DISEASES OF THE PULP

AND PERIAPICAL TISSUES

A Comprehensive Presentation Report

Submitted by:

Resmi Raju R L

2nd year BDS

Roll no: 25

[Date of Submission/Generation: October 26, 2023]

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TABLE OF CONTENTS
1. Introduction to Diseases of Pulp and Periapical Tissues
2. Apical Periodontitis
1. Definition and Manifestations
2. Causes of Apical Periodontitis
3. Acute Apical Periodontitis
1. Clinical Features
2. Radiographic Features
3. Histologic Features
4. Treatment and Prognosis
4. Chronic Apical Periodontitis (Periapical Granuloma)
1. Introduction
2. Clinical Features
3. Radiographic Features
4. Histologic Features
5. Microbiologic Features
6. Treatment and Prognosis
7. Complications
5. Comparison of Acute vs. Chronic Apical Periodontitis
6. Conclusion
7. References
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1. INTRODUCTION TO DISEASES OF PULP AND

PERIAPICAL TISSUES
Diseases of the dental pulp and periapical tissues represent a significant area
of study in dentistry, encompassing a range of inflammatory and infectious
conditions that can lead to severe pain, tooth loss, and systemic health issues
if left untreated. The dental pulp, residing within the tooth, is a highly
vascular and innervated connective tissue that supports the dentin. When the
pulp becomes inflamed or necrotic, it can trigger a cascade of events leading
to periapical pathosis, affecting the tissues surrounding the apex of the tooth
root. Understanding these conditions is crucial for accurate diagnosis,
effective treatment planning, and ultimately, preserving dental health. This
report focuses specifically on Apical Periodontitis, detailing its acute and
chronic forms, their causes, clinical manifestations, diagnostic features, and
management strategies.

2. APICAL PERIODONTITIS
2.1 DEFINITION AND MANIFESTATIONS

Apical periodontitis is characterized as an inflammatory response in the

periodontal ligament and the surrounding periapical tissues, occurring at the
apex of a tooth root. This inflammation is typically a direct consequence of
noxious stimuli emanating from an infected or necrotic dental pulp. The
body's immune system mounts a defense mechanism against these irritants,
leading to a localized inflammatory reaction at the root apex.

The manifestation of apical periodontitis can vary significantly, presenting as

either an acute or chronic condition. The classification into acute or chronic
forms is primarily based on the nature, intensity, and duration of the
underlying irritant or infection, as well as the host's immune response. Acute
forms typically present with severe symptoms, while chronic forms may be
asymptomatic or present with milder, persistent symptoms.

Image Placeholder for Slide 4: Illustration of Apical Periodontitis (Periapical

Periodontitis) showing inflammation at the root apex due to dental caries/
pulp infection.
Figure 2.1: Illustration of Apical Periodontitis indicating inflammation in the
periapical region.

2.2 CAUSES OF APICAL PERIODONTITIS

The etiology of apical periodontitis is multifactorial, primarily involving

microbial invasion and inflammatory reactions. Key causes include:

• Spread of Infection from Pulp Necrosis: This is the most common

cause. When the dental pulp undergoes necrosis (tissue death), typically
due to deep dental caries or trauma, the necrotic tissue serves as a
substrate for bacterial proliferation. These bacteria, along with their
toxins and metabolic by-products, can then egress through the apical
foramen into the periapical tissues, initiating an inflammatory response.
The bacterial invasion from a necrotic pulp into the periapical tissues is
the primary driver of apical periodontitis.
• Occlusal Trauma: Excessive or abnormal biting forces on a tooth,
known as occlusal trauma, can also lead to apical periodontitis, even in
the absence of pulp infection. This can occur in cases of:
◦ High restoration: A dental filling or crown that is too high can
cause premature contact and excessive pressure on the tooth.
◦ Sudden force from biting a hard object: Acute trauma can
damage the periodontal ligament, leading to inflammation.
The mechanical stress can cause sterile inflammation of the periodontal
ligament, leading to symptoms mimicking apical periodontitis.
• Iatrogenic Factors: These are factors caused by dental treatment
procedures. Certain aspects of root canal treatment, if not performed
meticulously, can induce or exacerbate periapical inflammation:
◦ Over-instrumentation: Accidental extension of endodontic
instruments beyond the apical foramen can push infected debris,
necrotic tissue, or irritants into the periapical region, leading to
acute inflammation.
◦ Pushing infected debris or irritants: Incomplete cleaning or
forceful irrigation during root canal preparation can force bacteria
and toxins into the periapical tissues.
◦ Chemical irritation from root canal medicaments: Certain root
canal filling materials or irrigants, if extruded into the periapical
space, can cause a chemical inflammatory reaction.
 • Anatomical Variations: Deviations in tooth anatomy can predispose to
periapical issues.
◦ Accessory root canals: These lateral canals, if present and not
adequately cleaned during root canal treatment, can harbor
bacteria. They allow infection to bypass the main apical opening
and spread laterally into the periodontal ligament, leading to
persistent inflammation or abscess formation even after seemingly
successful root canal therapy of the main canal.

