Ecological considerations in the treatment of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis periodontal infections.

The appearance of this issue of PERIODONTOLOGY 2000 is a tribute to the sustained efforts of an international group of oral microbiologists, immunologists and clinical investigators. When one of us (SSS) began work in this field in 1957, Actinobacillus actinomyceterncornitans was unknown in periodontal microbiology and Porphyromonas gingiualis was not known as such, although the “black-pigmented Bacteroides” had achieved some notoriety in studies of experimental mixed infections. In the late 1950s, the importance of plaque accumulation in the pathogenesis of periodontal diseases was once more re-established. With a few exceptions, most investigators appeared to subscribe to the notion of the nonspecific plaque hypothesis in terms of the causation of periodontal diseases. Plaque composition was thought to be similar from subject to subject and site to site within a subject. Abundant plaque formation was thought to lead to gingivitis and gingivitis eventually to periodontitis. The only studies seeking specific causative agents of disease were studies of mixed infections in animal model systems. Early studies of mixed infections focused on a fusospirochetal complex (85, 86, 981, whereas later studies emphasized infections in which “Bacteroides melaninogenicus” was a key component (65, 66, 100). This last group of studies was a precursor to the introduction of I? gingivalis as a key “player” in periodontal infections. The re-introduction of the concept of specificity in the causation of periodontal diseases gained impetus from the detection of a specific spirochete in lesions of acute necrotizing ulcerative gingivitis (59, 63) and the demonstration that transmission of periodontal disease in a hamster model system was due to infection by a specific species now known as Actinomyces uiscosus (43, 44, 47, 48). The key to the recognition of the role of A. actinomycetemcomitans in periodontal diseases and the firm re-establishment of the “specific plaque” hypothesis came from cultural studies of the subgingival microbiota detected in a clinical condition known at that time as periodontosis (now known as localized juvenile periodontitis). Studies in Copenhagen and Boston carried out by Slots (95) and Newman et d. (72, 73) demonstrated that the microbiota recovered from lesions in these subjects differed from that observed in healthy periodontal sites in the same subjects. Notable were the high levels of several unidentified gram-negative rod species (A. actinomycetemcomitans was not recognized as such until 1979 (105)). These studies indicated that lesion sites harbored different species than healthy sites in the same subject but did not determine whether the microorganisms caused the lesions or whether the habitat of the microbiota selected the detected species. Therapy studies reviewed in Slots & Ting in this volume (97) demonstrated that control of the species in the lesion led to disease remission indicating unequivocally that the resident species caused the infection. The focus on A. actinornyceterncomitans as the key organism in this infection came about primarily from studies of the local and serum antibody response in subjects with localized juvenile peri-