AIM: To determine the strength of association of type 2 diabetes mellitus and periodontal disease with the oral inflammatory burden, as assessed by markers of inflammation in saliva. MATERIAL AND METHODS: Unstimulated saliva samples were collected from 192 subjects with or without type 2 diabetes. β-glucuronidase (βG) was measured via a fluorometric array and interlukin-1β (IL-1β) via enzyme-linked immunosorbent assay. The concentration of both mediators was evaluated in relationship to clinical parameters, severity of periodontal disease and diabetes status. RESULTS: Regression analysis demonstrated that diabetes and periodontal disease was independently and positively correlated with increased concentration of βG in saliva (p < 0.001). Moreover, the relative association of periodontal disease with the level of βG in saliva was greater than the strength of association of the diabetic status. IL-1β concentration in saliva was primarily associated with the severity of periodontal disease (p < 0.01), but not the presence of diabetes (p = 0.50). CONCLUSIONS: This study examined the nature of the inflammatory response in the oral cavity as assessed by inflammatory markers in saliva. Both periodontal disease and diabetes mellitus were independently associated with the oral inflammatory burden, in which the effect of periodontal disease was more pronounced.
AIM: To determine the strength of association of type 2 diabetes mellitus and periodontal disease with the oral inflammatory burden, as assessed by markers of inflammation in saliva. MATERIAL AND METHODS: Unstimulated saliva samples were collected from 192 subjects with or without type 2 diabetes. β-glucuronidase (βG) was measured via a fluorometric array and interlukin-1β (IL-1β) via enzyme-linked immunosorbent assay. The concentration of both mediators was evaluated in relationship to clinical parameters, severity of periodontal disease and diabetes status. RESULTS: Regression analysis demonstrated that diabetes and periodontal disease was independently and positively correlated with increased concentration of βG in saliva (p < 0.001). Moreover, the relative association of periodontal disease with the level of βG in saliva was greater than the strength of association of the diabetic status. IL-1β concentration in saliva was primarily associated with the severity of periodontal disease (p < 0.01), but not the presence of diabetes (p = 0.50). CONCLUSIONS: This study examined the nature of the inflammatory response in the oral cavity as assessed by inflammatory markers in saliva. Both periodontal disease and diabetes mellitus were independently associated with the oral inflammatory burden, in which the effect of periodontal disease was more pronounced.
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