Page 3 Image Placeholder for Slide 6: Comparison of Chronic Apical

Periodontitis (Apical Granuloma) and Acute Apical Periodontitis (Widening of
PDL, exudate, gingiva redness).

Figure 2.2: Distinguishing features of Chronic vs. Acute Apical Periodontitis.

3. ACUTE APICAL PERIODONTITIS

Acute apical periodontitis (AAP) represents the initial and often symptomatic
phase of inflammation affecting the periapical tissues. It is characterized by a
rapid onset of pain and discomfort, typically in response to a newly initiated
or exacerbated inflammatory process originating from a diseased or necrotic
pulp.

3.1 Clinical Features

Patients suffering from acute apical periodontitis often present with distinct
clinical signs and symptoms:

• History of Pulpitis: Patients frequently report a preceding history of

pulpitis, which is inflammation of the dental pulp. This could have been
reversible or irreversible, leading to eventual pulp necrosis, which then
triggers the periapical inflammation.
• Pain upon Biting or Slight Touch: A hallmark symptom is pain elicited
by biting on the affected tooth or even by slight touch (palpation or
percussion). This is due to the inflammation and edema in the
periodontal ligament, which contains numerous nociceptors (pain
receptors). Any pressure on the tooth directly transmits force to the
inflamed ligament, causing sharp pain.
• Tooth Elevation: The tooth may feel elevated or "long" in its socket. This
sensation arises from the accumulation of inflammatory fluid and
exudate within the periodontal ligament space, which exerts pressure
and slightly extrudes the tooth from its alveolar socket.
 • Thermal Stimuli: Unlike pulpitis, thermal stimuli (hot or cold) typically
do not elicit pain in acute apical periodontitis. This is because the pulp,
the primary responder to thermal changes, is often necrotic or severely
compromised, thus unresponsive. The pain originates from the
periapical tissues, not the pulp itself.

3.2 Radiographic Features

Radiographic examination plays a crucial role in diagnosing apical

periodontitis, although early acute phases may present subtly:

• No Significant Changes in Early Stages: In the very early stages of

acute apical periodontitis, before significant bone resorption occurs,
radiographs may not show any notable changes. The periapical bone
may appear normal.
• Slight Widening of the Periodontal Ligament Space: As the
inflammation progresses, the most common early radiographic sign is a
slight widening of the periodontal ligament (PDL) space around the root
apex. This widening is indicative of fluid accumulation and inflammatory
cell infiltration within the ligament. It appears as a thin radiolucent line
surrounding the root, which is thicker than normal.

Image Placeholder for Slide 8: Diagrams showing Primary Acute Apical

Periodontitis (localized inflammation) and Secondary Acute Apical
Periodontitis (more diffuse inflammation/bone loss).

Figure 3.1: Diagrammatic representation of Primary and Secondary Acute

Apical Periodontitis (Source: Paul V. Abott, Endodontic Topics 2004).

Image Placeholder for Slide 9: Illustration of Apical Periodontitis Immunology,

showing dental caries, necrotic pulp, diseased apical tissues, and a magnified
view of immune cells (macrophages, neutrophils, lymphocytes, osteoclasts,
osteoblasts) and cytokines involved.

