- Email: [email protected]
Periodontitis
COMMENTARY
EDITORIAL
Editorials represent the opinions of the authors and not necessarily those of the American Dental Association.
EDITORIAL
Periodontitis The canary in the coal mine
Chances are good that a person prone to periodontitis— especially with severe periodontal breakdown—also may have systemic conditions related to a compromised immune system; that is, periodontal disease could be a marker of greater general health issues. Related information for the dental patient, page 860
Wenche S. Borgnakke, DDS, MPH, PhD; Michael Glick, DMD; Robert J. Genco, DDS, PhD
A
t a recent meeting organized by the European Federation of Periodontology and the American Academy of Perio dontology, a panel of experts reviewed existing evidence linking periodontal disease to general health. This was an important and timely conference that provided a forum for open and frank discussions about this much explored and debated topic. Twelve literature reviews and four consensus statements from this meeting were published and made publicly accessible in a special supplement circulated in April 2013.1 The experts attempted pri marily to answer two essential questions surrounding the potential clinical and public health relevance of the relationship between periodontal disease and general health: Does periodontal disease cause systemic disease? And does treatment of periodontal disease affect systemic diseases and conditions? The strongest evidence for periodontal disease potentially hav ing an effect on systemic disease exists for the relationship between periodontal disease and three conditions—diabetes mellitus (DM), atherosclerotic cerebrocardiovascular diseases (ACVD) and adverse pregnancy outcomes. Diabetes mellitus
Seventeen noninterventional, descriptive, epidemiologic studies were eligible for inclusion in the first-ever systematic review conducted of the effect of periodontal disease on DM.2 To be included, a study had to determine directionality; that is, the study had to be concerned with the effect of periodontal disease on the outcome measure of DM, namely hyperglycemia or diabetes complications, not on the effect of DM on periodontal disease. The systematic review concluded that there exists emerging (but nevertheless statistically significant) evidence inferring that periodontal disease adversely affects glycemic control in people with type 2 DM; increases blood glucose levels in people without DM; promotes development of new (incident) manifest type 2 DM; and is directly related in a dose-dependent manner to complications of type 1 and type 2 DM. Randomized controlled trials consistently demonstrate that mechanical periodontal therapy is associated with a three-month posttreatment reduction in glycosylat ed hemoglobin (HbA 1c) of approximately 0.4 percent, a clinical impact equivalent to adding a second drug to a pharmacological regime for diabetes.3 There is no current evidence to support adjunctive use of antimicrobials for periodontal management of patients with diabetes.3
764 JADA 144(7) http://jada.ada.org July 2013 Copyright © 2013 American Dental Association. All Rights Reserved.
COMMENTARY
EDITORIAL
designed longitudinal studies of periodontal disease and dia There is consistent and strong betes complications, including epidemiologic evidence that ACVD, that show periodontitis periodontitis is associated with precedes these systemic ACVD.4 Support of the asso conditions. ciation between periodontal Another criterion neces bacteria and ACVD stems from sary to establish causality is studies demonstrating a link biological plausibility, where Association or between the presence of bac known biological mechanisms causality? teremia and plaque/gingival can explain how a suspected indexes; presence of periodontal A multitude of study findings risk factor can possibly affect pathogens in atherothrombotic demonstrate associations be a disease or condition. Pres lesions and a correlation with tween periodontal disease and ently, it is thought that most periodontal status; a correla systemic health. An association periodontal-systemic links tion between subgingival flora simply shows that there are share an underlying mecha and pathogens detected in links or relationships between nism in susceptible people, atheromas; and live and viable two conditions studied, such namely the host immune periodontal bacteria within as both conditions being pres response in the form of acuteatheromas. Furthermore, perio ent in a population at the same phase and subsequent chronic dontal treatment reduces the time. However, associations do inflammatory responses to periosystemic level of inflammation not provide information about dontal pathogens and their by demonstrated by a decrease which of the two conditions products that are disseminated in levels of the proinflam effects (causes) the other, if at by the bloodstream. The likeli matory acute-phase protein all. Importantly, any associa hood of such bacteremia occur C-reactive protein and by an tion could potentially be due to ring from chewing, brushing, increase in and improvement another factor that influences flossing or scaling/root planing of endothelial function. The both conditions. may depend directly on an in link between periodontitis and Several criteria need to be dividual’s periodontal health, atherosclerotic heart disease satisfied to ascertain whether whereas the consequences of exists independently of other a suspected causative agent such bacteremia depend more known cerebrocardiovascular or potential risk factor (perio on the host’s inflammatory risk factors, such as smoking. response. dontal disease) can affect— This association is greater