These data suggest that periodontal status and oral mucosal health are better in those who have quit cigarette smoking compared to current smokers. However, the data further suggest that smoking may significantly lower both general proteolytic enzyme activity and MMP-8 levels in saliva. Thus, care should be taken in interpreting results revealing salivary/mouthrinse proteinases as diagnostic markers for oral/periodontal disease activity.

The profile of salivary proteases and their cellular origin, with special reference to polymorphonuclear leukocytes and bacteria, was studied in localized juvenile periodontitis and compared with adult periodontitis and healthy controls. General proteolytic activity in saliva as well as collagenase, elastase-like and trypsin-like activity was measured. In addition, the sensitivity of salivary collagenase of patients with localized juvenile periodontitis to doxycycline inhibition was studied. The saliva of localized juvenile periodontitis patients contained low amounts of collagenase compared with adult periodontitis saliva, and almost all salivary collagenase was found to exist in endogenously active form, as was found to be the case also in adult periodontitis patients and healthy controls. The salivary collagenase of localized juvenile periodontitis patients was relatively insensitive to 100 mumol/l doxycycline but was completely inhibited by 600 mumol/l doxycycline, reflecting rather matrix metalloproteinase-1 (fibroblast-type) than matrix metalloproteinase-8 (polymorphonuclear leukocyte) enzyme. The saliva of localized juvenile periodontitis patients also contained low amounts of elastase-like activity compared with the saliva of untreated adult periodontitis patients. Scaling and root planing caused a significant decrease in elastase-like activity in the saliva of adult periodontitis patients. General proteolytic and trypsin-like activities were also low in the saliva of localized juvenile periodontitis patients. Furthermore, the reducing agent beta-mercaptoethanol did not activate or inhibit the salivary trypsin-like activity of localized juvenile periodontitis or adult periodontitis patients, although the reductant readily activated partially purified Porphyromonas gingivalis trypsin-like protease in a characteristic manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Cigarette smoking leads to lowered elastase and neutrophil levels in the oral cavity. The oral neutrophil elastase assay, therefore, cannot be used to measure the periodontal status of smokers.

Alpha-tocopherol (vitamin E) may play a role in the treatment of arterial thromboembolic disease, possibly by inhibiting platelet aggregation. Thus far, no clinical evidence exists for this effect. The objective of this study was to assess the effect of alpha-tocopherol supplementation on gingival bleeding either in combination with acetylsalicylic acid (ASA) or without it. This study was an end-point examination of a random sample of male smokers who had participated in a controlled clinical trial, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) for 5-7 years. The study included 409 men aged 55-74 years of whom 191 received alpha-tocopherol supplementation (50 mg/day); 56 used ASA, 30 received both and 132 received neither. Gingival bleeding was examined by probing with a WHO probe and reported as a percentage of bleeding sites adjusted by the logistic regression model. Gingival bleeding was more common in those who received alpha-tocopherol compared with nonreceivers among subjects with a high prevalence of dental plaque (P < 0.05). ASA alone increased bleeding only slightly. The highest risk of gingival bleeding was among those who took both alpha-tocopherol and ASA (33.4% of probed sites bleeding vs 25.8% among subjects taking neither alpha-tocopherol nor ASA, P < 0.001). In the ATBC Study, more deaths from haemorrhagic stroke and fewer from ischaemic heart disease were observed among those participants who received alpha-tocopherol compared with those who did not. Based on the results of the present study and the ATBC Study, we conclude that alpha-tocopherol supplementation may increase the risk of clinically important bleedings, particularly when combined with ASA.

OBJECTIVE: To assess the effect of alpha‐tocopherol and beta‐carotene supplementation on the prevalence of oral mucosal lesions in smokers. DESIGN: An end‐point examination of a random sample of participants in a controlled trial for 5–7 years (Alpha‐Tocopherol Beta‐Carotene Cancer Prevention Study) in Helsinki, Finland. SUBJECTS: A total of 409 white male cigarette smokers, aged 55–74 years who received either alpha‐tocopherol (50 mg per day) or beta‐carotene (20 mg per day) supplementation, both of these or placebo capsules. METHODS: Clinical examination of oral mucosae, histological examination of lesions showing leukoplakia and cytological examination of buccal epithelium. Statistical analysis using Fisher's exact test. RESULTS: No statistically significant differences were found between the study groups either in the prevalence of oral mucosal lesions or in the cells of unkeratinized epithelium. Leukoplakia was present in 24 (5.9%) of the subjects. Seven lesions showed dysplasia. CONCLUSION: The present study on oral health does not support the hypothesis that alpha‐tocopherol or beta‐carotene supplementation plays an essential role in preventing oral mucosal changes in smokers.