A Review of the Relationship between Obesity and Periodontal Diseases
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 3
Abstract
Aim: To explore the influence of obesity/overweight on development and treatment outcome of periodontal diseases (PD), and to explore possible mechanisms of interaction between obesity and PD.Methods:A literature search was conducted using the PubMed and Go Pubmed databases.Conclusion: Obesity and PD can exert similar pathogenic effects via common pathways, and can influence each other bidirectionally. Elucidating the relationship between obesity and PD allows for the development of care guidelines and recommendations for clinicians and the public.Obesity and periodontal diseases (PD) are very prevalent among U.S. adults during recent years [1-4]. Since both can lead to severe chronic health conditions and impair people’s life quality by exerting similar influences [5-10], a clear understanding of the association between obesity and periodontal diseases is warranted to reduce health and medical costs in the U.S. [5] The objective of this review is to explore the influence of obesity/overweight on development and treatment outcome of PD, and to explore possible mechanisms of interaction between obesity and PD.PubMed and Go Pubmed were used to search for related preclinical, observational, clinical studies and meta-analyses that investigated the relationship between obesity and PD. They were reviewed to determine the association and to summarize mechanisms of interaction between the conditions. Combinations of “obesity” or”overweight” or “fat-induced obesity” or “weight changes” AND“gingivitis” or “periodontitis” or “periodontal diseases” were used as key terms. Studies conducted in the past six years.PD and obesity can cause and/or facilitate the development and progression of similar systemic diseases and conditions, which include metabolic syndrome [9-16], type 2 diabetes mellitus (T2DM) [17,18], cardiovascular diseases (CVD) [19-21], alveolar bone loss [22-24], rheumatic diseases[17,25-34], and a series of cancers [32-38]. Because of the pro-inflammatory cytokines and adipokines released by adipocytes [9-16], obesity has been consistently shown to be significantly associated with increased risk and worsened prognosis of metabolic syndrome, T2DM, CVD, breast cancer and pancreatic cancer. Meanwhile, PD has been found to have similar relationship with these diseases because of the pro-inflammatory effects caused by virulent factors and antigens of periodontal pathogens such as Fusobacterium species, T. denticolaand P.gingivalis [37-41]. Fusobacterium species have even been detected in pancreatic tissues of patients suffering from pancreatic ductal adenocarcinoma [38]. At the same time, although alveolar bone loss is the hallmark of PD [22], it has been found that each unit increase in BMI is associated with a 5% increase in the risk of alveolar bone loss, and that every 1% increase in waist circumference to height ratio is associated with 3% increase in risk of progression of alveolar bone loss [23,24].PD and obesity are very likely to interact through their shared inflammatory pathways to influence diseases mentioned above [42]. Although they initiate inflammation via different mechanisms [39,40,43-45], their similar effects on the same set of biomarkers involved in pathogenesis indicate that lots of common inflammatory pathways are involved in subsequent steps [14,40,42]. Among these biomarkers, resistin, TNF-alpha, and IL-6 are commonly tested for [46,47]. PD elevates levels of these biomarkers mainly through bacterial invasion [39,41,46,48,49].
Authors and Affiliations
Jiabao Sun BA, Kristin Williams, Leena Palomo
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