4/5/2020

Periodontal Pocket

Dr. MahMouD MuDalal

B.Sc. Dental surgery

M.Sc. Periodontology
Ph.D. Periodontology and Implantology
Asst. Professor at Arab American university
Member of ADEE.
Research fellow at Jilin Provincial Experimental School.
Google scholar. Mahmoud MUDALAL 22 citations.

Classification
• Gingival pocket (also called “peudo-pocket”) is
formed by gingival enlargement without
destruction of the underlying periodontal tissues.
• Periodontal pocket produces destruction of the
supporting periodontal tissues, leading to the
loosening and exfoliation of the teeth.
1- Suprabony (supracrestal or supraalveolar) occurs
when the bottom of the pocket is coronal to the
underlying alveolar bone.
2- Intrabony (infrabony, subcrestal, or intraalveolar)
occurs when the bottom of the pocket is apical to
the level of the adjacent alveolar bone.

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• Pockets can involve one, two, or more tooth

surfaces, and they can be of different depths
and types on different surfaces of the same
tooth and on approximal surfaces of the same
interdental space.
• Pockets can also be spiral (i.e., originating on
one tooth surface and twisting around the
tooth to involve one or more additional
surfaces) . These types of pockets are most
common in furcation areas.

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Simple Compound Complex

Features of Junctional Epithelium

• It acts as a physical barrier against plaque bacteria.
• It is stratified squamous nonkeratinized in nature,
which develops by the union of oral epithelium and
reduced enamel epithelium during tooth eruption.
• It is attached to the tooth by internal basal lamina
and to the connective tissue by external basal
lamina.
• It exhibits higher permeability to cells, gingival fluid,
and host-defense molecules to flow through.
• It has higher rate of cellular proliferation and
turnover.

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Role of Inflammation
• Cytokines are proteins secreted by cells that
interact with other cells and eventually lead to a
specific cellular response.
• Cytokines can be proinflammatory or anti-
inflammatory in nature. Proinflammatory
cytokines such as interleukin-1 (IL-1) and tumor
necrosis factor-alpha (TNF-α) are implicated
strongly in the pathogenesis of periodontal
disease progression.
• Anti-inflammatory cytokines such as IL-4 and IL-
10 counteract the effects of proinflammatory
cytokines.

• The transformation of a gingival sulcus into a

periodontal pocket creates an area in which
plaque removal becomes impossible, and a
feedback mechanism is established.
• The rationale for pocket reduction is based on
the need to eliminate areas of plaque
accumulation.

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Clinical Features
• Early concepts assumed that after the initial
bacterial attack, periodontal tissue destruction
continued to be linked to bacterial action.
• More recently it was established that the
host’s immunoinflammatory response to the
initial and persistent bacterial attack
unleashes mechanisms that lead to collagen
and bone destruction.

• The only reliable method of locating

periodontal pockets and determining their
extent is careful probing of the gingival margin
along each tooth surface.

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1. The gingival wall of the pocket presents

various degrees of bluish red discoloration;
flaccidity; a smooth, shiny surface; and
pitting on pressure.
2. Less frequently, the gingival wall may be pink
and firm.
3. Bleeding is elicited by gently probing the
soft-tissue wall of the pocket.
4. When explored with a probe, the inner
aspect of the pocket is generally painful.
5. In many cases, pus may be expressed with
the application of digital pressure.

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Histopathology
1. The discoloration is caused by circulatory
stagnation; the flaccidity by the destruction of
gingival fibers and surrounding tissues.
2. Fibrotic changes predominate over exudation
and degeneration, particularly in relation to the
outer surface of the pocket wall.
3. Ease of bleeding results from increased
vascularity, the thinning and degeneration of the
epithelium, and the proximity of engorged
vessels to the inner surface.
4. Pain on tactile stimulation is caused by the
ulceration of the inner aspect of the pocket wall.
5. Pus occurs in pockets with suppurative
inflammation of the inner wall.
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Bacterial Invasion
• Bacterial invasion of the apical and lateral areas of the
pocket wall has been described in human chronic
periodontitis.
• the presence of Porphyromonas gingivalis and
Prevotella intermedia in the gingiva of aggressive
periodontitis cases. Aggregatibacter
actinomycetemcomitans has also been found in the
tissues.
• The presence of bacteria in the gingival tissues has
been interpreted by different investigators as bacterial
invasion or as the “passive translocation” of plaque
bacteria.

