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Journal of Dental Research
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Clinical

Stimulation of Cells Derived from Nifedipine-induced Gingival Overgrowth with Porphyromonas gingivalis, Lipopolysaccharide, and Interleukin-1β

H.-K. Lu1,2, H.-P. Chou2, C.-L. Li2, M.-Y. Wang3 and L.-F. Wang4,*

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

Correspondence: * 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-1β). Human gingival fibroblasts from healthy tissues and nifedipine-induced gingival overgrowth tissues were stimulated with nifedipine, IL-1β, 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-1β, 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-1β only. Furthermore, the responses to IL-1β in the nifedipine-induced gingival overgrowth group were stronger than those of the healthy group. It can be concluded that IL-1β 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-1β

Journal of Dental Research, Vol. 86, No. 11, 1100-1104 (2007)
DOI: 10.1177/154405910708601115
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