Department of Rehabilitation, Faculty of Rehabilitation, Hiroshima International University, Higashi-Hiroshima, Hiroshima, Japan.
Major in Medical Engineering and Technology, Graduate School of Medical Technology and Health Welfare Sciences, Hiroshima International University, Higashi-Hiroshima, Hiroshima, Japan.
Cartilage. 2021 Dec;13(2_suppl):1570S-1582S. doi: 10.1177/19476035211014588. Epub 2021 May 24.
The process of anterior cruciate ligament (ACL) injury-induced meniscal tear formation is not fully understood. Clinical studies have shown that ACL reconstruction (ACLR) reduces the development of secondary meniscal tears, but it is difficult to gain insight into the protective effects of ACLR from clinical studies alone. Using rat ACL transection (ACLT) and ACLR models, we aimed to reveal (1) the formation process of meniscal tears secondary to ACLT and (2) the protective effects of ACLR on secondary meniscal tears.
ACLT surgery alone or with ACLR was performed on the knees of rats. Histomorphological and histopathological changes were examined in the posteromedial region of the meniscus in intact rats and in rats that received ACLT or ACLR up to 12 weeks postsurgery. In addition, anterior-posterior joint laxity was measured using the universal testing machine to evaluate the effects of ACLT and ACLR on joint laxity.
AAnterior-posterior laxity was significantly increased by ACLT compared to the intact knee. This ACLT-induced joint laxity was partially but significantly reduced by ACLR. Meniscal proliferation and hyaline cartilage-like tissue formation were detected in the medial meniscus at 4 weeks post-ACLT. At 12 weeks post-ACLT, hyaline cartilage-like tissue was replaced by ossicles and meniscal tears were observed. These ACLT-induced abnormalities were attenuated by ACLR.
Our results suggest that ACLT-induced joint laxity induces secondary medial meniscal tears through meniscal proliferation and ossicle formation via endochondral ossification. Joint re-stabilization by ACLR suppresses meniscal proliferation and ossicle formation and consequently prevents secondary meniscal tears.
前交叉韧带（ACL）损伤导致半月板撕裂的形成过程尚不完全清楚。临床研究表明，ACL 重建（ACLR）可减少继发性半月板撕裂的发生，但仅从临床研究很难深入了解 ACLR 的保护作用。本研究采用大鼠 ACL 切断（ACLT）和 ACLR 模型，旨在揭示（1）ACLT 后半月板继发性撕裂的形成过程，（2）ACLR 对继发性半月板撕裂的保护作用。
对大鼠膝关节行 ACLT 手术或 ACLR 手术。在术后 12 周内，观察未手术的大鼠、接受 ACLT 或 ACLR 的大鼠的半月板后内侧区域的组织形态学和组织病理学变化。此外，使用万能试验机测量前-后关节松弛度，以评估 ACLT 和 ACLR 对关节松弛度的影响。
与正常膝关节相比，ACLT 可显著增加前-后关节松弛度。ACLR 部分但显著减轻了 ACLT 引起的关节松弛。ACLT 后 4 周，内侧半月板可见增生和软骨样组织形成。ACLT 后 12 周，软骨样组织被骨赘取代，并出现半月板撕裂。ACLR 减轻了 ACLT 引起的这些异常。
我们的研究结果表明，ACLT 引起的关节松弛通过软骨内骨化诱导内侧半月板的继发性撕裂，导致半月板增生和骨赘形成。ACLR 实现关节再稳定，抑制半月板增生和骨赘形成，从而预防继发性半月板撕裂。
