ETIOLOGY/OTHER
ARTICLE ANALYSIS & EVALUATION ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION Daily smoking and 4-year caries increment in Finnish adults. Bernabe E, Delgado-Angulo EK, Vehkalahti MM, Aromaa A, Suominen AL. Community Dent Oral Epidemiol 2014.
REVIEWERS Takashi Hanioka, DDS, PhD, Miki Ojima, DDS, PhD, Keiko Tanaka, DDS, PhD
Daily Smoking May Independently Predict Caries Development in Adults SUMMARY Subjects The sample of the Health 2000 Survey conducted in 2000–2001 was representative of the Finnish population age 30 years or older. The data analyzed were gathered from 955 dentate adults who participated in both the Health 2000 Survey and the Follow-Up Study of Finnish Adults’ Oral Health and whose information on relevant variables was complete. Mean age was 48.4 years (SD: 11.9, range: 30–89 years).
Key Risk/Study Factor
This study assessed whether daily smoking predicts caries increment in adults over age 4 years.
Current tobacco smoking as reported in baseline home interviews. Smokers also reported the mean number of cigarettes or similar products smoked per day. The two indicators of smoking used were the prevalence of daily tobacco smoking and the level of tobacco consumption (0, 1–19, and 20 þ cigarettes per day).
SOURCE OF FUNDING
Main Outcome Measure
Finnish Dental Society Apollonia (nonprofit), Finnish Dental Association, National Institute for Health and Welfare, and Social Insurance Institution of Finland
The 4-year net increment in the numbers of decayed (DT), filled (FT), and missing (MT) teeth and the DMFT index were calculated using the data from baseline and follow-up clinical oral examinations.
PURPOSE/QUESTION
TYPE OF STUDY/DESIGN Cohort study: Data from subjects who participated in both the Health 2000 Survey and the Follow-Up Study of Finnish Adults’ Oral Health were analyzed
LEVEL OF EVIDENCE Level 2: Limited-quality, patientoriented evidence
STRENGTH OF RECOMMENDATION GRADE
Main Results Daily smokers reported less favorable behaviors than nonsmokers. Daily smoking was associated with net DT increment, but not with net DMFT, FT, or MT increments. A significant linear and positive relationship was found between baseline levels of tobacco consumption and net DT increment, but not with net DMFT, FT, or MT increments. Dental behavior only explained 20% of the effect on net DT increment. The associations with net DT increment remained significant after adjustments for baseline demographic, socioeconomic, and behavioral factors. Incidence rate ratio (IRR) and 95% CI of daily smoker regarding net DT increment was 1.70 and 1.07 to 2.70, respectively. A significant dose–response relationship was also found between levels of tobacco consumption and net DT increment after adjustments for the confounders. Although the difference between daily smokers consuming 1–19 cigarettes per day and nondaily smokers was not statistically significant (IRR: 1.48, 95% CI: 0.83–2.64), the IRR of consuming 20 or more cigarettes per day for the 4-year net DT increment was 2.00 (95% CI: 1.09–3.70).
Not applicable
Conclusions J Evid Base Dent Pract 2014;14:151-153 1532-3382/$36.00 Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jebdp.2014.07.005
Daily smoking as well as the level of tobacco consumption were independently related to caries development (net DT increment) in adults over a 4-year time period, but not to caries treatment (net FT and MT increments) or caries experience (net DMFT increment).
