The meniscus plays an important role in knee joint diseases such as osteoarthritis (OA). Meniscal injuries can be accompanied by joint catabolic events initiated by inflammation, leading to articular cartilage destruction, but the cellular events responsible for intrinsic meniscal injury and the extracellular matrix changes necessary for meniscal degradation are not well known.
To explore the cellular and matrix-related changes of menisci based on a mouse OA model of anterior cruciate ligament transection (ACLT).
Controlled laboratory study.
A mouse ACLT OA model was established by transection of anterior cruciate ligaments on the right knee joints of 8-week-old male (n = 34) and female (n = 34) C57 mice. The knee joints were collected at 1, 2, 4, and 8 weeks after ACLT surgery, and the meniscal changes were analyzed by radiography, histology, immunohistochemistry, immunoblot, and quantitative real-time polymerase chain reaction.
The deterioration of menisci was more extensive than that of articular cartilage and subchondral bone at 4 weeks after ACLT surgery. The rapid loss of collagen II and Sox9 in chondrocyte-like cells in the white-white zone of menisci was confirmed, and the activation of potential meniscus progenitor cells and chondroblasts was identified based on the increase of CD90, CD105, and Runx2. Further, the intrinsic inflammation in the bone marrow-like zone of menisci was activated by enhancement of dendritic cells (CD11c
This study provides support for better protection of menisci in ACL injury-induced conditions such as OA and indicates that menisci should be considered in the development of clinical pharmacological interventions.
ACLT-induced meniscal changes not only could explain the contribution of the meniscus to the progress of OA but also could provide a cue for initiation of preventive treatments in the early stages of OA.