Smoking will affect the periodontitis?

The relationship of smoking and periodontal disease has been inconclusive. Most data indicate that smoking promote calculus deposition and plaque accumulation, smokers gum disease is more important than non-smokers, mainly deep periodontal pocket, alveolar bone loss, loss of attachment level height and tooth loss. Suggesting that smoking and periodontitis prevalence is closely related, mainly through local and systemic factors pathogenic.

Local factors: poor oral health of smokers, plaque accumulation, calculus, increased debris can lead to gingivitis and periodontitis risk factors. The data show that: smokers DI, CI, and periodontitis prevalence rates than non-smokers. Heavy smoker’s periodontitis section is higher than that of light, moderate smokers and non smokers.

Calculus mechanical damage to the gums, creating good conditions for bacterial invasion. Detection rate of 100% of the anaerobic bacteria in the periodontal abscess. Smoking hypoxia within the oral cavity, periodontal redox potential drop, which is conducive to the survival of anaerobic bacteria. Studies have shown that as long as smoking a cigarette, gum at the redox potential significantly reduce oral pH value changes.

Systemic factors: smoking can cause the body's immune function. Cellular immunity to smokers, leukocyte chemo taxis is lower than non-smokers, the total number of leukocytes, Europhiles, lymphocytes and monocytes were lower than non-smokers. Humoral immune smoking reduces the dental instruments serum level of inhibition of helper T lymphocyte proliferation. Smoker’s Oral local immune function, the survey found lower than non-smokers smokers’ saliva.

Other aspects: It has been reported in tobacco nicotine into the bloodstream, leading to gingival vasoconstriction, decreased blood flow, resulting in gingival oxygen supply and blood gas exchange decreased. Waste removal capacity decreased, resulting in lower gum protection repair function. Animal experiments have proved the high temperature and chemical composition of the smoke to stimulate long-term gingival epithelium keratinized layer thickening, submucosal vascular congestion of the gums in the long-term chronic inflammatory state. Studies have shown: the absorption of nicotine through stimulation into bone alkaline phosphates activity, inhibition of cell proliferation, promotes alveolar bone.