Localization of Porphyromonas gingivalis and Treponema denticola in different areas of subgingival plaque from advanced adult periodontitis patients was studied immunohistochemically using sensitive immunogold-silver staining and immunoelectron microscopy. Fourteen periodontally diseased teeth were extracted without damaging the subgingival plaque, fixed, and embedded. The subgingival plaque samples were sectioned according to four different pocket depths (0-2 mm, 2-4 mm, 4-6 mm and > or = 6 mm). Serial thin sections were stained using specific antisera to P. gingivalis or T. denticola and then with secondary antibody labelled with colloidal-gold. Cells of both P. gingivalis and T. denticola were predominantly found in subgingival plaque located at depths of more than 4 mm in periodontal pockets. T. denticola cells were found in the surface layers of subgingival plaque, and P. gingivalis were predominant beneath them. However, in the deeper subgingival plaque, the coexistence of P. gingivalis and T. denticola was observed. The present findings suggest that P. gingivalis and T. denticola play important roles in the pathogenicity of periodontal disease and provide the useful information for elucidating the pattern of colonization of microorganisms in the periodontal pocket.

OBJECTIVE: The role of the S‐layer of Campylobacter rectus ATCC 33238 in complement‐mediated killing and interaction with leukocytes of the intraperitoneal cavity from guinea pigs and human peripheral blood was studied in vitro. MATERIALS AND METHODS: Rabbit polyclonal anti‐serum to whole C.rectus cells, a monoclonal antibody which recognizes 150KDa S‐layer protein antigen and a monoclonal antibody against lipopolysaccharide (LPS) were prepared. Sensitivities of C.rectus cells against complement mediated killing and phagocytic killing by peritoneal leukocytes of guinea pig and human peripheral leukocytes were examined in the presence or absence of a specific antibody. RESULTS: C.rectus ATCC 33238 cells were moderately sensitive to complement mediated killing in the presence of rabbit polyclonal antibody against whole cells, and slightly sensitive in the presence of monoclonal antibody against S‐layer. Ingestion and phagocytic killing of C.rec‐tus cells by leukocytes were enhanced by the rabbit anti‐serum and monoclonal antibody against S‐layer, but not by the monoclonal antibody against LPS, pre‐immune rabbit serum or control asciteS. Viability of leukocytes was dependent on the number of ingested C.rectus cellS. CONCLUSIONS: The present study demonstrates that S‐layer possessing C.rectus cells are resistant to complement mediated killing and phagocytic killing by leukocytes in the absence of specific antibody.

This report describes a case of chronic periodontitis requiring treatment including smoking cessation care and periodontal surgery in an elderly patient with a long-term smoking habit. The patient, a 79-year-old man, presented with the chief complaint of halitosis. He had a 56-year history of smoking cigarettes. An initial examination revealed that 34.5% of sites had a probing depth (PD) of ≥4 mm, with 24.1% of sites showing bleeding on probing (BOP). Open bite and loss of appropriate anterior and lateral guidance were also found. Radiographic examination revealed extensive horizontal bone resorption in the maxillary and mandibular molars. Based on a clinical diagnosis of severe generalized chronic periodontitis, initial periodontal therapy consisting of plaque control, smoking cessation care, scaling and root planing, and caries treatment of #47 was performed. Prosthetic treatment with a removable partial denture was planned for #26, which was missing. The patient quit smoking at the end of initial periodontal therapy. Subsequently, surgical periodontal therapy including open flap debridement was performed on #16, #17, #18, and #27. Following reevaluation, a full metal crown (#47) and removal partial denture (#26) were placed. The patient was then placed on supportive periodontal therapy (SPT). Periodontal treatment including surgical therapy resulted in an improvement in PD and a reduction in the number of sites with BOP. The patient has not started smoking again since initial treatment. Improvement has been adequately maintained over a 4-year period. The present results suggest that even when a patient has been exposed to a risk factor for a long time, periodontal treatment and control of that risk factor can contribute to stabilization of periodontal conditions. Some problems with occlusion have persisted, however. Additional care is necessary to retain stable periodontal conditions during SPT.

Recent studies have shown that invasive and non-invasive strains of Porphyromonas gingivalis can both be isolated from patients with periodontitis. We examined the interaction between an invasive 16-1 P. gingivalis strain and phagocytes obtained from human peripheral blood and guinea pig peritoneal cavity. Phagocytes from human peripheral blood, mainly polymorphonuclear leukocytes (PMNs) isolated by centrifugation in Ficoll Hypaque, and macrophages collected from the peritoneal cavity of guinea pigs, were exposed to P. gingivalis cells. After this exposure, greater numbers of the non-invasive P. gingivalis ATCC 33277 were observed in human PMNs and guinea pig macrophages compared with the invasive P. gingivalis 16-1. Electron microscopic observations showed that invasive 16-1 within phagosomes in human PMNs and guinea pig macrophages retained their surface fibrous structures as well as their outer membranes. Electron microscopic examination showed that destruction and damage to the cell membranes and inner structures were clear in human PMNs and guinea pig macrophages after exposure to invasive 16-1 for 6 and 24 hours; this was a clear difference from exposure to the non-invasive ATCC 33277. Release of lactate dehydrogenase (LDH) activities into the culture supernatant of PMNs after exposure to the invasive 16-1 for 4 and 6 hours was significantly greater than that after exposure to the non-invasive ATCC 33277 (pϽ0.05). On the other hand, the LDH activity after exposure for 21 hours to the invasive 16-1 was significantly lower than that of untreated cells and cells after exposure to the non-invasive ATCC 33277 strain (pϽ0.05). The PMN viabilities after exposure to cells of the invasive 16-1 for 3, 4, and 6 hours as evaluated by trypan blue staining were similar to those after exposure to cells of the non-invasive ATCC 33277, but that after exposure to the invasive 16-1 strain for 21 hours was significantly lower than that after exposure to cells of the noninvasive ATCC 33277 strain.

The aim of the present investigation was to determine the clinical and microbiological effects of long-term undisturbed plaque formation on the gingiva and peri-implant mucosa. Four mongrel