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Interleukin-1beta, clinical parameters and matched cellular-histopathologic changes of biopsied gingival tissue from
Lein-Tuan Hou1, Cheing-Meei Liu, Bu-Yuan Liu
1Department of Periodontology, College of Medicine, National Taiwan University Hospital, Taiwan. lthou@ha.mc.ntu.edu.tw
Objective:
The aim of the present study was to investigate whether interleukin (IL)-1beta in diseased tissues adjacent to periodontal pockets can reflect the degree of inflammation and destruction of these tissues pathologically.
Background:
IL-1beta-dependent mechanisms have been strongly implicated in contributing to inflammation and destruction of bone and attachment loss, which are characteristic features of periodontal disease. This biochemical mediator released during pro-inflammatory processes has not been objectively integrated with clinical and histopathologic features of periodontal disease.
Methods:
Periodontitis-affected inflamed tissue and clinically nonaffected healthy gingivae were harvested from 14 periodontal patients, respectively. The severity of tissue inflammation was illustrated by clinical parameters and cellular histologic changes and quantified by histometric assessments. IL-1beta in these extracted specimens was measured with an enzyme-linked immunosorbent assay (ELISA) technique. Pathogenic roles that IL-1beta plays in gingival inflammation and pathologic tissue changes in tissue sections were analyzed statistically.
Results:
The overall total tissue IL-1beta, tissue concentration of IL-1beta, and percentage of inflammatory cell infiltration (PICI) determined from diseased gingivae were obviously higher than those of controls from both healthy sites of periodontitis and non-periodontitis subjects. With increasing gingival index (GI), plaque index (PlI), and probing depth (PD), there was a marked elevation in total tissue IL-1beta. Total tissue IL-1beta was significantly correlated with GI, PlI, the PICI, and tissue alterations. Polymorphonuclear leukocytes (PMNs) and monocyte-macrophage cells seemed to predominate in heavily infiltrated areas of diseased gingiva. These cell types were confirmed by immunocytochemical localization with either monoclonal mouse antihuman neutrophil elastase antibody or monoclonal mouse antihuman macrophage (CD68) antibody, respectively. Total tissue IL-1beta and the PICI were also elevated in diseased gingivae near deeper PD, while neither total IL-1beta nor tissue concentration was statistically correlated with PD. Thus, correlation analysis indicates that IL-1beta level in inflamed periodontal tissues correlates highly with clinical parameters (GI and PlI) and PICI (the degree of inflammation).
Conclusions:
These observations suggest that IL-1beta plays a significant role in the pathogenic mechanisms of periodontal tissue destruction, and that measurement of tissue IL-1beta would be a valuable aid and useful for diagnostic markers of periodontal diseases.