The planning stage for aesthetic crown lengthening plays a vital role in
achieving a successful long-term outcome and aligning with patient
expectations. Initially, it is essential to establish or maintain periodontal
health and effective plaque control prior to the procedure. If a patient has
been diagnosed with gingivitis or periodontitis through a comprehensive
periodontal assessment, these conditions must be addressed before
proceeding. Additionally, local factors such as the crown-to-root ratio,
furcation entrance level, root proximity, and the tooth’s endodontic
condition should be evaluated and any necessary endodontic treatment
should be completed prior to crown lengthening.

Next, it is crucial to identify the reference point or finish line for the
procedure. In cases of altered passive eruption, the CEJ is typically used as
the reference point, but it can also be based on existing or provisional
restorations or guided by a surgical stent. For aesthetic cases, understanding
the principles of ‘pink’ aesthetics and assessing the current gingival
architecture will help you to determine the extent of crown lengthening
required for the relevant teeth. Considering facial symmetry, such as the
interpupillary line, can provide you with further insight.

The extent of crown lengthening may also depend on the restorative

treatment plan. Discussing with the patient their aesthetic expectations will
allow you to ensure that these are realistic before surgery. Visual aids like
annotated photographs, in-mouth composite mock-ups, and wax-ups can
assist in this process, along with digital smile design. Cone-beam computed
tomography (CBCT) scans can also be beneficial for diagnostic purposes,
although currently they are not commonly used solely for crown-
lengthening treatment planning.

Assessing the amount of keratinised tissue is critical, as it will inform the

surgical approach, whether resective, apically positioned, or a combination
of both. Ideally, at least 2 mm of keratinised tissue should remain after
surgery – which is more comfortable compared to having only lining
mucosa – to help the patient maintain optimal plaque control.

The position of the bone and the distance from the bone level to the
reference point will dictate whether any bone removal is necessary. The
supracrestal tissue attachment should ideally be about 2 mm, so when
considering the depth of the gingival sulcus, there should be approximately
3 mm between the reference point and the bone level. If this measurement
is already met, bone removal is not required; otherwise, it must be
performed to prevent invasion of the supracrestal tissue attachment and its
related negative effects. High-quality periapical radiographs and bone-
sounding techniques will aid you in assessing the bone position. You can
also use gutta-percha points alongside radiographs to obtain valuable
information regarding the clinical and anatomical crown height relative to
the bone level. In many cases, raising a flap will help to definitively
determine the bone level and its architecture.

The surgery
The procedure used for aesthetic crown lengthening typically involves
elevating only a buccal flap and necessitates the exclusive removal of
buccal bone. By contrast, restorative or functional crown lengthening
requires the elevation of both buccal and palatal/lingual flaps, as bone
removal is generally required on all surfaces. Initially, bleeding points are
managed, followed by a superficial scoring incision in the epithelium. Once
you are satisfied with the initial incision, make a full-thickness incision. To
minimise the risk of developing ‘black triangles’, the interproximal tissue
can be thinned instead of fully reflected or preserved by excluding it from
the flap design. Vertical incisions are typically avoided to reduce the
potential for scarring. You can use a 15c blade or a laser for the incisions,
depending on preference.

If bone removal, particularly ostectomy, is necessary, the objective is to

eliminate sufficient bone to re-establish the supracrestal tissue attachment.
Additionally, it is essential to create a gradual contour of the osseous crest
to restore positive architecture, which may also require osteoplasty. Any
visible bony exostoses that become apparent during smiling should also be
addressed through osteoplasty. Bone removal can be carried out using a
suitable anti-retraction micromotor or piezoelectric handpieces/burs,
potentially supplemented with hand chisels or curettes.

The suturing technique typically employed is either single interrupted or

mattress sutures. In aesthetic cases where eversion of the gingival tissue is
necessary (to prevent black triangles), an internal mattress suture is ideal. If
the papilla is wide or a diastema is present, a horizontal internal mattress
suture is preferred; for narrow papillae, a vertical internal mattress suture is
more appropriate. Fine sutures, such as 5–0 or 6–0, promote optimal
healing. The choice of suture material ultimately depends on your
preference.

Unlike restorative or functional crown lengthening, periodontal dressings

are not utilised in aesthetic crown-lengthening cases. Sutures are typically
removed about two weeks after the surgical procedure. Advise the patient to
take regular analgesics as needed, maintain a soft diet for four to five days,
and use an antiseptic mouth rinse while avoiding brushing the surgical site
for two weeks. In cases of altered passive eruption, only the crown of the
tooth is usually exposed, while in other situations, particularly restorative
cases, some root exposure may occur. Sensitivity is generally not a concern,
so no additional measures are typically necessary during the two-week
recovery period.

Further restorative treatment

In cases of altered passive eruption, restorative work after surgery is not
always necessary unless the patient has a specific desire to enhance the
aesthetics of the tooth. When crown lengthening has been performed for
other restorative purposes, such as addressing tooth wear due to
dentoalveolar extrusion, a subsequent restorative phase is generally
anticipated. Provisional restorations can be placed after the removal of
sutures; however, for teeth located in the aesthetic zone, it may be prudent
to delay definitive restorations for around six months, as the position of the
gingival crest may continue to evolve during this time. Consequently, lab-
fabricated provisional restorations are frequently utilised during this interim
period. For other restorative cases, waiting about three months before
proceeding with definitive restorations may be advisable.

Coronal displacement of the gingival margin tends to be more significant in

individuals with thick gingival phenotypes, but it is essential to obtain
informed consent from the patient regarding the possibility of revision
surgery. Typically, if revision is needed and the bone level is appropriately
positioned, a gingivectomy may suffice.
Conclusion

As we reach the conclusion of this comprehensive guide to modern

periodontics, I hope you feel armed with a robust foundation in the essential
concepts and practices that define this vital field. Throughout this book, I
have aimed to provide a clear, concise, and practical resource that enhances
your ability to deliver exceptional periodontal care.

