INFLAMMATORY MEDIATOR RESPONSE AS A POTENTIAL RISK MARKER FOR PERIODONTAL-DISEASES IN INSULIN-DEPENDENT DIABETES-MELLITUS PATIENTS

THE GINGIVAL CREVICULAR FLUID (GCF) and monocytic secretion of prostag landin E(2) (PGE(2)) and interleukin 1 beta (IL-1 beta) were measured in a group of 39 insulin-dependent diabetes mellitus (IDDM) patients a nd 64 systemically healthy individuals. Diabetics were divided into Gr oup A (gingivitis or mild periodontal disease) and Group B (moderate o r severe periodontal disease). Diabetics had significantly higher GCF levels of both PGE(2) and IL-1 beta was compared to non-diabetic contr ols who were matched with regard to periodontal disease severity (P < 0.00001 and P = 0.0005, respectively). Within the diabetic population, the GCF levels of these inflammatory mediators were almost 2-fold hig her in Group B as compared to Group A (P = 0.01, P = 0.006, respective ly for GCF-PGE(2) and IL-1 beta). Furthermore, diabetics as a group ha d a significantly higher monocytic PGE(2) and IL-1 beta production in response to various concentrations of both Escherichia coli and Porphy romonas gingivalis lipopolysaccharide (LPS) as compared to non-diabeti c patients with adult periodontitis (P = 0.0001). LPS dose-response cu rves demonstrated that monocytes from Group B diabetics produced appro ximately 3 times more PGE(2) than Group A monocytes; however, there wa s no significant difference in monocytic IL-1 beta secretion within th e IDDM patients. The levels of GCF or monocytic mediators did not corr elate with age, race, or glycosylated hemoglobin (HbA(1C)) levels. Our data suggest that the high GCF and monocytic secretion of PGE(2) and IL-1 beta in IDDM patients may be a consequence of a systemic response trait and that the presence of Gram-negative infections such as perio dontal diseases may interact synergistically to yield high local level s of these mediators and a more severe periodontal condition.