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Background: Arginine- and lysine-specific cysteine proteinases (arg-gingipain: Rgp, lys-gingipain: Kgp) are major virulence factors of Porphyromonas gingivalis. Recent reports have suggested that antibodies against gingipains can play a protective role against infection by P. gingivalis. The purpose of this study was to evaluate the IgG responses of patients with periodontitis to functional domains of gingipains.Methods: A group of 29 periodontitis patients and 10 periodontally healthy subjects (control group) were recruited into this study. We prepared three recombinant fragments of rgp A (catalytic domain; r-Rgp CAT) and two hemagglutinin domains (r-Rgp 44, and r-Rgps 15-27) corresponding to amino acid residues 228 to 719, 720 to 1136, and 1137 to 1704, respectively. One fragment of the Kgp catalytic domain (r-Kgp CAT) corresponding to amino acid residues 229 to 737 and expressed in Escherichia coli was also used. IgG antibody levels to these recombinant proteins in sera from the subjects were determined by an enzyme-linked immunosorbent assay (ELISA).Results: We found that IgG levels against r-Rgp 44 and r-Rgps 15-27 in sera obtained from the patients were significantly higher than those in the healthy group (P<0.01). In contrast, no significant differences in IgG levels against r-Rgp CAT and r-Kgp CAT were found between the control and patient groups. The IgG responses to P. gingivalis sonic extracts, r-Rgp 44 and r-Rgps 15-27, were related to probing depth in sera from patients, but those to r-Rgp CAT and r-Kgp CAT were not.Conclusion: The present findings suggest that the low responsiveness of IgG antibody against the catalytic domains of gingipain, r-Rgp CAT, and r-Kgp CAT is a key factor in infection by P. gingivalis. [ABSTRACT FROM AUTHOR]

Background: Porphyromonas gingivalis is one of the major microbial pathogens associated with chronic periodontitis. To eradicate such pathogens by periodontal therapy, it is essential to clarify the source of infection. Recent findings suggest that the genotype of the fimbriae is one of the important factors in infection by P. gingivalis. The objectives of the present study were to investigate the transmission of P. gingivalis between spouses and to determine the relationship between P. gingivalis fimA type and colonization. Methods: A total of 14 couples were selected to investigate the transmission of P. gingivalis and its association with the fimA types. To examine the distribution of fimA type in the general population. 32 subgingival plaque samples from 47 patients with periodontitis were also tested. The transmission of P. gingivalis strains was determined by using pulsed field gel electrophoresis (PFGE). P. gingivalis strains isolated from the couples and subgingival dental plaque samples were studied for fimA classification. Results: The PFGE patterns of P gingivalis strains from matched husbands and wives were identical for six of the 14 couples. In five of these six couples (B3.3%). P. gingivalis strains harboring the type II fimA gene were present. The proportion of type II fimA in the strains isolated from couples with probable intrafamilial transmission was significantly higher than that in patients with periodontitis or in the group of samples isolated from one member of a couple Conclusion: This study suggests that fimA type II, even though widely distributed in patients with periodontitis, may be an important factor in the transmission of P. gingivalis between spouses. [ABSTRACT FROM AUTHOR]

Increasing evidence has linked colonization by Helicobacter pylori with the development of gastritis and peptic ulcer disease. H. pylori resides primarily in the gastric mucosa without invading the gastric epithelium, causing persistent mild gastric inflammation. There are many reports examining the relationship between colonization by microorganisms in the stomach and oral cavity. We found that some oral bacteria are able to trap H. pylori cells, but oral bacteria inhibit H. pylori growth in vitro. In cases where H. pylori was detected in oral cavity samples, including oral cancer surface samples, we suggested that this species had colonized the stomach and were present in the oral cavity only as a transient organism. We demonstrated that periodontopathic Campylobacter rectus strains posses proteinaceous antigens, including heat shock proteins that share antigenicity with antigens of H. pylori strains. These cross-reactive antigens between H. pylori and C rectus may be related to the induction of immunopathological responses in periodontal tissues and the stomach. We concluded that H. pylori could not survive in the human oral cavity; however, there would be an interrelationship between periodontal disease due to C. rectux and stomach diseases due to H. pylori. [ABSTRACT FROM AUTHOR]

THE PURPOSE OF THIS STUDY WAS TO EXAMINE avidity of immunoglobulin G (IgG) antibody for surface antigens of Porphyromonas gingivalis in sera from patients with adult periodontitis. The antigens used were whole cell antigens, lipopolysaccharides (LPS), and fimbriae of non-invasive P. gingivalis ATCC 33277 and invasive 16-1. Serum IgG titers for the P. gingivalis antigens were measured by enzyme-linked immunosorbent assay (ELISA) before and after periodontal initial preparation. IgG avidity was measured by diethylamine dissociation ELISA. IgG titers for the whole cell antigens of 16-1, LPS, and the fimbria antigens from both P. gingivalis strains were significantly higher in the patient group than those in the control group, whereas values for avidities were significantly lower in patient sera. Although we found a statistically significant decrease in the IgG titers of patients following initial preparation, avidities against the fimbria antigen of invasive 16-1 strain increased. The present study showed that IgG antibodies elicited in patients were different in their ability to respond to invasive P. gingivalis 16-1 and to non-invasive 33277. The patient sera with high IgG titers demonstrated low values for avidity, suggesting that IgG responses in patients play a limited role in colonization inhibition or elimination of P. gingivalis. The data indicate that periodontally healthy individuals may have highly functional antibodies which may protect against P. gingivalis colonization. Our findings suggest that the ability to produce functional antibodies in the patient group is lower than that in the periodontally healthy group, but the functional antibodies can be induced by the initial preparation. [ABSTRACT FROM AUTHOR]