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BACKGROUND AND OBJECTIVE: Porphyromonas gingivalis is an oral pathogen strongly associated with destruction of the tooth-supporting tissues in human periodontitis. Gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) are functionally different cell types in the periodontium that can participate in the host immune response in periodontitis. This study aimed to investigate the effects of viable P. gingivalis on the expression of genes associated with inflammation and bone degradation by these fibroblast subsets.MATERIAL AND METHODS: Primary human GF and PDLF from six healthy donors were challenged in vitro with viable P. gingivalis W83 for 6 h. Gene expression of inflammatory cytokines in GF and PDLF was analyzed using real-time PCR, and protein expression was analyzed using ELISA.RESULTS: Viable P. gingivalis induced a strong in vitro inflammatory response in both GF and PDLF. We found increased gene expression of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor-alpha, monocyte chemotactic protein-1 and regulated upon activation, normal T-cell expressed and secreted (RANTES). Macrophage colony-stimulating factor was induced and the expression of osteoprotegerin was decreased in GF, but not in PDLF. In nonchallenged cells, a higher level of expression of IL-6 was observed in GF than in PDLF. Between individual donors there was large heterogeneity in responsiveness to P. gingivalis. Also, in each individual, either GF or PDLF was more responsive to P. gingivalis.CONCLUSION: Considerable heterogeneity in responsiveness to P. gingivalis exists both between GF and PDLF and between individuals, which may be crucial determinants for the susceptibility to develop periodontitis.

Recently van Winkelhoff et al. (1) described 3 novel serotypes in virulent Porphyromonas gingivalis strains, which were based on different polysaccharide antigens. These antigens probably represent capsular structures and have been designated K1, K2 and K3. In the present study we report on 3 novel capsular serotypes, which are represented by P. gingivalis strains ATCC 49417, HG 1690 and HG 1691. The strains, isolated from patients with periodontitis, showed obvious encapsulation in wet India ink preparations. Thermostable antigens could be detected in the supernatant fractions of autoclaved cells. These antigens appeared to be negatively charged, sensitive to periodate degradation, and resistant to proteinase K treatment. On the basis of these characteristics we conclude that the antigens are probably extra-cellular polysaccharides representing a bacterial capsular structure. These K-antigens did not cross-react with K1, K2 or K3 immune-sera of P. gingivalis, with the exception of the K2 antiserum, which partially recognized K5- and K6-antigens. In contrast, K5 and K6 antisera did not react with the K2-antigen. After absorbtion of the K2 antiserum with cells of strains HG 1690 (K5) and HG 1691 (K6) cross-reactivity was no longer present. We propose these novel serotypes to be designated: K4 (ATCC 49417), K5 (HG 1960) and K6 (HG 1691).

Actinobacillus actinomycetemcomitans is a suspected etiologic agent in destructive periodontal diseases. The detection of bacteriophages in A. actinomycetemcomitans in the subgingival plaque of patients with rapidly destructive forms of periodontitis led to the hypothesis that bacteriophage infection might increase the virulence of this bacterium (19). A. actinomycetemcomitans was isolated from 68 subjects from the Netherlands and Switzerland with localized juvenile periodontitis, rapidly progressing periodontitis, or adult periodontitis, and was tested for the presence of temperate bacteriophage with the overlay plate technique. More than half of the A. actinomycetemcomitans strains were found to release bacteriophage which formed individual plaques on indicator strains. Electron microscopy of preparations from 7 strains revealed virions with an icosahedral head and a contractile tail typical for double-stranded DNA bacteriophages. The presence of A. actinomycetemcomitans carrying temperate bacteriophage was not correlated with the composition of the subgingival microflora nor with the clinical form of periodontal disease. Destructive periodontal disease of subjects with phage-carrying A. actinomycetemcomitans was not more severe than of subjects with phage-free A. actinomycetemcomitans as determined by several clinical parameters. In contrast, the pocket depth and the attachment loss were significantly lower for adult periodontitis subjects with phage-carrying A. actinomycetemcomitans. It seems unlikely that the frequently occurring temperate bacteriophages increase significantly the virulence of A. actinomycetemcomitans.

The purpose of this study was to compare the microbiological flora on mucosal surfaces of the tongue and the tonsils of individuals with and without periodontal breakdown. Twenty-four adults were selected on the basis of clinical parameters. The study included evaluation for the presence of spirochetes and motile organisms by phase-contrast microscopy and blackpigmented Bacteroides by cultivation. Results showed statistically significant differences in the prevalence of various types of microorganism on the tongue and the tonsils between both groups. A positive correlation could be demonstrated between the presence of motile organisms and Bacteroides intermedius on the tongue and periodontal breakdown. Furthermore, a positive correlation was found between the presence of motile organisms on the tonsils and periodontal breakdown. From the results of this study, it was concluded that the microbial composition of the tongue and the tonsils is associated with periodontal breakdown.