Figure 3.2: Immunological cascade in Apical Periodontitis.

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3.3 Histologic Features

Histological examination of tissues affected by acute apical periodontitis

reveals specific microscopic changes indicative of acute inflammation:

• Vascular Dilatation and Infiltration of Polymorphonuclear

Leukocytes: A prominent feature is the significant dilatation of blood
vessels in the periodontal ligament, leading to increased blood flow and
permeability. This is accompanied by a dense infiltration of
polymorphonuclear leukocytes (PMNs), primarily neutrophils, which are
characteristic of acute inflammatory responses. These cells migrate from
the bloodstream into the inflamed tissue to combat infection.
• Localized Changes Around the Root Apex: Initially, these inflammatory
changes are highly localized around the root apex, precisely where the
noxious stimuli from the infected pulp exit. This localization is due to the
rich vascularity of the periapical region, which facilitates a rapid
inflammatory response.
• Inflammation Progression: If the acute inflammation is left untreated
or the irritant persists, it may lead to more severe tissue destruction,
including:
◦ Bone Resorption: The inflammatory process, driven by cytokines
and inflammatory mediators, can stimulate osteoclasts, leading to
localized resorption of the surrounding alveolar bone.
◦ Formation of an Abscess: In many cases, particularly with virulent
infections, the accumulation of pus (a collection of necrotic cells,
bacteria, and inflammatory exudate) results in the formation of an
acute periapical abscess, also known as an alveolar abscess. This is
a painful swelling that can spread into surrounding soft and hard
tissues.

3.4 Treatment and Prognosis

Effective management of acute apical periodontitis is critical to alleviate pain,

eliminate infection, and prevent progression to chronic forms or more severe
complications:

• Occlusal Trauma Management: If occlusal trauma is identified as a

primary or contributing factor, immediate relief is necessary. This is
typically achieved by selective occlusal grinding, where small amounts of
tooth structure or restoration are removed to eliminate premature
contacts and reduce biting forces on the affected tooth.
 • Infection Spread from Pulp (Root Canal Therapy): For cases stemming
from pulp necrosis and infection, the definitive treatment is root canal
therapy (RCT). This procedure involves:
◦ Draining Exudate: Initially, the root canal system is accessed to
allow drainage of any accumulated exudate or pus, which provides
immediate pain relief.
◦ Removal of Necrotic Tissue and Bacteria: The infected and
necrotic pulp tissue, along with bacteria and their by-products, are
meticulously removed from the root canal system. This step is
crucial for eliminating the source of inflammation.
◦ Sealing the System: After thorough cleaning and shaping, the
root canal system is filled with an inert material to prevent
reinfection.
◦ Tooth Extraction: In cases where root canal therapy is not feasible
due to severe tooth destruction, anatomical complexities, or
patient factors, extraction of the tooth may be the only viable
option to resolve the infection and associated symptoms.
• Prognosis and Prevention of Progression: Early and appropriate
treatment of acute apical periodontitis is associated with an excellent
prognosis. Timely intervention can effectively resolve the acute
inflammation and prevent its progression to a chronic apical
periodontitis (like a periapical granuloma) or the formation of a
widespread abscess, thus preserving the tooth.

4. CHRONIC APICAL PERIODONTITIS (PERIAPICAL

GRANULOMA)
Image Placeholder for Slide 16: Image of extracted teeth, potentially showing
periapical lesion.

Figure 4.1: Clinical appearance of extracted teeth potentially showing

periapical lesions.

4.1 INTRODUCTION

Chronic apical periodontitis, commonly referred to as a periapical granuloma,

represents a persistent, low-grade inflammatory lesion that develops at the
root apex. This condition typically arises as a sequela of untreated pulpitis
(where the pulp dies but the body's defenses manage to contain the infection
in a chronic state) or unresolved acute apical periodontitis. It is the most
common form of apical periodontitis.
The hallmark of chronic apical periodontitis is its characterization by the
formation of granulation tissue at the root apex. This granulation tissue is
essentially a reparative inflammatory tissue composed of fibroblasts,
capillaries, and chronic inflammatory cells (lymphocytes, plasma cells,
macrophages), aiming to wall off the infection and contain its spread.

