This study investigated the influence of different levels of exposure to smoking on periodontal healing for 12 mo after nonsurgical periodontal therapy and supportive periodontal care every third month. Eighty smokers willing to quit smoking and with periodontitis were included. Participants were offered an individualized voluntary smoking cessation program. Data collection included questionnaires and a full-mouth periodontal examination. Group-based trajectory modeling was used to model smoking trajectories over the follow-up. The effect of smoking trajectory on periodontal parameters over time was estimated with mixed effects modeling. Three smoking patterns were identified: light smokers/quitters ( n = 46), moderate smokers ( n = 17), and heavy smokers ( n = 17). For the periodontal data, the first factor, moderate periodontitis, included the number of sites with clinical attachment levels (CALs) of 4, 5, 6, and 7 mm; periodontal pocket depths (PPDs) of 4, 5, and 6 mm; and bleeding on probing. The second factor, severe periodontitis, consisted of the number of sites with a CAL ≥8 mm and PPD ≥7 mm. Heavy smokers commenced with a higher average CAL of 1.1 mm and 10 more sites with severe periodontitis than light smokers/quitters. While light smokers/quitters and moderate smokers obtained an average improvement of 0.6-mm PPD and 0.7-mm CAL, respectively, heavy smokers experienced 0.5-mm attachment loss. Heavy smokers had only a 50% reduction in the number of sites with moderate periodontitis when compared with light smokers/quitters and moderate smokers. While most participants benefited from nonsurgical periodontal therapy with results affected in a dose-response manner, the therapy had no effect on severe periodontitis among heavy smokers. Smoking cessation should be part of periodontal therapy; otherwise, limited benefits would be observed among heavy smokers, hindering the effect of treatment.
Information on smoking exposure obtained with self-reports may be inaccurate. Cotinine has a large half-life and its salivary levels correlate well with plasmatic levels. The influence of storage conditions on the validity and precision of salivary cotinine assessments has rarely been evaluated. Here, smokers donated saliva samples, which were sent for immediate analysis, mail posting, storage at 4 °C for 30 or 90 days, or storage at −20 °C for 30 or 90 days. Cotinine levels were determined using enzyme-linked immune-sorbent assay. Agreement of cotinine level measurements was assessed using Bland-Altman analyses. Average age (years), duration of smoking (years) and number of cigarettes smoked (/day) were 55.4 (±SD 9.4), 35.1 (±SD 11.3), and 15.3 (±SD 7.6). The mean immediate cotinine level was 457 ng/mL (range 11.3 to 1318 ng/mL). Mean cotinine levels in samples analyzed after delay ranged between 433 ng/mL (−20 °C 30 days) and 468 ng/mL (4 °C 30 days). A dose-response gradient was observed in the relationship between salivary cotinine level and self-reported smoking status. A good agreement between cotinine levels for all storage conditions compared with immediate analysis was observed, with average differences ranging from −11 to 24 ng/mL. Cotinine levels remained stable regardless of the tested condition. The stability of salivary cotinine may enable samples to be obtained in difficult-to-reach areas, reduce study costs, and improve the validity of the information on exposure to smoking.
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