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ORIGINAL ARTICLE - EVALUATIVE STUDY
Year : 2017  |  Volume : 7  |  Issue : 1  |  Page : 82-88

Reconstruction of drug-induced cleft palate using bone marrow mesenchymal stem cell in rodents


1 Department of Anatomy, Ponnaiyah Ramajayam Institute of Medical Sciences, Manamai Nallur, Kancheepuram, Tamil Nadu, India
2 VR Scientific Lab, Chennai, Tamil Nadu, India
3 Department of Anesthesia, Ponnaiyah Ramajayam Institute of Medical Sciences, Manamai Nallur, Kancheepuram, India

Correspondence Address:
Julie Christy Amalraj
No: 9 Ganga Kaveri Street, Ramakrishna Nagar Extn., Porur, Chennai - 600 116, Tamil Nadu
India
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DOI: 10.4103/ams.ams_140_16

PMID: 28713741

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Background: Triamcinolone acetonide (TAC) (Kenacort*) is a commonly used synthetic glucocorticoid in today's medical practice. The drug is also a potential agent in inducing cleft palates in rats. This drug has been used to induce cleft palate in the fetus of the pregnant rats to bring out a suitable animal model for human cleft lip and palate. The drug was given intraperitoneally to induce congenital cleft palate in pregnant mother rats. Aim: The aim of this study is to induce congenital cleft palate in pregnant Wister albino rats and reconstruct the defect with bone marrow mesenchymal stem cells (BMSCs) isolated from the same species along with PLGA (poly lactic co glycolic acid) scaffold. Methods: Twenty female animals were divided into two groups. Each group contains 10 animals. The animals were allowed to mate with male rat during the esterase period and the day, in hich vaginal plug was noticed was taken to be day 0. The pregnant rats were given triamcinolone acetonide (Kenacort* 10 mg/1 ml intramuscularly/intravenous [IM/IV] injections) injection intraperitoneally at two different dosages as the existing literature. The injection was given on the 10, 12, and 14th day of gestation. The clinical changes observed were recorded, and the change in the body weight was noted carefully. Group 1 which received 0.5 mg/kg body weight of TAC had many drug toxic effects. Group 2 which received 0.05 mg/kg body weight produced cleft palate in rat pups. The pups were divided into three groups. Group A control group without cell transplant, the cleft was allowed to close by itself. Group B containing palate reconstructed with plain PLGA scaffold (Bioscaffold, Singapore) without BMSC, Group C containing BMSC and PLGA scaffold (Bioscaffold, Singapore), Group C operated for the cleft palate reconstruction using BMSCs and PLGA scaffold. There was faster and efficient reconstruction of bone in the cleft defect in Group C while there was no defect closure in Group A and B. Results: There was complete reconstruction of the cleft palate in the group of rat pups which received BMSCs along with PLGA scaffold. Bone growth in the cleft defect was faster; complete fusion of the defect was achieved. Conclusion: The dosage of drug used for inducing cleft palate was standardized in rodents for a definitive congenital cleft palate model. The cleft palate induced was reconstructed using BMSCs and PLGA scaffold. This was compared with a control group and the other group with plain PLGA used for reconstruction of the palate. This study will invite future research in the effect of the drug on human beings, especially on pregnant mothers.


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