Image Placeholder for Slide 17: Illustration of Periapical Inflammatory

Disease showing pulp chamber, root canal, lateral accessory canals, periapical
region, and differentiating between granuloma and cyst.

Figure 4.2: Schematic representation of Periapical Inflammatory Disease.

4.2 CLINICAL FEATURES

Unlike its acute counterpart, chronic apical periodontitis is often insidious and
less symptomatic:

• Non-vital Tooth: The affected tooth is usually non-vital, meaning the

pulp is necrotic and does not respond to vitality tests (e.g., electric pulp
test, thermal tests).
• Symptoms May Include:
◦ Mild Tenderness to Percussion: While often asymptomatic, a mild
tenderness to percussion or palpation of the apical area might be
present, especially if the lesion is expanding or undergoing a minor
exacerbation.
◦ Occlusal Mild Pain: Patients may occasionally report mild pain or
discomfort during chewing or biting, particularly if the periapical
lesion is large enough to exert pressure on adjacent structures.
◦ Tooth Elongation: Similar to acute forms, the tooth may
occasionally feel slightly elongated due to inflammatory exudate,
though this is less common and less pronounced than in acute
cases.
• Asymptomatic and Incidental Discovery: A significant proportion of
chronic apical periodontitis cases are asymptomatic. They are frequently
discovered incidentally during routine radiographic examinations, as the
lesion develops slowly over time without causing significant discomfort.
• Fistula Formation: In some instances, if the lesion becomes large and
perforates the surrounding bone, it may create a pathway for pus
drainage. This leads to the formation of a fistula (also known as a sinus
tract) which opens onto the oral mucosa, often near the apex of the
affected tooth. This drainage often alleviates pain, making the lesion
asymptomatic.
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4.3 RADIOGRAPHIC FEATURES

Radiographic examination is the primary method for diagnosing chronic

apical periodontitis due to its often asymptomatic nature:

• Early Signs: The earliest radiographic sign may be a thickening of the

periodontal ligament (PDL) space at the root apex, indicating chronic
inflammation.
• Progression: As the lesion progresses and bone destruction occurs, the
characteristic radiographic appearance changes:
◦ Well-Defined Radiolucent Lesion: Typically, a well-defined,
circumscribed radiolucent (dark) lesion is observed at the root
apex, attached to the root. This lucency represents the bone
destruction and the presence of granulation tissue.
◦ Radiopaque Sclerotic Border: In long-standing lesions, the body's
attempt to wall off the infection can lead to the formation of a
dense, radiopaque (white) sclerotic border around the radiolucent
area. This indicates reactive bone formation.
◦ Diffuse Radiolucency: In more active or rapidly expanding chronic
lesions, the radiolucency may appear diffuse with ill-defined
borders, indicating an ongoing, less contained inflammatory
process.
• Root Resorption: Root resorption, where portions of the tooth root are
dissolved, is often present in chronic apical periodontitis. This occurs
due to the inflammatory cells (osteoclasts) directly or indirectly attacking
the root surface, leading to shortening or blunting of the root apex.

Image Placeholder for Slide 21: Radiograph showing periapical radiolucency

with possible root canal treatment.

Figure 4.3: Radiograph demonstrating features of chronic apical periodontitis.

4.4 HISTOLOGIC FEATURES

Microscopic examination of a periapical granuloma reveals a complex

inflammatory and reparative tissue:

