Tobacco and smoking: environmental factors that modify the host response (immune system) and have an impact on periodontal health.
This review summarizes the current data on the effects of smoking and tobacco on the immune system and its potential impact on periodontal health. Smokers are 2.5-6 times more likely to develop periodontal disease than non-smokers, and there is evidence for a direct correlation between the number of cigarettes smoked and the risk of developing disease. Tobacco users also tend to exhibit increased severity of periodontal disease. Direct correlations between tobacco use and increased attachment loss and pocket depth and reduced bone crest height have been reported. Although the correlation between tobacco use and periodontal disease is quite strong, the role of tobacco in the pathogenesis of periodontal disease is uncertain. Recent studies indicate that one potential mechanism is that tobacco use exacerbates periodontal disease because it alters the immune response to periodontal pathogens. Indeed, smokers exhibit increased numbers of peripheral blood mononuclear phagocytes which appear to be functionally compromised. Inadequate phagocyte activity could reduce the clearance of pathogens from the oral cavity and thereby facilitate the development of periodontal disease. Tobacco-exposed B- and T-lymphocytes exhibit reduced proliferative capacities which could limit the production of protective immunoglobulins against oral pathogens. The risk factors for periodontal disease can be broadly classified as genetic, environmental, host-response factors, and host-related factors such as age. Tobacco, an environmental factor, undermines the host response and may facilitate the development and progression of periodontal disease. This review highlights the inter-relatedness of two of the risk factors associated with periodontal disease.
Barbour
S E
SE
Clinical Research Center for Periodontal Diseases, School of Dentistry, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0566, USA.
Nakashima
K
K
Zhang
J B
JB
Tangada
S
S
Hahn
C L
CL
Schenkein
H A
HA
Tew
J G
JG
D016301:Alveolar Bone Loss / Q000209:etiology; D000907:Antibodies, Bacterial / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D001419:Bacteria / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D018450:Disease Progression; D006801:Humans; D007111:Immunity, Cellular; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D017622:Periodontal Attachment Loss / Q000209:etiology; D010510:Periodontal Diseases / Q000209:etiology* / Q000276:immunology / Q000382:microbiology; D010514:Periodontal Pocket / Q000209:etiology; D010519:Periodontium / Q000276:immunology* / Q000382:microbiology; D010586:Phagocytes / Q000276:immunology; D010947:Plants, Toxic; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014026:Nicotiana
D000907:Antibodies, Bacterial