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Mechanisms of Tissue Destruction

• The inflammatory response triggered by bacterial
plaque unleashes a complex cascade of events
aimed at destroying and removing bacteria,
necrotic cells, and deleterious agents.
• However, this process is nonspecific; in an
attempt to restore health, the host’s cells (e.g.,
neutrophils, macrophages, fibroblasts, epithelial
cells) produce proteinases, cytokines, and
prostaglandins that can damage or destroy the
tissues.

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Microtopography of the Gingival Wall

1. Areas of relative quiescence, showing a relatively flat surface with
minor depressions and mounds and occasional shedding of cells.
2. Areas of bacterial accumulation, which appear as depressions on
the epithelial surface, with abundant debris and bacterial clumps
penetrating into the enlarged intercellular spaces.
3. Areas of emergence of leukocytes, in which leukocytes appear in
the pocket wall through holes located in the intercellular spaces.
4. Areas of leukocyte–bacteria interaction, in which numerous
leukocytes are present and covered with bacteria in an apparent
process of phagocytosis.
5. Areas of intense epithelial desquamation, consisting of semi
attached and folded epithelial squames, which are sometimes
partially covered with bacteria.
6. Areas of ulceration, with exposed connective tissue.
7. Areas of hemorrhage, with numerous erythrocytes.

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• A- Area of quiescence.
• B- Bacteria.
• C- Leukocyte and
Bacteria.
• D- Desquamation.

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• Advances periodontitis,
desquamation of the
cells.

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Area of Ulceration

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Surface Morphology of Tooth Wall

1. Cementum covered by calculus, in which all of the
changes described in the preceding paragraphs can be
found.
2. Attached plaque, which covers calculus and extends
apically from it to a variable degree (typically 100 to 500
μm).
3. The zone of unattached plaque that surrounds attached
plaque and extends apically to it.
4. The zone of attachment of the junctional epithelium to
the tooth. The extension of this zone, which in normal
sulci is more than 500 μm, is usually reduced in
periodontal pockets to less than 100 μm.
5. A zone of semi destroyed connective tissue fibers may be
apical to the junctional epithelium (see the Pathogenesis
section earlier in this chapter).

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Relationship of Attachment Loss and

Bone Loss to Pocket Depth
• The severity of the attachment loss in pocket formation is
generally but not always correlated with the depth of the
pocket. This is because the degree of attachment loss
depends on the location of the base of the pocket on the
root surface, whereas pocket depth is the distance between
the base of the pocket and the crest of the gingival margin.
• Pockets of the same depth may be associated with different
degrees of attachment loss, and pockets of different depths
may be associated with the same amount of attachment
loss.

The severity of bone loss is generally but not always

correlated with pocket depth.

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Periodontal Abscess
• Periodontal abscess formation may occur in the following
ways:
1. Extension of infection from a periodontal pocket deep
into the supporting periodontal tissues.
2. Lateral extension of inflammation from the inner surface
of a periodontal pocket into the connective tissue of the
pocket wall.
3. Formation in a pocket with a tortuous course around the
root.
4. Incomplete removal of calculus during treatment of a
periodontal pocket.
5. After trauma to the tooth or with perforation of the
lateral wall of the root in endodontic therapy.

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• Periodontal abscesses are classified according

to location as follows:
1. Abscess in the supporting periodontal tissues
along the lateral aspect of the root.
2. Abscess in the soft-tissue wall of a deep
periodontal pocket.

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Distinguishing Features of Supra-

bony and Intra-bony Periodontal
Pockets

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Supra-bony
1. The pattern of destruction of the underlying
bone is horizontal.
2. Interproximal, transseptal fibers that are
restored during progressive periodontal disease
are arranged horizontally in the space between
the base of the pocket and the alveolar Bone.
3. On the facial and lingual surfaces, periodontal
ligament fibers beneath the pocket follow their
normal horizontal–oblique course between the
tooth and the bone.

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Intra-bony
1. The base of the pocket is apical to the crest of the
alveolar bone so that the bone is adjacent to the soft-
tissue wall
2. The pattern of bone destruction is vertical (angular)
3. Interproximal, transseptal fibers are oblique rather
than horizontal.
4. They extend from the cementum beneath the base of
the pocket along the alveolar bone
5. On the facial and lingual surfaces, periodontal
ligament fibers follow the angular pattern of the
adjacent bone.

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