Abstract
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 infectious-inflammatory 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 circulation 2 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 inflammation 3 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://onlinelibrary.wiley.com/doi/10.1111/jcpe.2013.40.issue-s14/issuetoc; or www.perioworkshop.org