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Limited evidence shows a possible causal relationship between secondhand smoke and caries in children
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Limited evidence shows a possible causal relationship between secondhand smoke and caries in children David Leader JADA 2014;145(2):179-181 10.14219/jada.2013.27 The following resources related to this article are available online at jada.ada.org (this information is current as of June 28, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/145/2/179
This article cites 2 articles, 0 of which can be accessed free: http://jada.ada.org/content/145/2/179/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
Critical Summaries
Limited evidence shows a possible causal relationship between secondhand smoke and caries in children A critical summary of Hanioka T, Ojima M, Tanaka K, Yamamoto M. Does secondhand smoke affect the development of dental caries in children? A systematic review (published online May 12, 2011). J Environ Res Public Health 2011;8(5):1503-1519. doi:10.3390/ijerph8051503. David Leader, DMD, MPH
Clinical question. Are children
who are exposed to secondhand smoke (SHS) at a higher risk of developing caries than children who are not exposed? Review methods. The authors searched a single database for articles published from January 1990 to September 2010 that met the inclusion criteria. Inclusion criteria were publication in English and an analysis of the relationship between SHS and dental caries by means of multivariate models. Two reviewers who underwent calibration screened results independently and resolved any disagreement by discussion until reaching a consensus. The reviewers considered caries in primary and permanent dentition separately; investigators in three studies reported findings for both. Study investigators defined SHS as exposure to maternal, paternal, parental or household smoking or maternal smoking during pregnancy. Investigators in one study measured participants’ serum cotinine level
as a marker for exposure to SHS. (Cotinine is a metabolite of nicotine and often is used as a marker for exposure to nicotine because it has a longer half-life.1) The authors of the systematic review considered the causal relationship between SHS and caries in light of three Bradford Hill criteria for experimental evidence: strength of association, biological gradient (dose response) and experimental evidence.2 The authors suggested that natural experiment, “a situation in nature that mimics an experimental study,”2(p77) which was examined in the included studies, satisfied the last of these criteria. The authors of the systematic review provided definitions of strong, moderate and limited evidence on the basis of quality and consistency. They rated the strength of the association as convincing, probable, possible or insufficient and defined each rating level clearly. In addition, the authors assessed the methodological quality of each study by using a modified eight-point Newcastle-Ottawa Scale
for observational studies.3 One reviewer performed data abstraction, and a second reviewer verified it. Effect sizes (the difference in the proportions of the outcomes of the control and experimental groups)4 were reported in terms of odds ratios, with a few reported as prevalence ratios. Main results. One cohort study and 14 case-control studies, consisting of 101,552 participants, were included in the systematic review. Investigators in 10 of 11 studies found an association between SHS and caries in primary teeth, with the overall association determined to be weak to moderate. Investigators in five of seven studies found an association between SHS and permanent dentition, with the overall association determined to be weak. Researchers in five studies examined dose response. The effect size was lower when there was a lower exposure to SHS than when the exposure to SHS was higher. However, the effect appeared to plateau in studies involv-
JADA 145(2) http://jada.ada.org February 2014 179 Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
ing more levels of exposure to SHS. This systematic review is unusual in that the authors suggest a causal relationship between SHS and caries in the primary dentition. However, the evidence for causality was insufficient in the permanent dentition. Conclusions. On the basis of the preponderance of data from 15 high-quality observational studies in which researchers adjusted for
low socioeconomic status and other related factors, the authors of the systematic review reported a possible causal relationship between SHS and caries in the primary dentition. The evidence is insufficient to demonstrate a causal relationship between SHS and caries in the permanent dentition. It is not yet time to declare that SHS is a risk factor for caries, but these authors advised the use
of methodological approaches to lead to better understanding of this possible association. In addition, the authors recommended further study of the relationship between maternal smoking when pregnant and caries in the permanent dentition. Funding for this systematic review was provided by grants from the Japanese Ministry of Health, Labor and Welfare and from the 8020 Promotion Foundation.
