Shigley Christian, Trivedi Jay, Meghani Ozair, Owens Brett D, Jayasuriya Chathuraka T
The Warren Alpert Medical School, Brown University, Providence, RI 02903, USA.
Department of Orthopaedics, Alpert Medical School of Brown University, Rhode Island Hospital, Providence, RI 02903, USA.
Bioengineering (Basel). 2023 Jun 20;10(6):741. doi: 10.3390/bioengineering10060741.
Current clinical strategies for restoring cartilage defects do not adequately consider taking the necessary steps to prevent the formation of hypertrophic tissue at injury sites. Chondrocyte hypertrophy inevitably causes both macroscopic and microscopic level changes in cartilage, resulting in adverse long-term outcomes following attempted restoration. Repairing/restoring articular cartilage while minimizing the risk of hypertrophic neo tissue formation represents an unmet clinical challenge. Previous investigations have extensively identified and characterized the biological mechanisms that regulate cartilage hypertrophy with preclinical studies now beginning to leverage this knowledge to help build better cartilage. In this comprehensive article, we will provide a summary of these biological mechanisms and systematically review the most cutting-edge strategies for circumventing this pathological hallmark of osteoarthritis.
目前修复软骨缺损的临床策略并未充分考虑采取必要措施来预防损伤部位肥厚组织的形成。软骨细胞肥大不可避免地会导致软骨在宏观和微观层面发生变化,从而在尝试修复后产生不良的长期后果。在将肥厚性新组织形成的风险降至最低的同时修复/恢复关节软骨是一项尚未解决的临床挑战。先前的研究已经广泛地确定并描述了调节软骨肥大的生物学机制,目前临床前研究开始利用这些知识来帮助构建更好的软骨。在这篇全面的文章中,我们将总结这些生物学机制,并系统地回顾规避骨关节炎这一病理特征的最前沿策略。