PASSIVE-IMMUNIZATION WITH MONOCLONAL-ANTIBODIES AGAINST PORPHYROMONAS-GINGIVALIS IN PATIENTS WITH PERIODONTITIS

Selective inhibition of recolonization by Porphyromonas gingivalis was investigated by topical application of monoclonal antibody (MAb). To select a MAb to P. gingivalis with the potential for recognizing most strains of P. gingivalis, we examined seven MAbs, one of which (MAb 61 BG 1.3) recognized all 22 laboratory strains and serotypes of P. gingi valis tested as well as 105 human clinical isolates. A comparative stu dy of the number of P. gingivalis bacteria identified by conventional culture and immunofluorescence with MAb 61BG 1.3 showed a very signifi cant correlation between the two methods (Spearman r = 0.85, P < 0.001 ). Fourteen patients with periodontitis, who harbored P. gingivalis in their subgingival plaque, were treated by root planing and with metro nidazole to suppress any detectable P. gingivalis. In this double-blin d study, the patients were then divided randomly into two groups; one was treated with MAb to P, gingivalis, and the other was treated with saline, Each patient had four subgingival applications of 3 mu g of MA b (or saline) per tooth at 1, 3, 7, and 10 days after P. gingivalis wa s suppressed. The number of P. gingivalis bacteria was then monitored, and significantly less recolonization of the sites with the most seve re periodontitis was found in the MAb-treated patients than in the con trol patients (P < 0.01). This was evident at 6 and 9 months after the application of MAb, but by 12 months, P. gingivalis was also found to recolonize these sites in two of the MAb-treated patients. The effect of MAb was specific to P. gingivalis, since the numbers of spirochete s were not significantly different between the two groups. However, no significant difference in any clinical periodontal indices between th e immunized and control patients at 6 and 12 months was observed. This is the first demonstration that a putative periodontal pathogen can b e selectively prevented from recolonization for up to 9 months in site s with the most severe periodontitis. This strategy could be used to e stablish directly in humans whether a microorganism is involved in the pathogenesis of periodontitis, by repeated application of the corresp onding MAb at about 6-month intervals and by comparing the clinical in dices between the MAb-treated and control patients.