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
COMMENTARY AND ANALYSIS To evaluate the reliability of findings, the methodological quality of the study was assessed based on the partially validated indicators of the Newcastle-Ottawa Scale (NOS) for observational studies.1 The grouping of items in the NOS consists of the three categories of selection, comparability, and exposure/outcome measurement. Because the original scale is comprehensive, the scale for the assessment of cohort studies was modified based on that of a previous review.2 In the selection category, both the representativeness of the sample in the community and the use of a secure record or structured interview to ascertain exposure in which the researcher was blinded to exposure status were satisfactory. Comparability can also be considered satisfactory because sociodemographic (including education) and behavioral factors (including dental attendance) were adjusted in the models of negative binomial regression. Regarding outcomes, dental caries was examined by well-calibrated dentists and the 4-year follow-up period was within the permissible range. Given that the participation rate was 84%, the dropout rate was satisfactory at less than 20%. However, the similarity in the rate between the exposure and control groups was not described. Given the high-quality methodology of the cohort study, the findings regarding the association between exposure and outcome can be considered highly reliable. The prospective study had high methodological quality, and its findings might affect daily dental care. Current practice is based on previous systematic reviews of the effect of tobacco smoking on dental caries.3,4 However, those reviews did not include this present article and fell short of making clinical recommendations. The present article stresses the necessity of including these findings in health promotion efforts aimed at the prevention of smoking initiation and facilitation of smoking cessation. However, because the effect of previous smoking was not separately evaluated in the prospective study, the epidemiological evidence for the reduced risk of developing dental caries following smoking cessation might be insufficient. The article also stresses the need for dental professionals to be aware of the potential link between smoking and dental caries to ensure well-prepared recommendations for smoking cessation. Discussion of a biological link might also help practitioners prepare to facilitate smoking cessation efforts. One article on biological associations, such as alterations in saliva and dental plaque, reported that nicotine enhances Streptococcus mutans biofilm formation and biofilm metabolic activity.5 Furthermore, that article introduced an animal study that found expansion of the caries-affected area in the molars of cigarette smokeexposed rats.6 The reviewed study defined decayed teeth as advanced lesions such that the carious lesion was cavitated, had penetrated the fissure and undermined the enamel, or had produced clear 152
softening of the dentin walls. Therefore the findings of these three studies might form a line of evidence through which the biological association is explained by the effect of environmental stress on the cariogenic microorganism. This speculation might be supported by the similar effect of tobacco smoke on the periodontal microbiome.7–9 The findings of this study strongly suggest a causal link between tobacco smoke exposure and dental caries in adults. The same mechanism can be applied to the potential association between second-hand smoke exposure and dental caries in children, which was recently reviewed.4,10 As stated in this article and elsewhere, further studies are required to fully understand the underlying causes of the association between the broad range of exposure types and dental caries in both dentition types.3,4,10
REFERENCES 1. Wells GA, Shea B, O’Connell D, et al. The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in metaanalyses. [http://www.ohri.ca/programs/clinical_epidemiology/ oxford.asp]. 2. Hanioka T, Ojima M, Tanaka K, Matsuo K, Sato F, Tanaka H. Causal assessment of smoking and tooth loss: a systematic review of observational studies. BMC Public Health 2011;11:221. 3. Benedetti G, Campus G, Strohmenger L, Lingstr€ om P. Tobacco and dental caries: a systematic review. Acta Odontol Scand 2013;71:363-71. 4. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2014. 5. Huang R, Li M, Gregory RL. Effect of nicotine on growth and metabolism of Streptococcus mutans. Eur J Oral Sci 2012;120: 319-25. 6. Fujinami Y, Nakano K, Ueda O, et al. Dental caries area of rat molar expanded by cigarette smoke exposure. Caries Res 2011;45:561-7. 7. Delima SL, McBride RK, Preshaw PM, Heasman PA, Kumar PS. Response of subgingival bacteria to smoking cessation. J Clin Microbiol 2010;48:2344-9. 8. Bagaitkar J, Daep CA, Patel CK, Renaud DE, Demuth DR, Scott DA. Tobacco smoke augments Porphyromonas gingivalis-Streptococcus gordonii biofilm formation. PLoS One 2011;6:e27386. 9. Matthews CR, Joshi V, de Jager M, Aspiras M, Kumar PS. Host-bacterial interactions during induction and resolution of experimental gingivitis in current smokers. J Periodontol 2013;84:32-40. 10. Hanioka T, Ojima M, Tanaka K, Yamamoto M. Does secondhand smoke affect the development of dental caries in children? A systematic review. Int J Environ Res Public Health 2011;8:1503-19.
REVIEWERS Takashi Hanioka, DDS, PhD Professor, Department of Preventive and Public Health Dentistry, Fukuoka Dental College, Fukuoka 814-0193, Japan [email protected] September 2014
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
Miki Ojima, DDS, PhD Assistant Professor, Department of Preventive Dentistry, Graduate School of Dentistry Osaka University, Osaka 565-0871, Japan [email protected]
Volume 14, Number 3
Keiko Tanaka, DDS, PhD Associate Professor, Department of Preventive Medicine and Public Health, Faculty of Medicine, Fukuoka University, Fukuoka 814-0180, Japan [email protected]
153
ARTICLE ANALYSIS & EVALUATION ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION Daily smoking and 4-year caries increment in Finnish adults. Bernabe E, Delgado-Angulo EK, Vehkalahti MM, Aromaa A, Suominen AL. Community Dent Oral Epidemiol 2014.