COMMENTARY Importance and context. According to Healthy People 2020, the prevalence of caries in American children aged 3 to 5 years in 1999-2004 was 33.3 percent. In that same time frame, the prevalence of caries in children aged 6 to 9 years was 54.4 percent, and in children aged 13 to 15 years, it was 53.7 percent.5 The U.S. Department of Health and Human Services’ objective is to reduce the prevalence of caries in children by 10 percent by 2020.6 The authors of this systematic review refer to caries as a disease. In fact, the Centers for Disease Control and Prevention refers to caries as the most prevalent chronic disease in children aged 6 to 11 years and in adolescents aged 12 to 19 years.7 Alternatively, there is a new paradigm that classifies caries as a physiologic process, a balance of demineralization and remineralization.8 Caries lesions develop when the balance tilts in favor of demineralization as a result of a preponderance of risk factors.8 Risk factors for high caries risk include low socioeconomic status, a diet high in refined carbohydrates, low fluoride exposure, and poor or infrequent oral hygiene. Researchers in this systematic review investigated whether SHS is another risk factor. If true, this risk factor would be within the ability of parents and guardians to moderate. SHS may simply be a marker for low socioeconomic status and poor health choices, because both are risk factors for caries. However, the authors of this systematic review asserted that investigators in the included studies demonstrated a statistically significant increase in caries risk after adjusting for environmental factors. Proposed mechanisms linking exposure to SHS with caries risk include influencing oral microbiota; influencing the mineralization of developing dentition; increasing environmental cadmium levels; decreasing vitamin C levels; decreasing immune function; decreasing the production and effectiveness of saliva by affecting the development and function of salivary glands; and by causing nasal congestion, which could increase mouth breathing.
Strengths and weaknesses of the systematic review. Overall, this systematic review was well conducted, with clear methods for quality assessment. The authors addressed strength of association, biological gradient and natural experiment (a substitute for experimental evidence), according to the Bradford Hill criteria2 and the surgeon general’s report5 to demonstrate causality. The authors applied straightforward inclusion criteria and exclusion criteria. However, they limited their search to reports published in English. They did not search the gray literature or identify excluded studies. The authors performed this study by using standard criteria from the surgeon general’s report5 that do not involve the use of meta-analysis for assessment of a causal relationship. However, although the authors stated that a meta-analysis could be of value to clarify the strength of the association, observational studies can be subject to bias and confounding. They did not evaluate the included studies’ reports of biological plausibility (that is, basic science supports the hypothesis), and they recommended further study to evaluate unmeas ured covariates such as the effect of SHS on salivary function. This systematic review provides evidence that there is a potential for a causal relationship—not only a statistically significant association—between SHS and caries in primary teeth. Strengths and weaknesses of the evidence. This systematic review included 15 studies. The effect of SHS on primary teeth was examined in 11 studies that involved 27,968 participants. Researchers in only seven studies examined the relationship between SHS and caries in the permanent dentition; however, these studies included 67,656 participants. The included studies comprised a wide range of facilities (such as public health clinics, schools and hospitals), participants, geographical areas and practice environments; therefore, results of this review are more likely to be generally applicable to many populations. The sources of data for all but one of the included studies were surveys, which are prone to recall and report-
180 JADA 145(2) http://jada.ada.org February 2014 Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
ing biases, and records reviews, which are prone to interviewer bias. Investigators in only one study used an objective measure of SHS exposure: serum cotinine levels. Researchers in the included studies reported regression analysis of data, adjusting for variables that might affect caries risk to reduce the effect of confounders. Adjusting for age or limiting a study to children of the same age was common among the studies. Most of the researchers did not adjust for some variables commonly associated with bias or caries risk, including sex and geographical location. Many did not adjust for factors associated with caries risk such as sugar intake, oral hygiene practice and use of fluoride. Researchers in some studies adjusted for uncommon variables, such as height or body mass index or the parent’s cleaning of the child’s pacifier in the parent’s mouth. Although the use of uncommon variables is interesting, it reduces commonality between studies. Implications for dental practice. As dentistry moves from surgical treatment of caries to prevention and risk-based medical management, it becomes more important to understand behaviors that are associated with a higher risk of developing caries. SHS may be such a risk, but more research is required to establish causality. Regardless of the nature of the association with caries, tobacco use and SHS are severe health risks, and oral health care providers are in an advantageous position to provide tobacco use– cessation counseling. n doi:10.14219/jada.2013.27 Dr. Leader is an associate clinical professor, School of Dental Medicine,
