Human soluble receptor for advanced glycation end products and tumor necrosis factor-α as gingival crevicular fluid and serum markers of inflammation in chronic periodontitis and type 2 diabetes

Abstract

The present study aimed to evaluate the levels of soluble receptor for advanced glycation end products (sRAGE) and tumor necrosis factor-α (TNF-α) in serum and gingival crevicular fluid (GCF) in chronic periodontitis (CP) patients with and without type 2 diabetes mellitus (T2DM). A total of 70 subjects were divided into four groups: group 1 (n = 15; subjects with healthy periodontium); group 2 (n = 20; CP patients); group 3 (n = 20; CP patients with T2DM); and group 4 (n = 15; CP patients without T2DM). The serum and GCF levels of human sRAGE and TNF-α were assessed using enzyme-linked immunosorbent assay and correlated with clinical parameters, including probing depth, gingival index and clinical attachment level. Both sRAGE and TNF-α levels varied with the inflammatory state of the patient; the highest levels of sRAGE were seen in group 1, whereas the lowest levels in group 3 (P < 0.05). Conversely, TNF-α levels were found to be the highest in group 3 and lowest in group 1 (P < 0.05). Thus, human sRAGE and TNF-α can be considered as possible GCF and serum markers of inflammatory activity in CP and T2DM. (J Oral Sci 58, 547-553, 2016)

Levels of advanced glycation end products in gingival crevicular fluid of chronic periodontitis patients with and without type‐2 diabetes mellitus

“…Results of an immunohistochemistry‐based study reported that expression of the receptors of AGEs (RAGE) in the basal and spinous layer and endothelium of the inflamed gingival epithelium is increased in CP patients with and without type‐2 DM. Interaction between AGEs and RAGE alters the physiologic function and tertiary structure of macromolecules and provokes fibrotic and tissue‐inflammatory reactions; Furthermore, AGEs‐RAGE interactions exacerbate CP by increasing the production of destructive inflammatory cytokines including interleukin (IL) 1 beta (β), IL‐6 and tumor necrosis factor‐alpha (TNF‐α) in the serum and gingival crevicular fluid (GCF) . In this regard, Katz et al .…”

“…Interaction between AGEs and RAGE alters the physiologic function and tertiary structure of macromolecules and provokes fibrotic and tissue-inflammatory reactions 8 ; Furthermore, AGEs-RAGE interactions exacerbate CP by increasing the production of destructive inflammatory cytokines including interleukin (IL) 1 beta ( ), IL-6 and tumor necrosis factor-alpha (TNF-) in the serum and gingival crevicular fluid (GCF). [13][14][15] In this regard, Katz et al 12 proposed that the AGEs-RAGE interface augments periodontal destruction in CP patients with and without type-2 DM.…”

Stability and bone loss around submerged and non-submerged implants in diabetic and non-diabetic patients: a 7-year follow-up

“…Research indicates that T2DM has been associated with the formation and accumulation of advanced glycation end products (AGEs), which contribute to its pathogenesis and to abnormal periodontal wound healing. 6,7 These end products reduce the production of matrix proteins such as collagen and osteocalcin by gingival and periodontal fibroblasts. 8 It has also been suggested that T2DM patients present with persistent inflammatory response, significant attachment loss, and increased alveolar bone resorption.…”

Survival of adjacent‐dental‐implants in prediabetic and systemically healthy subjects at 5‐years follow‐up

“…Our results showed that HbA1c levels at nearly 5‐years' after implant therapy were nearly 1.5 times elevated in group‐A than group‐B. It is well‐reported that persistent hyperglycemia induces oxidative stress in tissues by increasing the formation and accumulation of AGEs . Moreover, interactions between these endproducts and their receptors enhances the expression of proinflammatory cytokines including TNF‐α, IL‐1β, and IL‐6 in the bodily fluids including serum and GCF .…”

“…A state of CH is associated with deposition of advanced‐glycation‐endproducts (AGEs) in tissues, including the periodontium . Once AGEs interact with their specific receptors, proinflammatory cytokines such as interleukin (IL)‐1β and tumor‐necrosis‐factor‐α (TNF‐α) are produced that accumulate in the blood and gingival crevicular fluid (GCF) . These proinflammatory cytokines worsen periodontal inflammation, which may lead to alveolar bone loss around dentition and implants .…”