Deletion of Runx2 in condylar chondrocytes disrupts TMJ tissue homeostasis.

Autor: Liao L; Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Department of Implant Dentistry, Xi'an Jiaotong University College of Stomatology, Xi'an, Shaanxi, China.; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois., Zhang S; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois., Zhou GQ; Department of Medical Cell Biology and Genetics, Shenzhen Key Laboratory and the Center for Anti-Ageing and Regenerative Medicine, Shenzhen University Medical School, Shenzhen, China., Ye L; Department of Cariology and Endodonics West China Hospital of Stomatology, Sichuan University, Sichuan, China., Huang J; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois., Zhao L; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois., Chen D; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois.
Jazyk: angličtina
Zdroj: Journal of cellular physiology [J Cell Physiol] 2019 Apr; Vol. 234 (4), pp. 3436-3444. Date of Electronic Publication: 2018 Nov 01.
DOI: 10.1002/jcp.26761
Abstrakt: Runt-related transcription factor-2 (Runx2) is essential for chondrocyte maturation during cartilage development and embryonic mandibular condylar development. The process that chondrocytes, especially a subgroup of hypertrophic chondrocytes (HC), could transform into bone cells in mandibular condyle growth makes chondrocytes crucially important for normal endochondral bone formation. To determine whether Runx2 regulates postnatal condylar cartilage growth and tissue homeostasis, we deleted Runx2 in chondrocytes in postnatal mice and assessed the consequences on temporomandibular joint (TMJ) cartilage growth and remodeling. The cell lineage tracing data provide information demonstrating the role of chondrocytes in subchondral bone remodeling. The histologic and immunohistochemical data showed that Runx2 deficiency caused condylar tissue disorganization, including loss of HC and reduced hypertrophic zone, reduced proliferative chondrocytes, and decreased cartilage matrix production. Expression of Col10a1, Mmp13, Col2a1, Aggrecan, and Ihh was significantly reduced in Runx2 knockout mice. The findings of this study demonstrate that Runx2 is required for chondrocyte proliferation and hypertrophy in TMJ cartilage and postnatal TMJ cartilage growth and homeostasis, and that Runx2 may play an important role in regulation of chondrocyte-derived subchondral bone remodeling.
(© 2018 Wiley Periodicals, Inc.)
Databáze: MEDLINE
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