• Inflammatory Cells: The lesion is predominantly composed of chronic

inflammatory cells, including:
◦ Macrophages: Phagocytic cells that engulf debris and present
antigens.
 ◦ Lymphocytes: T-lymphocytes and B-lymphocytes, indicative of a
chronic immune response. B-lymphocytes may differentiate into
plasma cells.
◦ Plasma Cells: Antibody-producing cells, signifying an active
humoral immune response against microbial antigens.
◦ Occasional Mast Cells and Eosinophils: These cells may also be
present, contributing to the inflammatory milieu.
• Fibrous Tissue Formation: A key characteristic is the extensive
proliferation of fibrous connective tissue.
◦ Proliferation of Fibroblasts and Capillaries: Fibroblasts produce
collagen, and numerous new capillaries form (angiogenesis), which
are characteristic components of granulation tissue, aimed at
repair and containment.
◦ Collagen Bundles Forming a Capsule: Denser collagen bundles
may form a fibrous capsule around the lesion, effectively
separating it from the surrounding normal bone, which contributes
to its well-defined radiographic appearance in some cases.
• Bone and Root Resorption: The inflammatory process actively causes
resorption of the surrounding alveolar bone. This is primarily caused by
inflammatory mediators (e.g., cytokines like IL-1, TNF-α) produced by the
inflammatory cells. These mediators stimulate the differentiation and
activation of osteoclasts, leading to localized bone destruction. Similarly,
root resorption may occur, affecting the cementum and dentin of the
tooth.
• Cholesterol Crystals: These needle-like spaces are often observed
within the granuloma. They are derived from the breakdown of red
blood cells and lipid degeneration within the chronically inflamed tissue.
These crystals are typically surrounded by multinucleated giant cells
(foreign body giant cells) attempting to phagocytose them.
• Epithelial Proliferation: A significant finding is the proliferation of
epithelial rests of Malassez. These are remnants of Hertwig's epithelial
root sheath, naturally present in the periodontal ligament. In response
to chronic inflammation, these epithelial cells can proliferate and form
strands or islands within the granuloma. This epithelial proliferation is
crucial because it can lead to the formation of an apical periodontal cyst,
which is an epithelial-lined cavity filled with fluid, differentiating it from a
granuloma.
• Immune Features: The periapical granuloma is considered an immune-
type lesion.
◦ It is rich in lymphocytes, plasma cells, and macrophages, indicating
a sophisticated immune response.
 ◦ Immunoglobulins (IgG, IgA, IgE), produced by plasma cells, play a
significant role in mediating the immune response against
bacterial antigens within the lesion.

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4.5 MICROBIOLOGIC FEATURES

The microbial etiology of chronic apical periodontitis is complex,

predominantly involving polymicrobial infections:

• Bacteria: Bacteria are the primary culprits. Organisms commonly

associated with the oral cavity, such as various species of Streptococcus,
Enterococcus faecalis, and anaerobic bacteria (e.g., Porphyromonas,
Prevotella, Fusobacterium), are often present within the root canal system
and the periapical lesion. While E.coli is mentioned in the slide, it is less
commonly a primary pathogen in periapical lesions compared to strict
anaerobes and facultative anaerobes typically found in the root canal.
Mixed infections, involving multiple bacterial species, are common and
contribute to the persistence of the lesion.
• Viruses: Recent research suggests that certain viruses may also
contribute to the pathogenesis of chronic apical periodontitis:
◦ Human Cytomegalovirus (HCMV) and Epstein-Barr Virus (EBV):
These herpesviruses may contribute to pathogenesis by
modulating the host immune response.
◦ High Prevalence in Symptomatic Lesions: Studies have shown a
high prevalence of HCMV in symptomatic lesions of chronic apical
periodontitis, suggesting a potential role in exacerbating
inflammation or hindering healing.
◦ Modulating Cytokine Production: Viruses may exacerbate the
inflammatory response by modulating the production of cytokines,
influencing the balance between pro-inflammatory and anti-
inflammatory mediators, thereby contributing to the chronicity or
exacerbation of the lesion.
4.6 TREATMENT AND PROGNOSIS

The primary goal of treating chronic apical periodontitis is to eliminate the

source of infection and promote periapical healing:

