Patients' awareness of the potential benefit of smoking cessation. A study evaluating self-reported and clinical data from patients referred to an oral medicine unit

The present study analyzed history of smoking and willingness to quit smoking in patients referred for diagnosis and treatment of different oral mucosal lesions. Prior to the initial clinical examination, patients filled in a standardized questionnaire regarding their current and former smoking habits and willingness to quit. Definitive diagnoses were classified into three groups (benign/reactive lesions, premalignant lesions and conditions, and malignant diseases) and correlated with the self-reported data in the questionnaires. Of the 980 patients included, 514 (52%) described themselves as never smokers, 202 (21%) as former smokers, and 264 (27%) as current smokers. In the group of current smokers, 23% thought their premalignant lesions/conditions were related to their smoking habit, but only 15% of the patients with malignant mucosal diseases saw that correlation. Only 14% of the smokers wanted to commence smoking cessation within the next 30 days. Patients with malignant diseases (31%) showed greater willingness to quit than patients diagnosed with benign/reactive lesions (11%). Future clinical studies should attempt (1) to enhance patients' awareness of the negative impact of smoking on the oral mucosa and (2) to increase willingness to quit in smokers referred to a dental/oral medicine setting.

Tooth loss over five years

Objectives: To assess the ability to predict tooth loss on the basis of clinical and radiographic parameters. Methods: Clinical and radiographic data from a five year prospective cohort were studied to identify cause of progressive tooth loss in older subjects. Results: 363 subjects with a baseline mean age of 67.1 years (S.D. + 4.7, range : 60-75), and 51.4% women were studied including 59.5% never smokers, and 33.0% current smokers. At baseline the subjects had, on average, 22.4 teeth (S.D. + 6.4). Self-assessed tooth loss risk was identified by 16.0 % of subjects while 34% of subjects lost teeth. Tooth loss due to caries was found in 24.7% (178 teeth), periodontitis in 15.4% (133 teeth), peri-apical lesions 5.9% (32 teeth), combined periodontal/peri-apical in 3.4% (18 teeth), and teeth irrational to treat in 7.5% (58 teeth) of the subjects. 122 of the extracted teeth (34%) should have been possible to save but were extracted. At year five severe caries, periodontitis, peri-apical lesions, periodontal/peri-apical, irrational to treat were found in 6.3%, 7.2%, 2.6%, 4.6%, and 1.2% of subjects, respectively. Signs of osteoporosis increased by 11.2 % (Klemetti index). Linear regression analysis failed to include smoking habits as being explanatory. Explanatory factors were researcher prediction of extraction needs, subject self assessment of risk and change in ostoporosis status (r2 = 0.39, ANOVA, F=22.6, p< 0.001). Conclusions: Caries and periodontitis are primary causes for extraction. Progressive osteoporosis is associated with tooth loss. Radiographs, and subjects self-assessment of risk for tooth loss are robust predictors.

Multicenter phase II trial of gefitinib first-line therapy followed by chemotherapy in advanced non-small-cell lung cancer (NSCLC): SAKK protocol 19/03

BACKGROUND: Gefitinib is active in patients with pretreated non-small-cell lung cancer (NSCLC). We evaluated the activity and toxicity of gefitinib first-line treatment in advanced NSCLC followed by chemotherapy at disease progression. PATIENTS AND METHODS: In all, 63 patients with chemotherapy-naive stage IIIB/IV NSCLC received gefitinib 250 mg/day. At disease progression, gefitinib was replaced by cisplatin 80 mg/m(2) on day 1 and gemcitabine 1250 mg/m(2) on days 1, 8 for up to six 3-week cycles. Primary end point was the disease stabilization rate (DSR) after 12 weeks of gefitinib. RESULTS: After 12 weeks of gefitinib, the DSR was 24% and the response rate (RR) was 8%. Median time to progression (TtP) was 2.5 months and median overall survival (OS) 11.5 months. Never smokers (n = 9) had a DSR of 56% and a median OS of 20.2 months; patients with epidermal growth factor receptor (EGFR) mutation (n = 4) had a DSR of 75% and the median OS was not reached after the follow-up of 21.6 months. In all, 41 patients received chemotherapy with an overall RR of 34%, DSR of 71% and median TtP of 6.7 months. CONCLUSIONS: First-line gefitinib monotherapy led to a DSR of 24% at 12 weeks in an unselected patients population. Never smokers and patients with EGFR mutations tend to have a better outcome; hence, further trials in selected patients are warranted.

