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RESEARCH REPORT |
1 Periodontal Clinic of the Dental Department, Taipei Medical University Hospital, Taipei, Taiwan;
2 College of Oral Medicine, Taipei Medical University, Taipei, Taiwan;
3 School of Dentistry, College of Medicine, National Taiwan University, Taipei, Taiwan; and
4 Department of Biochemistry, College of Medicine, Taipei Medical University, 250, Wu-shing Street, Taipei, Taiwan
* corresponding author, wanglf{at}tmu.edu.tw
The purpose of this study was to clarify the main contributory factor of nifedipine-induced gingival overgrowth either by Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) or interleukin-1beta (IL-1ß). Human gingival fibroblasts from healthy tissues and nifedipine-induced gingival overgrowth tissues were stimulated with nifedipine, IL-1ß, Escherichia coli lipopolysaccharide (Ec-LPS), and Pg-LPS, and the gene expressions were analyzed by RT-PCR. Analysis of the data showed no strong evidence of a synergistic effect of nifedipine and Pg-LPS on IL-6, connective tissue growth factor (CTGF), and type 1 collagen gene expression of either healthy cells or nifedipine-induced gingival overgrowth cells. Among the three stimulants—IL-1ß, Pg-LPS, and Ec-LPS—androgen receptor and IL-6 gene expressions in both the healthy and nifedipine-induced gingival overgrowth groups were strongly up-regulated by the presence of IL-1ß only. Furthermore, the responses to IL-1ß in the nifedipine-induced gingival overgrowth group were stronger than those of the healthy group. It can be concluded that IL-1ß is an important mediator responsible for the higher IL-6 and androgen receptor expression of nifedipine-induced gingival overgrowth cells.
KEY WORDS: nifedipine-induced gingival overgrowth androgen receptor IL-6 Porphyromonas gingivalis IL-1ß
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