scholarly journals Effect of Smoking Cessation On Tooth Loss: A Systematic Review With Meta-Analysis

2019 ◽  
Author(s):  
Maria Luisa Silveira Souto ◽  
Emanuel Silva Rovai ◽  
Cristina Cunha Villar ◽  
Mariana Minatel Braga ◽  
Claudio Mendes Pannuti

Abstract Background: Smoking is a major risk factor for periodontitis and tooth loss. Smoking cessation has a positive impact in periodontal treatment. However, so far, no systematic reviewhas evaluatedthe effect of smoking cessation on tooth loss. Therefore, this review aimed to evaluate if smoking cessation reduces the risk of tooth loss. Methods: Observational (cross-sectional and longitudinal) studiesthat investigated the association between smoking cessation and tooth loss were included. MEDLINE, EMBASE and LILACS databases were searched for articles published up to November 2018. Pooled results for subgroups of current and former smokers were compared in meta-analysis. Meta-regression was used to test the influence of smoking status on estimates and explore the heterogeneity. Results: Of 230 potentially relevant publications, 21 studies were included in the qualitative review and 12 in the quantitative analysis. Meta-analysis of cross-sectional studies did not show any differences between former and current smokers in the chance of losing 1 or more teeth (OR = 1.00; 95% CI = 0.80 to 1.24, I 2 = 80%), losing more than 8 teeth (OR = 1.02; 95% CI = 0.78 to 1.32, I 2 = 0%) or being edentulous (OR = 1.37; 95% CI = 0.94 to 1.99, I 2 = 98%). Meta-analysis from longitudinal studies showed that, when compared to never smokers, former smokers presented no increased risk of tooth loss (RR = 1.15; 95% CI = 0.98 to 1.35, I 2 = 76%), while current smokers presented an increased risk of tooth loss (RR = 2.60; 95% CI = 2.29 to 2.96, I 2 = 61%). Meta-regression showed that, among former smokers, the time of cessation was the variable that better explained heterogeneity (approximately 60%). Conclusions: Risk for tooth loss in former smokers is comparable to that of never smokers. Moreover, former smokers have a reduced risk of tooth loss, when compared to current smokers.

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Maria Luisa Silveira Souto ◽  
Emanuel Silva Rovai ◽  
Cristina Cunha Villar ◽  
Mariana Minatel Braga ◽  
Cláudio Mendes Pannuti

Abstract Background Smoking is a major risk factor for periodontitis and tooth loss. Smoking cessation has a positive impact in periodontal treatment. However, so far, no systematic review has evaluated the effect of smoking cessation on tooth loss. Therefore, this review aimed to evaluate if smoking cessation reduces the risk of tooth loss. Methods Observational (cross-sectional and longitudinal) studies that investigated the association between smoking cessation and tooth loss were included. MEDLINE, EMBASE and LILACS databases were searched for articles published up to November 2018. Pooled results for subgroups of current and former smokers were compared in meta-analysis. Meta-regression was used to test the influence of smoking status on estimates and explore the heterogeneity. Results Of 230 potentially relevant publications, 21 studies were included in the qualitative review and 12 in the quantitative analysis. Meta-analysis of cross-sectional studies did not show any differences between former and current smokers in the chance of losing 1 or more teeth (OR = 1.00; 95% CI = 0.80 to 1.24, I2 = 80%), losing more than 8 teeth (OR = 1.02; 95% CI = 0.78 to 1.32, I2 = 0%) or being edentulous (OR = 1.37; 95% CI = 0.94 to 1.99, I2 = 98%). Meta-analysis from longitudinal studies showed that, when compared to never smokers, former smokers presented no increased risk of tooth loss (RR = 1.15; 95% CI = 0.98 to 1.35, I2 = 76%), while current smokers presented an increased risk of tooth loss (RR = 2.60; 95% CI = 2.29 to 2.96, I2 = 61%). Meta-regression showed that, among former smokers, the time of cessation was the variable that better explained heterogeneity (approximately 60%). Conclusions Risk for tooth loss in former smokers is comparable to that of never smokers. Moreover, former smokers have a reduced risk of tooth loss, when compared to current smokers.


