No abstract

The cleavage of complement may be an important immunopathologic mechanism in the development of gingival inflammation. Utilizing the experimental gingivitis model, cleavage of C3, C4 and B was assessed in gingival fluid following abstention from oral hygiene. 4 male dental students performed stringent oral hygiene measures until the gingival index approached 0, then refrained from any oral hygiene for 21 days. Gingival fluid, sampled with filter paper strips from the mesial surface of all maxillary premolars at 0, 7, 14, and 21 days, was assayed for C3, C4 and B cleavage by multilayer crossed-immunoelectrophoresis. Clinical indices were assessed following gingival fluid sampling. The subjects, who were plaque-free (PI = 0) at the beginning of the study, showed significant plaque accumulation at day 21 (87% of sites with PI greater than or equal to 2). Approximately 90% of the sites were free from clinical inflammation (GI = 0) at the start, but gingivitis increased with time such that 25% of the sites had GI scores of 2 at day 21. Bleeding on probing to the base of the pocket was not observed at day 0, but was observed at 62% of sites by day 21. Statistical analyses showed that all 3 indices significantly increased with time. The %C3 cleavage increased from a mean of 24% at day 0, to 35%, 45% and then 57% at days 7, 14 and 21, respectively, and both days 14 and 21 demonstrated significantly greater C3 conversion than that seen at day 0. The Spearman rank-order correlation coefficient for %C3 conversion versus time was p = 0.52, significant at the p less than 0.0001 level.(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship between probing attachment changes in treated periodontal pockets and the prevalence of selected periodontal pathogens was assessed in 10 patients with adult periodontitis 1 year following randomized therapy. All patients had at least 1 tooth in each quadrant with an inflamed pocket of probing depth > or =5 mm and clinical attachment loss and harbored at least one of the following 3 major periodontal pathogens: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, or Bacteroides forsythus. The number of target organisms per site was determined preoperatively; at 1 week; and at 1, 3, 6, and 12 months postoperatively utilizing DNA probes. The following clinical parameters were measured and recorded preoperatively and at 1, 3, 6, and 12 months post-treatment: gingival fluid flow, gingival index, plaque index, probing depth, probing attachment level, gingival recession, and bleeding on probing. One quadrant in each patient was randomly assigned to 1 of the following 4 treatments: 1) scaling and root planing; 2) pocket reduction through osseous surgery and apically-positioned flap; 3) modified Widman flap; and 4) modified Widman flap and topical application of saturated citric acid at pH 1 for 3 minutes. All 4 treatments were rendered in one appointment using local anesthesia. No postoperative antibiotics were used, but patients rinsed with 0.12% chlorhexidine for the first 3 months postoperatively and received a prophylaxis every 3 months. This investigation revealed: 1) 30.0% of the sites were infected by at least 1 species at 3, 6, and 12 months postoperatively. 2) Failing sites were infected by a high number of both Pg and Bf These sites had a mean of 24.2+/-9.0 x 10(3) Pg and 93.1+/-42.0 X 10(3) Bf while stable sites had a mean of 6.8+/-0.5 x 10(3) Pg and 7.2+/-1.2 x 10(3) Bf (P = 0.06 and P = 0.05, respectively). 3) The infected sites lost significantly more mean clinical attachment at 12 months (1.5+/-0.5 mm compared to a loss of 0.2+/-0.3 mm for uninfected sites, P = 0.017). 4) The infected sites had a significantly greater BOP (67+/-14% versus 25+/-8% for uninfected sites at 12 months, P = 0.012). 5) The choice of treatment modality did not affect the prevalence of the target species at 1 year post-treatment. These results suggest that prevalence of microbial pathogens negatively affects the 1 year outcome of periodontal surgical and nonsurgical therapy.

These data indicate that the prevalence of colonization of the sulcus by pathogenic bacterial species in periodontitis-free individuals is related to the quantity and duration of cigarette smoking.

Cell-mediated immunity in humans to antigens derived from oral plaque bacteria was investigated by using the lymphocyte blastogenesis assay. Subjects with varying severities of periodontal disease including normal, gingivitis, periodontitis, and edentulous were compared. Mononuclear leukocytes were separated from peripheral blood and cultured with antigens prepared by sonication of Actinomyces viscosus (AV), Actinomyces naeslundii (AN), Veillonella alcalescens (VA), Leptotrichia buccalis (LB), Bacteroides melaninogenicus (BM), and homologous dental plaque (DP). The lymphocyte response of subjects with gingivitis or periodontitis was significantly greater than that of normal subjects to antigens of AV, AN, and DP, but did not differ from the response of edentulous subjects. Periodontitis subjects were significantly more reactive than edentulous and normal subjects in response to VA, LB, and BM. These findings suggest that the tested gram-negative bacteria and the host response they evoke are associated with advanced periodontal destruction.