Correlation of periodontal inflamed surface area with glycemic status in controlled and uncontrolled type 2 diabetes mellitus

BACKGROUND: The bidirectional link between periodontitis and diabetes mellitus (DM) has been established. Periodontitis causes systemic inflammatory burden through inflammatory mediators. The currently utilized tools [clinical attachment loss (CAL) and probing pocket depth (PPD)] are linear measurements, that do not exactly quantify the inflammatory burden of periodontitis. Periodontal inflamed surface area (PISA) quantifies the surface area of bleeding pocket epithelium and estimates the inflammatory burden. Studies relating to the periodontal status of diabetic patients with and without microvascular complications are scarce. This study assessed the proportion of periodontitis and correlation of PISA with glycemic status in controlled, uncontrolled type 2 DM (T2DM) with and without microvascular complications. AIM: To assess the proportion of periodontitis and correlation of PISA with glycemic status in controlled, and uncontrolled T2DM with and without microvascular complications. METHODS: This study comprised 180 T2DM patients. Based on glycated hemoglobin (HbA1c) levels, they were grouped into: (1) Controlled T2DMgroup: (HbA1c ≤ 7%); (2) Uncontrolled T2DM group: (HbA1c > 7%) without microvascular complications; and (3) Uncontrolled T2DM group: (HbA1c > 7%) with microvascular complications. Each group comprised 60 patients. All patients were assessed for periodontal parameters (Bleeding on Probing, PPD, CAL, Oral hygiene index simplified and PISA), and systemic parameters (HbA1c, fasting plasma glucose and post prandial plasma glucose). RESULTS: The proportion of periodontitis among controlled T2DM group, uncontrolled T2DM group without microvascular complications, uncontrolled T2DM group with microvascular complications was 75%, 93.4% and 96.6% respectively. Extent and severity of periodontitis were high in the uncontrolled T2DM group. A significant positive correlation was found between PISA and HbA1c among all patients (r = 0.393, P < 0.001). The dose–response relationship between PISA and HbA1c was observed. An increase of PISA with 168 mm(2) was associated with a 1.0% increase of HbA1c. CONCLUSION: High proportion and severity of periodontitis, and increased inflamed surface area in uncontrolled T2DM may have contributed to the poor glycemic control and microvascular complications.