2018 ◽  
Vol 26 (3) ◽  
pp. 279-288 ◽  
Author(s):  
Dagfinn Aune ◽  
Sabrina Schlesinger ◽  
Teresa Norat ◽  
Elio Riboli

Background We conducted a systematic review and meta-analysis to clarify the association between smoking and the risk of developing heart failure. Methods PubMed and Embase databases were searched up to 24 July 2018. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) of heart failure associated with smoking. Summary RRs and 95% CIs were estimated using a random effects model. Results Twenty-six studies were included. The summary RR was 1.75 (95% CI: 1.54–1.99, I2 = 81%, n = 10) for current smokers, 1.16 (95% CI: 1.08–1.24, I2 = 51%, n = 9) for former smokers, and 1.44 (1.34–1.55, I2 = 83%, n = 10) for ever smokers compared with never smokers. The summary RR was 1.41 (95% CI: 1.01–1.96, I2 = 82%, n = 2) per 10 cigarettes per day, 1.11 (95% CI: 1.04–1.18, I2 = 70%, n = 3) and 1.08 (95% CI: 1.02–1.14, I2 = 34%, n = 2) per 10 pack-years among ever smokers and former smokers, respectively, and 0.79 (95% CI: 0.63–1.00, I2 = 96%, n = 2) per 10 years since quitting smoking. The association between smoking cessation and heart failure reached significance at 15 years of smoking cessation, and at 30 years the summary RR was 0.72 (95% CI: 0.57–0.90), only slightly higher than the summary RR for never smokers (0.64 (95% CI: 0.57–0.72)) when compared with current smokers. Conclusion Smoking is associated with increased risk of heart failure, but the risk decreases with increasing duration since smoking cessation. Any further studies should investigate the association between number of cigarettes per day, duration, pack-years and time since quitting smoking and risk of heart failure.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. J. MacDonald ◽  
A. L. Madika ◽  
G. Severi ◽  
A. Fournier ◽  
M. C. Boutron-Ruault

AbstractDyslipidaemia is a major risk factor for cardio-vascular disease, as it promotes atherosclerosis. While cross-sectional studies have identified higher serum cholesterol amongst individuals with the A blood group, there is less evidence from prospective studies whether this translates into a higher risk of dyslipidaemia that requires treatment, nor if this genetic factor interacts with smoking status. This study aimed to prospectively determine potential associations between smoking, ABO blood groups, and risk of incident dyslipidaemia requiring treatment, and to assess associations over strata of blood ABO group. We assessed associations between blood ABO group, smoking and dyslipidaemia in 74,206 women participating in the E3N cohort. We included women who did not have cardiovascular disease at baseline. Logistic regression was used to determine associations between ABO group, smoking and prevalent dyslipidaemia at baseline. Cox proportional hazard models were then used to determine if blood ABO group and smoking were associated with the risk of incident dyslipidaemia, amongst women free of dyslipidaemia at baseline. At baseline 28,281 women with prevalent dyslipidaemia were identified. Compared to the O-blood group, the non-O blood group was associated higher odds of with prevalent dyslipidaemia (ORnon-O = 1.09 [1.06: 1.13]). Amongst the women free of dyslipidaemia at baseline, 6041 incident cases of treated dyslipidaemia were identified during 454,951 person-years of follow-up. The non-O blood groups were associated with an increased risk of dyslipidaemia when compared to the O-group (HRnon-O = 1.16 [1.11: 1.22]), specifically the A blood-group (HRA = 1.18 [1.12: 1.25]). Current smokers were associated with an increased risk of incident dyslipidaemia (HR smokers = 1.27 [1.16: 1.37]), compared to never-smokers. No evidence for effect modification between smoking and ABO blood group was observed (p-effect modification = 0.45), although the highest risk was observed among AB blood group women who smoked (HR = 1.76 [1.22: 2.55]). In conclusion, the non-O blood groups, specifically the A group were associated with an increased risk of dyslipidaemia. Current smokers were associated with a 30% increased risk of dyslipidaemia. These results could aid in personalised approaches to the prevention of cardiovascular risk-factors.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Woncheol Lee ◽  
Yoosoo Chang ◽  
Hocheol Shin ◽  
Seungho Ryu

AbstractWe examined the associations of smoking status and urinary cotinine levels, an objective measure of smoking, with the development of new-onset HL. This cohort study was performed in 293,991 Korean adults free of HL who underwent a comprehensive screening examination and were followed for up to 8.8 years. HL was defined as a pure-tone average of thresholds at 0.5, 1.0, and 2.0 kHz ≥ 25 dB in both ears. During a median follow-up of 4.9 years, 2286 participants developed new-onset bilateral HL. Self-reported smoking status was associated with an increased risk of new-onset bilateral HL. Multivariable-adjusted HRs (95% CIs) for incident HL comparing former smokers and current smokers to never-smokers were 1.14 (1.004–1.30) and 1.40 (1.21–1.61), respectively. Number of cigarettes, pack-years, and urinary cotinine levels were consistently associated with incident HL. These associations were similarly observed when introducing changes in smoking status, urinary cotinine, and other confounders during follow-up as time-varying covariates. In this large cohort of young and middle-aged men and women, smoking status based on both self-report and urinary cotinine level were independently associated with an increased incidence of bilateral HL. Our findings indicate smoking is an independent risk factor for HL.


