The Effect of Smoking on Mechanical and Antimicrobial Periodontal Therapy

Abstract

The aim of this investigation was to evaluate the effect of smoking on the outcome of periodontal therapy. The study consisted of 54 patients who participated in a 4-group parallel-arm clinical trial on the efficacy of three locally delivered antimicrobial systems as adjuncts to scaling and root planing in the treatment of sites with persistent pocketing after a course of scaling and root planing. These groups included scaling and root planing either alone (S) (n = 3), or in conjunction with the application of 25% tetracycline fibers (S&T) (n = 13), 2% minocycline gel (S&Mi) (n = 14), or 25% metronidazole gel (S&Me) (n = 14). In each patient four pockets > 5 mm with bleeding on probing (BOP) and/or suppuration were studied. The number of subjects who smoked was: 8 (61.5%) in the S&T group, 8 (57.1%) in the S&Mi group, 6 (42.9%) in the S&Me group, and 6 (46.2%) in the S group. The probing depth, attachment level and other clinical parameters were assessed at baseline and 6 weeks after treatments. The clinical results of this comparative study have been previously reported. Regardless of the type of treatment, the change in the probing depth (delta PD) and attachment gain (delta AL) were greater in non-smoker subjects than smoker subjects. delta PD was 1.14 mm versus 0.76 mm (P = 0.019), and delta AL was 0.52 mm versus 0.50 mm at (P = 0.845) for non-smokers and smokers respectively. The analysis of variance using the general linear model (GLM) was used for delta PD and delta AL and took into account the variations in the treatments, number of smoker subjects per group, and baseline probing depth. There was a significant interaction between the "smoking" and the "baseline PD." Further analysis using linear regression indicated that, while there was a significant relationship between the baseline PD and the delta PD or delta AL among the non-smokers, weak and insignificant relationship existed among the smoker subjects. Thus, smoking may have an important role in determining the prognosis of periodontal treatment, particularly in persistent and deep pockets.

Smoking and Periodontal Disease

“…Kinane and Radvar (1997) found that the response to non-surgical mechanical therapy is particularly poor in deep pockets in smokers. Although the attachment gain was also greater among the non-smokers than the smokers, this was not significant.…”

Tobacco smoking and chronic destructive periodontal disease

“…[1][2][3][4] Studies during later years have confirmed these observations and contributed additional evidence that the gingival inflammatory response is altered by smoking. [5][6][7][8][9][10][11][12][13][14][15] The anti-hemorrhagic and anti-inflammatory effects imply that typical symptoms of inflammation, such as redness, bleeding, and edema appear comparably late in the disease process, if at all, in the average smoker patient. Interestingly, in smokers undergoing smoking cessation programs, gingival bleeding and gingival blood flow, as well as gingival crevicular fluid flow, increase and normalize toward non-smoker levels after quitting.…”

Relationship between Salivary Flow Rates and The Amount of Candida in Saliva in Smokers

“…This mechanism is possibly caused by chemical substances in cigarettes that can provide nutrition for candida, local changes in epithelium that which leads to candida colonization [12,14,16], decreased antibodies in saliva and hyposalivation [8,24,32,33]. Duration and amount of smoking would have a different impact on number of the candida colonies [12].…”