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Cyclops nodule formation is a serious complication after anterior cruciate ligament (ACL) reconstruction. The purpose of our study was to investigate whether an increase in thymol turbidity test (TTT) values is involved in the development of cyclops nodule formation or cyclopoid scar formation following ACL reconstruction.
Medial meniscus (MM) tears are associated with both acute and chronic anterior cruciate ligament (ACL) insufficiency and can lead to degenerative changes in the knee. ACL reconstruction (ACLR) combined with the meniscal repair was reported to result in decreased anterior knee joint laxity with evidence of improved patient-reported outcomes in the long term. However, a subtle tear of the MM posterior segment, also known as a ramp lesion, is difficult to detect on conventional magnetic resonance imaging (MRI) and is frequently missed in ACL-deficient knees. However, there are few studies about the associations between bone geometry and ramp lesion of the MM. This study aimed to compare sagittal medial tibial slope (MTS), medial tibial plateau depth (MTPD), and coronal tibial slope (CTS) between ACL-injured knees with and without ramp lesion of the MM. We hypothesised that patients with ramp lesion of the MM and a concomitant ACL injury have a steeper MTS and shallower MTPD than those without ramp lesion of the MM.
Chondrogenesis and subsequent endochondral ossification are processes tightly regulated by the transcription factor Sox9 (SRY-related high mobility group-Box gene 9), but molecular mechanisms underlying this activity remain unclear. Here we report that coactivator-associated arginine methyltransferase 1 (CARM1) regulates chondrocyte proliferation via arginine methylation of Sox9.
Aging is a major risk factor of osteoarthritis, which is characterized by the degeneration of articular cartilage. CCN3, a member of the CCN family, is expressed in cartilage and has various physiological functions during chondrocyte development, differentiation, and regeneration. Here, we examine the role of CCN3 in cartilage maintenance. During aging, the expression of Ccn3 mRNA in mouse primary chondrocytes from knee cartilage increased and showed a positive correlation with p21 and p53 mRNA. Increased accumulation of CCN3 protein was confirmed. To analyze the effects of CCN3 in vitro, either primary cultured human articular chondrocytes or rat chondrosarcoma cell line (RCS) were used. Artificial senescence induced by H2O2 caused a dose-dependent increase in Ccn3 gene and CCN3 protein expression, along with enhanced expression of p21 and p53 mRNA and proteins, as well as SA-β gal activity. Overexpression of CCN3 also enhanced p21 promoter activity via p53. Accordingly, the addition of recombinant CCN3 protein to the culture increased the expression of p21 and p53 mRNAs. We have produced cartilage-specific CCN3-overexpressing transgenic mice, and found degradative changes in knee joints within two months. Inflammatory gene expression was found even in the rib chondrocytes of three-month-old transgenic mice. Similar results were observed in human knee articular chondrocytes from patients at both mRNA and protein levels. These results indicate that CCN3 is a new senescence marker of chondrocytes, and the overexpression of CCN3 in cartilage may in part promote chondrocyte senescence, leading to the degeneration of articular cartilage through the induction of p53 and p21.
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