2007 ◽  
Vol 86 (4) ◽  
pp. 373-377 ◽  
Author(s):  
T. Dietrich ◽  
N.N. Maserejian ◽  
K.J. Joshipura ◽  
E.A. Krall ◽  
R.I. Garcia

Data on the dose-dependent effects of smoking and smoking cessation on tooth loss are scarce. We hypothesized that smoking has both dose- and time-dependent effects on tooth loss incidence. We used longitudinal data on tobacco use and incident tooth loss in 43,112 male health professionals, between 1986 and 2002. In multivariate Cox models, current smokers of 5 to 14 and 45+ cigarettes daily had a two-fold (HR, 1.94; 95% CI, 1.72, 2.18) and three-fold (HR, 3.05; 95% CI, 2.38, 3.90) higher risk of tooth loss, respectively, compared with never-smokers. Risk decreased with increasing time since cessation, but remained elevated by 20% (95% CI, 16%, 25%) for men who had quit 10+ years before. Current pipe/cigar smokers had a 20% (95% CI, 1.11, 1.30) increased risk of tooth loss compared with never- and former smokers of pipes/cigars.


2020 ◽  
Vol 30 (1) ◽  
pp. 108-110 ◽  
Author(s):  
Philip Gendall ◽  
Janet Hoek

BackgroundConcerns about the effects of vaping have prompted calls to restrict e-cigarette flavours. Vaping proponents have criticised these proposals, which they argue may discourage smokers from taking up vaping or trigger relapse to smoking. We explored the role flavours play in vaping uptake and cessation among New Zealand cigarette smokers and vaping-susceptible never smokers (VSNS), and examined current vapers’ preferred flavours.MethodsWe conducted an online survey of 1005 New Zealanders aged 18–70 years that included 324 current vapers (vaped in the last 30 days) and 302 ‘past’ vapers (reported past vaping, but not within the last month). We asked respondents their reasons for vaping and explored current vapers’ preferred e-cigarette flavours; we analysed the data using descriptive statistics and logistic regression.ResultsIrrespective of smoking status, flavour was one of the main reasons respondents gave for vaping (smokers 83%; former smokers 77%; VSNS 80%). Flavour was less important to former vapers; 47% of smokers, 57% of former smokers and 64% of VSNS cited flavour as a reason for originally taking up vaping. Fruit flavours were most popular among all three groups; smokers also favoured tobacco flavour, while former smokers also favoured mint or menthol, and never smokers also favoured confectionery/sweets/lolly flavours.ConclusionsFlavours play a major role in vaping initiation for current smokers, former smokers and vaping-susceptible non-smokers, and remain important to those who continue vaping. Our findings highlight the need for regulation that allows some flavour diversity without the extravagant marketing currently used to promote vaping and e-liquids.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Annette Kaufman ◽  
Erik M. Augustson ◽  
Heather Patrick

Research has shown that current smokers have a lower mean body mass index (BMI) than never and former smokers, with former smokers having the highest mean BMI. A number of physiological mechanisms have been hypothesized to explain this pattern, but few studies have explored the possible role of behavioral factors. Using data from the cross-sectional National Health and Nutrition Examination Survey 1999–2006, this descriptive study explored the associations among smoking status, sedentary behavior, and two anthropometric measures (BMI and waist circumference (WC)). Sedentary behavior was significantly higher among current smokers compared to never and former smokers; former smokers had higher levels of sedentary behavior compared to never smokers. The association between smoking status and anthropometric outcomes was moderated by sedentary behavior, with current smokers evidencing higher BMI and WC at higher levels of sedentary behavior compared to lower levels of sedentary behavior. Results are discussed in terms of their implications for interventions, particularly with respect to postcessation weight gain.


Author(s):  
Frazer J. Lowe ◽  
Evan O. Gregg ◽  
Michael McEwan

Abstract: The objective of this study was to obtain baseline data on biomarkers of exposure (BoE) and biomarkers of potential harm (BoPH) in smokers, former smokers and never-smokers.: This was a cross-sectional study of 80 healthy male and female volunteers over 21 years old, self-selected for smoking status. Subjects were pre-screened by medical staff at an independent clinical research unit, within 1 week prior to a single overnight residential visit and sample collection.: All BoE were able to differentiate between the two smoking groups and smokers from all non-smokers. There was a strong correlation between cigarettes smoked per day and total urinary nicotine equivalents (TNE; r=0.85). TNE correlated better with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels than cigarettes smoked per day (r=0.75 and r=0.56, respectively). Of the BoPH included in this study, seven (11-dehydro-thromboxane B2, 2, 3-dinorthromboxane B2, 8-epi prostaglandin F: While BoE clearly differentiate between groups based on self-declared smoking status, most BoPH examined could not do so in a consistent manner. The dynamics of BoPH levels are not well understood. Future studies of BoPH should eliminate potential confounding factors and increase the number of subjects to allow the investigation of genetic polymorphism in metabolic pathways.Clin Chem Lab Med 2009;47:311–20.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Ricky L Camplain ◽  
Michelle L Snyder ◽  
Priya Palta ◽  
Hanyu Ni ◽  
Kenneth R Butler ◽  
...  