By delving into the foundations of periodontal disease, mastering the art of

assessment and diagnosis, and exploring a wide range of treatment
strategies, you should now be well-equipped to address the myriad
challenges that may arise in your professional practice. The advanced topics
covered in the final sections ensure that you are well-versed in the latest
developments and techniques and can confidently handle even the most
complex cases.

My goal has been to empower you with knowledge and tools that will
translate directly into improved patient outcomes. Whether you are
integrating new techniques into your routine, managing a periodontal
emergency, or planning a surgical intervention, this guide is designed to
support you every step of the way.

Thank you for choosing this book as your trusted companion in your
professional journey. It will serve as a valuable reference, continually aiding
you in providing the highest standard of care to your patients. As you apply
these insights and techniques, may you find both professional fulfilment
and success in your ongoing commitment to excellence in periodontics.
References

The Periodontium And Beyond

Chapple, ILC, ‘Time to take periodontitis seriously', British Medical
Journal, 348 (2014), 2645
Chapple, ILC and Genco, R, ‘Diabetes and periodontal diseases:
consensus report of the Joint EFP/ AAP Workshop on Periodontitis
and Systemic Diseases’, Journal of Clinical Periodontology, 40/Suppl
14 (2013), S106–S112
GBD 2017 Disease and Injury Incidence and Prevalence
Collaborators, ‘Global, regional, and national incidence, prevalence,
and years lived with disability for 354 diseases and injuries for 195
countries and territories, 1990–2017: A systematic analysis for the
Global Burden of Disease Study 2017’, Lancet, 392, 10159 (2018),
1789–1858
Grossi, SG et al, ‘Assessment of risk for periodontal disease. I. Risk
indicators for attachment loss’, Journal of Periodontology, 65 (1994),
260–267
Hirschfeld, J and Chapple, ILC, Periodontitis and Systemic Diseases
(Quintessence Publishing, 2021)
Jakubovics, NS et al, ‘The dental plaque biofilm matrix’,
Periodontology 2000, 86/1 (2021), 32–56
Kassebaum, NJ et al, ‘Global burden of severe periodontitis in 1990–
2010: A systematic review and meta-regression’, Journal of Dental
Research, 93 (2014), 1045–1053
Lang, N and Lindhe, J, Clinical Periodontology and Implant Dentistry,
6th edition (Wiley Blackwell, 2015)
Preshaw, PM and Bissett, SM, ‘Periodontitis and diabetes’, British
Dental Journal, 227 (2019), 577–584
Simpson, TC et al, ‘Treatment of periodontal disease for glycaemic
control in people with diabetes’, Cochrane Database of Systematic
Reviews, 12/5 (2010), CD004714
Van Dyke, TE et al, ‘The nexus between periodontal inflammation
and dysbiosis’, Frontiers in Immunology, Mar 31/11 (2020), 511

Think Like A Detective

Ah, MK, Johnson, GK, Kaldahl, WB, Patil, KD, and Kalkwarf, KL,
‘The effect of smoking on the response to periodontal therapy’,
Journal of Clinical Periodontology, 21 (1994), 91–97
Action on Smoking and Health (ASH), ‘Use of e-cigarettes (vapes)
among adults in Great Britain’ (ASH, 2023),
https://ash.org.uk/uploads/Use-of-e-cigarettes-among-adults-in-
Great-Britain-2023.pdf, accessed 19 July 2024
Bergstrom, J and Bostrom, L, ‘Tobacco smoking and periodontal
hemorrhagic responsiveness’, Journal of Clinical Periodontology, 28
(2001), 680–685
Bostrom, L, Linder, LE, and Bergstrom, J, ‘Influence of smoking on
the outcome of periodontal surgery: A 5-year follow-up’, Journal of
Clinical Periodontology, 25 (1998), 194–201
Chapple, ILC and Genco, R, ‘Diabetes and periodontal diseases:
consensus report of the Joint EFP/ AAP Workshop on Periodontitis
and Systemic Diseases’, Journal of Clinical Periodontology, 40/Suppl
14 (2013), S106–S112
European Federation of Periodontology, ‘Oral health and pregnancy
– key messages for oral-health professionals’ (EFP),
www.efp.org/fileadmin/uploads/efp/Documents/Campaigns/Oral_Hea
lth_and_Pregnancy/Brochures/key-messages-dental.pdf, accessed
19 July 2024
Holliday, R et al, ‘Electronic cigarettes and oral health’, Journal of
Dental Research, 100/9 (2021), 906–913
Hugoson, A, Ljungquist, B, and Breivik, T, ‘The relationship of some
negative events and psychological factors to periodontal disease in
an adult Swedish population 50 to 80 years of age’, Journal of
Clinical Periodontology, 29 (2002), 247–253
International Diabetes Federation, ‘Facts and figures’ (IDF, 2021),
https://idf.org/about-diabetes/diabetes-facts-figures, accessed 7 July
2024
Michalowicz, BS et al, ‘Evidence of a substantial genetic basis for
risk of adult periodontitis’, Journal of Clinical Periodontology, 71
(2000), 1699–1707
Raindi, D, ‘Nutrition and periodontal disease’, Dental Update, 43/1
(2016), 66-8
Ramseier, CA et al, ‘Impact of risk factor control interventions for
smoking cessation and promotion of healthy lifestyles in patients with
periodontitis: A systematic review’, Journal of Clinical
Periodontology, 47 (2020), S22(90–106)
Ryder, MI et al, ‘Alterations of neutrophil oxidative burst by in vitro
smoke exposure: implications for oral and systemic disease’, Annals
of Periodontology, 3 (1998), 76–97
Simpson, TC et al, ‘Treatment of periodontal disease for glycaemic
control in people with diabetes’, Cochrane Database of Systematic
Reviews, 5 (2010), CD004714
Tomar, SL and Asma, S, ‘Smoking-attributable periodontitis in the
United States: Findings from NHANES III. National Health and
Nutrition Examination Survey’, Journal of Periodontology, 71 (2000),
743–751
Van Dyke, TE and Dave, S, ‘Risk factors for periodontitis’, Journal of
the International Academy of Periodontology, 7/1 (2005), 3–7
Wimmer, G, Janda, M, Wieselmann-Penkner, K, Jakse, N, Polansky,
R, and Pertl, C, ‘Coping with stress: Its influence on periodontal
disease’, Journal of Periodontology, 73 (2002), 1343–1351
Woelber, JP et al, ‘An oral health optimised diet can reduce gingival
and periodontal inflammation in humans: A randomised controlled
pilot study’, BMC Oral Health, 17 (2017), 28
Zoheir, N and Hughes, FJ, ‘The management of drug-influenced
gingival enlargement’, Primary Dental Journal, 8/4 (2020), 34–39

