摘要
Tobacco smoking has been found to be a major environmental factor associated with generalized forms of severe periodontitis. Altered serum and gingival crevicular fluid inflammatory cytokine profiles, immune cell function, and altered proteolytic regulations are noticed in smokers. These observations are not consistent, and to date, there has been no clear mechanism to explain how smoking may affect periodontal disease. Hence, the present study was undertaken to assess the impact of smoking on serum immunoglobulin G (IgG) levels in smokers with periodontitis and its potential role as a risk indicator of the disease process. 40 subjects (15 smokers and 15 non-smokers with chronic periodontitis, 10 healthy controls) were included in the study. Smoking history was assessed according to a standardized interview and a questionnaire, Fagerstom Test for Nicotine Dependence. Serum immunoglobulin IgG was estimated with immunoturbidimetric assay. IgG levels were significantly decreased with longer duration of smoking. In addition levels of serum IgG were significantly lower in smokers compared to non-smokers with chronic periodontitis and healthy controls (P < 0.001). Current observations indicate that cigarette smoking may be associated with the suppression of B-cell function and immunoglobulin production. The alteration of antibody levels further explains the potential mechanism by which smoking exacerbates periodontal disease. Further studies at the molecular level may highlight the specific mechanism by which tobacco can interact with cells of the immune system and its impact on periodontal disease process. Additional controlled, longitudinal studies may expound the significance of serum antibodies as potential markers for periodontal disease.
Tobacco smoking has been found to be a major environmental factor associated with generalized forms of severe periodontitis. Altered serum and gingival crevicular fluid inflammatory cytokine profiles, immune cell function, and altered proteolytic regulations are noticed in smokers. These observations are not consistent, and to date, there has been no clear mechanism to explain how smoking may affect periodontal disease. Hence, the present study was undertaken to assess the impact of smoking on serum immunoglobulin G (IgG) levels in smokers with periodontitis and its potential role as a risk indicator of the disease process. 40 subjects (15 smokers and 15 non-smokers with chronic periodontitis, 10 healthy controls) were included in the study. Smoking history was assessed according to a standardized interview and a questionnaire, Fagerstom Test for Nicotine Dependence. Serum immunoglobulin IgG was estimated with immunoturbidimetric assay. IgG levels were significantly decreased with longer duration of smoking. In addition levels of serum IgG were significantly lower in smokers compared to non-smokers with chronic periodontitis and healthy controls (P < 0.001). Current observations indicate that cigarette smoking may be associated with the suppression of B-cell function and immunoglobulin production. The alteration of antibody levels further explains the potential mechanism by which smoking exacerbates periodontal disease. Further studies at the molecular level may highlight the specific mechanism by which tobacco can interact with cells of the immune system and its impact on periodontal disease process. Additional controlled, longitudinal studies may expound the significance of serum antibodies as potential markers for periodontal disease.