REVIEWERS Takashi Hanioka, DDS, PhD, Miki Ojima, DDS, PhD, Keiko Tanaka, DDS, PhD
Daily Smoking May Independently Predict Caries Development in Adults SUMMARY Subjects The sample of the Health 2000 Survey conducted in 2000–2001 was representative of the Finnish population age 30 years or older. The data analyzed were gathered from 955 dentate adults who participated in both the Health 2000 Survey and the Follow-Up Study of Finnish Adults’ Oral Health and whose information on relevant variables was complete. Mean age was 48.4 years (SD: 11.9, range: 30–89 years).
Key Risk/Study Factor
This study assessed whether daily smoking predicts caries increment in adults over age 4 years.
Current tobacco smoking as reported in baseline home interviews. Smokers also reported the mean number of cigarettes or similar products smoked per day. The two indicators of smoking used were the prevalence of daily tobacco smoking and the level of tobacco consumption (0, 1–19, and 20 þ cigarettes per day).
SOURCE OF FUNDING
Main Outcome Measure
Finnish Dental Society Apollonia (nonprofit), Finnish Dental Association, National Institute for Health and Welfare, and Social Insurance Institution of Finland
The 4-year net increment in the numbers of decayed (DT), filled (FT), and missing (MT) teeth and the DMFT index were calculated using the data from baseline and follow-up clinical oral examinations.
PURPOSE/QUESTION
TYPE OF STUDY/DESIGN Cohort study: Data from subjects who participated in both the Health 2000 Survey and the Follow-Up Study of Finnish Adults’ Oral Health were analyzed
LEVEL OF EVIDENCE Level 2: Limited-quality, patientoriented evidence
STRENGTH OF RECOMMENDATION GRADE
Main Results Daily smokers reported less favorable behaviors than nonsmokers. Daily smoking was associated with net DT increment, but not with net DMFT, FT, or MT increments. A significant linear and positive relationship was found between baseline levels of tobacco consumption and net DT increment, but not with net DMFT, FT, or MT increments. Dental behavior only explained 20% of the effect on net DT increment. The associations with net DT increment remained significant after adjustments for baseline demographic, socioeconomic, and behavioral factors. Incidence rate ratio (IRR) and 95% CI of daily smoker regarding net DT increment was 1.70 and 1.07 to 2.70, respectively. A significant dose–response relationship was also found between levels of tobacco consumption and net DT increment after adjustments for the confounders. Although the difference between daily smokers consuming 1–19 cigarettes per day and nondaily smokers was not statistically significant (IRR: 1.48, 95% CI: 0.83–2.64), the IRR of consuming 20 or more cigarettes per day for the 4-year net DT increment was 2.00 (95% CI: 1.09–3.70).
Not applicable
Conclusions J Evid Base Dent Pract 2014;14:151-153 1532-3382/$36.00 Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jebdp.2014.07.005
Daily smoking as well as the level of tobacco consumption were independently related to caries development (net DT increment) in adults over a 4-year time period, but not to caries treatment (net FT and MT increments) or caries experience (net DMFT increment).