Clinical Examination
Ainamo, J and Bay, I, ‘Problems and proposals for recording
gingivitis and plaque’, International Dental Journal, 25/4 (1975), 229–
35
BSP, ‘BPE guidelines’ (BSP, 2019),
www.bsperio.org.uk/assets/downloads/BSP_BPE_Guidelines_2019.
pdf, accessed June 2024
Hamp, SE et al, ‘Periodontal treatment of multirooted teeth: Results
after 5 years’, Journal of Clinical Periodontology, 2/3 (1975), 126–35
Miller, SC, Textbook of Periodontia (Blakiston Co, 1950)
O’Leary et al, ‘The plaque control record’, Journal of Periodontology,
43/1 (1972), 38

Diagnosis
Berglundh, T et al, ‘Peri-implant diseases and conditions: Consensus
report of workgroup 4 of the 2017 World Workshop on the
Classification of Periodontal and Peri-Implant Diseases and
Conditions’, Journal of Clinical Periodontology, 45/Suppl 20 (2018),
S286–S291
Caton, JG et al, ‘A new classification scheme for periodontal and
peri-implant diseases and conditions: Introduction and key changes
from the 1999 classification’, Journal of Clinical Periodontology,
45/Suppl 20 (2018), S1–S8
Chapple, ILC et al, ‘Periodontal health and gingival diseases and
conditions on an intact and a reduced periodontium. Consensus
report of workgroup 1 of the 2017 World Workshop on the
Classification of Periodontal and Peri-Implant Diseases and
Conditions’, Journal of Clinical Periodontology, 45/Suppl 20 (2018),
S68–77
Dietrich, T et al, ‘Periodontal diagnosis in the context of the 2017
classification system of periodontal diseases and conditions:
Implementation in clinical practice’, British Dental Journal, 226/1
(2019), 16–22
Jepsen, S et al, ‘Periodontal manifestations of systemic diseases
and developmental and acquired conditions: Consensus report of
workgroup 3 of the 2017 World Workshop on the Classification of
Periodontal and Peri-Implant Diseases and Conditions’, Journal of
Clinical Periodontology, 45/Suppl 20 (2018), S219–S229
Papapanou, PN et al, ‘Periodontitis: Consensus report of workgroup
2 of the 2017 World Workshop on the Classification of Periodontal
and Peri-Implant Diseases and Conditions’, Journal of Clinical
Periodontology, 45/Suppl 20 (2018), S162–S170

Prognosis
Mordohai, N et al, ‘Factors that affect individual tooth prognosis and
choices in contemporary treatment planning’, British Dental Journal,
202/2 (2007), 63–72
Nibali, L et al, ‘A retrospective study on periodontal disease
progression in private practice’, Journal of Clinical Periodontology,
44/3 (2016), 290–297

Treatment Planning
BSP, ‘BSP guidelines for patient referral’ (BSP, 2020),
www.bsperio.org.uk/assets/downloads/BSP_Guidelines_for_Patient_
Referral_2020.pdf, accessed June 2024
Herrera, D et al, ‘Treatment of stage IV periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
49/S24 (2022), 4–71
Sanz, M et al, ‘Treatment of stage I–III periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
47/S22 (2020), 4–60
West, N et al, ‘BSP implementation of European S3-level evidence-
based treatment guidelines for stage I–III periodontitis in UK clinical
practice’, Journal of Dentistry, 106 (2021), 103562

Educating And Empowering Patients

Michie, S, Van Stralen, MM, and West, R, ‘The behaviour change
wheel: A new method for characterising and designing behaviour
change interventions’, Implementation Science, 6/1 (2011), 1–12
Sanz, M et al, ‘Treatment of stage I–III periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
47/S22 (2020), 4–60
Scottish Dental Effectiveness Programme – Oral Hygiene TIPPS
(SDCEP), www.periodontalcare.sdcep.org.uk/supporting-tools/oral-
hygiene-tipps, accessed 27 July 2024
Slot, DE, Valkenburg, C, and Van der Weijden, F, ‘Mechanical plaque
removal of periodontal maintenance patients: A systematic review
and network meta-analysis’, Journal of Clinical Periodontology,
47/Suppl 22 (2020), 107–124
Tonetti, MS et al, ‘Principles in prevention of periodontal diseases:
Consensus report of group 1 of the 11th European Workshop on
Periodontology on effective prevention of periodontal and peri-
implant diseases’, Journal of Clinical Periodontology, 42/S16 (2015),
S5–11
Yaacob, M et al, ‘Powered versus manual toothbrushing for oral
health’, Cochrane Database of Systematic Reviews, 6 (2014),
CD002281

