Regeneration of cementum, ligament, bone and new attachment was achieved by introducing mixtures of recombinant human platelet-derived growth factor and insulin-like growth factor into debrided lesions of experimentally induced periodontitis in monkeys. This growth factor therapeutic regimen induced the regeneration of nearly 50% of the lost attachment within 4 weeks. New attachment in some cases included regeneration of horizontally resorbed interdental septa. These observations suggest that predictable, clinically significant gains in new attachment may be possible through the use of highly purified human recombinant growth factors delivered to debrided lesions of adult periodontitis in appropriate, inert carrier vehicles.

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 activation of the complement system is an important host‐mediated mechanism in the initiation and progression of inflammation. Complement cleavage products have been reported in gingival fluid obtained from periodontitis lesions suggesting a potential role for the activation of the alternative and/or classical complement pathways in the pathogenesis of periodontitis. Using the multi‐layer crossed immunoelectrophoresis technique, the effect of periodontal therapy on complement conversion of C3, C4, and B was assessed in 37 sites in 9 patients. Patients selected for study had moderate‐severe periodontitis as confirmed by clinical measurements of plaque, gingival inflammation, bleeding on probing, suppuration, pocket depth, and loss of attachment. Gingival fluid and clinical indices were obtained from representative sites prior to treatment and again 2–4 weeks following extensive periodontal scaling and root planing. Periodontal therapy resulted in a statistically significant decrease in all clinical parameters of inflammation. The percentage of C3 conversion decreased significantly from 70.0% to 37.5% with therapy (p=0.0001) while the reference protein, transferrin, did not significantly change. C4 conversion to C4c was never observed and total C4 was not significantly altered by therapy. Changes in B conversion to Bb could not be evaluated because the Bb precipitate was too small to measure reproducibly. These results suggested that complement activation, as measured by C3 conversion to C3c, decreased in gingival fluid following periodontal therapy and suggested a role for complement activation in the pathogenesis of inflammatory periodontal disease.

Octenidine, a new bispyridine mouthrinse, has been shown to prevent plaque formation in humans over a seven‐day period. The purpose of the present study was to determine the effects of octenidine on plaque and gingivitis development in humans using a 21‐day experimental gingivitis model. Eighty‐eight subjects with a Plaque Index (PII) and Gingival Index (GI) ≤ 0.4 were randomly assigned to 4 coded formulations: 1) 0.1% octenidine in mouthwash vehicle used 3 times a day (TID), 2) 0.1% octenidine in mouthwash vehicle used twice a day (BID), placebo rinse once a day, 3) 0.1% octenidine in water used 3 times a day, and 4) mouthwash vehicle alone used 3 times a day (VEH). Each subject refrained from all mechanical plaque control and rinsed morning, noon, and evening under supervision with 15 ml of assigned formulation for 60 s. At 0, 7, 14, and 21 days, Pit, GI, and mucosal tolerance were assessed. Tooth stain was measured at day 0 and twice at day 21 (prior to and immediately following a single toothbrushing). By day seven of the rinse phase, significant mucosal irritation had occurred in several subjects in the octenidine in water group. Therefore, that group was discontinued from the study and the remaining 66 subjects continued. The mean PII increased in the VEH group from a mean of 0.13 at day 0 to 1.08, 1.39, and 1.69 at days 7, 14, and 21, respectively. In contrast, the mean PII of the TID and BID groups did not increase over the 21 day period (0.14 and 0.10, 0.18 and 0.22, 0.15 and 0.16, 0.12 and 0.16 at day 0, 7, 14, and 21 for TID and BID, respectively). Although the TID and BID groups did not statistically differ at any point, both groups demonstrated significantly less plaque accumulation than the VEH group at days 7, 14, and 21 (p < 0.000001). Gingivitis, as measured by GI, increased significantly in the VEH group from a mean of 0.14 at day 0, to 0.58, 0.84 and 0.98 at day 7, 14, and 21. Both the TID and BID groups demonstrated a small increase in mean GI, rising from 0.12 and 0.16 at day 0 to 0.21 and 0.24, 0.29 and 0.27, and 0.32 and 0.31 at days 7, 14, and 21 for TID and BID, respectively. Again, the TID and BID groups were not different while both had significantly less gingivitis than the VEH group at days 7, 14, and 21 (p 0.000002). Stain, observed in 26 subjects in the TID and BID groups at day 21, was removed by a single toothbrushing in all but 5 subjects. No significant adverse reactions were observed in the remaining subjects. These results demonstrate that octenidine, when used as the only means of oral hygiene for 21 days, will significantly inhibit the development of plaque and gingivitis.

The activation of the complement system is an important host-mediated mechanism in the initiation and progression of inflammation. Complement cleavage products have been reported in gingival fluid obtained from periodontitis lesions suggesting a potential role for the activation of the alternative and/or classical complement pathways in the pathogenesis of periodontitis. Using the multi-layer crossed immunoelectrophoresis technique, the eflect of periodontal therapy on complement conversion of C3, C4, and B was assessed in 37 sites in 9 patients. Patients selected for study had moderate-severe periodontitis as confirmed by clinical measurements of plaque, gingival inflammation, bleeding on probing, suppuration, pocket depth, and loss of attachment. Gingival fluid and clinical indices were obtained from representative sites prior to treatment and again 2-4 weeks following extensive periodontal scaling and root planing.Periodontal therapy resulted in a statistically significant decrease in all clinical parameters of inflammation. The percentage of C3 conversion decreased significantly from 70.0% to 37.5% with therapy (p = 0.0001) while the reference protein, transferrin, did not significantly change. C4 conversion to C4c was never observed and total C4 was not significantly altered by therapy. Changes in B conversion to Bb could not be evaluated because the Bb precipitate was too small to measure reproducibly. These results suggested that complement activation, as measured by C3 conversion to C3c, decreased in gingival fluid following periodontal therapy and suggested a role for complement activation in the pathogenesis of inflammatory periodontal disease.anisms including chemotactic attraction of Address: