Abstract
Nifedipine (NF), a calcium channel blocker commonly used for treatming essential hypertension, has been reported in many studies to cause gingival hyperplasia. To clarify the mechanism of NF-induced gingival overgrowth in animals, we examined angiotensin II levels in gingiva and the expression of transforming growth factor (TGF) -β protein in relation to the tissue renin-angiotensin (RA) system in spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs) with normal blood pressure. We also studied the inhibitory effect of captopril, an angiotensin-converting enzyme (ACE) inhibitor, on NF-induced gingival overgrowth in both hypertensive and normotensive animals.
1) Ang II levels in gingiva were significantly higher in the SHR group than in the WKY group.
2) Although hyperplasia of the gingival endothelium and connective tissue was enhanced in both groups receiving NF (SHR NF and WKY NF) compared to that in animals not receiving it (SHR and WKY controls), gingival hyperplasia tended to be more marked in the SHR NF group than in the WKY NF group.
3) TGF-β protein expression was higher in the SHR control group than in the WKY control group. The expression of this protein was significantly higher in both groups receiving NF than in control groups (SHR and WKY).
4) No tendency toward gingival overgrowth was observed in animals receiving NF plus CP or CP alone in either the SHR or WKY group. In both groups, TGF-β protein expression was inhibited more significantly in animals receiving NF plus CP than in those receiving NF alone.
These findings suggest that the tissue RA system may result from overexpression of the TGF-β protein due to an increase in tissue Ang II, and thus also in the pathogenesis of gingival overgrowth in SHRs receiving NF. J Jpn Soc Periodontol 45 : 289-299, 2003.