for An additional criterion that cause, intensify or attenuate— cerebrovascular disease than strongly implies a causative nonoral diseases or conditions. for coronary heart disease, and relationship is the elimination Exposure to a risk fac greater for men and for people or diminished presence of a tor needs to occur before the younger than 65 years.4 suspected risk factor, result outcome that is being studied Still, no intervention studies (onset or change of the disease/ ing in direct elimination or at have tested any potential effect condition). This temporal re tenuation of a systemic disease of periodontal treatment direct lationship is the sine qua non or condition. This criterion ly on preventing initial ACVD obviously would be easier to of causality. As this condition events (primary prevention) or satisfy if only a single risk fac must be met, epidemiologic, on preventing recurrence (sec tor rather than a multitude of descriptive studies of crossondary prevention). sectional (providing a onepotential risk factors existed; point-in-time snapshot) or unfortunately, the latter is the Adverse pregnancy case-control (looking back in case for both periodontitis and outcomes time for potential reasons that the systemic conditions men Epidemiologic study findings may have caused differences be tioned above.6 show associations between tween groups) designs are un What can we tell our maternal periodontitis and low able to demonstrate causality. patients? birth weight, preterm birth and Unfortunately, the vast major preeclampsia.5 Nevertheless, ity of studies exploring the rela The current body of scientific the strength of the observed tionships between periodontal evidence, as expressed in the associations is modest and disease and systemic health are published literature reviews seems to depend on the study of exactly these designs. How and summarized in the con population and the choice of ever, there are several wellsensus reports, shows strong Atherosclerotic cardiovascular disease
case definitions for periodontal disease. Furthermore, treatment studies have not consistently demonstrated that treating periodontal disease has an ef fect on decreasing rates of pre term birth or low birth weight.5
JADA 144(7) http://jada.ada.org July 2013 765 Copyright © 2013 American Dental Association. All Rights Reserved.
COMMENTARY
EDITORIAL
associations between perio dontal disease and nonoral diseases and conditions. But current evidence does not substantiate that periodontal disease can cause the develop ment of any systemic disease or condition, although DMrelated evidence is emerging. Randomized controlled trials that would strongly suggest causality are expensive and difficult to conduct. It is hoped that these types of studies will be funded, performed and pub lished in the future. However, until then, telling our patients that periodontal infections cause a plethora of nonoral diseases and conditions cannot be supported by existing evi dence, even though periodontal pathogens do contribute to the cumulative bacterial burden that subsequently causes an inflammatory response in the host. Nonsurgical, mechanical periodontal treatment (with out adjuvant antibiotics) in people with type 2 DM has been confirmed to contribute to improved glycemic control in the short run in different populations. However, there still are no confirmatory stud ies applicable to the general population that would suggest
that treatment of periodontal disease would prevent or at tenuate other systemic diseas es. Nonetheless, the results of some studies suggest there may be individuals with particular susceptibilities for whom elimi nation of periodontal disease may benefit specific diseases and conditions. Who these individuals are is yet to be determined. Chances are good that a per son prone to periodontitis— especially with severe perio dontal breakdown—also may have systemic conditions re lated to a compromised immune system; that is, periodontal disease could be a marker of greater general health issues. There is ample evidence that treatment of periodontal disease is safe and effective in managing periodontal infection and inflammation—and that good oral health is an essential, integral part of overall health. That is an important message for our patients—and for policy makers as well. So don’t forget to look for that canary. n
LETTERS
that appeared in April JADA usu ally will be considered for accept ance only until the end of July. You may submit your letter via e-mail to [email protected]; by fax to 1-312-440-3538; or by mail to 211 E. Chicago Ave., Chicago, Ill. 60611-2678. By sending a letter to the editor, the author acknowl edges and agrees that the letter and all rights of the author in the letter sent become the property of The Journal. Letter writers are asked to disclose any personal or professional affiliations or conflicts of interest that readers may wish to take into consideration in as sessing their stated opinions. The
J
ADA welcomes letters from readers on articles that have appeared in The Journal. The Journal reserves the right to edit all communications and requires that all letters be signed. Letters must be no more than 550 words and must cite no more than five references. No illustrations will be accepted. A letter concerning a recent JADA article will have the best chance of acceptance if it is received within two months of the article’s publication. For instance, a letter about an article
Dr. Borgnakke is an adjunct clinical assistant professor, School of Dentistry, University of Michigan, 1011 North University Ave., Room G049, Ann Arbor, Mich. 48109-1078, e-mail [email protected]. Address reprint requests to Dr. Borgnakke.
