Faculty Bibliography

INTRODUCTION: Adherence to smoking cessation treatment is generally low, especially among socio-economically disadvantaged groups including individuals experiencing homelessness and those with mental illnesses. Despite the high smoking rates in homeless populations (~70%) no study to date has systematically examined predictors of adherence to nicotine replacement therapy (NRT) in this population. OBJECTIVE: The aim of this secondary analysis was to identify predictors of adherence to NRT in a smoking cessation trial conducted among homeless smokers. METHODS: Secondary analysis of data from a randomized controlled trial enrolling 430 persons who were homeless and current cigarette smokers. Participants were assigned to one of the two study conditions to enhance smoking cessation: Motivational Interviewing (MI; 6 sessions of MI + 8 weeks of NRT) or Standard Care (Brief advice to quit+ 8 weeks of NRT). The primary outcome for the current analysis was adherence to NRT at end of treatment (8 weeks following randomization). Adherence was defined as a total score of zero on a modified Morisky adherence scale). Demographic and baseline psychosocial, tobacco-related, and substance abuse measures were compared between those who did and did not adhere to NRT. RESULTS: After adjusting for confounders, smokers who were depressed at baseline (OR=0.58, 95% CI, 0.38-0.87, p=0.01), had lower confidence to quit (OR=1.10, 95% CI, 1.01-1.19, p=0.04), were less motivated to adhere (OR=1.04, 95% CI, 1.00-1.07, p=0.04), and were less likely to be adherent to NRT. Further, age of initial smoking was positively associated with adherence status (OR= 0.83, 95% CI, 0.69-0.99, p=0.04). CONCLUSION: These results suggest that smoking cessation programs conducted in this population may target increased adherence to NRT by addressing both depression and motivation to quit. TRIAL REGISTRATION: clinicaltrials.gov: NCT00786149.

Competency-based education, introduced approximately 10 years ago, has become the preferred method and generally the accepted norm for delivering and assessing the outcomes of undergraduate (European) or predoctoral (North America) dental education in many parts of the world. As a philosophical approach, the competency statements drive national agencies in external programme review and at the institutional level in the definition of curriculum development, student assessment and programme evaluation. It would be presumptuous of this group to prescribe competences for various parts of the world; the application of this approach on a global basis may define what is the absolute minimum knowledge base and behavioural standard expected of a 'dentist' in the health care setting, while respecting local limitations and values. The review of documents and distillation of recommendations is presented as a reference and consideration for dental undergraduate programmes and their administration

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-1 beta and TNF alpha. 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 < or = p < or = 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

Ligature-induced periodontitis was monitored for 6 months in eight Macaca mulatta monkeys to examine clinical status, radiographic bone level, and crevicular fluid (CF) levels of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha, and leukotriene B4 (LTB4). A split-mouth design was used, with eight ligated teeth and eight contralateral nonligated teeth which develop soft-chow-promoted (spontaneous) disease. Ligated sites experienced an average attachment loss of 0.94 mm per site and linear bone loss of 0.88 mm per site, with spontaneous-periodontitis sites experiencing approximately half the loss of ligated sites. The CF mediator levels showed increased levels of PGE2 and TxB2 at the ligated sites, as compared with the spontaneous sites, with no significant contralateral differences in the IL-1 beta or LTB4 responses. The concentrations of LTB4 in CF reached an early threefold peak over the baseline level at 1 month. By 2 months there was a statistically significant threefold elevation in CF-PGE2 in the ligated sites and a twofold elevation in the spontaneous sites as compared to the baseline level (P = 0.041 and 0.008, respectively). The monocyte product IL-1 beta increased sharply at 2 months and returned to the baseline level by 6 months at both ligated and nonligated sites. Tumor necrosis factor alpha in CF was below the limit of detection at all sites throughout the experiment (i.e., < 2 ng/ml). The selective elevation of both PGE2 and TxB2 in ligated sites, compared with levels in spontaneous sites, in the presence of similar levels of LTB4 and IL-1 beta provides further evidence that these molecules regulate the magnitude of the tissue-destructive response in progressive periodontitis.

Previous studies have indicated that non-steroidal anti-inflammatory drugs administered prior to oral surgery procedures are effective in reducing postoperative pain. The purpose of the present study was to compare the efficacy of medicating with ibuprofen immediately presurgically to medicating immediately postsurgically on postoperative pain associated with periodontal surgery. Sixty patients who were to undergo periodontal surgery were randomly divided into 3 groups: the I-pretreatment group received 600 mg ibuprofen immediately presurgically and placebo immediately after the surgery; the I-post-treatment group received placebo before surgery and 600 mg ibuprofen postsurgically; the placebo group received placebo at both time periods. Responses from an 8-hour pain diary completed by each subject were quantified and statistically evaluated non-parametrically. Results indicated that dosing with ibuprofen either immediately before or immediately after periodontal surgery significantly delays onset of pain as compared to placebo, with dosing after surgery demonstrating a significantly greater delay of onset of pain as compared to dosing presurgically. In addition, unlike the presurgical dosing, dosing postsurgically significantly decreases mean pain intensity for a combined 8-hour period following periodontal surgery as compared to placebo

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 x 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

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