Letter Journal of the Royal Society of Medicine; 2014, Vol. 107(3) 94 DOI: 10.1177/0141076813518770
To submit a letter in response to a JRSM article, please visit http://jrsm.sagepub.com to find the article concerned, then click on the ‘Submit a comment’ link found in the Reader Responses section. Comments will automatically be submitted for consideration to be published in print.
Periodontal disease and systemic disease We were intrigued to read the editorial by Bains and Rashid, ‘Junk food and heart disease: the missing tooth’.1 The authors correctly emphasise the importance of oral health to general health/wellbeing, and specifically cardiovascular risk. However, we wish to highlight significant misunderstandings within the editorial concerning periodontitis and emerging biologically plausible mechanisms underpinning its association with atherogenic cardiovascular disease (ACVD). Periodontitis is a ubiquitous chronic infectiousinflammatory disease initiated by the accumulation of a plaque biofilm at/below the gum margin. The majority of host tissue damage (bone destruction around teeth) is caused by a dysregulated (exaggerated) inflammatory-immune response to pathogenic bacteria within the biofilm. Periodontitis is not, as stated in the editorial, a disease that ‘occurs as a result of untreated dental caries’. It is a completely separate disease with a distinctly different aetiology, pathogenesis, natural history and outcome. Dental caries is not associated with ACVD. Large-scale epidemiological studies consistently and independently associate periodontitis with ACVD. Periodontitis drives elevations in acute-phase reactants (CRP/ IL-6) and oxidative stress within the circulation2 and plausible mechanisms for this emanate from the entry of pathogenic bacteria at periodontally diseased sites into the circulation during eating/tooth brushing which subsequently trigger: (1) the liver’s acute-phase response; and (2) oxidative stress responses by priming/stimulating peripheral blood neutrophils to release reactive oxygen species and cytokines.2 Contrary to the editorial, there is no evidence that sugar intake and junk food drive ‘caries-mediated’ periodontitis pathways. However, there is emerging evidence in humans that refined sugars drive periodontal inflammation3 and calorie restriction by reverting to a ‘hunter-gatherer’ diet/lifestyle may substantially reduce gum inflammation.4 Mechanisms likely involve meal-induced inflammation from
refined sugar and/or saturated fat, mediated via oxidative stress pathways.5 Periodontitis therefore likely contributes to elevated ACVD risk through co-morbidity due to an elevated systemic inflammatory burden. A European/American expert consensus recently summarised contemporary evidence: http://online library.wiley.com/doi/10.1111/jcpe.2013.40.issue-s14/ issuetoc; or www.perioworkshop.org Declarations Competing interests: None declared
References 1. Bains A and Rashid MA. Junk food and heart disease: the missing tooth. J R Soc Med 2013; 106: 472–3. 2. Tonetti MS and Van Dyke TE; on behalf of working group 1 of the joint EFP/AAP workshop. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013; 40(Suppl 14): S24–9. 3. Chapple ILC. Potential mechanisms underpinning the nutritional modulation of periodontal inflammation. JADA 2009; 140: 178–84. 4. Baumgartner S, Imfeld T, Schicht O, et al. The impact of the Stone Age diet on gingival conditions in the absence of oral hygiene. J Periodontol 2009; 80: 759–68. 5. Esposito K, Ciotola M and Carleo D. Post-meal glucose peaks at home associate with carotid intima-media thickness in type 2 diabetes. JCEM 2008; 93: 1345–50.
Iain LC Chapple Periodontal Research Group, MRC Centre for Immune Regulation, MRC Centre for Musculo-skeletal Ageing, College of Medical & Dental Sciences, School of Dentistry, St Chads Queensway, Birmingham, B4 6NN, UK Email: [email protected]
Michael Busby, Henry Clover and Roger Matthews Denplan Ltd, Denplan Court, Victoria Road, Winchester, SO23 7RG, UK
Downloaded from jrs.sagepub.com at Mount Royal University on June 9, 2015
To submit a letter in response to a JRSM article, please visit http://jrsm.sagepub.com to find the article concerned, then click on the ‘Submit a comment’ link found in the Reader Responses section. Comments will automatically be submitted for consideration to be published in print.
