Does nifedipine aggravate cyclosporin-induced gingival overgrowth? An experiment in rats

Background: Nifedipine (NIF) may aggravate cyclosporin A (CsA)-induced ging ival overgrowth because the potentiated gingival overgrowth has been observ ed in the patients treated with CsA and NIF The purpose of this study was t o evaluate whether NIF could aggravate the CsA-induced gingival overgrowth in a rat model. Methods: Ninety male Sprague-Dawley rats were divided into 6 groups: the fi rst group received 8 mg/kg of CsA daily by gastric feeding for 6 weeks; the second and third groups received NIF daily at a dosage of 10 or 50 mg/kg; the fourth and fifth groups received CsA (8 mg/kg) and NIF (10 or 50 mg/kg) ; and the sixth group received solvents as a negative control. Gingival dim ensions (including bucco-lingual depth, mesio-distal width, and vertical he ight) were assessed bi-weekly from impressed stone models of the mandibular incisal region. At the end of the experiment, the animals were sacrificed. Following histopathological procedures, serial horizontal sections were ob tained at the base of the central incisal papilla. Two tissue levels were s elected for histometric analysis. Level 1 was defined as the point where th e lingual gingiva embraced the bucco-lingual midpoint of the roots and the level 2 as the point where the lingual gingiva at the enamel-dentinal junct ion approximated the bucco-proximal angle of the roots. The bucco-lingual d epth and the mesio-distal width of the papilla were recorded on 5 consecuti ve sections at the 2 levels, respectively. Results: At the 6-week observations, the gingival dimensions (including the depth, width, and height) significantly increased after CsA therapy and th e increasing treatment duration; however, only the mesio-distal width incre ased after NIF therapy. For NIF therapy alone, a positive linear relation w as noted by increased NIF treatment dosages in all gingival dimensions at w eek 6. But, this relationship was not found in the combined therapies. By h istometry, tissue dimensions increased following single drug therapy, eithe r CsA or NIF, at both levels. In animals with the combined therapies, the t issue dimensions decreased if the animals received 10 mg NIF, while they re bounded to control levels with the 50 mg dosage. A dose-dependent positive pattern by NIF was noted in tissue dimensions, but the pattern did not occu r in animals that received combined therapy. Conclusions: The gingival dimensions increased after CsA or NIF therapy, al though they were more prevalent with CsA. But the augmenting pattern in gin gival morphology observed with CsA therapy decreased when the animals recei ved additional NIF Therefore, we question whether NIF is a critical factor in aggravating the CsA-induced gingival overgrowth.