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Notes: Ketoprofen creams were evaluated for the treatment of periodontal disease in a placebo-controlled, double-blind study in the rhesus monkeys, Macaca mulatta. Two formulations containing ketoprofen (1%), with or without vitamin E, were evaluated against appropriate controls (8 monkeys per group). Two weeks prior to treatment, the animals received prophylaxis on only the left side of the mouth (spontaneous model). Selected teeth on the right side of the mouth were ligated (ligature model). The creams were administered to the gingiva once daily at a standard dose of 1.8 ml per monkey for 6 months. Clinical assessments were made 2 wk before initiation, at baseline and 1, 2, 3 and 6 months post-treatment. The clinical parameters included plaque formation, gingival redness, edema, bleeding on probing and Ramfjord Attachment Level measurements (RAL). Radiographs were taken at 2 wk before initiation, baseline and at 3 and 6 months post-treatment. Digital subtraction radiography was used to measure vertical linear bone loss along the interproximal root surfaces of the left and right mandibular first molars. Gingival crevicular fluid (GCF) was collected for biochemical assays on PGE2, TxB2, LTB4, IL-1β and TNFα. There were no significant differences among groups with respect to gingival indices. Radiographic data demonstrated significant positive effects on bone activity in both groups treated with ketoprofen formulations with improvement over time in the ligature model (0.01 ≤p≤ 0.04). The placebo group exhibited bone loss of 1.96±0.48 and 1.40±0.56 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream showed an apparent bone gain of 0.28±0.41 and 0.78±0.47 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream containing vitamin E showed a mean bone loss of 0.41–0.48 mm per site at 3 months with improvement to an apparent bone gain of 0.31±0.44 mm per site at 6 months. The biochemical data demonstrated early and significant suppression of GCF-LTB4 by both ketoprofen formulations at 1 month, which preceded the significant suppression of GCF-PGE2 at 2 and 3 months in the ligature model (p≤0.003) and at 2 to 6 months in the spontaneous model (p≤0.02). We conclude that ketoprofen at 1% level in suitable topical vehicles can effectively inhibit GCF-LTB4 and GCF-PGE2 and positively alter alveolar bone activity in the ligature-induced model of periodontitis in the monkey.

Notes: The effect of zinc sulfadiazine (ZnSD) and silver sulfadiazine (AgSD) on developing plaque formation and gingivitis was studied in 12 beagle dogs over a 14-week period. Plaque and gingival indices were used to measure plaque formation and gingivitis. During a 2-wk baseline period each dog was brought to optimal gingival health with prophylaxis and tooth brushing. Thereafter, 4 dogs were treated twice daily with topical application of 3.0% zinc sulfadiazine; 4 dogs were treated with 2.0% silver sulfadiazine while 4 dogs treated with placebo gel served as controls over a 12-wk treatment period. At wk 2 of treatment, all three groups of dogs showed an increase in plaque build-up on their teeth from baseline. By wk 6, plaque accumulation on the teeth was significantly less in dogs treated with either ZnSD or AgSD compared to control dogs. At wk 2 of treatment, gingival inflammation was increased from baseline in all three groups. Thereafter, over the course of the 12-wk treatment period, gingival inflammation in the ZnSD and the AgSD treated dogs was significantly less than the placebo treated dogs. The data indicate that both ZnSD and AgSD inhibit developing plaque formation in beagles. This significant inhibition of plaque formation was accompanied by a significant reduction in gingival inflammation.

Notes: The purpose of this study was to determine the effect of hydrogen peroxide delivered into periodontal pockets on gingival fluid flow and myeloperoxidase activity in the gingival fluid. Twenty systemically healthy human subjects presenting with moderate to advanced periodontitis were utilized. One side of the maxilla served as the control and the contralateral segment served as the experimental side. Measurements were made 0.5, 24, and 168 hours postoperatively. The experimental side was treated with 0.03 % hydrogen peroxide and the control side received distilled water. Five milliliters of fluid was delivered into the periodontal pockets either by sonication or passive dispersion. The 30 minute results indicated a mean increase in gingival fluid myeloperoxidase of 8.08 units per milliliter (U/ml) for the sonicated hydrogen peroxide, 2.05 U/ml for the passively dispersed hydrogen peroxide, 1.31 U/ml for the sonicated distilled water, and 0.60 U/ml for the passively dispersed distilled water. The values for hydrogen peroxide both sonicated and passively dispersed were significantly greater than baseline readings (p 〈 0.01), and the sonicated value was significantly larger than the passively dispersed value.

Notes: Although a well known barrier effect against the penetration of macromolecules exists at the basement membrane region of epithelial tissues, recent reports suggest that the penetration of smaller molecules may also be impeded by this region. Considering the probable importance of the permeability of gingival crevicular tissues in the etiology of inflammatory periodontal disease, the present study was designed to evaluate the barrier function of the basement membrane region of non-keratinized oral mucosal epithelium to a series of radiolabelled penetrating molecules of increasing molecular weight. Tritium labeled inulin (ℳ 5,000), dextran 20 (ℳ 20,000) and dextran 70 (ℳ 70,000) were used as penetrating molecules, and autoradiographic tracer techniques were used to evaluate the barrier function. The study was conducted in vitro to eliminate vascular “wash-out” effects and to facilitate study of penetration across the basement membrane region in both directions. The results indicated that although the penetration of inulin and dextran 70 was impeded by the basement membrane region, the penetration of dextran 20 was not affected. Therefore, the barrier function of the basement membrane region is not solely dependent on the molecular weight of the penetration molecule. Mechanisms to account for the findings are described and the significance to periodontal disease is discussed.

Notes: Abstract The effect of zinc sulfadiazine (ZnSD) and silver sulfadiazine (AgSD) on reducing plaque formation and gingivitis was studied in 12 beagle dogs over a 14-week period. 12 beagle dogs were scaled, root planed and pumiced to bring them to a similar level of gingival health, prior to placing them on a diet of Purina Dog Chow softened with canned gravy and molasses to promote the build-up of plaque and the initiation of gingivitis. At the end of 8 weeks, the dogs were determined to have substantial bacterial plaque accumulation and apparent gingivitis. Thereafter, 4 dogs were treated 2 × daily with topical applications of 3% zinc sulfadiazine; 4 dogs were treated with 2% silver sulfadiazine while 4 dogs were treated with placebo gel serving as control over a 14-week treatment period. By week 2, the zinc and silver sulfadiazine dogs showed a significant decrease in gingival index which was maintained throughout the study. Additionally, by week 2, the % of sites with bleeding was also seen to decrease significantly in the experimental groups. The plaque index remained consistent in all 3 groups until week 6 when the 2 experimental groups indicated significant decrease in plaque accumulation as compared to controls. Probing depths were also seen to decrease significantly in the experimental groups after 10 weeks of therapy. The mean stain index was similar in all 3 groups of dogs throughout the study. Data indicate that both zinc and silver sulfadiazine inhibit plaque formation and reduce existing gingivitis in beagle dogs.