Tufts University, Boston. He also is an evidence reviewer for the American Dental Association. Address correspondence to Dr. David Leader, Tufts University, 1 Kneeland St., Fourth Floor, Boston, Mass. 02111, e-mail david. [email protected]. Disclosure. Dr. Leader did not report any disclosures. These summaries, published under the auspices of the American Dental Association Center for Evidence-Based Dentistry, are prepared by practitioners trained in critical appraisal of published systematic reviews who work under the mentorship of experts. The summaries are not intended to, and do not, express, imply or summarize standards of care, but rather provide a concise reference for dentists to aid in understanding and applying evidence from the referenced systematic review in making clinically sound decisions as guided by their clinical judgment and by patient needs. For more information on the evidence quality rating provided above and additional critical summaries, please visit http://ebd.ada.org. 1. Centers for Disease Control and Prevention. National biomonitoring program. Biomonitoring summary. Continine. www.cdc.gov/biomonitoring/Cotinine_BiomonitoringSummary.html. Accessed Dec. 27, 2013. 2. Oleckno W. Epidemiology Concepts and Methods. Long Grove, Ill.: Waveland Press; 2008:188-189. 3. Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses (published online ahead of print July 22, 2010). Eur J Epidemiol 2010;25(9):603605. doi:10.1007/s10654-010-9491-z. 4. Oleckno W. Glossary. In: Epidemiology Concepts and Methods. Long Grove, Ill.: Waveland Press; 2008:580. 5. U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta: 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; 2004:22-23. 6. U.S. Department of Health and Human Services, Office of Disease Prevention and Health Promotion. Healthy People 2020. Oral health of children and adolescents. www.healthypeople.gov/2020/ topicsobjectives2020/objectiveslist.aspx?topicId=32. Accessed Dec. 27, 2013. 7. Centers for Disease Control and Prevention. Hygiene-related diseases. Dental caries (tooth decay). www.cdc.gov/healthywater/hygiene/disease/ dental_caries.html. Accessed Dec. 27, 2013. 8. Kidd E. The implications of the new paradigm of dental caries. J Dent 2011;39(suppl 2):S3-S8.
JADA 145(2) http://jada.ada.org February 2014 181 Copyright © 2014 American Dental Association. All Rights Reserved.
Limited evidence shows a possible causal relationship between secondhand smoke and caries in children David Leader JADA 2014;145(2):179-181 10.14219/jada.2013.27 The following resources related to this article are available online at jada.ada.org (this information is current as of June 28, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/145/2/179
This article cites 2 articles, 0 of which can be accessed free: http://jada.ada.org/content/145/2/179/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
Critical Summaries
Limited evidence shows a possible causal relationship between secondhand smoke and caries in children A critical summary of Hanioka T, Ojima M, Tanaka K, Yamamoto M. Does secondhand smoke affect the development of dental caries in children? A systematic review (published online May 12, 2011). J Environ Res Public Health 2011;8(5):1503-1519. doi:10.3390/ijerph8051503. David Leader, DMD, MPH
Clinical question. Are children
who are exposed to secondhand smoke (SHS) at a higher risk of developing caries than children who are not exposed? Review methods. The authors searched a single database for articles published from January 1990 to September 2010 that met the inclusion criteria. Inclusion criteria were publication in English and an analysis of the relationship between SHS and dental caries by means of multivariate models. Two reviewers who underwent calibration screened results independently and resolved any disagreement by discussion until reaching a consensus. The reviewers considered caries in primary and permanent dentition separately; investigators in three studies reported findings for both. Study investigators defined SHS as exposure to maternal, paternal, parental or household smoking or maternal smoking during pregnancy. Investigators in one study measured participants’ serum cotinine level
