Disease of the periodontal tissues constitutes the chief reason, more prevalent even than dental caries, for the loss of teeth. It is almost universally present among adults. Epidemiologic studies have shown an association between the development of coronary artery disease and the presence of periodontal disease. This is presumed to be independent of the close association between tobacco smoking and each of these conditions.
Periodontitis manifests as a chronic inflammation resulting from endogenous plaque bacteria, which arise from a worsening gingivitis culminating in the loss of dentition. A marginal periodontitis is usually the sequel to long-standing marginal gingivitis and generally includes all the signs of marginal gingivitis plus alveolar crestal bone and adjacent peridental membrane resorption. The formation of a periodontal pocket, a pathologic alteration of the gingival attachment, is pathognomonic for this condition. Periodontal disease is defined by pocket depth and loss of attachment. The epithelial lining of the gingival crevice is ulcerated, and the peridental membrane fibers are destroyed, generating an inflammatory cell infiltrate in the corium which may produce a purulent discharge. The epithelial attach- ment is displaced and takes successively deeper positions as the pocket increases. Beginning with notching of the alveolar crest, bone resorption continues, with destruction of the cribriform plate (lamina dura). Under the influence of occlusal trauma, the pocket penetrates toward the apex of the root; such pocket formation is seen in radiographic images as “vertical” in type, indi- cating advanced periodontal disease, compared with the simpler “horizontal” resorption. The local factors that contribute to the development of these pockets include deposition of plaque and calculi from saliva; food debris, which creates an environment for incubation of bacteria and a resulting microbiofilm in the mouth; poor oral hygiene; and mouth breathing. Tobacco is the most significant risk factor associated with the development of periodontal disease. Patients with diabetes mellitus, HIV infection, or cancer or who have undergone radia- tion therapy to the head and neck region are also at increased risk for periodontal disease. Medications that reduce salivary production can also contribute to the development of this condition. Some individuals are genetically susceptible to the development of periodontal disease; when they also have other high-risk factors, there is a greater likelihood of the development of severe periodontal disease.
Eighty-five percent of patients with periodontitis have mild disease, and less than 5% have aggressive periodontitis. Rapidly progressive chronic periodontitis can develop in young children, resulting in bone and possibly tooth loss by early adulthood. Aggressive periodontitis in healthy adolescents is typically a result of colonization by Aggregatibacter actinomycetemcomitans. A less common form of aggressive periodontitis affects the deciduous teeth, resulting in acute proliferative gingivitis with rapid alveolar destruction, which resolves before the eruption of the permanent teeth.
HIV infection is associated with a particularly virulent form of rapidly progressive periodontitis (see Plate 2-53).
Occlusal trauma, most often as a result of grinding (bruxism), clenching, or similar habits producing repetitive and excessive contacts of tooth on tooth, can result in an augmentation of lateral stresses on a tooth. The malpositioned, nonfunctional contacts result in dental abrasions on the surfaces and a widening of the periodontal membrane within the infrabony pockets, leading to tooth mobility.
A missing tooth permits an open contact, with food impaction causing an interproximal pocket, typically associated with caries on the distal tooth surface. The stress of occlusion on such a tooth may further accelerate the formation of a pocket on the mesial surface.
Migration of teeth, a late symptom in periodontitis, is a consequence of open contacts, wedging of food particles, extrusion of teeth through the pressure of granulation tissues, and other traumatic relationships in the deranged occlusion. Mobility of the teeth becomes marked as bone resorption increases the ratio of dental parts supported by bone to those not supported. The gingiva in this phase of periodontitis is typically soft and spongy and is duskier in color than normal, and there is retraction of the margin and abundant accretions of calculus.
Regardless of disease severity, the initial phase of treatment requires removal of plaque and calculus deposits through professional scaling and root planing, followed by proper oral hygiene.