The Periodontal Pocket Formation
The periodontal pocket, which is defined as a
pathologically deepened gingival sulcus may occur as
a result of coronal movement of the gingival margin,
apical displacement of the gingival attachment, or a
combination of the two processes
It is one of the most important clinical features of
periodontal diseases.
Classification:
A) Gingival pocket (also called “pseudo-pocket”)
B) Periodontal pocket (true pocket)
I) Based on the location of the base of the pocket
in relation to the underlying bone
a) Suprabony (supracrestal or supra-alveolar)
b) Intrabony (infrabony, subcrestal or intraalveolar)
II) According to involved tooth surfaces
a) Simple pocket
b) Compound pocket
c) Complex pocket
Clinical signs
a bluish-red thickened marginal gingiva,
a bluish-red vertical zone from the gingival margin to the
alveolar mucosa,
gingival bleeding and suppuration,
tooth mobility,
• diastema formation,
• symptoms such as localized pain or pain “deep in the
bone.”
PATHOGENESIS
INFLAMMATION
PLAQUE (COCCOID & STRAIGHT RODS) – HEALTHY GINGIVA
PLAQUE (SPIROCHETES & MOTILE RODS) – DISEASED GINGIVA
ACCUMULATION OF CELLULAR & INFLAMMATORY FLUID EXUDATE
DESTRUCTION OF COLLAGEN FIBERS
ACCUMULATION OF INFLAMMATORY CELLS
APICAL MIGRATION OF JE POCKET FORMATION
Pus is a common feature of
periodontal diseases,
but it is only a secondary sign.
HISTOPATHOLOGY
Bacterial Invasion
Mechanisms of Tissue Destruction
Microtopography of the Gingival Wall
Periodontal Pockets as Healing Lesions
Pocket Contents
Root Surface Walls
Micrograph of gingival wall
• Areas of quiescence
• Areas of bacterial accumulation
• Areas of emergence of leukocytes
• Areas of leukocyte-bacteria interaction
• Areas of intense epithelial desquamation
• Areas of ulceration
• Areas of hemorrhage
Root surface wall
Necrotic Cementum
Bacterial Endotoxin
Active root caries
Inactive lesions
Root caries – Actinomyces viscosus
Surface Morphology of tooth wall
Surface Morphology of tooth
wall
1. Cementum covered by calculus
2. Attached plaque
3. The zone of unattached plaque
4. The zone of attachment of the junctional
epithelium to the tooth
5. A zone of semi destroyed connective tissue
fibers
3, 4 and 5 PLAQUE FREE ZONE
PERIODONTITIS ACTIVITY
With the studies of the specificity of plaque
bacteria, the concept of periodontitis activity has
evolved.
Periodontal pockets go through
periods of exacerbation and quiescence
Periods of quiescence are
characterized by:
➢ A reduced inflammatory response
➢ A little or no loss of bone
and connective tissue attachment
➢ Proliferation of gram-positive bacteria
➢ A more stable condition is established.
A period of exacerbation
characterized by:
• bone and connective tissue attachment loss
• deepening of pocket
• . This period may last for days, weeks, or months.
• It is followed by a period of remission or quiescence
These periods of
quiescence and
exacerbation are also known
as
periods of inactivity and
periods of activity
Clinically, active periods show:
1. bleeding, either spontaneously
or with probing
2. greater amounts of gingival
exudate.
SITE SPECIFICITY
1. the severity of periodontitis
increases with the development
of new disease sites
2. with the increased
breakdown of existing sites.
Pulp Changes Associated
With Periodontal Pockets
•Involvement of the pulp in periodontitis
occurs through
- either the apical foramen
- or the lateral pulp canals
Atrophic and inflammatory pulpal
changes occur in such cases
Relationship of attachment loss
and bone loss to pocket depth
Pockets of the
same depth may
be associated with
different degrees
of attachment loss
pockets of
different
depths may
be associated
with the same
amount of
attachment
loss
Severity of bone loss not always
correlated with pocket depth
Extensive attachment and bone loss -- shallow
pockets if the attachment loss is accompanied
by recession of the gingival margin
Slight bone loss -- deep pockets, if it is
accompanied by gingival enlargement.
loss of attach ment can be
equated with loss of bone,
although attachment loss
precedes bone loss by
about 6 to 8 months
Transseptal fibers protect interdental
bone from the inflammatory process.
