Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Methods Mol Biol. 2023;2598:337-344. doi: 10.1007/978-1-0716-2839-3_24.
Chondral defects are common and disabling. The development of pharmacological approaches for cartilage repair requires the availability of in vivo models which are amenable for gain and loss of function and ideally to genetic modification. In this chapter, we describe a method to induce full-thickness cartilage defects which, in young DBA/1 mice, heal spontaneously, but fail to heal in C57BL/6 mice of the same age or in aged DBA/1 mice. This model (or variants) has been used for genetic screenings to identify genes associated to repair capacity, to study stem cells involved in cartilage repair, and to study the function of molecules involved in repair mechanisms.
软骨缺损很常见且会导致功能障碍。开发用于软骨修复的药理学方法需要有适合进行功能获得和功能丧失的体内模型，理想情况下还需要有基因修饰的模型。在本章中，我们描述了一种诱导全层软骨缺损的方法，该方法可在年轻的 DBA/1 小鼠中自发愈合，但在相同年龄的 C57BL/6 小鼠或老年 DBA/1 小鼠中无法愈合。该模型（或其变体）已被用于遗传筛选，以鉴定与修复能力相关的基因，研究参与软骨修复的干细胞，并研究参与修复机制的分子的功能。