Cigarette smoking is a preventable cause of cardiovascular disease and is associated with arterial stiffening among young adults. While smoking cessation lowers the risk of cardiovascular morbidity and mortality, evidence for a relationship between time since smoking cessation and arterial stiffness is limited in older adults. We assessed the association of smoking status and time since smoking cessation with arterial stiffness, measured by carotid-femoral (cfPWV) and brachial-ankle (baPWV) pulse wave velocity, conditional on intensity and duration of exposure to smoking (pack-years). Analyses included 1,996 men and 2,767 women aged 67 to 90 years examined in the ARIC study in 2011-2013. Smoking status was ascertained at all five ARIC examinations and during annual telephone interviews. Information on age at initiation of smoking, smoking intensity and duration were also collected. Pack-years were calculated as the product of the average number of cigarettes smoked per day and years smoked divided by 20. Two measures of baPWV and cfPWV were obtained then averaged. Multivariable linear regression was used to estimate the association between smoking status and time since smoking cessation with PWV by gender, adjusted for age, hypertension, body mass index (BMI), and heart rate. Estimates of the association between smoking cessation and PWV were further adjusted for pack-years. Among women, former smokers and current smokers had a lower baPWV when compared to never smokers [β = -40.9 (95% confidence interval (CI): -64.2, -17.6) and β = -119.7 (95%CI: -168.7, -70.7), respectively]. Similar patterns were observed for cfPWV; however, the relationship was only significant among former smokers [β = -25.3 (95%CI: -48.0, -2.5)]. Association of smoking status and PWV was not significant in men. Among men who were former smokers there was a negative and significant association between smoking cessation and cfPWV [β = -1.4 (-2.7, -0.4)]; however, this same relationship was not observed for baPWV. BMI modified the association between smoking cessation and PWV in women. Time since smoking cessation was positively associated with PWV in women with a BMI <25 kg/m 2 [baPWV: β = 3.8 (95%CI: 1.2, 6.5); cfPWV: β = 2.5 (0.3, 4.7)], but not in women with a BMI ≥25 kg/m 2 . In these cross-sectional analyses, ever smokers had lower PWV compared to never smokers among older women, but not among older men. Greater time since smoking cessation was positively associated with arterial stiffness among normal or underweight women, but not among women who were overweight or obese, or among men. Accounting for cumulative exposure to smoking over the life course, gender-specific and arterial segment-specific patterns were observed in the association between time since smoking cessation and arterial stiffness measured in community-dwelling older adults, as well as a modification of these associations by excess weight among women.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4829-4829
Author(s):  
Sheila Pascual ◽  
Cannon Milani ◽  
Joanna Mitri ◽  
Jorge Castillo

Abstract INTRODUCTION: The etiology of Hodgkin lymphoma (HL) is largely unknown. However, certain associations have been noted, such as familial factors and infection with viruses. Smoking has been associated with the development of multiple malignancies and some studies have reported an association between HL and smoking but the relationship of tobacco use with lymphomas in largely unclear. OBJECTIVE: To investigate the potential relationship between tobacco use and the development of HL using a meta-analysis methodology of retrospective, case-control studies. METHODS: An extensive search was conducted using Pubmed/MEDLINE through July 2008. Case-control studies that reported odds ratio (OR) and 95% confidence intervals (CI) or allow for those values to be calculated were included in our analysis. Case reports, editorials, letters to the editor, review articles and prospective studies were excluded. The smoking status was then subdivided in three groups: never smokers, former smokers and current smokers. Meta-analyses were performed comparing the risks of former and current smokers against the risk of never smokers of developing HL. Fixed and random effects models were used to assess for heterogeneity. RESULTS: Seven case-controls studies, accounting for 3201 cases and 15268 controls were included in the analysis. Most of the articles reported OR adjusted for age, sex and educational level. In former smokers, the OR was 0.73 (95% CI, 0.65 – 0.82) when compared to never smokers; no heterogeneity was detected. The current smoker group had an OR of 1.70 (95% CI, 1.36 – 2.13) when compared to the never smoker group; some heterogeneity was detected in this group (p &lt; 0.003, I2 = 69.6%). CONCLUSIONS: Despite the heterogeneity observed in the analysis, the current smoker group seems to have a 70% increased risk of developing HL. Although a cause-effect linkage between tobacco use and HL is difficult to prove, further basic and translational research is necessary to clarify the potential etiological role of smoking in HL.


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