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Front. Bioeng. Biotechnol. | doi: 10.3389/fbioe.2018.00018

Recent insights into the contribution of the changing hypertrophic chondrocyte phenotype in the development and progression of osteoarthritis.

  • 1Orthopedic Surgery, Maastricht University Medical Centre, Netherlands

Osteoarthritis is an extremely prevalent age-related condition. The economic and societal burden due to the cost of symptomatic treatment, inability to work, joint replacement and rehabilitation is huge and increasing. Currently there are no effective medical therapies that delay or reverse the pathological manifestations of osteoarthritis. Current treatment options are, without exception, focused on slowing down progression of the disease to postpone total joint replacement surgery for as long as possible and keeping the associated pain and joint immobility manageable. Alterations in the articular cartilage chondrocyte phenotype might be fundamental in the pathological mechanisms of osteoarthritis development. In many ways the changing chondrocyte phenotype in osteoarthritic cartilage resembles the process of endochondral ossification as seen, for instance, in developing growth plates. However, the relative contribution of endochondral ossification to the changing chondrocyte phenotype in the development and progression of osteoarthritis remains poorly described. In this review we will discuss the current knowledge regarding the cartilage endochondral phenotypic changes occurring during osteoarthritis development and progression, as well as the molecular and environmental effectors driving these changes. Understanding how these molecular mechanisms determine the chondrocyte cell fate in osteoarthritis will be essential in enabling cartilage regenerative approaches in future treatments of osteoarthritis.

Keywords: Chondrocytes, Osteoarthritis, Hypertrophy, Cartilage, phenotype, endochondral ossification

Received: 18 Dec 2017; Accepted: 08 Feb 2018.

Edited by:

Eric Farrell, Erasmus University Rotterdam, Netherlands

Reviewed by:

Katherine A. Staines, Edinburgh Napier University, United Kingdom
Andrea Lolli, Erasmus Medical Center, Erasmus University Rotterdam, Netherlands  

Copyright: © 2018 Ripmeester, Tan Timur, Caron and Welting. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: PhD. Tim J. Welting, Maastricht University Medical Centre, Orthopedic Surgery, PO Box 5800, Maastricht, 6202 AZ, Netherlands, t.welting@maastrichtuniversity.nl