Abstract
Cigarette smoking is a significant risk factor for the initiation and progression of periodontal disease. Studies have shown altered serum and gingival crevicular fluid inflammatory cytokine profiles, immune cell function, and altered proteolytic regulation in smokers. The observations are not consistent, and to date, there is no clear mechanism to explain how smoking may affect periodontal disease. Hence, the present study was undertaken to assess the alterations of serum immunoglobulin levels in smokers with periodontitis and its potential role as a risk indicator of the disease process.
In this study, 30 patients who smoked and 30 patients who did not smoke with chronic periodontitis and 30 healthy subjects were enrolled. Serum immunoglobulin (Ig) G, IgA, and IgM levels were estimated with immunoturbidimetric assay. The IgG subclass (IgG1, IgG2, IgG3, and IgG4) levels were performed using single radial immunodiffusion assay.
Levels of serum IgG and IgA were significantly lower in smokers compared to non-smokers and healthy controls (P <0.001). Although IgM levels were low in smokers, it was not significant. Of the four subclasses of IgG studied, the IgG2 was found to be significantly lower among smokers with periodontitis.
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.