Dr. Glick is the dean, School of Dental Medicine, University at Buffalo, The State University of New York. He also is the editor of The Journal of the American Dental Association. Dr. Genco is Distinguished Professor of Oral Biology and Microbiology, School of Dental Medicine and School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York. 1. Tonetti M, Kornman KS, eds. Periodon titis and systemic diseases: proceedings of a workshop jointly held by the European Federation of Periodontology and American Academy of Periodontology. J Clin Periodon tol 2013;40(suppl 14):S1-S215. http:// onlinelibrary.wiley.com/doi/10.1111/ jcpe.2013.40.issue-s14/issuetoc?dmmsm id=73654&dmmspid=17129767&dmmsu id=1955451. Accessed May 27, 2013. 2. Borgnakke WS, Ylöstalo PV, Taylor GW, Genco RJ. Effect of periodontal disease on diabetes: systematic review of epidemiologic observational evidence. J Clin Periodontol 2013;40(suppl 14):S135-S152. doi:10.1111/ jcpe.12080. 3. Engebretson S, Kocher T. Evidence that periodontal treatment improves diabetes outcomes: a systematic review and metaanalysis. J Clin Periodontol 2013;40(suppl 14):S153-S163. doi:10.1111/jcpe.12084. 4. Tonetti MS, Van Dyke TE; Working Group 1 of the Joint EFP/AAP Workshop. Periodontitis and atherosclerotic cardio vascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013;40(suppl 14):S24-S29. doi:10.1111/ jcpe.12089. 5. Sanz M, Kornman K; Working Group 3 of the Joint EFP/AAP Workshop. Periodontitis and adverse pregnancy outcomes: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013;40(suppl 14):S164-S169. doi:10.1111/jcpe.12083. 6. Glick M. Causation: a loosely founded concept in epidemiology. JADA 2007;138(12): 1532-1533.
views expressed are those of the letter writer and do not necessar ily reflect the opinion or official policy of the Association. Brevity is appreciated. HUMAN DENTITION
I applaud Dr. Bruce Pihlstrom for his efforts in choosing a Schour and Massler article to highlight in JADA’s land mark articles series in April (Messer LB, Till MJ. A land mark report on understanding the human dentition. JADA 2013;144[4]:357-361). Certainly Drs. Schour and
766 JADA 144(7) http://jada.ada.org July 2013 Copyright © 2013 American Dental Association. All Rights Reserved.
EDITORIAL
Editorials represent the opinions of the authors and not necessarily those of the American Dental Association.
EDITORIAL
Periodontitis The canary in the coal mine
Chances are good that a person prone to periodontitis— especially with severe periodontal breakdown—also may have systemic conditions related to a compromised immune system; that is, periodontal disease could be a marker of greater general health issues. Related information for the dental patient, page 860
Wenche S. Borgnakke, DDS, MPH, PhD; Michael Glick, DMD; Robert J. Genco, DDS, PhD
A
t a recent meeting organized by the European Federation of Periodontology and the American Academy of Perio dontology, a panel of experts reviewed existing evidence linking periodontal disease to general health. This was an important and timely conference that provided a forum for open and frank discussions about this much explored and debated topic. Twelve literature reviews and four consensus statements from this meeting were published and made publicly accessible in a special supplement circulated in April 2013.1 The experts attempted pri marily to answer two essential questions surrounding the potential clinical and public health relevance of the relationship between periodontal disease and general health: Does periodontal disease cause systemic disease? And does treatment of periodontal disease affect systemic diseases and conditions? The strongest evidence for periodontal disease potentially hav ing an effect on systemic disease exists for the relationship between periodontal disease and three conditions—diabetes mellitus (DM), atherosclerotic cerebrocardiovascular diseases (ACVD) and adverse pregnancy outcomes. Diabetes mellitus
Seventeen noninterventional, descriptive, epidemiologic studies were eligible for inclusion in the first-ever systematic review conducted of the effect of periodontal disease on DM.2 To be included, a study had to determine directionality; that is, the study had to be concerned with the effect of periodontal disease on the outcome measure of DM, namely hyperglycemia or diabetes complications, not on the effect of DM on periodontal disease. The systematic review concluded that there exists emerging (but nevertheless statistically significant) evidence inferring that periodontal disease adversely affects glycemic control in people with type 2 DM; increases blood glucose levels in people without DM; promotes development of new (incident) manifest type 2 DM; and is directly related in a dose-dependent manner to complications of type 1 and type 2 DM. Randomized controlled trials consistently demonstrate that mechanical periodontal therapy is associated with a three-month posttreatment reduction in glycosylat ed hemoglobin (HbA 1c) of approximately 0.4 percent, a clinical impact equivalent to adding a second drug to a pharmacological regime for diabetes.3 There is no current evidence to support adjunctive use of antimicrobials for periodontal management of patients with diabetes.3