as a marker for exposure to SHS. (Cotinine is a metabolite of nicotine and often is used as a marker for exposure to nicotine because it has a longer half-life.1) The authors of the systematic review considered the causal relationship between SHS and caries in light of three Bradford Hill criteria for experimental evidence: strength of association, biological gradient (dose response) and experimental evidence.2 The authors suggested that natural experiment, “a situation in nature that mimics an experimental study,”2(p77) which was examined in the included studies, satisfied the last of these criteria. The authors of the systematic review provided definitions of strong, moderate and limited evidence on the basis of quality and consistency. They rated the strength of the association as convincing, probable, possible or insufficient and defined each rating level clearly. In addition, the authors assessed the methodological quality of each study by using a modified eight-point Newcastle-Ottawa Scale
for observational studies.3 One reviewer performed data abstraction, and a second reviewer verified it. Effect sizes (the difference in the proportions of the outcomes of the control and experimental groups)4 were reported in terms of odds ratios, with a few reported as prevalence ratios. Main results. One cohort study and 14 case-control studies, consisting of 101,552 participants, were included in the systematic review. Investigators in 10 of 11 studies found an association between SHS and caries in primary teeth, with the overall association determined to be weak to moderate. Investigators in five of seven studies found an association between SHS and permanent dentition, with the overall association determined to be weak. Researchers in five studies examined dose response. The effect size was lower when there was a lower exposure to SHS than when the exposure to SHS was higher. However, the effect appeared to plateau in studies involv-
JADA 145(2) http://jada.ada.org February 2014 179 Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
ing more levels of exposure to SHS. This systematic review is unusual in that the authors suggest a causal relationship between SHS and caries in the primary dentition. However, the evidence for causality was insufficient in the permanent dentition. Conclusions. On the basis of the preponderance of data from 15 high-quality observational studies in which researchers adjusted for
low socioeconomic status and other related factors, the authors of the systematic review reported a possible causal relationship between SHS and caries in the primary dentition. The evidence is insufficient to demonstrate a causal relationship between SHS and caries in the permanent dentition. It is not yet time to declare that SHS is a risk factor for caries, but these authors advised the use
of methodological approaches to lead to better understanding of this possible association. In addition, the authors recommended further study of the relationship between maternal smoking when pregnant and caries in the permanent dentition. Funding for this systematic review was provided by grants from the Japanese Ministry of Health, Labor and Welfare and from the 8020 Promotion Foundation.
COMMENTARY Importance and context. According to Healthy People 2020, the prevalence of caries in American children aged 3 to 5 years in 1999-2004 was 33.3 percent. In that same time frame, the prevalence of caries in children aged 6 to 9 years was 54.4 percent, and in children aged 13 to 15 years, it was 53.7 percent.5 The U.S. Department of Health and Human Services’ objective is to reduce the prevalence of caries in children by 10 percent by 2020.6 The authors of this systematic review refer to caries as a disease. In fact, the Centers for Disease Control and Prevention refers to caries as the most prevalent chronic disease in children aged 6 to 11 years and in adolescents aged 12 to 19 years.7 Alternatively, there is a new paradigm that classifies caries as a physiologic process, a balance of demineralization and remineralization.8 Caries lesions develop when the balance tilts in favor of demineralization as a result of a preponderance of risk factors.8 Risk factors for high caries risk include low socioeconomic status, a diet high in refined carbohydrates, low fluoride exposure, and poor or infrequent oral hygiene. Researchers in this systematic review investigated whether SHS is another risk factor. If true, this risk factor would be within the ability of parents and guardians to moderate. SHS may simply be a marker for low socioeconomic status and poor health choices, because both are risk factors for caries. However, the authors of this systematic review asserted that investigators in the included studies demonstrated a statistically significant increase in caries risk after adjusting for environmental factors. Proposed mechanisms linking exposure to SHS with caries risk include influencing oral microbiota; influencing the mineralization of developing dentition; increasing environmental cadmium levels; decreasing vitamin C levels; decreasing immune function; decreasing the production and effectiveness of saliva by affecting the development and function of salivary glands; and by causing nasal congestion, which could increase mouth breathing.
