Association Between Metabolic Syndrome and Periodontitis: A Systematic Review and Meta-analysis

Department of Internal Medicine (M.R.), University of Palermo, 90133 Palermo, Italy
The Journal of Clinical Endocrinology and Metabolism (Impact Factor: 6.21). 02/2013; 98(3). DOI: 10.1210/jc.2012-3552
Source: PubMed


Several epidemiological studies have reported an association between metabolic syndrome (MetS) and periodontal diseases (PDs). The aim of this systematic review was to investigate the existence and magnitude of this association.

Materials and methods:
A systematic search of the literature was conducted looking for case-control, cross-sectional, cohort studies and population surveys including patients with measures of MetS and PD. Ovid MEDLINE, EMBASE, LILACS, and Cochrane library databases were used for the search by 2 independent reviewers. A meta-analysis was conducted to investigate the association for coexistence of MetS and PD.

A total of 20 studies were included in the review, from an initial search of 3486 titles. Only 1 study reported longitudinal data on the onset of MetS components in association with periodontal measures. However, several studies investigated coexistence. A random effects meta-analysis showed that the presence of MetS is associated with the presence of periodontitis in a total of 36 337 subjects (odds ratio = 1.71; 95% confidence interval = 1.42 to 2.03). When only studies with "secure" diagnoses were included (n = 16 405), the magnitude of association increased (odds ratio = 2.09; 95% confidence interval = 1.28 to 3.44). Moderate heterogeneity was detected (I(2) = 53.6%; P = .004).

This review presents clear evidence for an association between MetS and periodontitis. The direction of the association and factors influencing it should be investigated by longitudinal and treatment studies. Periodontal diagnostic procedures should be routinely carried out in MetS patients.

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    • "Interestingly, several meta-analyses have revealed that periodontitis is associated with obesity, diabetes type II, and metabolic syndrome [7–10]. Even though the underlying mechanisms for these associations are yet to be determined, it has been speculated that adipokines might represent an important pathomechanistic link between periodontitis and the aforementioned systemic diseases [11]. "
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    ABSTRACT: Adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), are molecules, which are produced in adipose tissue. Recent studies suggest that NAMPT might also be produced in the tooth-supporting tissues, that is, periodontium, which also includes the gingiva. The aim of this study was to examine if and under what conditions NAMPT is produced in gingival fibroblasts and biopsies from healthy and inflamed gingiva. Gingival fibroblasts produced constitutively NAMPT, and this synthesis was significantly increased by interleukin-1 β and the oral bacteria P. gingivalis and F. nucleatum. Inhibition of the MEK1/2 and NF κ B pathways abrogated the stimulatory effects of F. nucleatum on NAMPT. Furthermore, the expression and protein levels of NAMPT were significantly enhanced in gingival biopsies from patients with periodontitis, a chronic inflammatory infectious disease of the periodontium, as compared to gingiva from periodontally healthy individuals. In summary, the present study provides original evidence that gingival fibroblasts produce NAMPT and that this synthesis is increased under inflammatory and infectious conditions. Local synthesis of NAMPT in the inflamed gingiva may contribute to the enhanced gingival and serum levels of NAMPT, as observed in periodontitis patients. Moreover, local production of NAMPT by gingival fibroblasts may represent a possible mechanism whereby periodontitis may impact on systemic diseases.
    Mediators of Inflammation 02/2014; 2014(4):912821. DOI:10.1155/2014/912821 · 3.24 Impact Factor
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    • "Many epidemiological studies have examined the relationship between oral health and different systemic conditions such as metabolic syndrome (21-23). At present, research focuses on the identification of possible mechanisms underlying this association, and on establishing whether the treatment of oral disease leads to improvement in the systemic disease markers (24,25). "
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    ABSTRACT: The components of the human body are closely interdependent; as a result, disease conditions in some organs or components can influence the development of disease in other body locations. The effect of oral health upon health in general has been investigated for decades by many epidemiological studies. In this context, there appears to be a clear relationship between deficient oral hygiene and different systemic disorders such as cardiovascular disease and metabolic syndrome. The precise relationship between them is the subject of ongoing research, and a variety of theories have been proposed, though most of them postulate the mediation of an inflammatory response. This association between the oral cavity and disease in general requires further study, and health professionals should be made aware of the importance of adopting measures destined to promote correct oral health. The present study conducts a Medline search with the purpose of offering an update on the relationship between oral diseases and cardiovascular diseases, together with an evaluation of the bidirectional relationship between metabolic syndrome and periodontal disease. Most authors effectively describe a moderate association between the oral cavity and cardiovascular diseases, though they also report a lack of scientific evidence that oral alterations constitute an independent cause of cardiovascular diseases, or that their adequate treatment can contribute to prevent such diseases. In the case of metabolic syndrome, obesity and particularly diabetes mellitus may be associated to an increased susceptibility to periodontitis. However, it is not clear whether periodontal treatment is able to improve the systemic conditions of these patients. Key words:Cardiovascular diseases, periodontitis, metabolic syndrome, obesity, diabetes mellitus.
    Medicina oral, patologia oral y cirugia bucal 10/2013; 19(3). DOI:10.4317/medoral.19563 · 1.17 Impact Factor
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    • "Metabolic syndrome is also positively correlated with destructive periodontal disease [9–22]. A recent meta-analysis reported that the odds of destructive periodontal disease to occur was 1.71 to 2.09 higher in individuals with metabolic syndrome compared to those without this syndrome [47]. Despite all these evidence indicating the higher risk of destructive periodontal disease in obesity and metabolic syndrome, the underlying biological mechanism(s) is yet to be fully understood. "
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    ABSTRACT: Obesity has become a worldwide health burden in the last two decades. Obesity has been associated with increased comorbidities, such as coronary artery disease, diabetes, and destructive periodontal disease. Obesity is also part of a group of risk factors occurring together in an individual, which is referred to as metabolic syndrome. Clinical studies have shown higher risk for destructive periodontal disease in obesity and metabolic syndrome. However, the role of obesity and metabolic syndrome in the onset and development of destructive periodontal disease has not yet been fully understood. In this review, we discuss a working model, which focuses on interorgan inflammation as a common etiological factor for destructive periodontal disease associated with obesity and metabolic syndrome. Specifically, we suggest that elevated levels of tumor necrosis factor- α (TNF- α ) or interleukin 6 (IL-6)-both adipokines and known risk factors for destructive periodontal disease-in obesity and metabolic syndrome contribute to the onset and development of destructive periodontal disease. The connections between destructive periodontal disease and systemic conditions, such as obesity or metabolic syndrome, are complex and potentially multidirectional. This review largely focuses on TNF- α and IL-6, inflammatory mediators, as potential common risk factors and does not exclude other biological mechanisms.
    Mediators of Inflammation 08/2013; 2013:728987. DOI:10.1155/2013/728987 · 3.24 Impact Factor
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