BMJ 2014;348:g2645 doi: 10.1136/bmj.g2645 (Published 10 April 2014)

Page 1 of 2

Editorials

EDITORIALS Time to take periodontitis seriously The benefits of treatment are likely to exceed the costs Iain L C Chapple professor of periodontology University of Birmingham Periodontal Research Group and MRC Centre for Immune Regulation, Dental School, Birmingham B4 6NN, UK

Periodontitis is the most common chronic inflammatory disease seen in humans, affecting nearly half of adults in the United Kingdom and 60% of those over 65 years.1 It is a major public health problem, causing tooth loss, disability, masticatory dysfunction, and poor nutritional status.2 Periodontitis also compromises speech, reduces quality of life,3 and is an escalating burden to the healthcare economy. In the UK alone it was estimated to cost £2.8bn (€3.4bn; $4.6bn) in 2008,4 not including raised all cause mortality, an association that has been noted in several populations.5 Worryingly, the disease is often silent, being present for decades before diagnosis and treatment. It can leave a substantial pathological footprint on multiple organ systems, as well as the oral cavity.

Periodontitis follows the development of a pathogenic microbial biofilm at and below the gingival (gum) margin. In susceptible patients, this triggers an exaggerated and dysfunctional inflammatory immune response, which destroys the bone surrounding the teeth, causing tooth loss.6 The host’s immune response to the initiating microbiota is largely genetically determined, but environmental and lifestyle factors such as smoking, suboptimally controlled diabetes, obesity, poor nutrition (high intake of refined sugar and low intake of antioxidant micronutrients), and stress play important modifying roles.7 However, the most important modifiable risk factor is oral hygiene, and removing the initiating factor avoids activating the chronic non-resolving inflammation that characterises periodontitis. Moving beyond the mouth, periodontitis is significantly and independently associated with most chronic inflammatory diseases of ageing, including atherogenic cardiovascular disease,8 type 2 diabetes,9 rheumatoid arthritis,10 chronic kidney disease,11 obesity, and chronic obstructive pulmonary disease.12 This is unsurprising given that these conditions all have complex causes and are characterised by chronic inflammation. Although debate about unifying explanatory hypotheses (“common risk hypothesis” or “comorbidity”) is ongoing, there is no longer debate about the value of a stratified medical approach to understanding common disease pathways and using periodontitis as a model chronic inflammatory disease. The levels of evidence implicating periodontitis in the causal pathway of chronic diseases and conditions vary from strong

in the case of diabetes and its complications to weak in the case of adverse pregnancy outcomes.9 13 The European Federation of Periodontology (EFP) and American Academy of Periodontology (AAP) therefore held a joint workshop in 2012 to look at the evidence base. Consensus reports were developed and published in 2013, underpinned by 11 comprehensive systematic reviews (http://onlinelibrary.wiley.com/doi/10.1111/ jcpe.2013.40.issue-s14/issuetoc; summarised at: www. perioworkshop.org). The findings are summarised below. With regard to epidemiological associations between periodontitis and incident atherosclerotic cardiovascular disease (ACVD), data from 12 longitudinal studies consistently show an association between pre-existing periodontitis and incident ACVD. The strongest association was found in younger men, and no association was seen in those over 65 years.8 The associations were evident for various ACVD measures and were independent of traditional cardiovascular risk factors.

Treatment for periodontal disease also has effects on biomarkers and ACVD outcomes. Studies suggest that treatment can trigger short term inflammatory sequelae within the circulation, probably as a result of bacterial inoculation during treatment. Although the importance of this is unknown, staged treatment is recommended over that provided in one episode. Periodontal treatment resulted in consistent and progressive reductions in systemic inflammation and biomarkers of ACVD risk, including improvements in vascular endothelial function and flow mediated dilation. However, no studies have used hard outcomes such as primary or secondary cardiovascular events. There were no studies on the effects of periodontal treatment on primary prevention of ACVD and only one feasibility trial on secondary prevention of ACVD. Periodontitis might contribute to the development of ACVD through several biologically plausible mechanisms. Firstly, periodontal pathogens enter the circulation during daily function (eating and tooth brushing) and disseminate to vascular tissues. The prevalence, incidence, and biodiversity of these bacteria are higher in gums that are affected by periodontitis than in healthy gums or those affected by gingivitis. Periodontal pathogens are found within atheromatous plaques and, in animal models, can invade endothelium, remain viable, and induce a pro-atherogenic phenotype through endothelial-monocyte

[email protected] For personal use only: See rights and reprints http://www.bmj.com/permissions

Subscribe: http://www.bmj.com/subscribe

BMJ 2014;348:g2645 doi: 10.1136/bmj.g2645 (Published 10 April 2014)

Page 2 of 2

EDITORIALS

interactions. Non-invasive mutants seem to be less pathogenic than wild-type bacteria in vitro and in vivo; however, bacterial isolates from human atheromas have not yet been shown to induce atheromas in animal models.14

