Relationship of Bacteria to the Etiology of Periodontal Disease

Introduction In introducing a discussion of the bacterial etiology of human periodontal disease, it is worthwhile to discuss some of the unique problems confronting the investigator. First, periodontal disease is a chronic disease in many of its forms. If the alveolar bone supporting a tooth root that is approximately 20 mm in length were lost in 20 years, the rate of bone destruction would average approximately 1 mm/year, or less than one tenth of 1 mm/month. It is unlikely that destruction would occur at a constant rate, but there would probably be periods of exacerbation and remission. The slow rate of periodontal destruction and the difficulty in distinguishing periodontal disease activity combine to complicate the demonstration of determinants of the disease. A second problem in studying the bacterial etiology of periodontal disease is variation in host "resistance." A noxious stimulus that causes severe destruction in one individual might have little or no effect in another individual. When this problem is coupled with the complexity of the microbiota, it becomes difficult to assign an etiologic role to any organism. A third problem is the lack of a good animal model system. Each animal model system currently in use has certain drawbacks. A major drawback common to all is the presence of a resident oral microbiota that is different from the human microbiota. Because of this difference, results obtained in animals are not directly transferrable to man. In addition, in many instances the indigenous microbiota of the animals appears to prevent the establishment of human oral organisms in the oral cavity of test animals. A fourth problem facing the microbiologist is the complexity of the microbiota inhabiting the human periodontal pocket. A great number of microbiota of perhaps 50 or more species can be commonly isolated from this site. Many of the isolates are difficult to cultivate because of a sensitivity to atmospheric oxygen or a dependence on unusual growth requirements provided by other bacteria or living mammalian cells. Finally, periodontal disease in humans could be a disease of single etiology with clinical variations that are principally due to differences in host response. Or alternatively, "periodontal disease" could be a group of diseases with differing etiology. In the latter instance, periodontal disease is a collective term for a number of diseases affecting an organ system. This is analogous to using "lung disease" as an inclusive term to cover infections caused by pneumococci, tubercle bacilli, staphylocci, and so on. If periodontal disease is a group of diseases, the sorting out of the etiologic agents in a complex, continually present microbiota would be a challenging task. The purpose of the present report is to (1) cite evidence that bacteria play a role in the etiology of periodontal disease, (2) indicate the nature of the microorganisms that reside in the human gingival crevice region, (3) discuss attempts to determine which of these organisms may be responsible for periodontal disease(s) and, (4) indicate some potential mechanisms of periodontal destruction.