Even after initial destruction these
fibers can continually re-form.
They are the fibers found during
periodontal flap surgery.
Mechanisms of Bone
Destruction
Bone Formation in
Periodontitis
• Areas of bone formation -- immediately adjacent to sites of
active bone resorption and along trabecular surfaces at a
distance from the inflammation in an apparent effort to
reinforce the remaining bone (i.e., buttressing bone
formation)
• The basic aim of periodontal therapy is the elimination of
inflammation to inhibit the stimulus for bone resorption and
therefore to allow the inherent constructive tendencies to
predominate.
Area between base of the
pocket and alveolar bone
•The distance between the apical extent
of calculus and the alveolar crest is
1.97mm
•The distance from attached plaque to
bone <0.5 mm and > 2.7 mm
Relationship of pocket to
bone
infrabony pockets -- base of the pocket is apical to
the crest of the alveolar bone -- pocket wall lies
between the tooth and the bone – vertical bone loss
-- transseptal fibers orientes obliquely along the
alveolar bone -- necessitates treatment
modifications.
Suprabony pocket -- alveolar
crest gradually attains a more
apical position in relation to the
tooth --morphology not altered –
transseptal fibers orient
horizontally following the alveolar
crest
Bone destruction caused by the
extension of gingival
inflammation
Periodontitis is always preceded by gingivitis,
but not all gingivitis progresses to periodontitis.
•Fibroblasts and lymphocytes predominatein
stage 1 gingivitis
• plasma cells and blast cells increases gradually
as the disease progresses.
Seymour and
colleagues have postulated
a stage of “contained”
gingivitis,
in which T lymphocytes are
preponderant
Pathways of in ammation
Bone destruction in periodontitis is not a
process of bone necrosis. It involves the
activity of living cells along viable bone.
Radius of Action
Accor ding to Waerhaug, a range of
effectiveness of about 1.5 to 2.5 mm in
which bacterial biofilm can induce loss
of bone.
Periodontal abscess
•It is a localized purulent inflammation in
the periodontal tissues .
•Other names : lateral abscess
or parietal abscess.
Reasons of formation
• 1. Extension of infection
•2. Lateral extension of inflammation
•3. In a pocket with a tortuous course around
the root
•4. Incomplete removal of calculus
•5. After trauma to the tooth or with perforation
of the lateral wall of
the root in endodontic therapy
Classification of
periodontal abscess
•Abscess in the supporting periodontal
tissues along the lateral aspect of the root.
•Abscess in the soft-tissue wall of a deep
periodontal pocket.
The PMNs liberate enzymes that
digest the cells and other tissue
structures,
thereby forming the liquid product
known as pus, which constitutes
the center of the abscess
The localized acute abscess ---- a
chronic abscess when its purulent
content drains through a fistula -
i) into the outer gingival surface
ii) into the periodontal pocket
iii) the infection that is causing
the abscess is not resolved.
The invading organisms
were identified as gram-
negative cocci,
diplococci,
fusiforms,
spirochetes.
Lateral periodontal cyst
•It is an uncommon lesion that produces
localized destruction of the periodontal
tissues along a lateral root surface,
most often in the mandibular canine–
premolar area.
• It is considered to be derived from the
rests of Malassez or other proliferating
odontogenic rests
•Usually asymptomatic, but it may present
as a localized, tender swelling.
•Radiographically, at the side of the root as
a radiolucent area bordered by a
radiopaque line. Can not be differentiated
from periodontal abscess.
Microscopically, the cystic
lining may be
(1) a loosely arranged,
thin, nonkeratinized epithelium,
sometimes with thicker
proliferating areas,
or
(2) an odontogenic keratocyst
