The periodontal pocket, defined as a pathologically deepened
gingival sulcus, is one of the most important clinical features of periodontal
disease. All different types of periodontitis share histopathologic features
such as tissue changes in the periodontal pocket, mechanisms of tissue
destruction, and healing mechanisms. They differ, however, in their etiology,
natural history, progression, and response to therapy.
CLASSIFICATION
Deepening of the gingival sulcus may occur by coronal movement
of the gingival margin, apical displacement of the gingival attachment, or a
combination of the two processes.
Illustration of pocket formation indicating expansion in two directions (arrows) from the normal gingival sulcus (left) to the periodontal pocket (right) |
Pockets
can be classified as follows:
Gingival pocket (pseudo pocket):
This type of pocket is formed by gingival enlargement
without destruction of the underlying periodontal tissues. The sulcus is deepened
because of the increased bulk of the gingiva
Periodontal pocket:
This type of pocket occurs with destruction of the
supporting periodontal tissues. Progressive pocket deepening leads to
destruction of the supporting periodontal tissues and loosening and exfoliation
of the teeth.
Two
types of periodontal pockets exist:
Suprabony
(supracrestal or supraalveolar), in which the bottom of the pocket is coronal
to the underlying alveolar bone.
Intrabony
(infrabony, subcrestal or intraalveolar), in which the bottom of the pocket is
apical to the level of the adjacent alveolar bone. In this second type, the lateral
pocket wall lies between the tooth surface and the alveolar bone.
Pockets can involve one, two, or more tooth surfaces and
can be of different depths and types on different surfaces of the same tooth
and on approximating 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.
Classification of pockets according to involved tooth surfaces. A, Simple pocket. B, Compound pocket. C, Complex pocket |
CLINICAL FEATURES
Clinical signs such as bluish-red, thickened marginal
gingiva;
A bluish-red vertical zone from the gingival margin to
the alveolar mucosa;
Gingival bleeding, suppuration,or both;
Tooth mobility;
And diastema formation and symptoms such as localized
pain or pain "deep in the bone" are suggestive of the presence of
periodontal pockets.
The only reliable method of locating periodontal pockets
and determining their extent is careful probing of the gingival margin along
each tooth surface.
Correlation of Clinical and Histopathologic Features of the Periodontal Pocket
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Clinical Features
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Histopathologic Features
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1. The gingival wall of the periodontal
pocket presents various degrees of bluish-red discoloration; flaccidity; a
smooth, shiny surface; and pitting on pressure.
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1. The discoloration is caused by
circulatory stagnation; the flaccidity, by destruction of the gingival fibers
and surrounding tissues; the smooth, shiny surface, by the atrophy of the
epithelium and edema; the pitting on pressure, by edema and degeneration.
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2. Less frequently, the gingival wall may
be pink and firm.
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2. In such cases, fibrotic changes
predominate over exudation and degeneration, particularly in relation to the
outer surface of the pocket wall. However, despite the external appearance of
health, the inner wall of the pocket invariably presents some degeneration
and is often ulcerated.
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3. Bleeding is elicited by gently probing
the soft tissue wall of the pocket.
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3. Ease of bleeding results from increased
vascularity, thinning and degeneration of the epithelium, and the proximity
of the engorged vessels to the inner surface.
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4. When explored with a probe, the inner
aspect of the periodontal pocket is generally painful.
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4. Pain on tactile stimulation is due to
ulceration of the inner aspect of the pocket wall.
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5. In many cases, pus may be expressed by
applying digital pressure.
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5. Pus occurs in pockets with suppurative inflammation
of the inner wall.
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On the basis of depth alone, however, it is sometimes
difficult to differentiate between a deep normal sulcus and a shallow
periodontal pocket. In such borderline cases, pathologic changes in the gingival
distinguish the two conditions.
PATHOGENESIS
The initial lesion in the development ofperiodontitis is
the inflammation of the gingiva in response to a bacterial challenge. Changes
involved in the transition from the normal gingival sulcus to the pathologic
periodontal pocket are associated with different proportions of bacterial cells
in dental plaque. Healthy gingiva is associated with few microorganisms, mostly
coccoid cells and straight rods. Diseased gingiva is associated with increased
numbers of spirochetes and motile rods. However, the microbiota of diseased
sites cannot be used as a predictor of future attachment or bone loss because
their presence alone is not sufficient for disease to start or progress.
Extension of the junctional epithelium along the root
requires the presence of healthy epithelial cells. Marked degeneration or
necrosis of the junctional epithelium retards rather than accelerates pocket
formation. Degenerative changes seen in the junctional epithelium at the base
of periodontal pockets are usually less severe than those in the epithelium of
the lateral pocket wall. Because migration of the junctional epithelium
requires healthy, viable cells, it is reasonable to assume that the degenerative
changes seen in this area occur after the junctional epithelium reaches its
position on the cementum.
The transformation of a gingival sulcus into a periodontal
pocket creates an area where plaque removal becomes impossible, and the following
feedback mechanism is established:
The rationale for pocket reduction is based on the need
to eliminate areas of plaque accumulation.
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