Non-Surgical Periodontal Therapy

Badersten, A et al, ‘Effect of nonsurgical periodontal therapy. I.
Moderately advanced periodontitis’, Journal of Clinical
Periodontology, 8 (1981), 57–72
Cobb, CM, ‘Non-surgical pocket therapy: Mechanical’, Annals of
Periodontology, 1 (1996), 443–490
Da Costa, LFNP et al, ‘Chlorhexidine mouthwash as an adjunct to
mechanical therapy in chronic periodontitis: A meta-analysis’,
Journal of the American Dental Association, 148/5 (2017), 308–318
Drisko, CH, ‘Root instrumentation: Power-driven versus manual
scalers, which one?’, Dental Clinics of North America, 42 (1998),
229–244
Graziani, F et al, ‘Acute-phase response following full-mouth versus
quadrant non-surgical periodontal treatment: A randomised clinical
trial’, Journal of Clinical Periodontology, 42/9 (2015), 843–852
Graziani, F et al, ‘Acute-phase response following one-stage full-
mouth versus quadrant non-surgical periodontal treatment in
subjects with comorbid type 2 diabetes: A randomised clinical trial’,
Journal of Clinical Periodontology, 50/4 (2023), 487–499
Herrera, D et al, ‘Adjunctive effect of locally delivered antimicrobials
in periodontitis therapy: A systematic review and meta-analysis’,
Journal of Clinical Periodontology, 47 (2020), 239–256
Loos, B et al, ‘An evaluation of basic periodontal therapy using sonic
and ultrasonic scaler’, Journal of Clinical Periodontology, 14 (1987)
29–33
Mehta, J et al, ‘Minimally invasive non-surgical periodontal therapy of
intrabony defects: A prospective multi-centre cohort study’, Journal
of Clinical Periodontology, 51/7 (2024), 905–914
Nibali, L et al, ‘Minimally invasive non-surgical vs surgical approach
for periodontal intrabony defects: A randomised controlled trial’,
Trials, 20/1 (2019), 461
Sanz, M et al, ‘Treatment of stage I–III periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
47/S22 (2020), 4–60
Suvan, J et al, ‘Subgingival instrumentation for treatment of
periodontitis: A systematic review’, Journal of Clinical
Periodontology, 47/Suppl 22 (2020), 155–175
Tomasi, C et al, ‘A randomised multi-centre study on the
effectiveness of non-surgical periodontal therapy in general practice’,
Journal of Clinical Periodontology, 49/11 (2022), 1092–1105

Periodontal Challenges

Occlusal trauma and splinting

Cortellini, P et al, ‘The simplified papilla preservation flap in the
regenerative treatment of deep intrabony defects: Clinical outcomes
and postoperative morbidity’, Journal of Periodontology, 72/12
(2001), 1702–1712
Fan, J and Caton, JG, ‘Occlusal trauma and excessive occlusal
forces: Narrative review, case definitions and diagnostic
considerations’, Journal of Periodontology, 89/S1 (2018), S214–
S222
Ferencz, J, ‘Splinting’, Dental Clinics of North America, 313 (1987),
383–393
Hirschfield, I, ‘The individual missing tooth: A factor in dental and
periodontal disease’, Journal of the American Dental Association, 24
(1937), 67–82
Jepsen, S et al, ‘Periodontal manifestations of systemic diseases
and developmental and acquired conditions: Consensus report of
workgroup 3 of the 2017 World Workshop on the Classification of
Periodontal and Peri-Implant Diseases and Conditions’, Journal of
Clinical Periodontology, 45/Suppl 20 (2018), S219–S229
Nyman, SR and Lang, NP, ‘Tooth mobility and the biologic rationale
for splinting teeth’, Periodontology 2000, 4 (1994), 15–22
Passanezi, E and Sant’Ana, ACP, ‘Role of occlusion in periodontal
disease’, Periodontology 2000, 79 (2019), 129–150

Furcations
American Academy of Periodontology, Glossary of Periodontal
Terms, 4th edition (American Academy of Periodontology, 2001),
https://members.perio.org/libraries/glossary, accessed 1 August
2024
Hughes, FJ, Clinical Problem Solving in Periodontology and
Implantology, 1st edition (Churchill Livingstone Elsevier, 2013)
Jepsen, S et al, ‘Regenerative surgical treatment of furcation
defects: A systematic review and Bayesian network meta-analysis of
randomised clinical trials’, Journal of Clinical Periodontology, 47/S22
(2020), 352–374

Dentine hypersensitivity
Holland, GR et al, ‘Guidelines for the design and conduct of clinical
trials on dentine hypersensitivity’, Journal of Clinical Periodontology,
24 (1997), 808–813
West, NX et al, ‘Prevalence of dentine hypersensitivity and study of
associated factors: A European population-based cross-sectional
study’, Journal of Dentistry, 41 (2013), 841–851
West, N et al, ‘Management of dentine hypersensitivity: Efficacy of
professionally and self-administered agents’, Journal of Clinical
Periodontology, 42/S16 (2015), S256–S302.
Halitosis
Eli, I et al, ‘Attribution of bad breath to halitosis and its impact on
social interactions’, Journal of Dental Research, 80/8 (2001), 2083–
2086
Friedman, M et al, ‘Management of halitosis’, Dental Clinics of North
America, 59/1 (2015), 159–178
Greenman, J et al, ‘The science of bad breath: Overview of causes
and treatments’, Journal of Dental Research, 84/7 (2005), 606–614
Kumar, P et al, ‘Halitosis: A review’, International Journal of Oral
Health Sciences, 4/1 (2014), 22–26
Miller, D and Dyer, J, ‘Halitosis: An overview’, Dental Clinics of North
America, 55/4 (2011), 771–782
Outhouse, TL et al, ‘Tongue scraping for treating halitosis’, Cochrane
Database of Systematic Reviews, 19/2 (2006), CD005519
Roldán, S et al, ‘The role of tongue coating in halitosis’, BMC Oral
Health, 13 (2013), 23
Rosenberg, M et al, ‘Halitosis: A review of the literature’, Journal of
Clinical Dentistry, 17/1 (2006), 8-12
Sanz, M et al, ‘Effect of professional mechanical plaque removal on
secondary prevention of periodontitis and the complications of
gingival and periodontal preventive measures: Consensus report of
group 4 of the 11th European workshop on periodontology on
effective prevention of periodontal and peri-implant diseases’,
Journal of Clinical Periodontology, 42/Suppl 16 (2015), S214–S220
Scully, C et al, ‘Halitosis (bad breath): A review’, Oral Diseases, 7/6
(2001), 230–233
Slot, DE et al, ‘Management of oral mal-odour. Efficacy of
mechanical and/or chemical agents: A systematic review’, Journal of
Clinical Periodontology, 42/16 (2015), S303–16
Van Dorsten, FA and Van der Weijden, GA, ‘Prevalence of halitosis:
A review of the literature’, Journal of Clinical Periodontology, 34/6
(2007), 415–422
Yoshida, Y et al, ‘Clinical evaluation of halitosis: An organoleptic
approach’, Journal of Oral Rehabilitation, 41/1 (2014), 70–76

