The Effect of Smoking on Mast Cells Density and Angiogenesis in Chronic Periodontitis

Abstract

Background and objective: Gingival bleeding reduction in smokers has been associated with decreased blood vessel density. The mechanism of suppressive effect of cigarette smoking on blood vessel density is not precisely defined. The aim of this study was to evaluate the impact of smoking on angiogenesis by assessing mast cells density and VEGF expression in chronic periodontitis. Materials& Methods: 52 paraffin embedded block of gingiva tissues with periodontitis obtained from 30 nonsmokers and 22 smokers undergoing flap surgery were examined immunohistochemically for VEGF expression. Mast cell counts was completed on toluidine blue stained slides. Exposure to cigarette smoking was calculated by the number of packs × year. Patients were classified into 4 groups based on the number of smoked cigarettes. The correlation between VEGF expression and mast cell counts was evaluated and compared in nonsmokers and smokers. Results: The mean number of mast cells (p=0.004) and average value of VEGF expression (p = 0.000) in nonsmokers was significantly higher than smokers. No correlation was noted between VEGF expression / mast cell counts and number of smoked cigarettes in four groups of smokers (p=0.29,0.12 , 0.20 and 0.11, respectively). Conclusion: Mast cells and VEGF expression may account for suppressive effect of cigarette smoking on blood vessels in periodontitis.

The effects of smoking on genotoxic and histopathologic damage in exfoliated oral epithelial cells and the periodontium: A cross-sectional study

“…While our inflammatory cell density results are similar to several studies, [38,39] they are inconsistent with the results of other investigations that either did not find a significant difference between study groups [13,25,40] or found inflammatory cell density more intense in nonsmokers. [12,41] The vascular density results in our study align with observations from the existing literature. [25,42–44] However, some studies [12,13,45,46] have observed no significant differences in vascular characteristics among their study groups.…”

“…[12,41] The vascular density results in our study align with observations from the existing literature. [25,42–44] However, some studies [12,13,45,46] have observed no significant differences in vascular characteristics among their study groups. In one recent study [25] that compared gingival biopsies taken from an area with periodontitis with those from another area that showed no clinical signs of gingival inflammation (each taken from smokers and nonsmokers), the authors reported that while small differences in inflammatory cell density and cellular components were found in the periodontitis tissues of both the nonsmokers and smokers, the nonsmoker’s vascular density was significantly higher than that of the smokers.…”

“…Studies have reported that smokers with periodontitis have lower gingival bleeding indices than nonsmokers with periodontitis owing to nicotine’s vasoconstrictive property. [12,25] We believe that the BOP score did not differ significantly between periodontitis groups as a result of the pressure exerted by the periodontal probe while placed it in the constricted periodontal pocket in the smokers group, and the excessive PD caused by the severe periodontal inflammation.…”

“…Clinical signs and symptoms of gingival inflammation tend to decrease in smokers, [3,12,13] and this finding can be confused with gingival health. [14–16] Moreover, a histopathologic approach is not used in routine periodontal disease assessment in clinical practice as the tissue biopsy must be examined in a histology laboratory.…”

Study on painless gastroscopy and POCD of smoking patients under general anesthesia

“…Studies have shown that mast cells stimulated by long‐term COVID syndrome after novel coronavirus infection release neuroinflammation, which activates microglia and leads to hypothalamic inflammation 16 . Smoking is likely to stimulate mast cells in the oral cavity and lung, resulting in chronic periodontitis and pneumonia, and then migrate and cause chronic inflammation 17 . Further evolution of various types of chronic inflammation leads to the occurrence of central chronic insidious inflammation.…”