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ORIGINAL HYPOTHESIS
Year : 2013  |  Volume : 4  |  Issue : 4  |  Page : 122-126

Transforming growth factor-β1/Smad/connective tissue growth factor axis: The main pathway in radiation-induced fibrosis of osteoradionecrosis?


Department of Oro-Maxillofacial Head and Neck Oncology, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University, School of Medicine, Shanghai - 200 011, China

Correspondence Address:
Yue He
Department of Oro-Maxillofacial Head and Neck Oncology, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University, School of Medicine, 639 Zhi Zao Ju Road, Shanghai - 200 011
China
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Source of Support: This work was supported by grants of the National Natural Science Foundation of China (NSFC 81271112), and “ShuGuang” project (10SG19) supported by Shanghai Municipal Education Commission and Shanghai Education Development Foundation., Conflict of Interest: None


DOI: 10.4103/2155-8213.122673

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Introduction: Osteoradionecrosis (ORN) of the mandible is a serious complication following radiation therapy for malignancies of the head and neck. Radiation-induced fibrosis (RIF) is a new theory that accounts for the damage to normal tissues after radiotherapy, and the radiation-induced fibroatrophic mechanism includes the free-radical formation, endothelial dysfunction, inflammation, microvascular thrombosis, fibrosis and remodeling, and finally bone and tissue necrosis. The Hypothesis: Previous studies revealed that transforming growth factor-β1 (TGF-β1) is the master switch cytokine responsible for the regulation of fibroblast proliferation and differentiation that result in RIF. Among the targets of TGF-β1, connective tissue growth factor (CTGF) is a downstream mediator through the Smad3/4 pathway and plays an important role in connective tissue homeostasis and fibroblast proliferation. Studies have proved that the TGF-β1/Smad/CTGF signaling pathway is involved in the RIF of soft tissues, so the authors put forward a hypothesis that the TGF-β1/Smad/CTGF axis is also the main pathway in RIF of ORN. Evaluation of the Hypothesis: The validation of our hypothesis may provide new insights for better understanding the pathogenesis of ORN and open new perspectives for anti-fibrotic therapies, and pioneer novel approaches to treat ORN.


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