Tobacco smoking and chronic destructive periodontal disease.
Tobacco smoking is the main risk factor associated with chronic destructive periodontal disease. No other known factor can match the strength of smoking in causing harm to the periodontium. The harmful effects manifest themselves by interfering with vascular and immunologic reactions, as well as by undermining the supportive functions of the periodontal tissues. The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the ensuing clinical symptoms of bone loss, attachment loss, pocket formation, and eventually tooth loss. A review of the international literature that has accumulated over the past 20 years offers convincing evidence that smokers exhibit greater bone loss and attachment loss, as well as more pronounced frequencies of periodontal pockets, than non-smokers do. In addition, tooth loss is more extensive in smokers. Smoking, thus, considerably increases the risk for destructive periodontal disease. Depending on the definition of disease and the exposure to smoking, the risk is 5- to 20-fold elevated for a smoker compared to a never-smoker. For a smoker exposed to heavy long-life smoking, the risk of attracting destructive periodontal disease is equivalent to that of attracting lung cancer. The outcome of periodontal treatment is less favorable or even unfavorable in smokers. Although long-term studies are rare, available studies unanimously agree that treatment failures and relapse of disease are predominantly seen in smokers. This contention is valid irrespective of treatment modality, suggesting that smoking will interfere with an expected normal outcome following commonplace periodontal therapies. The majority of available studies agree that the subgingival microflora of smokers and non-smokers are no different given other conditions. As a consequence, the elevated morbidity in smokers does not depend on particular microflora. The mechanisms behind the destructive effects of smoking on the periodontal tissues, however, are not well understood. It has been speculated that interference with vascular and inflammatory phenomena may be one potential mechanism. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing. Smoking research over the past two decades has brought new knowledge into the domains of periodontology. Even more so, it has called into question the prevailing paradigm that the disease is primarily related to intraoral factors such as supra- and subgingival infection. Smoking research has revealed that environmental and lifestyle factors are involved in the onset and progression of the disease. Being the result of smoking, destructive periodontal disease shares a common feature with some 40 other diseases or disorders. As a consequence, periodontal disease should be regarded as a systemic disease in the same way as heart disease or lung disease. Thus, chronic destructive periodontal disease in smokers is initiated and driven by smoking. Its progression may or may not be amplified by unavoidable microbial colonization.
Bergström
Jan
J
Karolinska Institutet, Stockholm, Alfred Nobels allé 8, Box 4064, S141 04 Huddinge, Sweden. Jan.Bergstrom@ofa.ki.se.
D016301:Alveolar Bone Loss / Q000209:etiology; D002908:Chronic Disease; D006801:Humans; D017622:Periodontal Attachment Loss / Q000209:etiology; D010510:Periodontal Diseases / Q000209:etiology* / Q000382:microbiology / Q000628:therapy; D010514:Periodontal Pocket / Q000209:etiology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D016388:Tooth Loss / Q000209:etiology; D016896:Treatment Outcome