764 JADA 144(7) http://jada.ada.org July 2013 Copyright © 2013 American Dental Association. All Rights Reserved.
COMMENTARY
EDITORIAL
designed longitudinal studies of periodontal disease and dia There is consistent and strong betes complications, including epidemiologic evidence that ACVD, that show periodontitis periodontitis is associated with precedes these systemic ACVD.4 Support of the asso conditions. ciation between periodontal Another criterion neces bacteria and ACVD stems from sary to establish causality is studies demonstrating a link biological plausibility, where Association or between the presence of bac known biological mechanisms causality? teremia and plaque/gingival can explain how a suspected indexes; presence of periodontal A multitude of study findings risk factor can possibly affect pathogens in atherothrombotic demonstrate associations be a disease or condition. Pres lesions and a correlation with tween periodontal disease and ently, it is thought that most periodontal status; a correla systemic health. An association periodontal-systemic links tion between subgingival flora simply shows that there are share an underlying mecha and pathogens detected in links or relationships between nism in susceptible people, atheromas; and live and viable two conditions studied, such namely the host immune periodontal bacteria within as both conditions being pres response in the form of acuteatheromas. Furthermore, perio ent in a population at the same phase and subsequent chronic dontal treatment reduces the time. However, associations do inflammatory responses to periosystemic level of inflammation not provide information about dontal pathogens and their by demonstrated by a decrease which of the two conditions products that are disseminated in levels of the proinflam effects (causes) the other, if at by the bloodstream. The likeli matory acute-phase protein all. Importantly, any associa hood of such bacteremia occur C-reactive protein and by an tion could potentially be due to ring from chewing, brushing, increase in and improvement another factor that influences flossing or scaling/root planing of endothelial function. The both conditions. may depend directly on an in link between periodontitis and Several criteria need to be dividual’s periodontal health, atherosclerotic heart disease satisfied to ascertain whether whereas the consequences of exists independently of other a suspected causative agent such bacteremia depend more known cerebrocardiovascular or potential risk factor (perio on the host’s inflammatory risk factors, such as smoking. response. dontal disease) can affect— This association is greater for An additional criterion that cause, intensify or attenuate— cerebrovascular disease than strongly implies a causative nonoral diseases or conditions. for coronary heart disease, and relationship is the elimination Exposure to a risk fac greater for men and for people or diminished presence of a tor needs to occur before the younger than 65 years.4 suspected risk factor, result outcome that is being studied Still, no intervention studies (onset or change of the disease/ ing in direct elimination or at have tested any potential effect condition). This temporal re tenuation of a systemic disease of periodontal treatment direct lationship is the sine qua non or condition. This criterion ly on preventing initial ACVD obviously would be easier to of causality. As this condition events (primary prevention) or satisfy if only a single risk fac must be met, epidemiologic, on preventing recurrence (sec tor rather than a multitude of descriptive studies of crossondary prevention). sectional (providing a onepotential risk factors existed; point-in-time snapshot) or unfortunately, the latter is the Adverse pregnancy case-control (looking back in case for both periodontitis and outcomes time for potential reasons that the systemic conditions men Epidemiologic study findings may have caused differences be tioned above.6 show associations between tween groups) designs are un What can we tell our maternal periodontitis and low able to demonstrate causality. patients? birth weight, preterm birth and Unfortunately, the vast major preeclampsia.5 Nevertheless, ity of studies exploring the rela The current body of scientific the strength of the observed tionships between periodontal evidence, as expressed in the associations is modest and disease and systemic health are published literature reviews seems to depend on the study of exactly these designs. How and summarized in the con population and the choice of ever, there are several wellsensus reports, shows strong Atherosclerotic cardiovascular disease
case definitions for periodontal disease. Furthermore, treatment studies have not consistently demonstrated that treating periodontal disease has an ef fect on decreasing rates of pre term birth or low birth weight.5
JADA 144(7) http://jada.ada.org July 2013 765 Copyright © 2013 American Dental Association. All Rights Reserved.
