Internet-delivered cognitive cognitive-behavioural therapy should be pursued further as a complement or treatment alternative for mild-to-moderate depression.

The results suggest that periodontal health is compromised by chronic smoking as evidenced by an increase of periodontally diseased sites concomitant with loss of periodontal bone height, as compared to non-smokers whose periodontal health condition remained unaltered throughout the 10-year period of investigation. The periodontal health condition in former smokers, similar to that of non-smokers, remained stable, suggesting that smoking cessation is beneficial to periodontal health.

Patients admitted to the School of Dentistry, Stockholm, for treatment of chronic periodontal disease during the years 1980-82 were retrospectively investigated with respect to their smoking habits. The investigation was designed as a case control study and covered all patients 30, 40, or 50 yr of age upon admission, in all 155. As control served a random sample of the Stockholm population. The periodontal variables under scrutiny were frequency of periodontally diseased teeth, frequency of periodontally diseased sites (probing depth greater than 4 mm), gingival index, and plaque index. The overall occurrence rate of smokers in the sample of cases was 56%, which is significantly greater than the population at large. This held true for all three age cohorts and for men as well as women. The risk ratio was 2.5, indicating more prevalent disease among smokers. Further, significantly greater frequencies of periodontally involved teeth and diseased sites were found in smokers, indicating more severe disease among smokers. Gingival index and plaque index did not notably differ between smoking groups. The results suggest increased prevalence as well as severity in smokers. Smoking, therefore, should be considered a risk factor for chronic 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 unavoida...

Altogether, the present observations identify a negative impact from smoking on periodontal health and provide further evidence that tobacco smoking is an avoidable risk for periodontal disease.