The periodontal pocket Logien Al Ghazal 3/11/2015

CONTENT CLASSIFICATION CLINICAL FEATURES PATHOGENESIS HISTOPATHOLOGY 4.1 Soft Tissue Wall 4.2 Microtopography of the Gingival Wall of the Pocket 4.3 Periodontal Pockets as Healing Lesions 4.4 Pocket Contents 4.5 Root Surface Wall SITE SPECIFICITY PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKETS RELATION OF ATTACHMENT LOSS AND BONE LOSS TO POCKET DEPTH AREA BETWEEN THE BASE OF THE POCKET AND THE ALVEOLAR BONE PERIODONTAL ABSCESS PERIODONTAL CYST

Definition of periodontal pocket: Defined as a pathologically deepened gingival sulcus, is one of the most important clinical features of periodontal disease. 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: 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 according to the relation of the pocket to the adjacent alveloar bone crest: 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.

Suprabony Pocket Intrabony Pocket The base of the pocket is coronal to the level of the alveolar bone. The base of the pocket is apical to the crest of the alveol ar bone so that the bone is adjacent to the soft tissue wall The pattern of destruction of the underlying bone is horizontal. The base of the pocket is apical to the crest of the alveolar bone so that the bone is adjacent to the soft tissue Interproximally, the 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 the facial and lingual surfaces, the periodontal ligament fibers follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join with the outer periosteum. On the facial and lingual surfaces, the periodontal ligament fibers beneath the pocket follow their normal horizontal-oblique course between the tooth and the bone. the facial and lingual surfaces, the periodontal ligament fibers follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join with the outer periosteum.

Classification of pockets according to involved tooth surfaces. A. Simple pocket: one tooth surface B. Compound pocket. Two tooth surfaces C. Complex pocket (Spiral) 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.

Bluish-red, thickened marginal gingiva; 2. CLINICAL FEATURES Signs : Bluish-red, thickened marginal gingiva; Bluish-red vertical zone from the gingival margin to the alveolar mucosa Gingival bleeding, suppuration, or both; tooth mobility diastema formation. Symptoms Localized pain or pain "deep in the bone" are suggestive of the presence of periodontal pockets. Dull aching pain (itching pain).

The only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface. 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 gingiva 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 is mainly caused by 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.

The transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes Impossible. The rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

HISTOPATHOLOGY Soft tissue wall The connective tissue wall is edematous and densly infiltrated with plasma cells. Blood vesssels are engorged and dilated and increase in their number. The connective tissue (C.T) exhibits varying degree of necrotic foci The c.t exhibits degenrative and proliferative change including new endothelium, fibroblast and collagen fibers. The junctional epithelium is much shorter that a normal sulcus. The most striking degenerative changes are found in the lateral wall, with epithelial projections apical to J.E and infiltrated with leukocytes and edema. These cells undergo vacuolar degeneration and rupture to form vesicles. The degeneration showed more prominent in aggressive periodontitis that chronic periodontitis. The rupture causes ulceration in the lateral wall. The ulcertaion are present in both shallow and deep pockets. The epitelium at the gingival crest is generally intact and thickened by rete pegs.

Microtopography of the Gingival Wall of the Pocket 1. Areas of relative quiescence, showing a relatively flat surface with shedding of cells. 2. Areas of bacterial accumulation, abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. Cocci, rods, and filaments, with a few spirochetes. 3. Areas of emergence of leukocytes. 4. Areas of leukocyte-bacteria interaction, where numerous leukocytes are present and covered with bacteria in an apparent process of phagocytosis. 5. Areas of intense epithelial desquamation, which consist of semi-attached and folded epithelial squames, sometimes partially covered with bacteria. 6. Areas of ulceration, with exposed connective tissue. 7. Areas of hemorrhage, with numerous erythrocytes.

Periodontal pockets are chronic inflammatory lesions Periodontal Pockets as Healing Lesions Periodontal pockets are chronic inflammatory lesions and as such are constantly undergoing repair. Complete healing does not occur. Soft tissue wall of the periodontal pocket results from the interplay of the destructive and constructive tissue changes. Their balance determines clinical features such as color, consistency, and surface texture of the pocket wall.

Edematous pocket: wall The pocket wall is bluishred, soft, spongy, and friable, with a smooth, shiny surface. fibrotic pocket wall :If there is a relative predominance of newly formed connective tissue cells and fibers, the pocket wall is more firm and pink. Fibrotic pocket walls may be misleading because they do not necessarily reflect what is taking place throughout the pocket wall.

Periodontal pockets contain debris consisting principally: Pocket Contents Periodontal pockets contain debris consisting principally: Microorganisms and their products (enzymes, endotoxins, and other metabolic products. Gingival fluid. Food remnants. Salivary mucin. Desquamated epithelial. Leukocytes. Plaque-covered calculus usually projects from the tooth surface. Purulent exudate, if present, consists of living, degenerated, and necrotic leukocytes; living and dead bacteria; serum; and a scant amount of fibrin.