COMMENTARY
EDITORIAL
associations between perio dontal disease and nonoral diseases and conditions. But current evidence does not substantiate that periodontal disease can cause the develop ment of any systemic disease or condition, although DMrelated evidence is emerging. Randomized controlled trials that would strongly suggest causality are expensive and difficult to conduct. It is hoped that these types of studies will be funded, performed and pub lished in the future. However, until then, telling our patients that periodontal infections cause a plethora of nonoral diseases and conditions cannot be supported by existing evi dence, even though periodontal pathogens do contribute to the cumulative bacterial burden that subsequently causes an inflammatory response in the host. Nonsurgical, mechanical periodontal treatment (with out adjuvant antibiotics) in people with type 2 DM has been confirmed to contribute to improved glycemic control in the short run in different populations. However, there still are no confirmatory stud ies applicable to the general population that would suggest
that treatment of periodontal disease would prevent or at tenuate other systemic diseas es. Nonetheless, the results of some studies suggest there may be individuals with particular susceptibilities for whom elimi nation of periodontal disease may benefit specific diseases and conditions. Who these individuals are is yet to be determined. Chances are good that a per son prone to periodontitis— especially with severe perio dontal breakdown—also may have systemic conditions re lated to a compromised immune system; that is, periodontal disease could be a marker of greater general health issues. There is ample evidence that treatment of periodontal disease is safe and effective in managing periodontal infection and inflammation—and that good oral health is an essential, integral part of overall health. That is an important message for our patients—and for policy makers as well. So don’t forget to look for that canary. n
LETTERS
that appeared in April JADA usu ally will be considered for accept ance only until the end of July. You may submit your letter via e-mail to [email protected]; by fax to 1-312-440-3538; or by mail to 211 E. Chicago Ave., Chicago, Ill. 60611-2678. By sending a letter to the editor, the author acknowl edges and agrees that the letter and all rights of the author in the letter sent become the property of The Journal. Letter writers are asked to disclose any personal or professional affiliations or conflicts of interest that readers may wish to take into consideration in as sessing their stated opinions. The
J
ADA welcomes letters from readers on articles that have appeared in The Journal. The Journal reserves the right to edit all communications and requires that all letters be signed. Letters must be no more than 550 words and must cite no more than five references. No illustrations will be accepted. A letter concerning a recent JADA article will have the best chance of acceptance if it is received within two months of the article’s publication. For instance, a letter about an article
Dr. Borgnakke is an adjunct clinical assistant professor, School of Dentistry, University of Michigan, 1011 North University Ave., Room G049, Ann Arbor, Mich. 48109-1078, e-mail [email protected]. Address reprint requests to Dr. Borgnakke.
Dr. Glick is the dean, School of Dental Medicine, University at Buffalo, The State University of New York. He also is the editor of The Journal of the American Dental Association. Dr. Genco is Distinguished Professor of Oral Biology and Microbiology, School of Dental Medicine and School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York. 1. Tonetti M, Kornman KS, eds. Periodon titis and systemic diseases: proceedings of a workshop jointly held by the European Federation of Periodontology and American Academy of Periodontology. J Clin Periodon tol 2013;40(suppl 14):S1-S215. http:// onlinelibrary.wiley.com/doi/10.1111/ jcpe.2013.40.issue-s14/issuetoc?dmmsm id=73654&dmmspid=17129767&dmmsu id=1955451. Accessed May 27, 2013. 2. Borgnakke WS, Ylöstalo PV, Taylor GW, Genco RJ. Effect of periodontal disease on diabetes: systematic review of epidemiologic observational evidence. J Clin Periodontol 2013;40(suppl 14):S135-S152. doi:10.1111/ jcpe.12080. 3. Engebretson S, Kocher T. Evidence that periodontal treatment improves diabetes outcomes: a systematic review and metaanalysis. J Clin Periodontol 2013;40(suppl 14):S153-S163. doi:10.1111/jcpe.12084. 4. Tonetti MS, Van Dyke TE; Working Group 1 of the Joint EFP/AAP Workshop. Periodontitis and atherosclerotic cardio vascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013;40(suppl 14):S24-S29. doi:10.1111/ jcpe.12089. 5. Sanz M, Kornman K; Working Group 3 of the Joint EFP/AAP Workshop. Periodontitis and adverse pregnancy outcomes: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013;40(suppl 14):S164-S169. doi:10.1111/jcpe.12083. 6. Glick M. Causation: a loosely founded concept in epidemiology. JADA 2007;138(12): 1532-1533.
views expressed are those of the letter writer and do not necessar ily reflect the opinion or official policy of the Association. Brevity is appreciated. HUMAN DENTITION
I applaud Dr. Bruce Pihlstrom for his efforts in choosing a Schour and Massler article to highlight in JADA’s land mark articles series in April (Messer LB, Till MJ. A land mark report on understanding the human dentition. JADA 2013;144[4]:357-361). Certainly Drs. Schour and
766 JADA 144(7) http://jada.ada.org July 2013 Copyright © 2013 American Dental Association. All Rights Reserved.