Resistin Levels in Gingival Crevicular Fluid of Patients With Chronic Periodontitis and Type 2 Diabetes Mellitus

• Localización: Journal of periodontology, ISSN 0022-3492, Nº. 4, 2014, págs. 610-617
• Idioma: inglés
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• Resumen

  • Background: Resistin is associated with local and systemic inflammatory conditions with a direct correlation with type 2 diabetes mellitus (T2DM). The aim of this clinico-biochemical study is to estimate and compare the levels of resistin in the gingival crevicular fluid (GCF) in health, chronic periodontitis (CP), and T2DM.

    Methods: Sixty patients (aged >35 years) who participated in this study were divided into four groups of 15 patients each: healthy individuals (group 1), patients with CP (group 2), patients with T2DM (group 3), and patients with T2DM and CP (group 4). The parameters assessed included plaque index (PI), gingival index (GI), probing depth (PD), periodontal index, body mass index, random blood sugar (RBS), and glycated hemoglobin (HbA1c). GCF (4 µL) was collected and analyzed for resistin levels using an enzyme-linked immunosorbent assay.

    Results: Resistin was detected in the GCF of all patients. A significant difference was observed in GCF resistin concentrations from group 1 versus group 2 (P = 0.0093), group 3 (P = 0.0341), and group 4 (P = 0.0002); in group 2 versus group 4 (P = 0.0032); and in group 3 versus group 4 (P = 0.0008). When all the samples were analyzed together, GCF resistin levels positively correlated with GI, PD, PI, RBS, and HbA1c and were predictable with PD and HbA1c.

    Conclusions: Resistin levels are increased in CP and T2DM. Hence, GCF resistin levels may be considered as a potential inflammatory marker for periodontitis with T2DM.

    The initiation and progression of periodontitis is mainly governed by the microbial onslaught and the host response in the form of an inflammatory reaction that ensues to combat it.1 Characterized by a breakdown of tooth-supporting tissues, periodontitis has been causally associated with several microorganisms, some definitively and some putatively. To deal with the microbial load, a gamut of mediators of the host response orchestrates the inflammatory reaction.

    Having being described as the sixth complication of diabetes mellitus (DM), periodontitis has been directly correlated with the level of glycemic control.2 Alterations in the microflora3 and neutrophil functioning4 as well as compromised wound healing5 make DM a risk factor for periodontal disease. At the same time, the effect of periodontal infections on the pathogenesis of certain systemic conditions has also been studied with equal fervor. A continuous low-grade infectious state is said to exist because of chronic periodontitis (CP).6 This has been attributed to both: 1) direct effects of disseminated periodontal pathogens and their toxins and 2) the altered metabolic changes that they can bring about indirectly, e.g., increased insulin sensitivity.7 In chronic infectious states, several immunologic and enzymatic factors recognized as mediators and/or biomarkers, of both bacterial and host origin, have been and are being studied to elaborate on the disease activity in addition to striving to establish their diagnostic and prognostic importance. Monitoring the response to treatment can be another application of such biomarkers.

    Resistin, a putative adipocyte-derived signaling polypeptide, is named after its proposed function of resisting insulin. This cysteine-rich molecule, also known as FIZZ3 (found in inflammatory zone-3) or ADSF (adipocyte-specific secretory factor), belongs to the group of adipokines (others being adiponectin, leptin, adiponutrin) whose protein was found originally in mouse adipose tissue.8 Although the expression of resistin in mice was originally restricted to adipocytes, there is much speculation about the source of resistin expression in humans. Human studies suggest that very little resistin is expressed in adipocytes, it being largely expressed in neutrophils, macrophages, and monocytes.9 Although there is evidence suggesting a role for resistin in the etiology of insulin resistance and type 2 DM (T2DM) by an exhibited impaired insulin-mediated glucose transport,8 it remains controversial with inconsistent results.10 Human resistin also acts as a proinflammatory molecule and stimulates the synthesis and secretion of proinflammatory cytokines: tumor necrosis factor (TNF)-a, interleukin (IL)-6, IL-12, and monocyte chemoattractant protein (MCP)-1.11 The association of resistin with periodontitis has been recently investigated, and a positive correlation with bleeding on probing (BOP) was observed when evaluated from the serum of patients with CP.12 Resistin has also been studied in the gingival crevicular fluid (GCF) as an inflammatory mediator during the induction and resolution of experimental gingivitis in humans.13 Other chronic inflammatory conditions, such as rheumatoid arthritis,14 inflammatory bowel disease,15 and asthma,16 have been correlated directly with resistin concentrations.

    The biologic association of DM and periodontal disease, though well documented in the literature, offers scope in research to better understand the commonalities governing the pathobiology of these two interrelated diseases. Resistin may hold value as an inflammatory mediator because it has been associated with insulin resistance and periodontitis. This may advance the biologic link between DM and periodontal disease.

    Hence, the aim of this study is to estimate and compare the levels of resistin in the GCF in health, CP, and T2DM.