The classic progression of the development of periodontitis with its associated formation of an inflammatory lesion is characterized by a highly reproducible microbiological progression of a Gram-positive microbiota to a highly pathogenic Gram-negative one. While this Gram-negative microbiota is estimated to consist of at least 300 different microbial species, it appears to consist of a very limited number of microbial species that are involved in the destruction of periodontal diseases. Among these "putative periodontopathic species" are members of the genera Porphyromonas, Bacteroides, Fusobacterium, Wolinella, Actinobacillus, Capnocytophaga, and Eikenella. While members of the genera Actinomyces and Streptococcus may not be directly involved in the microbial progression, these species do appear to be essential to the construction of the network of microbial species that comprise both the subgingival plaque matrix. The temporal fluctuation (emergence/disappearance) of members of this microbiota from the developing lesion appears to depend upon the physical interaction of the periodontal pocket inhabitants, as well as the utilization of the metabolic end-products of the respective species intimately involved in the disease progression. A concerted action of the end-products of prokaryotic metabolism and the destruction of host tissues through the action of a large number of excreted proteolytic enzymes from several of these periodontopathogens contribute directly to the periodontal disease process. Important to the role of these prokaryotes in attacking the host is the ability of several of them to directly attack host tissues by proteolytic digestion, as well as their ability to elaborate large amounts and types of "virulence factors" - LPS, outer membrane proteins, and vesicles, toxins, enzymes, which act both directly and indirectly through the activation of a variety of macromolecules that themselves are destructive to the host. The elaboration of several of these virulence factors appears to be closely regulated by the expression of host factors (i.e., hemin) that appear in several in vivo animal models of pathogenesis to control the virulence of the specific microbial species. Recent studies in a number of laboratories involved in studies of both oral and nonoral diseases indicate that those observations relevant to pathogenesis and virulence in in vitro models may have little if any applicability to that which occurs in vivo.
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