Strengths and weaknesses of the systematic review. Overall, this systematic review was well conducted, with clear methods for quality assessment. The authors addressed strength of association, biological gradient and natural experiment (a substitute for experimental evidence), according to the Bradford Hill criteria2 and the surgeon general’s report5 to demonstrate causality. The authors applied straightforward inclusion criteria and exclusion criteria. However, they limited their search to reports published in English. They did not search the gray literature or identify excluded studies. The authors performed this study by using standard criteria from the surgeon general’s report5 that do not involve the use of meta-analysis for assessment of a causal relationship. However, although the authors stated that a meta-analysis could be of value to clarify the strength of the association, observational studies can be subject to bias and confounding. They did not evaluate the included studies’ reports of biological plausibility (that is, basic science supports the hypothesis), and they recommended further study to evaluate unmeas ured covariates such as the effect of SHS on salivary function. This systematic review provides evidence that there is a potential for a causal relationship—not only a statistically significant association—between SHS and caries in primary teeth. Strengths and weaknesses of the evidence. This systematic review included 15 studies. The effect of SHS on primary teeth was examined in 11 studies that involved 27,968 participants. Researchers in only seven studies examined the relationship between SHS and caries in the permanent dentition; however, these studies included 67,656 participants. The included studies comprised a wide range of facilities (such as public health clinics, schools and hospitals), participants, geographical areas and practice environments; therefore, results of this review are more likely to be generally applicable to many populations. The sources of data for all but one of the included studies were surveys, which are prone to recall and report-
180 JADA 145(2) http://jada.ada.org February 2014 Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
ing biases, and records reviews, which are prone to interviewer bias. Investigators in only one study used an objective measure of SHS exposure: serum cotinine levels. Researchers in the included studies reported regression analysis of data, adjusting for variables that might affect caries risk to reduce the effect of confounders. Adjusting for age or limiting a study to children of the same age was common among the studies. Most of the researchers did not adjust for some variables commonly associated with bias or caries risk, including sex and geographical location. Many did not adjust for factors associated with caries risk such as sugar intake, oral hygiene practice and use of fluoride. Researchers in some studies adjusted for uncommon variables, such as height or body mass index or the parent’s cleaning of the child’s pacifier in the parent’s mouth. Although the use of uncommon variables is interesting, it reduces commonality between studies. Implications for dental practice. As dentistry moves from surgical treatment of caries to prevention and risk-based medical management, it becomes more important to understand behaviors that are associated with a higher risk of developing caries. SHS may be such a risk, but more research is required to establish causality. Regardless of the nature of the association with caries, tobacco use and SHS are severe health risks, and oral health care providers are in an advantageous position to provide tobacco use– cessation counseling. n doi:10.14219/jada.2013.27 Dr. Leader is an associate clinical professor, School of Dental Medicine,
Tufts University, Boston. He also is an evidence reviewer for the American Dental Association. Address correspondence to Dr. David Leader, Tufts University, 1 Kneeland St., Fourth Floor, Boston, Mass. 02111, e-mail david. [email protected]. Disclosure. Dr. Leader did not report any disclosures. These summaries, published under the auspices of the American Dental Association Center for Evidence-Based Dentistry, are prepared by practitioners trained in critical appraisal of published systematic reviews who work under the mentorship of experts. The summaries are not intended to, and do not, express, imply or summarize standards of care, but rather provide a concise reference for dentists to aid in understanding and applying evidence from the referenced systematic review in making clinically sound decisions as guided by their clinical judgment and by patient needs. For more information on the evidence quality rating provided above and additional critical summaries, please visit http://ebd.ada.org. 1. Centers for Disease Control and Prevention. National biomonitoring program. Biomonitoring summary. Continine. www.cdc.gov/biomonitoring/Cotinine_BiomonitoringSummary.html. Accessed Dec. 27, 2013. 2. Oleckno W. Epidemiology Concepts and Methods. Long Grove, Ill.: Waveland Press; 2008:188-189. 3. Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses (published online ahead of print July 22, 2010). Eur J Epidemiol 2010;25(9):603605. doi:10.1007/s10654-010-9491-z. 4. Oleckno W. Glossary. In: Epidemiology Concepts and Methods. Long Grove, Ill.: Waveland Press; 2008:580. 5. U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta: 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; 2004:22-23. 6. U.S. Department of Health and Human Services, Office of Disease Prevention and Health Promotion. Healthy People 2020. Oral health of children and adolescents. www.healthypeople.gov/2020/ topicsobjectives2020/objectiveslist.aspx?topicId=32. Accessed Dec. 27, 2013. 7. Centers for Disease Control and Prevention. Hygiene-related diseases. Dental caries (tooth decay). www.cdc.gov/healthywater/hygiene/disease/ dental_caries.html. Accessed Dec. 27, 2013. 8. Kidd E. The implications of the new paradigm of dental caries. J Dent 2011;39(suppl 2):S3-S8.
JADA 145(2) http://jada.ada.org February 2014 181 Copyright © 2014 American Dental Association. All Rights Reserved.