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Updated: Aug 7, 2026

Trans-vivo Delayed Type Hypersensitivity Assay for Antigen Specific Regulation
Published on: May 2, 2013
Cyclosporin A specifically affects nuclear PLCbeta1 in immunodepressed heart transplant patients with gingival
A Ruggeri1, L Montebugnoli, A Matteucci
1Department of SAU&FAL, University of Bologna, c/o IOR, Bologna, Italy.
Abstract:
One of the most commonly observed adverse effects of cyclosporin A (CsA) is the development of gingival overgrowth (GO). Fibroblasts are involved in GO, but the question why only a percentage of patients undergoing CsA treatment shows this side-effect remains unanswered. In a previous study, CsA has been demonstrated to induce over-expression of phospholipase C (PLC) beta(1) in fibroblasts of patients with clinical GO, in cells from both enlarged and clinically healthy gingival sites. In this work, we assessed the expression of PLCbeta isoforms to investigate whether the exaggerated fibroblast response to CsA related to increased PLCbeta(1) expression could also be detected in CsA-treated patients without clinical signs of GO. Our results support the hypothesis of a multi-factorial origin of gingival overgrowth, including specific changes within the gingival tissues orchestrating fibroblastic hyper-responsiveness as a consequence of a long-term in vivo exposure to cyclosporin A.
Insights
Cyclosporin A (CsA) can cause gingival overgrowth (GO). This study investigated phospholipase C beta (PLCbeta) isoform expression in patients without GO, suggesting multi-factorial origins for this CsA side effect.
Area of Science:
- Pharmacology
- Cell Biology
- Oral Medicine
Background:
- Gingival overgrowth (GO) is a common adverse effect of cyclosporin A (CsA).
- Fibroblasts play a role in GO, but the reason for variable patient susceptibility is unknown.
- Previous research linked CsA to phospholipase C beta 1 (PLCbeta1) over-expression in fibroblasts of patients with GO.
Purpose of the Study:
- To investigate PLCbeta isoform expression in CsA-treated patients without clinical signs of GO.
- To determine if increased PLCbeta1 expression contributes to CsA-induced fibroblast hyper-responsiveness in patients without GO.
- To explore the multi-factorial origins of CsA-induced gingival overgrowth.
Main Methods:
- Assessed PLCbeta isoform expression in fibroblasts.
- Compared expression levels between patients with and without clinical signs of GO.
- Analyzed fibroblast response to CsA in vitro.
Main Results:
- Results suggest that specific gingival tissue changes may predispose fibroblasts to hyper-responsiveness.
- Increased PLCbeta1 expression might be a factor even in patients without visible GO.
- The study supports a multi-factorial etiology for CsA-induced gingival overgrowth.
Conclusions:
- Gingival overgrowth in response to CsA is likely multifactorial.
- Individual patient factors and cellular changes orchestrate fibroblastic hyper-responsiveness.
- Long-term CsA exposure may induce specific gingival tissue alterations contributing to GO.
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