Background: Chronic periodontitis is the inflammation within the supporting tissues of the teeth resulting in attachment loss and bone loss. There are certain environmental factors such as smoking that can modify the host response to plaque organisms; hence can account for the aggressive progression of the disease. Smokers show a decreased expression of clinical inflammation even in the presence of abundant plaque accumulation. Neutrophils are the predominant host defense cells which protect the periodontal tissues from plaque organisms, deficiencies of neutrophil function, such as chemotaxis and phagocytosis, often result in increased susceptibility to periodontitis. Smoking can induce alteration in the neutrophil function; therefore, it is of importance to know the changes caused by smoking on neutrophil chemotaxis. This study will provide an essential basis for evaluating the role of nicotine in pathogenesis of periodontal disease by assessing the neutrophil activity.
Materials and methods: A total of 60 smokers and 60 non smokers were examined for this study. Both the groups included 20 subjects with gingivitis, periodontitis, and healthy periodontium. The periodontal status of the study subjects were assessed by gingival index, Russels periodontal index, sulcus bleeding index, and clinical attachment level. The blood sample was taken from each individual for the chemotactic analysis using agarose method.
Results: In this study, there was a significant decrease in the neutrophil chemotaxis in smokers with gingivitis, periodontitis, and healthy periodontium, compared to non smokers with similar findings.
Conclusion: Delayed neutrophil chemotaxis was found in smokers compared to non smokers with same periodontal status.
Keywords: Chemotaxis; nicotine; polymorphonuclear cells; smoking.