Periodontal disease and the complete dental prophylaxis (Proceedings)


Periodontal disease and the complete dental prophylaxis (Proceedings)

Aug 01, 2011

Pathogenesis of periodontal disease

Periodontal disease begins as an infiltrate subjacent to the epithelium of the gingival margin and rapidly extends throughout the marginal gingiva to affect the connective tissue underlying both the oral and the sulcular epithelium. In addition, there are pathologic alterations of both the sulcular and the oral epithelium of the marginal gingiva. The inflammatory lesion is found throughout the entire thickness of the marginal gingival tissue.

There is a significant correlation between deposit amounts and pocket depths and between deposits and hyperplastic tissues with the additional factor of infection by periodontal pathogens. The size of hyperplastic tissue mass and pocket depth increases concurrently as the disease becomes more severe.

Bone loss begins at the bifurcation of the second premolars and around the first premolars. As the disease progresses, the third and fourth premolars and then the first molars become involved. Bone resorption appears sooner and more severely in the bifurcation regions than interproximally. The first and second premolars are the teeth most frequently lost from periodontitis usually exhibiting bilateral symmetry in the disease process. The predilection for bone loss at the bifurcation of totally normal teeth is located at the base of the gingival sulcus and is readily accessible.

The clinical features and pathogenesis of periodontitis is characterized by conversion of the normal gingiva to acutely inflamed, highly vascular, collagen poor granulation tissue. The disease begins as an acute vasculitis upon which a lymphoid cell response becomes superimposed. However, at an early stage, proliferation of the tissues of the gingival margin and the soft tissue wall of the gingival sulcus occurs and enlargement becomes apparent. With the passage of time, this structure, which presents clinically as a rolled margin, enlarges and, in cross section, presents a mushroom-like appearance with a cauliflower-like surface. The structure is comprised of collagen poor, highly vascular granulation tissue with a dense infiltrate of lymphoid cells and a variable population of PMNs - vasculitis persists.

With time, this structure becomes smaller although in general there is a clear line of demarcation between the normal and the disease tissue. Enlargement continues until no normal gingiva remains. During this process, extensive bone resorption occurs. The soft tissues behave in one of two ways, either the hyperplastic granulation tissue remains located near the cemento-enamel junction and a deep periodontal pocket forms comparable to the situation usually seen around human teeth, or alternatively, the soft tissue retreats along the root surface as the bone resorbs. In cases of the latter type, the disease may progress to the point of tooth exfoliation without significant pocket formation.