Periodontal Emergencies And Their

American Academy of Periodontology, ‘Parameter on acute
periodontal diseases, parameters of care (supplement)’, Journal of
Periodontology, 71 (2000), 863–866
Creath, CJ et al, ‘A case report: Gingival swelling due to a fingernail-
biting habit’, Journal of the American Dental Association, 126 (1995),
1019–1021
De Bruyne, MA et al, ‘Necrosis of the gingiva caused by calcium
hydroxide: A case report’, International Endodontic Journal, 33
(2000), 67–71
Dello Russo, NM, ‘The post-prophylaxis periodontal abscess:
Etiology and treatment’, International Journal of Periodontics &
Restorative Dentistry, 1985; 5 (1985), 28–37
Fine, DH, ‘Microbial identification and antibiotic sensitivity testing, an
aid for patients refractory to periodontal therapy: A report of 3 cases’,
Journal of Clinical Periodontology, 21 (1994), 98–106
Garrett, S et al, ‘Comparison of a bioabsorbable GTR barrier to a
non-absorbable barrier in treating human class II furcation defects. A
multi-center parallel design randomised single-blind trial’, Journal of
Periodontology, 68 (1997), 667–675
Gillette, WB and Van House, RL, ‘Ill effects of improper oral hygiene
procedure’, Journal of the American Dentistry Association, 101
(1980), 476
Helovuo, H et al, ‘Changes in the prevalence of subgingival enteric
rods, staphylococci and yeasts after treatment with penicillin and
erythromycin’, Oral Microbiology and Immunology, 8 (1993), 75–79
Herrera, D et al, ‘The periodontal abscess (I): Clinical and
microbiological findings’, Journal of Clinical Periodontology, 27
(2000), 387–394
Herrera, D et al, ‘Acute periodontal lesions’, Periodontology 2000, 65
(2014), 149–177
Krejci, CB, ‘Self-inflicted gingival injury due to habitual fingernail
biting’, Journal of Periodontology, 71 (2000), 1029–1031
Loesche, WJ et al, ‘The bacteriology of acute necrotising ulcerative
gingivitis’, Journal of Periodontology, 53 (1982), 223–30
Sapir, S and Bimstein, E, ‘Cholinsalicylate gel induced oral lesion:
Report of case’, Journal of Clinical Paediatric Dentistry, 24 (2000),
103–106

Supportive Periodontal Care

Cortellini, P and Tonetti, MS, ‘Periodontal risk assessment in clinical
practice: A review’, International Journal of Periodontics and
Restorative Dentistry, 25/4 (2005), 397–404
Genco, R et al, ‘Relationship of stress, distress, and inadequate
coping behaviors to periodontal disease’, Journal of Periodontology,
70/7 (1999), 711–723
Heasman, L et al, ‘The effect of smoking on periodontal treatment
response: A review of clinical evidence’, Journal of Clinical
Periodontology, 33/4 (2006): 241–253
Kornman, KS et al, ‘The interleukin-1 genotype as a severity factor in
adult periodontal disease’, Journal of Clinical Periodontology, 24/1
(1997), 72–77
Löe, H, ‘Periodontal disease: The sixth complication of diabetes
mellitus’, Diabetes Care, 16/1 (1993), 329–334
Mavridis, I and Mavridis, K, ‘The significance of tooth type and
periodontal maintenance in the prognosis of multi-rooted teeth’,
Journal of Periodontology, 89/11 (2018), 1346–1355
Meyer, DH and Lewis, RA, ‘Assessing periodontal disease risk: An
evaluation of the DEPPA tool’, Journal of Periodontal Research, 53/5
(2018), 683–689
Rosling, B et al, ‘Longitudinal periodontal tissue alterations during
supportive therapy’, Journal of Clinical Periodontology, 28 (2001),
241–249
Tomar, SL and Asma, S, ‘Smoking-attributable periodontitis in the
United States: Findings from NHANES III’, Journal of
Periodontology, 7/5 (2000), 743–751
Trombelli, L et al, ‘The role of bleeding on probing in periodontal
diagnosis: A systematic review’, Journal of Periodontology, 86/6
(2015), 665–676

Dental Implants
Brånemark, PI et al, ‘Osseointegration and its clinical significance’,
Journal of Oral Rehabilitation, 4/4 (1977), 277–291
Feine, JS et al, ‘The McGill consensus statement on overdentures
recommends mandibular two-implant overdentures choice standard
of care for edentulous patients’, Gerodontology, 19/1 (2002), 3–4
Friedman, N et al, ‘Interventions for the management of peri-
implantitis’, Cochrane Database of Systematic Reviews, 12 (2012),
CD008811
Herrera, D et al, ‘Treatment of stage IV periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
49/S24 (2022), 4–71
Jung, RE and Ganeles, J, ‘Periodontal and peri-implant tissues:
Differences in anatomy and physiology’, Periodontology 2000, 63/1
(2013), 101–112
Kumar, S et al, ‘Comparative analysis of the longevity of retained
natural teeth versus dental implants’, International Journal of
Prosthodontics, 28/3 (2015), 287–292
Lang, NP et al, ‘Peri-implantitis: A complication of dental implants in
patients with periodontitis’, Periodontology 2000, 55/1 (2011), 47–56
Misch, CE et al, ‘The importance of preserving teeth in patients with
periodontal disease’, Dental Clinics of North America, 58/3 (2014),
437–454
Nishihara, Y et al, 'Comparative histological study of peri-implant and
periodontal tissues’, Journal of Periodontology, 86/4 (2015), 508-516
Pjetursson, BE and Lang, NP, ‘Comparative survival and
complication rates of tooth-supported fixed dental prostheses and
implant-supported fixed dental prostheses’, Clinical Oral Implants
Research, 19/2 (2008), 97–109
Pjetursson, BE et al, ‘Peri-implantitis susceptibility as it relates to
periodontal therapy and supportive care’, Clinical Oral Implants
Research, 23/7 (2012), 888–94
Roccuzzo, A et al, ‘Longitudinal assessment of peri-implant diseases
in patients with and without history of periodontitis: A 20-year follow-
up study’, International Journal of Oral Implantology, 16/3 (2023),
211–222
Salgado, JM et al, ‘Influence of cement excess on the development
of peri-implant diseases: A review’, International Journal of Oral &
Maxillofacial Implants, 31/3 (2016), 594–599
Sanz, M et al, ‘Periodontal and peri-implant diseases: A
comprehensive review’, Journal of Clinical Periodontology, 42/S16
(2015), S30–S50
Schwarz, F et al, ‘Peri-implant diseases: A review of the literature’,
International Journal of Oral & Maxillofacial Implants, 26/5 (2011),
110–118
Schwarz, F et al, ‘The influence of inter-implant distance on the long-
term success of dental implants’, Clinical Oral Implants Research,
26/6 (2015), 692–699
Sgolastra, F et al, ‘Periodontitis, implant loss and peri-implantitis. A
meta-analysis’, Clinical Oral Implants Research, 26/4 (2015), e8–e16
Zitzmann, NU and Marinello, CP, ‘Patient satisfaction with implant-
supported overdentures compared with conventional dentures’,
International Journal of Prosthodontics, 14/6 (2001), 596–602
Multidisciplinary Care

