Bacteria are present throughout life in a myriad of sites on and in the human body. The bacteria may be beneficial for the host, or of no consequence (commensal), or injurious. In the oral cavity, over 530 different species of microorganisms have so far been identified; fortunately, for the most part these organisms remain in ecological balance and do not cause disease. Certain facultatively pathogenic (“opportunistic”) bacteria are occasionally observed in high numbers, e.g., in cases of disease (periodontitis, mucosal infection). It remains unclear whether these bacteria alone represent the cause of the diseases, or whether they simply find favorable living conditions in the disease milieu. Non-specific supragingival plaque (mixed flora) will elicit gingivitis within ca. seven days. If the plaque is removed, gingivitis regresses in a short period of time (“reversibility”). On the other hand, for the various forms of periodontitis, especially the aggressive, rapidly-progressing forms, specific bacteria are associated.
Biofilm—Plaque Formation on Tooth and Root Surfaces
The oropharynx is an open ecosystem wherein bacteria are always present; bacteria attempt to colonize in all favorable locations. Most bacteria, however, can only persist after the formation of a biofilm upon desquamation-free surfaces, i.e., hard substances (tooth and root surfaces, restorative materials, implants, prostheses etc.). In the presence of healthy dental and gingival relationships, there is a balance between the additive and retentive mechanisms of biofilms vis-à-vis the abrasive forces that tend to reduce biofilm formation, e.g., self-cleansing by the cheeks and tongue, diet and mechanical oral hygiene measures.
The existence of a biofilm results within a matter of hours or days, in the phases described below (Darveau et al. 1997, Descouts & Aronsson 1999, Costerton et al. 1999).
The establishment and stabilization of bacteria within a biofilm are important not only for the etiology of periodontitis, but also for adjunctive systemic and topical medicinal treatment for periodontitis (p. 287): Biofilm bacteria imbedded within a matrix of extracellular polysaccharides are more than 1,000 times less sensitive to antimicrobials (e.g., antibiotics) than free-floating (“planktonic”) bacteria.
… and its Initial Subgingival Expansion
The first bacteria that accumulate supragingivally on the tooth surface are mostly gram-positive (Streptococcus sp, Actinomyces sp.). In the course of the following days, gramnegative cocci as well as gram-positive and gram-negative rods and the first filamentous forms begin to colonize (Listgarten et al. 1975, Listgarten 1976). By means of a variety of metabolic products, the bacterial flora provoke the tissue to increased exudation and migration of PMN leukocytes into the sulcus (“leukocyte walls” against the bacteria).
The increase in PMN diapedesis and the flow of sulcus fluid lead to initial disintegration of the junctional epithelium. This makes it possible for bacteria to more easily invade between the tooth and the junctional epithelium, and invade the subgingival area (gingivitis, gingival pocket formation). In the total absence of oral hygiene, plaque formation and an initial host defensive response within gingival tissue occur. With optimum—including interdental—oral hygiene, the formation of biofilm is repeatedly disrupted and gingival health is maintained.
Natural Factors Favoring Plaque Retention
The formation of a plaque biofilm can be enhanced by natural retention factors, which can also render biofilm removal by means of oral hygiene more difficult. These retention factors include:
Supra- and subgingival calculus
Cementoenamel junctions and enamel projections
Furcation entrances and irregularities
Tooth fissures and grooves
Cervical and root surface caries
Crowding of teeth in the arch.
By itself, calculus is not pathogenic. However, its rough surface presents a retention area for vital, pathogenic bacteria. At the microscopic level, the cementoenamel junction is very irregular, and offers retentive roughness. Enamel projections and “pearls” also inhibit soft tissue attachment.
Furcation entrances, fissures, etc. are retentive niches for plaque. Carious lesions represent a huge bacterial reservoir. Crowding of teeth reduces self-cleansing and renders oral hygiene more difficult.
Iatrogenic Factors Favoring Plaque Retention
Restorative dentistry—from a simple restoration to a fullmouth reconstruction—can do more harm than good to the patient’s oral health if performed improperly! Placing only optimum restorations is synonymous with preventive periodontics (tertiary prevention, p. 198).
Fillings and crowns that appear to be perfect clinically and macroscopically almost always exhibit deficiencies at the margins when viewed microscopically. When margins are located subgingivally, they always present an irritation for the marginal periodontal tissues.
Overhanging margins of restorations and crowns accumulate additional plaque. Gingivitis ensues. The composition of the plaque changes. The number of gram-negative anaerobes (e.g., Porphyromonas gingivalis), the organisms responsible for initiation and progression of periodontitis, increases rapidly (Lang et al. 1983).
Gross iatrogenic irritants such as poorly designed clasps and prosthesis saddles may exert a direct traumatic influence upon periodontal tissues.
Extending apically from the supragingival region, a subgingival plaque biofilm will often form within the existing gingival sulcus/pocket; this was previously called the “adherent” plaque. In addition to gram-positive bacteria such as streptococci, actinomyces, etc., as the probing depth increases so does the number of anaerobic gram-negative bacteria (p. 36).
This subgingival biofilm can also calcify. A dark, hard and difficult to remove calculus (“serum calculus”) accumulates. In addition, the gingival pocket also contains loose agglomerates of non-adherent, often mobile bacteria (with a high concentration of gram-negative anaerobes and spirochetes). In acute phases, periodontopathic bacteria often increase dramatically. These include Actinobacillus actinomycetemcomitans, P. gingivalis, T. forsythia, spirochetes etc. (pp. 30, 33, 38). Despite these alterations in the subgingival plaque, periodontitis, even in the acute stage, cannot be characterized as a “highly specific” infection because large differences have been reported in the bacterial composition between patients and even within different pocket locations in the same patient (Dzink et al. 1988, Slots & Taubmann 1992, Lindhe 1997).