Pathogenesis

The pathogenesis or sequence of events in the development of a gingivitis-periodontitis lesion is very complex. It involves not only local phenomena in the gingiva, PDL, tooth surface, and alveolar bone but also a number of complex host response mechanisms modified by the bacterial infection and behavioral factors.21 Implicated in the pathogenic mechanism are phagocytic cells, the lymphoid system, antibodies and immune complexes, complement and clotting cascades, immune reactions, and the microcirculation. Detailed descriptions of host response in the gingivitis-periodontitis lesion can be obtained by referring to standard periodontal texts .

The chronic plaque-induced lesion has been investigated- 22 in great detail clinically, histopatho-logically, and ultrastructurally, and the model of disease activity has remained consistent over time. From these analyses, an indistinct division into initial, early, established, and advanced stages has been put forth. The salient features and approximate time frame for each stage are presented here.

Initial Lesion. The initial lesion (Fig. 5-5) is localized in the region of the gingival sulcus and is evident after approximately 2 to 4 days of undisturbed plaque accumulation from a baseline of gingival health. The vessels of the gingiva become enlarged, and vasculitis occurs, allowing a fluid exudate of polymorphonuclear leukocytes to form in the sul-cus. Collagen is lost perivascularly, and the resultant space is filled with proteins and inflammatory cells. The most coronal portion of the junctional epithelium becomes altered.

Early Lesion. Although there is no distinct division between the stages of lesion formation, the early lesion (Fig. 5-6) generally appears within 4 to 7 days of plaque accumulation. This stage of devel opment exhibits further loss of collagen from the marginal gingiva. In addition, an increase in gingival sulcular fluid flow occurs with increased inflammatory cells and the accumulation of lymphoid cells subjacent to the junctional epithelium. The basal cells of the junctional epithelium begin to proliferate, and significant alterations are seen in the connective tissue fibroblasts.

Established Lesion. Within 7 to 21 days the lesion enters the established stage (Fig. 5-7). It is still

Junctional Epithelium

Fig. 5-6. Early lesion of gingivitis-periodontitis. The predominant inflammatory cells are lymphocytes subjacent to the junctional epithelium. The epithelium is beginning to proliferate into rete ridges.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

Fig. 5-6. Early lesion of gingivitis-periodontitis. The predominant inflammatory cells are lymphocytes subjacent to the junctional epithelium. The epithelium is beginning to proliferate into rete ridges.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

Pathogenesis Periodontal Disease

Fig. 5-5. Initial lesion of gingivitis-periodontitis. There is a predominance of polymorphonuclear leukocytes in the beginning stages of inflammation.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

Fig. 5-5. Initial lesion of gingivitis-periodontitis. There is a predominance of polymorphonuclear leukocytes in the beginning stages of inflammation.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

Initial Gingival Lesion

Fig. 5-7. Established lesion of gingivitis-periodontitis. The junctional epithelium is converted into pocket epithelium. Pocket formation may begin. The predominant inflammatory cells are plasma cells.

(Redrawn from Schluger S et al: Periodontal disease, ed2, Philadelphia, 1990, Lea & Febiger.)

Fig. 5-7. Established lesion of gingivitis-periodontitis. The junctional epithelium is converted into pocket epithelium. Pocket formation may begin. The predominant inflammatory cells are plasma cells.

(Redrawn from Schluger S et al: Periodontal disease, ed2, Philadelphia, 1990, Lea & Febiger.)

Bulbous Gingiva
Fig. 5-8. Gingivitis. The interproximal gingiva is bulbous and inflamed. Note the erythematous and edematous tissue extending onto the labial portions of the lateral incisors.

Fig. 5-10. Periodontitis. Plaque and calculus accumulation has resulted in a loss of connective tissue attachment apical to the CEJ.

Periodontal Pocket Formation

Fig. 5-9. Advanced lesion of gingivitis-periodontitis. Pocket formation has begun, with a loss of connective tissue attachment apical to the CEJ. Bone is converted into fibrous connective tissue and is subsequently lost. The predominant inflammatory cells are plasma cells, and there are scattered lymphocytes present.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

Fig. 5-9. Advanced lesion of gingivitis-periodontitis. Pocket formation has begun, with a loss of connective tissue attachment apical to the CEJ. Bone is converted into fibrous connective tissue and is subsequently lost. The predominant inflammatory cells are plasma cells, and there are scattered lymphocytes present.

(Redrawn from Schluger S et al: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.)

located at the apical portion of the gingival sulcus, and the inflammation is centered in a relatively small area. There is continuing loss of connective tissue, with persistence of the features of the early lesion. This stage exhibits a predominance of plasma cells, the presence of immunoglobulins in the connective tissue, and a proliferation of the functional epithelium (Fig. 5-8). Pocket formation, however, does not necessarily occur.

Advanced Lesion. It is difficult to pinpoint the time at which the established lesion of gingivitis results in a loss of connective tissue attachment to the tooth structure and becomes an advanced lesion or overt periodontitis (Fig. 5-9). Upon conversion to the advanced stage, the features of an established lesion persist. The connective tissue continues to lose collagen content, and fibroblasts are further altered. Periodontal pockets are formed, with increased probing depths, and the lesion extends into alveolar bone. The bone marrow converts to fibrous connective tissue, with a significant loss of connective tissue attachment to the root of the tooth. This is accompanied by the manifestations of im-munopathologic tissue reactions and inflammatory responses in the gingiva.

Periodontitis. When a loss of connective tissue attachment occurs, the lesion transforms from gingivitis into periodontitis (Fig. 5-10), a disease that may be characterized by alternating periods of quiescence and exacerbation. The extent to which the lesion progresses before it is treated will determine the amount of bone and connective tissue attachment loss that occurs. It will subsequently affect the prognosis of the tooth with regard to restorative demands.

(*] EXAMINATION, DIAGNOSIS,

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