The perio–endo interface

Friedman, S and Stabholtz, A, ‘Endodontic and periodontal
interrelationships’, Endodontic Topics, 3/1 (1999), 87–97
Kumar, P, and Nisha K, ‘Endodontic-periodontic interrelationship: A
review’, Journal of Clinical and Diagnostic Research, 9/2 (2015),
ZE01–ZE05
Papapanou, PN et al, ‘Periodontitis: Consensus report of workgroup
2 of the 2017 World Workshop on the Classification of Periodontal
and Peri-Implant Diseases and Conditions’, Journal of Clinical
Periodontology, 45/Suppl 20 (2018), S162–S170
Santos, JC et al, ‘The association between endodontic and
periodontal lesions: A review’, Journal of Clinical Periodontology,
44/11 (2017), 1064–1072

The perio–ortho interface

Bishara, SE et al, ‘Relapse in orthodontics: A review of the literature’,
American Journal of Orthodontics and Dentofacial Orthopedics,
154/2 (2018), 184–193
Diem, V et al, ‘The role of temporary anchorage devices in
orthodontics for periodontally compromised patients’, European
Journal of Orthodontics, 41/3 (2019), 304–311
García, J et al, ‘Gingival overgrowth in orthodontics: A review’,
European Journal of Orthodontics, 42/5 (2020), 509–515
Hassan, M et al, ‘Monitoring periodontal health during orthodontic
therapy’, American Journal of Orthodontics and Dentofacial
Orthopedics, 156/5 (2019), 685–691
Herrera, D et al, ‘Treatment of stage IV periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
49/S24 (2022), 4–71
Keller, M et al, ‘The impact of orthodontic treatment on periodontal
health: A systematic review’, Orthodontics & Craniofacial Research,
24/3 (2021), 180–192
Kloukos, D et al, ‘Effect of combined periodontal and orthodontic
treatment of tilted molars and of teeth with intrabony and furcation
defects in stage-IV periodontitis patients: A systematic review’,
Journal of Clinical Periodontology, 49/Suppl 24 (2021), S121–S148
Kothiwale, S et al, ‘Orthodontic considerations in patients with
periodontal disease: A review’, Journal of Indian Orthodontic Society,
54/1 (2020), 24–31
Kumar, P et al, ‘Oral hygiene and periodontal management during
orthodontic treatment’, Journal of Clinical Orthodontics, 54/6
(2020a), 365–372
Kumar, P et al, ‘Lifelong retention protocols in orthodontics: A clinical
perspective’, Journal of Clinical Orthodontics, 54/5 (2020b), 273–279
Lindhe, J et al, ‘Periodontal health and orthodontics: Considerations
for tooth movement in patients with periodontitis’, Periodontology
2000, 68/1 (2015), 187–203
Martín, C et al, ‘Effect of orthodontic therapy in periodontitis and non-
periodontitis patients: A systematic review with meta-analysis’,
Journal of Clinical Periodontology, 49/Suppl 24 (2021), S72–S101
Mason, A et al, ‘Efficacy of different retention strategies after
orthodontic treatment: A systematic review’, European Journal of
Orthodontics, 41/3 (2019), 238–247
Miller, D et al, ‘Clear aligners vs traditional braces: A review of the
literature’, Journal of Clinical Orthodontics, 55/5 (2021), 283–290
O’Leary, C et al, ‘Understanding the cone effect in orthodontics’, The
Angle Orthodontist, 91/1 (2021), 27–32
Papageorgiou, SN et al, ‘Effect of periodontal-orthodontic treatment
of teeth with pathological tooth flaring, drifting and elongation in
patients with severe periodontitis: A systematic review with meta-
analysis’, Journal of Clinical Periodontology, 49/Suppl 24 (2021),
S102–S120
Sanz, M et al, ‘Treatment of stage I–III periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
47/S22 (2020), 4–60
Watanabe, H et al, ‘Orthodontic treatment for patients with
periodontitis: a systematic review’, American Journal of Orthodontics
and Dentofacial Orthopedics, 157/1 (2020), 17–25