Periodontal disease and systemic disease We were intrigued to read the editorial by Bains and Rashid, ‘Junk food and heart disease: the missing tooth’.1 The authors correctly emphasise the importance of oral health to general health/wellbeing, and specifically cardiovascular risk. However, we wish to highlight significant misunderstandings within the editorial concerning periodontitis and emerging biologically plausible mechanisms underpinning its association with atherogenic cardiovascular disease (ACVD). Periodontitis is a ubiquitous chronic infectiousinflammatory disease initiated by the accumulation of a plaque biofilm at/below the gum margin. The majority of host tissue damage (bone destruction around teeth) is caused by a dysregulated (exaggerated) inflammatory-immune response to pathogenic bacteria within the biofilm. Periodontitis is not, as stated in the editorial, a disease that ‘occurs as a result of untreated dental caries’. It is a completely separate disease with a distinctly different aetiology, pathogenesis, natural history and outcome. Dental caries is not associated with ACVD. Large-scale epidemiological studies consistently and independently associate periodontitis with ACVD. Periodontitis drives elevations in acute-phase reactants (CRP/ IL-6) and oxidative stress within the circulation2 and plausible mechanisms for this emanate from the entry of pathogenic bacteria at periodontally diseased sites into the circulation during eating/tooth brushing which subsequently trigger: (1) the liver’s acute-phase response; and (2) oxidative stress responses by priming/stimulating peripheral blood neutrophils to release reactive oxygen species and cytokines.2 Contrary to the editorial, there is no evidence that sugar intake and junk food drive ‘caries-mediated’ periodontitis pathways. However, there is emerging evidence in humans that refined sugars drive periodontal inflammation3 and calorie restriction by reverting to a ‘hunter-gatherer’ diet/lifestyle may substantially reduce gum inflammation.4 Mechanisms likely involve meal-induced inflammation from
refined sugar and/or saturated fat, mediated via oxidative stress pathways.5 Periodontitis therefore likely contributes to elevated ACVD risk through co-morbidity due to an elevated systemic inflammatory burden. A European/American expert consensus recently summarised contemporary evidence: http://online library.wiley.com/doi/10.1111/jcpe.2013.40.issue-s14/ issuetoc; or www.perioworkshop.org Declarations Competing interests: None declared
References 1. Bains A and Rashid MA. Junk food and heart disease: the missing tooth. J R Soc Med 2013; 106: 472–3. 2. Tonetti MS and Van Dyke TE; on behalf of working group 1 of the joint EFP/AAP workshop. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013; 40(Suppl 14): S24–9. 3. Chapple ILC. Potential mechanisms underpinning the nutritional modulation of periodontal inflammation. JADA 2009; 140: 178–84. 4. Baumgartner S, Imfeld T, Schicht O, et al. The impact of the Stone Age diet on gingival conditions in the absence of oral hygiene. J Periodontol 2009; 80: 759–68. 5. Esposito K, Ciotola M and Carleo D. Post-meal glucose peaks at home associate with carotid intima-media thickness in type 2 diabetes. JCEM 2008; 93: 1345–50.
Iain LC Chapple Periodontal Research Group, MRC Centre for Immune Regulation, MRC Centre for Musculo-skeletal Ageing, College of Medical & Dental Sciences, School of Dentistry, St Chads Queensway, Birmingham, B4 6NN, UK Email: [email protected]
Michael Busby, Henry Clover and Roger Matthews Denplan Ltd, Denplan Court, Victoria Road, Winchester, SO23 7RG, UK
Downloaded from jrs.sagepub.com at Mount Royal University on June 9, 2015
