Eighty‐two periodontal patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous resection surgery (FO) which were randomly assigned to various quadrants in the dentition. Therapy was performed in 3 phases: non‐surgical, surgical, and supportive periodontal treatment (SPT) ≤ 7 years. Clinical data consisted of probing depth (PD), clinical attachment level (CAL), gingival recession (REC), bleeding on probing (BOP), suppuration (SUP), and supragingival plaque (PL). Because of the necessity to exit many CS treated sites due to breakdown, data for CS were reported only up to 2 years. All therapies produced mean PD reduction with FO > MW > RP > CS following the surgical phase for all probing depth severities. By the end of year 2 there were no differences between the therapies in the 1 to 4 mm sites. There were no differences in PD reduction between MW and RP treated sites by the end of year 3 in the 5 to 6 mm sites and by the end of year 5 in the ≥ 7 mm sites. FO produced greater PD reduction in ≥ 5 mm sites through year 7 of SPT. Following the surgical phase, FO produced a mean CAL loss and CS and RP produced a slight gain in 1–4 mm sites. RP and MW produced a greater gain of CAL than CS and FO following the surgical phase in 5 to 6 mm sites, but the magnitude of difference decreased during SPT. Similar CAL gains were produced by RP, MW, and FO in sites ≥ 7 mm. These gains were greater than that produced by CS and were sustained during SPT. Recession was produced with FO > MW > RP > CS. This relationship was maintained throughout SPT. The prevalences of BOP, SUP, and PL were greatly reduced throughout the study and were comparable between sites treated by RP, MW, and FO while the CS sites had more BOP and SUP. J Periodontol 1996;67:93–102.

Seventy-four patients with moderate to advanced periodontitis were classified by cigarette consumption at the initial exam: heavy smokers (HS) > or = 20 cigarettes/day (n = 31); light smokers (LS) < or = 19 cigarettes/day (n = 15); past smokers (PS) had a history of smoking but had quit by the initial exam (n = 10); and non-smokers (NS) had never smoked (n = 18). All patients were treated with four modalities of periodontal therapy followed by supportive periodontal treatment (SPT) for a period of up to 7 years. Clinical parameters including probing depth (PD), clinical attachment level (CAL), recession (REC), presence of bleeding on probing (BOP), and supragingival plaque (PL) were assessed at six sites around each tooth. Horizontal probing attachment level (HAL) was obtained at molar furcation sites. Data were collected initially, 4 weeks after non-surgical therapy, 10 weeks after surgical therapy, and yearly during SPT. HS and LS demonstrated less PD reduction and less CAL gain than PS and NS following active treatment and throughout SPT. Following active treatment, HAL changes were similar for all groups, but during 7 years of SPT, HS and LS experienced greater loss of HAL. There were no differences in BOP among the four groups. HS demonstrated a higher percentage of PL positive sites compared to the other groups. In summary, HS and LS responded less favorably to therapy than PS and NS. A past history of smoking was not deleterious to the response to therapy.

Eighty-two patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous surgery (FO) which were randomly assigned to the various quadrants in the dentition. Following phase I and phase II therapy, the patients received supportive periodontal treatment (SPT) at 3-month intervals for up to 7 years. Clinical attachment level (CAL) was determined initially, post-phase I, post-phase II and prior to each SPT appointment. If a site lost > or = 3 mm of CAL from its baseline, it was classified as a breakdown site. Baselines were the initial exam for sites treated by CS and 10 weeks post-phase II for sites treated by RP, MW, and FO. Data were grouped by probing depth (PD) severity at the initial exam and at post-phase II. The breakdown for CS sites was assessed separately from RP, MW, and FO sites because of different baselines and retreatment protocols. Sites treated by CS had a higher incidence of breakdown than the other therapies through year 1 of SPT. The breakdown incidences/year for RP and MW sites were similar and greater than for FO sites in 1 to 4 mm and 5 to 6 mm PD categories. Breakdown incidence of RP sites was greater than MW sites which was greater than FO sites initially > or = 7 mm. Differences in incidence of breakdown between therapies after recategorizing data by post-phase II PD were the same as above, except no difference was present between RP and MW sites > or = 7 mm. Breakdown incidences were greater in increasing PD severities regardless of when they were categorized. There was no further loss of CAL one year after retreatment in 88% of sites. Patients with higher breakdown incidences tended to be smokers at the initial exam.

Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post-active treatment clinical attachment loss (> 2% sites/year lost > or = 3 mm) were compared to 10 age-, race-, and supragingival plaque-matched patients with low post-treatment clinical attachment loss (< 0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL-1 alpha, IL-1 beta, IL-6) as determined by two-site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patient produced significantly more IL-6 (30.1 +/- 4.0 versus 15.4 +/- 2.8 nM, p < 0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL-1 concentrations. These data suggest that gingival IL-1 and IL-6 production is different in response to local and systemic factors associated with periodontitis, and that IL-6 may play a role in the identification and mechanisms of refractory periodontitis.

Academic dentists and members of the practice community have been hearing, for more than a decade, that our educational system is in trouble and that the profession has lost its vision and may be wavering in the achievement of its goals. A core of consistently recommended reforms has framed the discussion of future directions for dental education, but as yet, most schools report little movement toward implementation of these reforms in spite of persistent advocacy. Provision of faculty development related to teaching and assessment strategies is widely perceived to be the essential ingredient in efforts to introduce new curricular approaches and modify the educational environment in academic dentistry. Analyses of the outcomes of efforts to revise health professions curricula have identiied the availability and effectiveness of faculty development as a predictor of the success or failure of reform initiatives. This article will address faculty development for purposes of enhancing teaching effectiveness and preparing instructors for potential new roles associated with curriculum changes. Its overall purpose is to provide information and insights about faculty development that may be useful to dental schools in designing professional growth opportunities for their faculty. Seven questions are addressed: 1) What is faculty development? 2) How is faculty development accomplished? 3) Why is faculty development particularly important in dental education? 4) What happens when faculty development does not accompany educational reform? 5) Why are teaching attitudes and behaviors so dificult to change? 6) What outcomes can be expected from faculty development? and 7) What does the available evidence tell us about the design of faculty development programs? Evidence from systematic reviews pertaining to the teaching of evidence-based dentistry, strategies for continuing professional education, and the Best Evidence in Medical Education review of faculty development outcomes are presented to answer this question: does faculty development enhance teaching effectiveness? Characteristics consistently associated with effective faculty development are described.