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Diabetes and Periodontal Disease Periodontitis in Patients with Diabetes— A Complication that Impacts on Metabolic Control Corneliu Sima, DMD, DSc 1 and Michael Glogauer, DDS, PhD 2 1. Post-doctoral Fellow and Senior Resident in Periodontology, Faculty of Dentistry; 2. Associate Professor, Faculty of Dentistry and Faculty of Medicine, University of Toronto, Ontario, Canada Abstract Diabetes and periodontal diseases (PDs) exhibit a bidirectional relationship centered on an enhanced inflammatory response that manifests both locally and systemically. Diabetes is an established risk factor for PD, whereas the treatment of the latter has been shown to improve glycemic control in diabetic patients. Although compelling evidence from in vitro and animal studies supports a plausible biological explanation for the relationship between the two conditions centered on systemic low-grade inflammation, the limited number of comparable large randomized clinical trials is reflected in the limited specific guidelines offered by the international organizations for diabetes and periodontitis regarding the management of the two diseases in an individual. Further understanding of the biological phenomena underlying PDs and diabetes is critical for individual therapeutic approaches to patients with both conditions by endocrinologists and periodontists. Keywords Diabetes, periodontal diseases, inflammation, glycemic control Disclosure: The authors have no conflicts of interest to declare. Received: June 5, 2012 Accepted: June 27, 2012 Citation: US Endocrinology, 2012;8(1):35–9 Correspondence: Michael Glogauer, DDS, PhD, Associate Professor, Faculty of Dentistry and Faculty of Medicine, University of Toronto, Room 221, Fitzgerald Building, 150 College Street, Toronto, Ontario, M5S 3E2, Canada. E: michael.glogauer@utoronto.ca Diabetes is a multifactorial, life-threatening chronic disease characterized by a dysregulation of the endocrine and metabolic pathways involved in the control of blood glucose levels resulting in hyperglycemia. Uncontrolled diabetes gradually impacts on the nervous and circulatory systems, resulting in irreversible long-term complications. In 2010, approximately 8.3 % of the US population—or 25.8 million people—had diabetes either diagnosed (18.8 million) or undiagnosed (7.0 million) and a further 79 million people were estimated to have pre-diabetes according to the Centers for Disease Control and Prevention. 1 Chronic hyperglycemia is a hallmark of diabetes regardless of the pathophysiological mechanism of the disease and is regarded as a central player in the development of acute complications—such as hypoglycemic coma, ketoacidotic coma, hyperosmolar non-ketonic coma, myocardial infarction (MI), and stroke—and chronic complications—such as diabetic nephropathy, retinopathy, neuropathy, cardiovascular diseases, peripheral vascular diseases, and periodontal diseases (PDs). PDs are chronic, microbially induced inflammatory disorders of the tooth-supporting tissues (periodontium) characterized by the progressive destruction of those tissues and ultimately resulting in tooth loss. PDs are the most common inflammatory and bone lytic diseases of humans. Up to 75 % of North American adults experience the morbidity and decreased oral function associated with alveolar bone destruction and subsequent edentulism during their lifetime. Oral bone © TOUCH BRIEFINGS 2012 loss takes on additional importance because of recent evidence linking PDs with systemic health conditions including diabetes, cardiovascular disease, and cancer as well as with giving birth to premature children. Periodontitis, like several other bone diseases (e.g., osteoporosis), is not usually diagnosed until bone loss is well established and damage to skeletal structures has already occurred. Chronic inflammation of gingival tissues called gingivitis represents the initial reversible stage of PD. Although, in some individuals, gingivitis never progresses to PD, 2 data suggest that gingivitis always precedes PD and, more importantly, that it represents a clinically relevant risk factor for periodontal attachment loss. 3 PD represents the advancement of tissue destruction in the underlying periodontal structures—including the periodontal ligament (PDL), cementum covering the root surfaces, and alveolar bone—compromising tooth stability in the socket (see Figure 1). In general, three parameters are used to evaluate periodontal status: bleeding on probing (BOP) as indicator of gingivitis, and clinical attachment level (CAL) and alveolar bone loss (ABL) as indices for monitoring PD progression. The quality and quantity of gingival crevicular fluid (GCF), a pseudo-inflammatory exudate found in the gingival crevice, may also be assessed for diagnostic and disease monitoring purposes. Progression of gingivitis to PD is characterized by dysregulated host–biofilm interactions and a failure to resolve local inflammation induced by periodontopathogenic bacteria. 35