Periodontal disease is an infectious disease caused by the presence of bacterial plaque (Timmerman et al 2001). Bacterial plaque is a nonmineralized accumulation of microbes that is able to adhere firmly to dental, restorative, and prosthetic surfaces. Bacterial plaque has been found to have structural organization. It cannot be displaced by mouth rinsing or by a high-pressure water spray (Listgarten 1994). Its growth is regulated by a dynamic balance between the oral microbiota and a number of factors that may either promote or inhibit the development of specific bacterial populations. Supragingival plaque essentially contains aerobic bacteria. In subgingival plaque, the proportion of gram-negative anaerobes increases.
Different forms of periodontitis have different bacteriologic etiologies. Features of periodontal disease are also determined by factors that modify host response or those that modulate individual host susceptibility, whether systemic, genetic, environmental, or acquired. These modifiers can activate or inhibit mechanisms involved in host response.
The protagonists of the response to bacterial insult are normally involved in tissue protection, but they also may be involved in the processes resulting in tissue destruction. This means that an episode of tissue regeneration may follow an episode of tissue destruction. From a treatment standpoint, this justifies the use of conservative techniques that utilize the potential for repair and regeneration, rather than using more aggressive, irreversible approaches in treating periodontal disease.
Three bacterial species seem to be involved in most forms of periodontal disease (except in necrotizing ulcerative periodontitis): Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Tannerella forsythensis (formerly Bacteroides forsythus). Intrafamilial transmission is possible and seems to be associated with individual susceptibility factors. When these bacterial forms are present, all the infected members of a given family carry the same clonal type. Usually, this same clonal type occurs in a given pocket, family member, and family (Socransky and Haffajee 1994). This has multiple consequences in formulating strategies for prevention and treatment.
Two fundamental features of bacterial plaque explain the difficulty in controlling its growth and eliminating it. First, subgingival plaque is organized as a biofilm and, second, the bacterial species it harbors interact specifically to form bacterial complexes.
The biofilm is formed by the association of bacterial populations adhering to one another or to the surfaces found in their vicinity (Costerton et al 1994). Its specific features account for the resistance of bacterial plaque to the host’s usual defense mechanisms (Page et al 1997). Ecologic communities develop and contribute to the survival of the entire host of bacterial populations. Several types of cooperation take place inside these bacterial populations.
Biofilms are resistant to the host’s defense mechanisms and to the action of antimicrobial agents.
The gingival crevicular fluid has been shown to contain consistent levels of the molecular components of the complement, high levels of immunoglobulins and of the cellular blood constituents, including leukocytes and polymorphonuclear neutrophils; these systems are all involved in the control and prevention of infectious processes. The gingival crevicular fluid is found in periodontal pockets and therefore lies in close contact with the biofilm. However, bacterial populations resist and thrive; they are able to spread laterally and apically along the root surfaces, causing tissue destruction and an increase in pocket depth.
Like all other biofilms, subgingival microbial plaque is surprisingly resistant and difficult to eradicate. Through the mutual protection they provide to one another, bacterial populations achieve abnormal resistance to the effects of antibiotics and other antimicrobial agents, whether applied locally or administered systemically.
Mechanical debridement is the only efficacious means for disorganizing the biofilm. This is why the combination of scaling and root planing represents a remarkably efficient technique in the treatment of periodontal disease, prior even to any pharmacologic attempt at controlling infection.
The different bacterial species interact by facilitating or inhibiting the progression of periodontal disease. They form bacterial complexes. An understanding of the relations between these bacteria is necessary to further comprehend the biologic features of subgingival plaque and to formulate coherent strategies for plaque control. Among these species, there is a limited number of pathogenic types and a significant number of saprophytic bacteria. Some are exogenous, while others are normally present in dental plaque (Socransky et al 1998). Socransky et al proposed a classification system that attributes four bacterial complexes to distinct color categories, and it has since become a reference.
A actinomycetemcomitans is an exogenous pathogenic microorganism, which means that it is not considered part of the commensal flora. It is a gram-negative facultative anaerobic rod. This microbe is associated with aggressive, localized forms of periodontitis—previously called localized juvenile periodontitis—as well as with generalized periodontitis.
These exogenous species are found in great numbers in subgingival plaque, deep pockets, and advanced lesions. They invade periodontal tissues and the cementum and produce proteolytic enzymes. The different species belonging to this complex, including A actinomycetemcomitans, which has not been classified within any complex, are all found within active periodontopathic lesions.
P gingivalis is an exogenous, strictly anaerobic gram-negative rod. It is predominantly found in the gingival sulcus. It is known to alter the local response of neutrophils recruited through inflammatory processes. Many virulence factors are produced by bacterial pathogens and have been studied extensively (Ishikawa et al 1997).
These toxins are harmful to leukocytes. Bacteria-derived lipopolysaccharides promote and maintain tissue destruction. Other bacterial by-products modify both immune response and cell growth–regulating mechanisms. Finally, bacterial proteases induce tissue destruction and cause damage to the components of host immune response—specific antibodies and complement-activating compounds. However, none of these factors considered alone seems to play a decisive role in the pathogenesis of periodontal disease.
On the other hand, rapid development of pathogenic microorganisms such as P gingivalis in the subgingival flora seems to have many consequences: this microorganism plays an important role in the organization of the biofilm and in colonization of host tissues; it also promotes growth of other bacterial populations. By neutralizing the initial phase of the acute inflammatory response, P gingivalis alters the host’s response potential to in/>