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.