• Root Canal Therapy (RCT): This is the gold standard treatment. It

involves:
◦ Removal of Necrotic Tissue and Bacteria: Thorough debridement
and disinfection of the entire root canal system are performed to
eliminate the microbial irritants.
◦ Apicoectomy: If the lesion persists after conventional root canal
therapy, or in cases of complex anatomy/failed treatment, surgical
removal of the root apex (apicoectomy) along with the periapical
lesion may be required.
• Tooth Extraction: If root canal therapy is not feasible (e.g., due to
severe structural compromise of the tooth, irreparable fractures, or
complex anatomy that prevents proper disinfection) or if the lesion is
very large and unresponsive, extraction of the tooth may be necessary.
• Transformation of Untreated Granulomas: Untreated periapical
granulomas can evolve or transform over time:
◦ Apical Periodontitis Cyst: Due to epithelial proliferation within the
granuloma (from the epithelial rests of Malassez), a true apical
periodontal cyst (radicular cyst) may form. Cysts have an epithelial
lining and often require more extensive treatment than
granulomas.
◦ Abscess: If the chronic infection suddenly overwhelms the host
defenses or a new virulent bacterial strain colonizes, the chronic
granuloma can undergo an acute exacerbation, transforming into
an acute periapical abscess, presenting with severe pain and
swelling.

4.7 COMPLICATIONS

If left untreated, chronic apical periodontitis can lead to various

complications:

• Acute Exacerbation: As mentioned, a chronic granuloma can transform

into an acute abscess, leading to severe pain, swelling, and potential
spread of infection.
• Cyst Formation: The epithelial proliferation within the granuloma can
lead to the formation of an apical periodontal cyst, which typically
requires surgical enucleation in addition to root canal treatment.
 • Systemic Effects: Persistent localized infection can have systemic
implications. Bacteria and inflammatory mediators can spread via the
bloodstream, potentially leading to:
◦ Systemic Inflammation: Contributing to overall inflammatory
burden in the body.
◦ Spread to Distant Sites: In rare but serious cases, the infection
can spread to distant anatomical sites, leading to conditions like
osteomyelitis (bone infection) in adjacent bones, cavernous sinus
thrombosis, or even life-threatening conditions like sepsis in
immunocompromised individuals.

5. COMPARISON OF ACUTE VS. CHRONIC APICAL

PERIODONTITIS

Chronic Apical Periodontitis

Features Acute Apical Periodontitis
(Granuloma)

Onset Sudden Gradual

Severe pain, tenderness, tooth Mild or asymptomatic; occasional

Symptoms
elevation mild tenderness/pain on biting

Normal in early stages; slight Well-defined or diffuse radiolucency;

Radiographic
widening of periodontal possible sclerotic border; root
Appearance
ligament (PDL) space resorption common

Vascular dilation, Granulation tissue; predominantly

polymorphonuclear leukocytes macrophages, lymphocytes, plasma
Histology
(PMNs), edema; acute cells; fibrous tissue, cholesterol
inflammatory cells crystals, epithelial proliferation

Root canal therapy (RCT),

Root canal therapy (RCT),
Treatment occlusal adjustment, drainage,
apicoectomy if needed, extraction
extraction

6. CONCLUSION
Diseases of the pulp and periapical tissues, particularly apical periodontitis,
represent a spectrum of inflammatory conditions primarily driven by
microbial infection from a compromised dental pulp. Acute apical
periodontitis presents with rapid onset and severe symptoms, characterized
by a distinct inflammatory cellular infiltrate and early radiographic signs of
PDL widening. In contrast, chronic apical periodontitis, or periapical
granuloma, is often asymptomatic, developing slowly with characteristic
radiographic lucencies and a histological profile of chronic inflammatory and
granulation tissue. Accurate diagnosis, based on thorough clinical and
radiographic examinations, is paramount for effective management. Root
canal therapy remains the cornerstone of treatment for both conditions,
aiming to eliminate the microbial etiology and promote periapical healing.
Understanding the distinct features and potential complications of these
diseases is essential for dental practitioners to provide timely intervention,
prevent systemic complications, and preserve dental health.

7. REFERENCES
• Paul V. Abott, Classification, diagnosis and clinical manifestations of
apical Periodontitis. Endodontic Topics 2004, 8, 36-54.
• Grossman's Endodontic Practice: 11th Edition.
• Estrela, C., et al. (2018). Apical Periodontitis: A Review of Pathogenesis,
Diagnosis, and Treatment. Journal of Endodontics, 44(8), 1259–1271.
• Nair, P. N. R. (2004). Pathogenesis of Apical Periodontitis and the Causes
of Periapical Lesions. Oral Radiology and Endodontology, 98(3), 395-400.
• (Additional relevant endodontic textbooks and peer-reviewed articles
would be cited here in a complete formal report)

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