Smoking, apolipoprotein E genotypes, and mortality (the Ludwigshafen RIsk and Cardiovascular Health study).

AIMS The genetic polymorphism of apolipoprotein E (APOE) has been suggested to modify the effect of smoking on the development of coronary artery disease (CAD) in apparently healthy persons. The interaction of these factors in persons undergoing coronary angiography is not known. METHODS AND RESULTS We analysed the association between the APOE-genotype, smoking, angiographic CAD, and mortality in 3263 participants of the LUdwigshafen RIsk and Cardiovascular Health study. APOE-genotypes were associated with CAD [ε22 or ε23: odds ratio (OR) 0.56, 95% confidence interval (CI) 0.43-0.71; ε24 or ε34 or ε44: OR 1.10, 95% CI 0.89-1.37 compared with ε33] and moderately with cardiovascular mortality [ε22 or ε23: hazard ratio (HR) 0.71, 95% CI 0.51-0.99; ε33: HR 0.92, 95% CI 0.75-1.14 compared with ε24 or ε34 or ε44]. HRs for total mortality were 1.39 (95% CI 0.39-0.1.67), 2.29 (95% CI 1.85-2.83), 2.07 (95% CI 1.64-2.62), and 2.95 (95% CI 2.10-4.17) in ex-smokers, current smokers, current smokers without, or current smokers with one ε4 allele, respectively, compared with never-smokers. Carrying ε4 increased mortality in current, but not in ex-smokers (HR 1.66, 95% CI 1.04-2.64 for interaction). These findings applied to cardiovascular mortality, were robust against adjustment for cardiovascular risk factors, and consistent across subgroups. No interaction of smoking and ε4 was seen regarding non-cardiovascular mortality. Smokers with ε4 had reduced average low-density lipoprotein (LDL) diameters, elevated oxidized LDL, and lipoprotein-associated phospholipase A2. CONCLUSION In persons undergoing coronary angiography, there is a significant interaction between APOE-genotype and smoking. The presence of the ε4 allele in current smokers increases cardiovascular and all-cause mortality.

Compliance of cigarette smokers with scheduled visits for supportive periodontal therapy.

AIM To evaluate the compliance of cigarette smokers with scheduled visits for supportive periodontal therapy (SPT). MATERIALS AND METHODS Qualitative and quantitative analyses of compliance with scheduled SPT visits were performed using retrospective data from patients undergoing dental hygiene treatment at the Medi School of Dental Hygiene (MSDH), Bern, Switzerland 1985-2011. RESULTS A total of 1336 patients were identified with 32.1% (n = 429) being smokers, 23.1% (n = 308) former smokers and 44.8% (n = 599) non-smokers. Qualitatively, significantly less smokers returned for SPT than non-smokers or former smokers (p = 0.0026), whereas 25.9% (n = 346) never returned for SPT. Further quantitative analysis of patients returning twice or more (n = 883) revealed that the overall mean %-compliance was 69.8% (SD ±22.04),whereas smokers complied with 67.0% (SD ±22.00), former smokers with 69.7% (SD ±22.03), and non-smokers with 71.7% (SD ±21.92) reaching statistical significance (p = 0.0111). Confounder adjusted analysis, however, revealed that older age (p = 0.0001), female gender (p = 0.0058), longer SPT intervals (p < 0.0001) and higher severity of periodontal disease (p < 0.0001) had a much greater impact on %-compliance than smoking (p = 0.7636). CONCLUSIONS This study suggests that qualitatively, smokers return less likely for SPT than non-smokers or former smokers while quantitatively, a lower mean %-compliance of smokers attending scheduled SPT visits may be attributed to confounders.

A 10-year retrospective analysis of marginal bone-level changes around implants in periodontally healthy and periodontally compromised tobacco smokers

to compare the 10-year marginal bone loss rates around implants supporting single-unit crowns in tobacco smokers with and without a history of treated periodontitis.

Reactive oxygen species mediate functional differences in human radial and internal thoracic arteries from smokers

Smoking not only increases the risk that coronary heart disease will develop but also morbidity and mortality in patients with known coronary atherosclerosis and after coronary artery bypass grafting. Excessive generation of reactive oxygen species (ROS) has been implicated as the final common pathway for the development of endothelial dysfunction in various cardiovascular risk factors. This study assessed the influence of smoking on two different human arteries routinely used as coronary artery bypass graft conduits.

