Abstract
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.
Highlights
Chronic periodontitis is the result of a response of the host to bacterial aggregations on the tooth surfaces
A total of 40 systemically healthy male patients were included in this study of which 15 patients in Group 1, 15 in Group 2 and 10 patients were in Group 3
The mean Plaque Index (PI), gingival index (GI) and modified sulcular bleeding index in non-smoker with periodontitis was higher as compared to smoker with periodontitis and healthy individuals
Summary
Chronic periodontitis is the result of a response of the host to bacterial aggregations on the tooth surfaces. Epidemiological studies on the relationship between tobacco use and periodontal diseases consistently reported that cigarette smokers are five times more likely to develop severe periodontitis than non-smokers [8]-[10] These investigators reported a relationship between the duration of smoking and increased clinical attachment loss. The current understanding of the pathogenesis of periodontal disease suggests that periodontal tissue is destroyed by the modulation of host defences by bacterial products [4] This stimulates the host inflammatory process and releases cytokines and enzymes capable of destroying the host tissues. This does not preclude a role for bacteria and virulence factors, but suggests that in most forms of periodontal disease, destruction is a consequence of the host response to these factors [11]. This suggests that the most relevant virulence factors are those that strongly stimulate the destruction of host tissues by host-derived molecules [12]
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