Gingivitis—Periodontitis

The general term “periodontal diseases” encompasses inflammatory as well as recessive alterations within the gingiva and the periodontium (Page & Schroeder 1982; AAP 1989, 1996; Ranney 1992, 1993; Lindhe et al. 1997; Armitage 1999).

While gingival recession may have various etiologies, including morphologic, mechanical (improper oral hygiene) and even functional (p. 155), gingivitis and periodontitis are plaque-associated diseases. Today it is becoming more and more clear that bacteria alone, including even the so-called periodontopathic bacteria, can always elicit gingivitis, but not periodontitis in every case. The initiation of periodontitis, its speed of progress and the expression of its clinical picture also involve the responsibility of negative host factors and additional so-called risk factors (Clark & Hirsch 1995). One of the most important are defects of the acute host response resulting from functional disturbances of polymorphonuclear granulocytes (PMN), other insufficient immunologic reactions, and the predominance of pro-inflammatory mediators, many of which are genetically determined. The now well established alterable risk factors include, particularly, “unhealthy” habits such as smoking, alcohol consumption and a less than well-rounded diet (p. 22).

Furthermore, systemic disorders and syndromes are usually unalterable, obligate or facultative risk factors for periodontitis. In this regard, especially Diabetes mellitus is viewed as prejudicial (p. 132). Finally, the entire social environment of an individual can play an important role for the initiation and propagation of periodontitis (pp. 22, 51).

All of the factors discussed in the chapter “Etiology and Pathogenesis” (p. 21) enhance the occurrence of all diseases, including periodontitis. Thus, periodontitis is considered to be of multifactorial etiology. It remains difficult in the face of a manifest disease process to differentiate the “etiologic weight” of bacteria on the one hand and the host response and risk factors on the other hand, or to differentiate between and among such etiologic factors. The contemporary, on-going search for responsible “risk markers” is therefore very important.

Today, clinicians can use additional clinical parameters such as bleeding on probing, the severity of the disease in relation to patient age, as well as microbiologic and genetic tests in order to establish some semblance of a proper diagnosis and prognosis (p. 165).

In the future, more precise research into the reduced host defense occasioned by immunologic defects, as well as the type and quantity of participating cytokines and inflammatory mediators (e.g., in sulcus fluid, blood or saliva) will simplify diagnosis and permit more definitive predictions about the probable course of the disease, as well as indicating more targeted therapy.