Placa Supragingival

Periodontology 2000. Val. 8, 1995, 42-59 Printed in Denmark All rights reserued

Coavrizht 0 Munkspaard 1995

PERIODONTOLOGY 2000
ISSN 0906-6713

Supragingival dental plaque i the n etiology of oral diseases
OTHMAN SHIBLY, SUSAN RIFAI& J O S E P H J. ZAMBON
Dental plaque bacteria play a key role in what is now understood to be the complex process by which the most common types of oraldisease occur - dental caries and periodontal diseases (Fig. 1) (114). The conceptual framework for these oral diseases, like other infectious diseases, is that of a balance between host immune responses on the one hand and microbial pathogenesis on the other hand. In health, host immune responses are sufficient to hold in check the pathogenic potential of both the normal resident microbial flora orexogenous microbial pathogens. Infectious diseases such as dental caries and periodontal disease occur when this equilibrium is disturbed (29). If, for example, the host response is suppressed as the result of infection, as in acquired immunodeficiency syndrome or as the result of chemotherapy for cancer treatment or for transplantation, then opportunistic or other microbial pathogens can causedisease. Conversely, exogenous pathogens having significant virulence can overwhelm normal host defense mechanisms to cause disease. Against the background of this conceptual framework, this chapter briefly reviews dental plaque formation, discusses the role of dental plaque in dental caries and various types of periodontal disease and examines the role of supragingival plaque control in modulatingsubgingival plaque bacteria. tute distinct microbial ecological systems (82).Supragingival plaque can further be differentiated into coronal plaque and marginal plaque (901, and subgingiVal plaque can be differentiated into either adherent or nonadherent plaque (82). The development of supragingival plaque on exposed tooth surfaces as well as on artificial surfaces can be divided into threedistinct phases; salivary pellicle formation, initial bacterial colonization and the development of a complex plaque flora. Starting with a clean tooth surface as after dental prophylaxis, within minutes the tooth surface becomes covered with a 0.1- to 0.8-pm-thick layer of selectively absorbed, proteinaceous material derived from saliva known as pellicle (13, 60, 82, 92). Initial bacterialcolonization follows pellicle formation. Within 24 hours, gram-positive bacteria, mainly streptococci and Actinomyces, colonize the pelliclecoated tooth (82). Left undisturbed, the plaque mass develops into a complex ecology - a bacterial climax community - as is seen throughout nature. This occurs, first, through subsequent colonization of the pellicle-coated tooth by other bacteria and, second, by thegrowth and adherence of bacteria to each other (42, 89, 110). The ability of certain bacteria to colonize depends primarily on adherence mechanisms rather than on growth rate (60). Actinomyces viscosus and Streptococcus sanguis are the initial colonizers of dental pellicle: pioneer species. These ordinarily nonpathogenic bacteria form a monolayer. They facilitate the attachment of subsequent bacteria,other grarnnegative cocci as well as gram-negative rods and filaments (821, by altering the local environment. For example, they produce changes in local oxygen tension, facilitating colonization by facultative and anaerobic species. They also produce substrates as a consequence of their bacterial metabolism that can be utilized by other bacterial species (89, 92). The formation of dental plaqueis a dynamic process. Bacterial cell adherence, growth, removal and re-

Dental plaque formation
As generally understood, microbial dental plaque is a very dense, structured bacterial aggregation in a complex matrix comprised in part of extracellular polysaccharides (13).Approximately 75% of plaque volume is composed of bacterial cells. The other 25% consists of epithelial cells, leukocytes...