Secondly, patients with periodontitis have raised levels of inflammatory mediators within the circulation, including acute phase reactants such as C reactive protein and interleukin 6, as well as oxidative stress markers caused by activation of circulating neutrophils (for example, shorter leucocyte telomeres).15 Other inflammatory mediators that are raised in these patients include prothrombotic and haemostatic markers (fibrinogen and plasminogen activator inhibitor 1); cross reactive systemic antibodies that promote inflammation and interact with atheromas; and pro-inflammatory lipid classes/dyslipidaemia.14 The consensus view of the EFP/AAP was that in periodontitis, increased bacteraemia during daily function activates multiple inflammatory pathways, which may act in concert to promote or exacerbate the risk for atherogenesis.16 A role for periodontal disease in ACVD and its sequelae therefore seems to be biologically plausible, with strong evidence from association studies independent of confounding risk factors. However, direct evidence for a causal role has not been proved, and the impact of successful periodontal treatment on ACVD outcomes, although promising, requires longer term studies using hard endpoints. Recently, data have emerged from US based insurance companies on the health economic savings of managing periodontitis in patients with different systemic comorbidities.17 18 In one study, annual health cost savings of $2183 (25.4%) per patient were reported for patients with heart disease and $2831 (34.7%) for those with stroke.17 Annual overall savings per patient were $1020 after periodontal care, irrespective of comorbidity, largely due to a 67% reduction in hospital admissions and a 54% reduction in emergency room activity. Overall, it seems that it is time to put the mouth back into the body. Periodontitis is common, preventable, and treatable at relatively low cost to the healthcare economy. Irrespective of the results of longitudinal intervention studies using hard cardiovascular outcomes, the economic benefits to patients with heart disease and other healthcare stakeholders of attaining and maintaining periodontal health seem likely to outweigh the costs.

Provenance and peer review: Commissioned; not externally peer reviewed. 1 2 3

4 5 6 7 8 9 10 11

12 13 14 15 16 17 18

White DA, Tsakos G, Pitts NB, Fuller E, Douglas GVA, Murray JJ, et al. Adult Dental Health Survey 2009: common oral health conditions and their impact on the population. Br Dent J 2012;213:567-72. United Nations. Political declaration of the high level meeting of the General Assembly on the Prevention and Control of NCDs. A/66/L.1. www.who.int/nmh/events/un_ncd_ summit2011/political_declaration_en.pdf. Eke PI, Dye BA, Wei L, Thornton-Evans GO, Genco RJ. CDC Periodontal Disease Surveillance workgroup: James Beck (University of North Carolina, Chapel Hill, USA), Gordon Douglass (Past President, American Academy of Periodontology), Roy Page (University of Washington). Prevalence of periodontitis in adults in the United States: 2009 and 2010. J Dent Res 2012;91:914-20. PR Newswire. Britain’s plaque plague costing NHS more than GBP 2 billion. 2008. www. prnewswire.co.uk/cgi/news/release?id=224265. Garcia RI, Krall EA, Vokonas PS. Periodontal disease and mortality from all causes in the VA Dental Longitudinal Study. Ann Periodontol 1999;3:339-49. Dias HK, Chapple ILC, Milward MR, Grant MM, Hill E, Brown J, et al. Sulforaphane restores cellular glutathione levels and reduces chronic periodontitis neutrophil hyperactivity in vitro. PLoS One 2013;8:e66407. Tonetti MS, Chapple ILC. Biological approaches to the development of novel periodontal therapies—consensus of the seventh European workshop on periodontology micronutritional approaches to periodontal therapy. J Clin Periodontol 2011;38(S11):114-8. Dietrich T, Sharma P, Walter C, Weston P, Beck J. The epidemiological evidence behind the association between periodontitis and incident atherosclerotic cardiovascular disease. J Clin Periodontol 2013;40(S14):70-84. Chapple ILC, Genco RJ. Diabetes and periodontal diseases: consensus report of the joint EFP/AAP workshop on periodontitis and systemic diseases. J Clin Periodontol 2013;40(S14):106-12. DePablo P, Chapple ILC, Buckley CD, Dietrich T. Periodontitis and systemic rheumatic diseases. Nat Rev Rheumatol 2009;5:218-24. Sharma P, Dietrich T, Sidhu A, Vithlani V, Raman M, Stringer S, et al. The periodontal health component of the Renal Impairment In Secondary Care (RIISC) cohort study: a description of the rationale, methodology and initial baseline results. J Clin Periodontol 2014 [forthcoming]. Linden G, Herzberg MC. Periodontitis and systemic diseases: a record of discussions of working group 4 of the joint EFP/AAP workshop on periodontitis and systemic diseases. J Clin Periodontol 2013;40(S14):20-3. Sanz M, Kornman K. Periodontitis and adverse pregnancy outcomes: consensus report of the Joint EFP/AAP workshop on periodontitis and systemic diseases. J Clin Periodontol 2013;40(S14):164-9. Schenkein HA, Loos BG. Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases. J Clin Periodontol 2013;40(S14):51-69. Masi S, Salpea KD, Li KW, Parkar M, Nibali L, Donos N, et al. Oxidative stress, chronic inflammation, and telomere length in patients with periodontitis. Free Rad Biol Med 2011;50:730-5. Tonetti MS, Van Dyke TE. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the joint EFP/AAP workshop on periodontitis and systemic diseases. J Clin Periodontol 2013;40(S14):24-9. Cigna Health and Life Insurance Company. 2013. Improved health and lower medical costs: why good dental care is important. http://kb.previser.com/wp-content/uploads/2013/ 12/Cigna-Possible-Medical-Savings-from-Improved-Dental-Care.pdf. PR Newswire Association. New research continues to show medical cost savings and reduced hospitalizations possible with gum disease treatment. 2014. http:// insurancenewsnet.com/oarticle/2014/03/21/new-research-continues-to-show-medicalcost-savings-and-reduced-hospitalizations-a-477675.html.

Cite this as: BMJ 2014;348:g2645 © BMJ Publishing Group Ltd 2014

Competing interests: I have read and understood the BMJ Group policy on declaration of interests and declare the following interests: None.

For personal use only: See rights and reprints http://www.bmj.com/permissions

Subscribe: http://www.bmj.com/subscribe

Time to take periodontitis seriously.

Time to take periodontitis seriously. - PDF Download Free
187KB Sizes 0 Downloads 3 Views