Abstract

The effect of nifedipine and interleukin-alpha (IL-1alpha) on the cell proliferation and DNA synthesis was studied in human gingival fibroblasts derived from 5 patients who developed gingival overgrowth (nifedipine responders) and 5 patients who did not develop gingival overgrowth (nifedipine non-responders) in response to nifedipine. Epidermal growth factor was used as a positive control. The fibroblasts derived from nifedipine responders tended to have a numerically greater rate of cell proliferation and DNA synthesis (3H-thymidine incorporation) than those from nifedipine nonresponders in the presence of nifedipine and IL-lalpha. Fibroblasts derived from nifedipine responders showed significantly higher cell proliferation rate in the presence of nifedipine and IL-1alpha, than nifedipine or IL-lalpha alone on both the second and the fourth day of incubation (P < 0.05). A combination of IL-1alpha and epidermal growth factor also showed significantly greater cell proliferation than IL-lalpha alone on the second day (P < 0.05). The DNA synthesis rate with a combination of nifedipine and IL-1alpha was higher than that for nifedipine alone on the second day (P < 0.01), and IL-1alpha alone on the fourth day (P < 0.05) in gingival fibroblasts originating from nifedipine responders. These results suggest that the interaction between nifedipine and gingival inflammation might play an important role in the pathogenesis of nifedipine-induced gingival overgrowth.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.