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Evidence that cyclosporine inhibits periodontal prostaglandin I 2 synthesis
Author(s) -
Nell A.,
Matejka M.,
Solar P.,
Ulm C.,
Sinzinger H.,
Sinzinger H.
Publication year - 1996
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1996.tb00474.x
Subject(s) - in vivo , pharmacology , in vitro , nifedipine , phenytoin , drug , prostaglandin , prostaglandin e2 , hyperplasia , chemistry , medicine , endocrinology , biochemistry , biology , calcium , microbiology and biotechnology , psychiatry , epilepsy
Cyclosporine (CsA) is a selective immunosuppressant widely used in clinical therapy. Like phenytoin and nifedipine, the drug is associated with gingival overgrowth. This study considers the interaction of CsA and prostaglandin I 2 (PGI 2 ), in particular the action of the drug on gingival tissue in vitro and in vivo . The PGI 2 ‐synthesis of rat, rabbit and human gingival tissue was examined by bioassay. In vivo CsA‐therapy reduces gingival PGI 2 ‐synthesis. The results furthermore show a dose‐dependent inhibition of PGI 2 ‐synthesis by CsA (1–100 μg/ml) in vitro. PGI 2 ‐synthesis from in vivo CsA‐pretreated probes was further dose‐dependently diminished by in vitro addition of CsA. As PGI 2 exerts an antiproliferative activity via cAMP‐elevation, the drug‐induced inhibition of PGI 2 production is claimed to be responsible for gingival hyperplasia in CsA‐treated patients.