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Comparison of the microbiological features of chronic and aggressive periodontitis.

Any discussion of the comparative microbiology of chronic and aggressive forms of periodontitis must begin with the premise that our knowledge of the microbiota associated with these infections is incomplete. This does not mean that the field of oral microbiology has neglected the study of periodontal infections. On the contrary, the microbiota associated with periodontal health and disease has been intensely studied for well over a century by several generations of skilled scientists and clinicians (9, 15, 23, 42, 47, 48, 60, 65, 82, 101, 102, 105, 113, 114, 122, 123, 135, 145, 147, 149, 171, 175, 177, 181, 184, 206). The basic problem is that the oral microbiota is an enormously complex and dynamic entity that is profoundly affected by perpetually changing local environments and host-mediated selective pressures. In addition, the microorganisms live in hard-to-study biofilms comprising organized polymicrobial communities that are elegantly adapted to thriving and surviving in the multiple micro-ecosystems of the oral cavity. Another complication in any discussion of periodontal microbiology is the educational bias regarding the nature of infectious diseases that healthcare professionals develop during their training. Most dentists and physicians were taught the classical features of infectious diseases in their basic courses in medical microbiology. The dominant paradigm taught in these courses is that an exogenous pathogen overcomes the innate and adaptive immune defenses of the host, replicates within the body, and causes disease through a variety of virulence factors. Diagnosis of these classical infections often involves submitting a clinical specimen obtained from the infected patient to a clinical laboratory for isolation and identification of the pathogen by growing it in pure culture on artificial medium. These cultures are then used to determine the sensitivity of the isolated pathogen to a panel of antibiotics. Treatment of the infection involves administration of an appropriate regimen of antibiotics that is intended to suppress or eliminate the pathogen. This model for infectious diseases is certainly not the only one that is taught at most medical or dental schools, as it is widely known that some infections can be caused by multiple bacteria (i.e. mixed infections) and some diseases can be due to commensal opportunistic pathogens (82). Nevertheless, the one pathogen ⁄ one disease model dominates the thinking of most physicians and many dentists. Unfortunately, this dominant paradigm does not apply in cases of periodontal infections. These infections are caused by an extremely diverse consortium of microorganisms that are part of the endogenous microbiota of most people (82, 157). Many individuals who are periodontally healthy carry or harbor some periodontal pathogens as part of their normal supragingival and subgingival microbiota (4, 26, 32, 35, 43, 61, 62, 77, 94, 119, 129, 143, 150, 153, 155, 179, 180, 189, 196, 200, 203, 207). When detectable at healthy sites, the pathogens are usually present in very low numbers and show a limited range of phylotypes. It is quite clear that many individuals can harbor potential pathogens for long periods of time without developing periodontal disease. Carriage of putative periodontal pathogens at low levels as part of the commensal or normal oral microbiota is probably beneficial, since it is likely that their