The root surface wall of periodontal pockets often undergoes changes that are significant because they may perpetuate the periodontal infection, cause pain. The bacteria growth and invasion to cementum may lead to the necrotic cementum separated from the tooth by masses of bacteria. Significance of Pus Formation. There is a tendency to overemphasize the importance of the purulent exudate and to equate it with severity of periodontal disease. Pus is a common feature of periodontal disease, but it is only a secondary sign. The presence of pus reflects the nature of the inflarnmatory changes in the pocket wall. It is not an indication of the depth of the pocket or the severity of the destruction of the supporting tissues.

Surface Morphology of the Tooth Wall of Periodontal Pockets. 1. Cementum covered by calculus. 2. Attached plaque 3. The zone of unattached plaque that surrounds attached plaque and extends apically to it. 4. The zone where the junctional epithelium is attached to the tooth. 5. Apical to the junctional epithelium, there may be a zone of semidestroyed connective tissue fibers

Periodontal pockets go through periods of exacerbation and quiescence. PERIODONTAL DISEASE ACTIVITY Periodontal pockets go through periods of exacerbation and quiescence. Periods of quiescence (Inactivity) are characterized by a reduced inflammatory response and little or no loss of bone and connective tissue attachment. Periods of exacerbation (activity) A buildup of unattached plaque, with its gram-negative, motile, and anaerobic bacteria. which bone and connective tissue attachment are lost and the pocket deepens.

SITE SPECIFICITY Periodontal destruction does not occur in all parts of the mouth at the same time. Few teeth at a time or even only some aspects of some teeth at any given time. This is referred to as the site specificity of periodontal disease. It is very common to find sites of periodontal destruction next to sites with little or no destruction. Therefore the severity of periodontitis increases by the development of new disease sites, the increased breakdown of existing sites, or both.

PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKETS The spread of infection from periodontal pockets may cause pathologic changes in the pulp. Rises painful symptoms or adversely affect the response of the pulp to restorative procedures. Involvement of the pulp in periodontal disease occurs through either the apical foramen or the lateral canals in the root after infection spreads from the pocket through the periodontal Ligament.

Pocket formation causes loss of attachment of the gingiva RELATION OF ATTACHMENT LOSS AND BONE LOSS TO POCKET DEPTH Pocket formation causes loss of attachment of the gingiva and denudation of the root surface. The severity of the attachment loss is generally, but not always, correlated with the depth of the pocket. Attachment loss depends on the location of the base of the pocket on the root surface. Pocket depth is the distance between the base of the pocket and the crest of the gingival margin. Severity of bone loss is generally, but not always, correlated with pocket depth. Extensive attachment and bone loss may be associated with shallow pocket recession of the gingival margin and (Vice versa).

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.

Normally, the distance between the apical end of the functional AREA BETWEEN THE BASE OF THE POCKET AND THE ALVEOLAR BONE Normally, the distance between the apical end of the functional epithelium and the alveolar bone is relatively constant. The distance between the apical extent of calculus and the alveolar crest in human periodontal pockets is most Constant. The distance from attached plaque to bone is never less than 0.5mm. These findings suggest that the bone-resorbing activity induced by the bacteria is exerted within these distances.

A periodontal abscess is a localized purulent inflammation PERIODONTAL ABSCESS , LATERAL OR PARIETAL ABSCESS. A periodontal abscess is a localized purulent inflammation in the periodontal tissues. Gingival abscesses Abscesses localized in the gingiva, caused by injury to the outer surface of the gingiva, and not involving the supporting structures.

Formation of the periodontal abscess 1.Extension of infection from a periodontal pocket deeply into the supporting periodontal tissues and localization of the suppurative inflammatory process along the lateral aspect of the root. 2. Lateral extension of inflammation from the inner surface of a periodontal pocket into the connective tissue of the pocket wall. 3. In a pocket that describes a tortuous course around the root, a periodontal abscess may form in the cul de- sac, the deep end of which is shut off from the surface. 4. Incomplete removal of calculus during treatment of a periodontal pocket. In this instance, the gingival wall shrinks, occluding the pocket orifice. 5. A periodontal abscess may occur in the absence of periodontal disease after trauma to the tooth or perforation of the lateral wall of the root in endodontic treatment.

PERIODONTAL CYST The periodontal cyst 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. The following possible etiologies have been suggested: Odontogenic cyst Lateral dentigerous cyst. 3. Primordial cyst of supernumerary tooth germ. 4. Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal abscess or the pulp through an accessory root canal. A periodontal cyst is usually asymptomatic, but it may present as a localized tender swelling. Radiographically, an interproximal periodontal cyst appears on the side of the root as a radiolucent area bordered by a radiopaque line.