Marked global reduction in mGluR5 receptor binding in smokers and ex-smokers determined by [11C]ABP688 positron emission tomography

Nicotine addiction is a major public health problem, resulting in primary glutamatergic dysfunction. We measured the glutamate receptor binding in the human brain and provided direct evidence for the abnormal glutamate system in smokers. Because antagonism of the metabotropic glutamate receptor 5 (mGluR5) reduced nicotine self-administration in rats and mice, mGluR5 is suggested to be involved in nicotine addiction. mGluR5 receptor binding specifically to an allosteric site was observed by using positron emission tomography with [(11)C]ABP688. We found a marked global reduction (20.6%; P < 0.0001) in the mGluR5 distribution volume ratio (DVR) in the gray matter of 14 smokers. The most prominent reductions were found in the bilateral medial orbitofrontal cortex. Compared with 14 nonsmokers, 14 ex-smokers had global reductions in the average gray matter mGluR5 DVR (11.5%; P < 0.005), and there was a significant difference in average gray matter mGluR5 DVR between smokers and ex-smokers (9.2%; P < 0.01). Clinical variables reflecting current nicotine consumption, dependence and abstinence were not correlated with mGluR5 DVR. This decrease in mGluR5 receptor binding may be an adaptation to chronic increases in glutamate induced by chronic nicotine administration, and the decreased down-regulation seen in the ex-smokers could be due to incomplete recovery of the receptors, especially because the ex-smokers were abstinent for only 25 wk on average. These results encourage the development and testing of drugs against addiction that directly target the glutamatergic system.

EEG reactivity and EEG activity in never-treated acute schizophrenics, measured with spectral parameters and dimensional complexity

Our approaches to the use of EEG studies for the understanding of the pathogenesis of schizophrenic symptoms are presented. The basic assumptions of a heuristic and multifactorial model of the psychobiological brain mechanisms underlying the organization of normal behavior is described and used in order to formulate and test hypotheses about the pathogenesis of schizophrenic behavior using EEG measures. Results from our studies on EEG activity and EEG reactivity (= EEG components of a memory-driven, adaptive, non-unitary orienting response) as analyzed with spectral parameters and "chaotic" dimensionality (correlation dimension) are summarized. Both analysis procedures showed a deviant brain functional organization in never-treated first-episode schizophrenia which, within the framework of the model, suggests as common denominator for the pathogenesis of the symptoms a deviation of working memory, the nature of which is functional and not structural.

Ascorbate is depleted by smoking and repleted by moderate supplementation: a study in male smokers and nonsmokers with matched dietary antioxidant intakes

BACKGROUND: Lack of reliable dietary data has hampered the ability to effectively distinguish between effects of smoking and diet on plasma antioxidant status. As confirmed by analyses of comprehensive food-frequency questionnaires, the total dietary intakes of fruit and vegetables and of dietary antioxidants were not significantly different between the study groups in the present study, thereby enabling isolation of the effect of smoking. OBJECTIVE: Our objective was to investigate the effect of smoking on plasma antioxidant status by measuring ascorbic acid, alpha-tocopherol, gamma-tocopherol, beta-carotene, and lycopene, and subsequently, to test the effect of a 3-mo dietary supplementation with a moderate-dose vitamin cocktail. DESIGN: In a double-blind, placebo-controlled design, the effect of a vitamin cocktail containing 272 mg vitamin C, 31 mg all-rac-alpha-tocopheryl acetate, and 400 microg folic acid on plasma antioxidants was determined in a population of smokers (n = 37) and nonsmokers (n = 38). The population was selected for a low intake of fruit and vegetables and recruited from the San Francisco Bay area. RESULTS: Only ascorbic acid was significantly depleted by smoking per se (P < 0.01). After the 3-mo supplementation period, ascorbic acid was efficiently repleted in smokers (P < 0.001). Plasma alpha-tocopherol and the ratio of alpha- to gamma-tocopherol increased significantly in both supplemented groups (P < 0.05). CONCLUSIONS: Our data suggest that previous reports of lower concentrations of plasma vitamin E and carotenoids in smokers than in nonsmokers may primarily have been caused by differences in dietary habits between study groups. Plasma ascorbic acid was depleted by smoking and repleted by moderate supplementation.