Etiology and Pathogenesis

The most common diseases of the tooth-supporting apparatus are plaque-induced, usually chronic, inflammatory alterations in the gingiva and the subjacent periodontal structures.

Gingivitis may persist for many years without progressing to periodontitis. With good oral hygiene and effective professional removal of plaque and calculus, gingivitis is completely reversible.

Periodontitis usually develops out of a more or less pronounced gingivitis. Periodontitis is only partially reversible (see periodontal healing, p. 205/regenerative therapies).

The reasons why gingivitis develops into periodontitis (or does not) are still incompletely understood. As with all infections, it appears that the proliferation of pathogenic microorganisms, their toxic potency, their capacities to invade tissues, and above all the individual host response to such infections are the determining factors (p. 55; Kornman et al. 1997, Page & Kornman 1997, Salvi et al. 1997).

An absolutely plaque-free condition in the oral cavity, with prevention of any biofilm formation on tooth surfaces is unachievable, and illusion, and probably even unphysiologic. Nevertheless, gingival and periodontal health can be maintained if the accumulation of plaque is small and if the biofilm contains only weakly virulent organisms (gram-positive, facultative anaerobes), and if an effective host response is mounted.

If the bacterial flora takes on periodontally pathogenic characteristics (e.g., certain gram-negative microorganisms), the result will be inflammation and specific immunologic responses; these responses may represent not only defense mechanisms, but—especially in long-term chronic infection—also destructive potential (cytotoxic, immunopathologic; p. 34).

Inflammation-inducing products of bacteria include enzymes, antigens, toxins, and “signal” substances that activate macrophages and T-cells (Birkedal-Hansen 1998). It is likely that bacterial enzymes, other metabolic products and toxins can directly elicit injury to the periodontal tissues even without immediate host response (inflammation). Bacterial products including hyaluronidase, chondroitin sulfatase, proteolytic enzymes, as well as cytotoxins in the form of organic acids, ammonia, hydrogen sulfide and endotoxins (e.g., lipopolysaccharides, LPS) have been demonstrated in periodontal tissues.

Periodontitis—A Multifactorial Disease

In recent years, the conceptual view concerning the etiology of periodontitis has evolved. Early on, it was the bacteria that were viewed as the determining factor. Certain pathogenic microorganisms were shown to be associated with various forms of periodontal disease, as well as the speed of progression. However, the existence and distribution of pathogenic bacteria did not always correlate with the inception and clinical progression of periodontitis. Furthermore, it was demonstrated that the presence of pathogenic bacteria in a periodontal pocket is not necessarily the cause of that pocket; rather, it seemed much more important that the pocket milieu presents a favorable environment for the existence and proliferation of pathogenic organisms. The stage would then be set—like a vicious cycle—for the progression of the disease processes (Mombelli et al. 1991).

Nevertheless, the old adage “no bacteria = no periodontitis” still holds true, but on the other hand it is also a fact that bacteria, including periodontopathic bacteria, do not without exception cause periodontitis.

In addition to specific microorganisms, diverse host factors are critical for the development of periodontitis from a preexisting gingivitis (cf. Fig. 41, modified from Clarke & Hirsch 1995). Such factors include the immune responses triggered by pathogens, and these are well understood today. Such defense reactions may be disproportional to the insult, resulting in immunopathologic tissue injury.

Recently, however, in addition to the genetically determined immune reactions, a great number of other individual risk factors have been identified, which may be responsible for the initiation and the degree of severity of the clinical course of periodontitis (p. 51).

Of the risk factors listed in Figures 41 and 104, only a few are capable of damaging the periodontium directly (e.g., smoking); of much greater importance is the influence of such factors on the patient’s own immune system. The delicate balance between “attack/destruction” (bacteria) and defense (host response) is disturbed. It is only logical to assume that the most severe, early-onset and aggressive forms of periodontitis will occur when particularly virulent bacteria are present in a weak (immunodeficient) host.

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