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
COMMENTARY AND ANALYSIS To evaluate the reliability of findings, the methodological quality of the study was assessed based on the partially validated indicators of the Newcastle-Ottawa Scale (NOS) for observational studies.1 The grouping of items in the NOS consists of the three categories of selection, comparability, and exposure/outcome measurement. Because the original scale is comprehensive, the scale for the assessment of cohort studies was modified based on that of a previous review.2 In the selection category, both the representativeness of the sample in the community and the use of a secure record or structured interview to ascertain exposure in which the researcher was blinded to exposure status were satisfactory. Comparability can also be considered satisfactory because sociodemographic (including education) and behavioral factors (including dental attendance) were adjusted in the models of negative binomial regression. Regarding outcomes, dental caries was examined by well-calibrated dentists and the 4-year follow-up period was within the permissible range. Given that the participation rate was 84%, the dropout rate was satisfactory at less than 20%. However, the similarity in the rate between the exposure and control groups was not described. Given the high-quality methodology of the cohort study, the findings regarding the association between exposure and outcome can be considered highly reliable. The prospective study had high methodological quality, and its findings might affect daily dental care. Current practice is based on previous systematic reviews of the effect of tobacco smoking on dental caries.3,4 However, those reviews did not include this present article and fell short of making clinical recommendations. The present article stresses the necessity of including these findings in health promotion efforts aimed at the prevention of smoking initiation and facilitation of smoking cessation. However, because the effect of previous smoking was not separately evaluated in the prospective study, the epidemiological evidence for the reduced risk of developing dental caries following smoking cessation might be insufficient. The article also stresses the need for dental professionals to be aware of the potential link between smoking and dental caries to ensure well-prepared recommendations for smoking cessation. Discussion of a biological link might also help practitioners prepare to facilitate smoking cessation efforts. One article on biological associations, such as alterations in saliva and dental plaque, reported that nicotine enhances Streptococcus mutans biofilm formation and biofilm metabolic activity.5 Furthermore, that article introduced an animal study that found expansion of the caries-affected area in the molars of cigarette smokeexposed rats.6 The reviewed study defined decayed teeth as advanced lesions such that the carious lesion was cavitated, had penetrated the fissure and undermined the enamel, or had produced clear 152
softening of the dentin walls. Therefore the findings of these three studies might form a line of evidence through which the biological association is explained by the effect of environmental stress on the cariogenic microorganism. This speculation might be supported by the similar effect of tobacco smoke on the periodontal microbiome.7–9 The findings of this study strongly suggest a causal link between tobacco smoke exposure and dental caries in adults. The same mechanism can be applied to the potential association between second-hand smoke exposure and dental caries in children, which was recently reviewed.4,10 As stated in this article and elsewhere, further studies are required to fully understand the underlying causes of the association between the broad range of exposure types and dental caries in both dentition types.3,4,10
REFERENCES 1. Wells GA, Shea B, O’Connell D, et al. The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in metaanalyses. [http://www.ohri.ca/programs/clinical_epidemiology/ oxford.asp]. 2. Hanioka T, Ojima M, Tanaka K, Matsuo K, Sato F, Tanaka H. Causal assessment of smoking and tooth loss: a systematic review of observational studies. BMC Public Health 2011;11:221. 3. Benedetti G, Campus G, Strohmenger L, Lingstr€ om P. Tobacco and dental caries: a systematic review. Acta Odontol Scand 2013;71:363-71. 4. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2014. 5. Huang R, Li M, Gregory RL. Effect of nicotine on growth and metabolism of Streptococcus mutans. Eur J Oral Sci 2012;120: 319-25. 6. Fujinami Y, Nakano K, Ueda O, et al. Dental caries area of rat molar expanded by cigarette smoke exposure. Caries Res 2011;45:561-7. 7. Delima SL, McBride RK, Preshaw PM, Heasman PA, Kumar PS. Response of subgingival bacteria to smoking cessation. J Clin Microbiol 2010;48:2344-9. 8. Bagaitkar J, Daep CA, Patel CK, Renaud DE, Demuth DR, Scott DA. Tobacco smoke augments Porphyromonas gingivalis-Streptococcus gordonii biofilm formation. PLoS One 2011;6:e27386. 9. Matthews CR, Joshi V, de Jager M, Aspiras M, Kumar PS. Host-bacterial interactions during induction and resolution of experimental gingivitis in current smokers. J Periodontol 2013;84:32-40. 10. Hanioka T, Ojima M, Tanaka K, Yamamoto M. Does secondhand smoke affect the development of dental caries in children? A systematic review. Int J Environ Res Public Health 2011;8:1503-19.
REVIEWERS Takashi Hanioka, DDS, PhD Professor, Department of Preventive and Public Health Dentistry, Fukuoka Dental College, Fukuoka 814-0193, Japan [email protected] September 2014
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
Miki Ojima, DDS, PhD Assistant Professor, Department of Preventive Dentistry, Graduate School of Dentistry Osaka University, Osaka 565-0871, Japan [email protected]
Volume 14, Number 3
Keiko Tanaka, DDS, PhD Associate Professor, Department of Preventive Medicine and Public Health, Faculty of Medicine, Fukuoka University, Fukuoka 814-0180, Japan [email protected]
153
