Interrelationships of periodontitis and diabetes: A review of the current literature

Abstract

Diabetes and periodontitis are common chronic diseases in the world, and abundant epidemiological evidence implies a bidirectional relationship between the two diseases. It appears that diabetes is a risk factor for greater periodontal destruction, whereas managing periodontitis can also contribute to better glycemic control. The underlying regulatory mechanisms are also bidirectional. The hyperglycemic status may directly alter subgingival microbial compositions, impair cellular function, and change collagen metabolism. The formation of advanced glycation end-products (AGEs) can further modify the extracellular matrix, and establishment of cellular receptor binding can amplify inflammation. Moreover, periodontitis also induces hyperlipidemia and insulin resistance. This cyclical relationship converges via overproduction of proinflammatory cytokines, such as tumor necrosis factor-a and interleukin-1b. Thus, this article highlights the importance of maintaining periodontal health to eliminate systemic complications and meticulous metabolic control to prevent further periodontal destruction. From a systemic aspect, targeting proinflammatory cytokines or receptors of AGEs could be a potential modality for treating periodontitis.

Metagenome Analysis of Buccal Mucosal Biofilms to Identify Bacterial Prevalence in Subjects with and without type II Diabetes

“…Recent works of literature displayed a bidirectional relationship between diabetes and periodontitis in which subjects with controlled glycemic metabolic level as measured by HbA1c demonstrated a slower attachment loss than uncontrolled subjects, in contrast, few studies showed an improvement in glycemic control following periodontal treatment (Chang and Lim, 2012).…”

“…The main virulence factor of the microorganisms involved in periodontitis is lipo, 125 Polysaccharides (LPSs) an endotoxin, the pathogenesis is activated by identi ication of pathogen-associated molecular structures from Toll-like receptors (TLRs), release of ROS from defending cells by correspondingly inducing oxidative stress, proinlammatory cytokines, and immunoregulatory complexes through the NF-kB pathway (Chang and Lim, 2012).…”

“…Hyperglycemic status has a direct effect on the microbial composition, collagen metabolism and cellular function. By devel-opment of advanced glycation end-products (AGEs) contributing to the modi ication of the extracellular matrix with the binding to a cellular receptor, further exaggerating in lammation (Abass and Omer, 2011;Chang and Lim, 2012) Various complications such as retinopathy with potential blindness, nephropathy leading to renal failure, neuropathy with increased risk of nonhealing necrotic ulcers, cardiovascular, perivascular, cerebrovascular, autonomic dysfunction including sexual dysfunction may accompany diabetic individuals in the long run.…”

Relationship between Periodontal Disease and Diabetes: A Survey among Internal Medicine Residents in Saudi Arabia

“…Various forms of periodontitis with differing clinical manifestations, responses to treatment result from differences in the microbial etiology among individuals and/or factors that modify host response mechanisms [1]. Of many risk factors associated with the development of periodontal disease (PD), diabetes has long been confirmed as a major risk factor, increasing the chances of its occurrence threefold among type I and II diabetic patients [2,3]. PD has been reported as the sixth complication of diabetes, along with neuropathy, nephropathy, retinopathy, and micro-and macrovascular diseases [4].…”

Low Serum Zinc and Increased Acid Phosphatase Activity in Type 2 Diabetes Mellitus with Periodontitis Subjects

“…Periodontal disease is a microbially initiated chronic inflammatory disease, in which dysregulated immune-inflammatory processes are responsible for the majority of host tissue destruction, and ultimately tooth loss [7]. Periodontal disease is associated with increased incident diabetes risk, poor glycemic control, and diabetic complications, probably due to the higher levels of systemic proinflammatory mediators that exacerbate insulin resistance [8,9].…”