Pocket Reduction Surgery

Aapeng, F et al, ‘Factors influencing the healing of periodontal
tissues after surgical treatment’, International Journal of Oral
Science, 15/1 (2023), 10–19
Aroca, E and Mombelli, A, ‘Periodontal regeneration: The role of
mobility’, Periodontology 2000, 68/1 (2015), 46–56
Bartlett, JD, ‘Amelogenins: Structure, function and role in tooth
development’, Nature Reviews: Molecular Cell Biology, 14/12 (2013),
829–844
Bichara, DA et al, ‘The role of enamel matrix proteins in wound
healing’, Journal of Tissue Engineering, 8 (2017),
2041731417710421
Buser, D et al, ‘Guided bone regeneration with Bio-Gide and bone
grafts in the maxilla’, International Journal of Oral & Maxillofacial
Implants, 30/3 (2015), 505–512
Caffesse, RG et al, ‘A comparison of non-surgical and surgical
periodontal therapy’, Journal of Periodontology, 57/4 (1986), 232–
238
Cobb, CM, ‘Non-surgical pocket therapy: A review of the literature’,
Journal of Periodontology, 67/9 (1996), 933–949
Cortellini, P et al, ‘Long-term outcomes of surgical periodontal
therapy: A systematic review’, Periodontology 2000, 75/1 (2017),
70–80
Cortellini, P and Tonetti, MS, ‘A minimally invasive surgical approach
to the management of intra-bony defects’, Journal of Clinical
Periodontology, 32/S6 (2005), 190–196
Friedman, N, ‘A technique for periodontal surgery’, Journal of
Periodontology, 33/1 (1962), 66–72
Garg, V, Ranjan, R, and Ranjan, R, ‘The role of non-surgical
periodontal therapy in treating periodontitis: A review’, Journal of
Periodontology, 93/5 (2022), 633–642
Greenstein, G and Cavallaro, J, ‘Surgical and nonsurgical treatment
of furcation involvement: A review’, International Journal of
Periodontics & Restorative Dentistry, 26/5 (2006), 455–461
Haffajee, AD and Socransky, SS, ‘The effect of periodontal therapy
on the microbiological composition of subgingival plaque’, Journal of
Clinical Periodontology, 21/1 (1994), 33–41
Hämmerle, CHF and Trombelli, L, ‘Guided bone regeneration in
implant dentistry’, Periodontology 2000, 73/1 (2017), 145–157
Huang, TH et al, ‘Minimally invasive techniques in periodontal
surgery: A review’, Journal of Dental Sciences, 12/2 (2017), 107–114
Karnik, A et al, ‘The importance of the role of gingival contours in
periodontal therapy’, Journal of Clinical Dentistry, 10/1 (1999), 29–34
Kirkland, L, 'A method of periodontal surgery’, The Dental Review,
58/6 (1931), 505–510
Lindhe, J et al, ‘Critical probing depths in periodontal therapy’,
Journal of Clinical Periodontology, 9/4 (1982), 323–36
Löe, H, ‘Periodontal disease: The sixth complication of diabetes
mellitus’, Diabetes Care, 11/3 (1988), 275–276
McGuire, MK and Nunn, ME, ‘Prognosis versus actual treatment
outcomes’, International Journal of Periodontics and Restorative
Dentistry, 16/1 (1996), 1–11
Müller, HP and Heine, S, ‘Critical probing depth: An important
concept in periodontal therapy’, Clinical Oral Investigations, 23/4
(2019), 1797–1806
Nanci, A et al, ‘The role of enamel matrix derivative in periodontal
regeneration’, Periodontology 2000, 81/1 (2019), 185–202
Neumann, M, ‘Die operativen Möglichkeiten in der
Parodontaltherapie’, Dtsch Zahnarztl Z, 22 (1920), 1013–1018
Nibali, L et al, ‘Surgical and non-surgical management of intra-bony
defects: A systematic review’, Journal of Clinical Periodontology,
46/1 (2019), 29–44
Nyman, S et al, ‘Periodontal surgery in plaque-infected dentitions’,
Journal of Clinical Periodontology, 4/4 (1977), 240–9
Nyman, S et al, ‘Healing of human periodontal tissues after
treatment’, Journal of Clinical Periodontology, 9/4 (1982), 259–271
Ramfjord, SP and Nissle, RR, ‘The modified Widman flap’, Journal of
Periodontology, 45/10 (1974), 613–617
Sanz, M et al, ‘Treatment of stage I–III periodontitis: The EFP S3
level clinical practice guideline’, Journal of Clinical Periodontology,
47/S22 (2020), 4–60
Scabbia, A et al, ‘Cigarette smoking negatively affects healing
response following flap debridement surgery’, Journal of
Periodontology, 72/1 (2001), 43–9
Schlegel, K et al, ‘Bone regeneration in dental applications:
Biological effects of Bio-Oss’, Clinical Oral Implants Research, 26/4
(2015), 424–430
Sgolastra, F et al, ‘Minimally invasive surgery in periodontology: A
systematic review’, Journal of Clinical Periodontology, 43/4 (2016),
282–293
Socransky, SS et al, ‘The role of the microbiota in the pathogenesis
of periodontal disease’, Journal of Clinical Periodontology, 11/4
(1984), 168–178
Stern, R et al, ‘Enamel matrix derivative in the treatment of
periodontal defects’, Journal of Clinical Periodontology, 36/1 (2009),
12–21
Tornes, K et al, ‘Smoking and the treatment of periodontitis: A review
of the literature’, Journal of Periodontology, 76/11 (2005), 2050–2057
Trombelli, L et al, ‘Surgical treatment of intrabony defects: A
systematic review’, Journal of Clinical Periodontology, 40/1 (2013),
1–15
Trombelli, L et al, ‘Periodontal regeneration: A critical review of the
literature’, Periodontology 2000, 66/1 (2014), 153–171
Vignoletti, F and Sanz, M, ‘Influence of endodontic status on the
outcomes of regenerative periodontal therapy’, Journal of Clinical
Periodontology, 41/9 (2014), 913–920
Wagner, W and Gmür, R, ‘The critical probing depth in predicting the
outcome of non-surgical and surgical periodontal therapy’, Journal of
Clinical Periodontology, 20/7 (1993), 431–434
Widman, G, ‘Über die Entfernung des Zahnhalteapparates’, Dtsch
Zahnarztl Z, 22 (1918)
Yamada, Y et al, ‘Impact of papilla preservation flaps on periodontal
regeneration: A systematic review’, Journal of Clinical
Periodontology, 47/9 (2020), 1037–1049

