Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: A study with mast cell-deficient mice

Citation
Y. Asahara et al., Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: A study with mast cell-deficient mice, J PERIODONT, 71(7), 2000, pp. 1117-1120
Citations number
18
Categorie Soggetti
Dentistry/Oral Surgery & Medicine","da verificare
Journal title
JOURNAL OF PERIODONTOLOGY
ISSN journal
00223492 → ACNP
Volume
71
Issue
7
Year of publication
2000
Pages
1117 - 1120
Database
ISI
SICI code
0022-3492(200007)71:7<1117:MCANII>2.0.ZU;2-H
Abstract
Background: A previous study suggested that mast cells (MC) are involved in the development of cyclosporin A-induced gingival hyperplasia, since an in creased number of MC were observed in the tissue sections of enlarged gingi va. To determine the role of MC in gingival hyperplasia, an MC-deficient mo use model was used in the current study. Methods: MC-deficient mice (WBB6F1xW/W-V) and their littermates (+/+) were fed sucrose-containing diets supplemented with or without varying concentra tions (300, 400, 500, 600 mg) of cyclosporin A/kg of diet. After 30 days, t he mice were sacrificed and the degree of gingival hyperplasia was evaluate d by the appearance of the gingiva. Tissue MC were stained with toluidine b lue to confirm the presence or absence of MC in the enlarged gingiva. Results: Both W/W-V and +/+ mice, when fed with 600 mg cyclosporin A/kg die t for 30 days, exhibited a similar degree of gingival hyperplasia, while ot her test mice or control mice did not, Toluidine blue staining of the tissu e sections confirmed the presence of MC in the enlarged gingiva of the +/mice, but not the W/WV mice. Conclusions: These results indicate that mast cells are not necessary in th e development of cyclosporin A-induced gingival hyperplasia, and that the i ncreased number of MC observed in the enlarged gingiva may be a secondary e ffect of gingival hyperplasia. We also conclude that a study of mice lackin g certain molecules or cells would be quite useful in determining the molec ules or cell types responsible for the pathogenesis of drug-induced gingiva l hyperplasia.