Gingival Recession And Surgery

Allen, A, ‘Use of the supraperiosteal envelope in soft tissue grafting
for root coverage. II. Clinical results’, International Journal of
Periodontics and Restorative Dentistry, 14 (1994), 302–315
Baker, SR et al, ‘Periodontal phenotypes: What do we know and
what do we need to know?’, Journal of Clinical Periodontology, 45/5
(2018), 498–507
Baldi, C et al, ‘Coronally advanced flap procedure for root coverage.
Is flap thickness a relevant predictor to achieve root coverage? A 19-
case series’, Journal of Periodontology, 70 (1999), 1077–1084
Cairo, F et al, ‘Aesthetic surgical correction of gingival recession:
Case reports and scientific evidence’, Journal of Esthetic and
Restorative Dentistry, 30/4 (2018), 332–340
Cortellini, P and Bissada, NF, ‘Mucogingival conditions in the natural
dentition: Narrative review, case definitions, and diagnostic
considerations’, Journal of Periodontology, 89/S1 (2018), S204–
S213
Jepsen, S et al, ‘Periodontal manifestations of systemic diseases
and developmental and acquired conditions: consensus report of
workgroup 3 of the 2017 World Workshop on the Classification of
Periodontal and Peri-Implant Diseases and Conditions’, Journal of
Clinical Periodontology, 45/Suppl 20 (2018), S219–S229
Khan, S et al, ‘Gingival recession: Its causes and management’,
International Journal of Health Sciences, 10/1 (2016), 265–278
Miller, PD, ‘A classification of marginal tissue recession’,
International Journal of Periodontics and Restorative Dentistry, 5
(1985), 8–13
Tinti, C et al, ‘Guided tissue regeneration in the treatment of human
facial recession: A 12-case report’, Journal of Periodontology, 64/3
(1992), 119–124
Tonetti, MS and Jepsen, S, ‘Clinical efficacy of periodontal plastic
surgery procedures: Consensus report of Group 2 of the 10th
European Workshop on Periodontology’, Journal of Clinical
Periodontology, 41/S15 (2014), S36–S43
Trombelli, L, ‘Periodontal regeneration in deep intrabony defects: A
systematic review’, Journal of Clinical Periodontology, 42/S16
(2015), S116–S132
Zhang, Y et al, ‘Impact of oral hygiene on the success of periodontal
plastic surgery: A systematic review’, Journal of Periodontology, 92/4
(2021), 436–446
Zucchelli, G and De Sanctis, M, ‘Treatment of multiple recession-
type defects in patients with aesthetic demands’, Journal of
Periodontology, 71/9 (2000), 1506–1514
Crown-Lengthening Surgery
Cairo, F et al, ‘Aesthetic surgical correction of gingival recession:
Case reports and scientific evidence’, Journal of Esthetic and
Restorative Dentistry, 30/4 (2018), 332–340
Chu, SJ et al, ‘Aesthetic parameters for gingival zenith position: A
review of the literature’, Journal of Esthetic and Restorative
Dentistry, 21/6 (2009), 373–384
Cohen, ES, Atlas of Cosmetic & Reconstructive Periodontal Surgery,
Vol 3 (Hamilton, 2007)
Cortellini, P and Bissada, NF, ‘Mucogingival conditions in the natural
dentition: Narrative review, case definitions, and diagnostic
considerations’, Journal of Periodontology, 89/S1 (2018), S204–
S213
Coslet, GJ, Vanarsdall, R, and Weisgold, A, ‘Diagnosis and
classification of delayed passive eruption of the dentogingival
junction in the adult’, Alpha Omegan, 10 (1977), 24–8
Garber, DA and Salama, MA, ‘The aesthetic smile: Diagnosis and
treatment’, Periodontology 2000, 11/1 (1996), 18–28
Garguilo, AW, Wentz, FM, and Orban, B, ‘Dimensions and relations
of the dentogingival junction in humans’, Journal of Periodontology,
32 (1961), 321
Gargiulo, AW et al, ‘The importance of tooth proportion in the
aesthetics of the smile’, Journal of Esthetic and Restorative
Dentistry, 18/1 (2006), 43–52
Goldman, HM and Cohen, DW, ‘The effect of altered passive
eruption on periodontal health’, Journal of Periodontology, 42/1
(1971), 28–32
Jepsen, S et al, ‘Periodontal manifestations of systemic diseases
and developmental and acquired conditions: consensus report of
workgroup 3 of the 2017 World Workshop on the Classification of
Periodontal and Peri-Implant Diseases and Conditions’, Journal of
Clinical Periodontology, 45/Suppl 20 (2018), S219–S229
The Author

Dr Reena Wadia is the founder and principal periodontist at RW Perio,

which she set up and grew into an established, state-of-the-art, four-clinic
surgery on Harley Street. Today, RW Perio is one of the top specialist
periodontal clinics in the UK.

Dr Reena’s mission is to highlight the importance of gum health,

incorporating it into a healthy overall lifestyle. This focus has been
celebrated regularly in the press, including Forbes, Financial Times How To
Spend It, Vogue, Harper’s Bazaar, The Times, and the BBC. She has
developed her own award-winning product range, By Dr Reena, which
combines specialist dentistry with luxury lifestyle. Her podcast, Life &
Smile, was launched in 2022, featuring guests including Sarah Harris
(British Vogue), Lydia Slater (Harper’s Bazaar), and Harpz Kaur (BBC).
As well as being passionate about acquiring new knowledge, Dr Reena has
always encouraged and supported other entrepreneurs, dentists, and
hygienists/therapists by sharing her own learning and experiences. She is
the founder of Perio School, which is now the leading global teaching
academy for periodontal courses, having taught dental students, dentists,
and hygienists for over ten years.

Dr Reena endeavours to contribute to the profession through her role as an

expert advisor on the BDA Indemnity Board, as co-editor of the ‘Other
Journals in Brief’ section of the British Dental Journal, and as trustee of the
Oral and Dental Research Trust.

www.perio.school
www.rwperio.com
www.bydrreena.com
www.linkedin.com/in/reenawadia
@reenawadia
www.youtube.com/rwperio