Osteoarthritis (OA) is one of the most prevalent pain-inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4-week-old rats), natural degeneration (16-week-old rats) or induced degeneration (IL-1β-treated chondrocytes from 4-week-old rats) groups. Immunocytochemical analysis with β-galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism.

Knee osteoarthritis (KOA) is a chronic joint disorder involving the articular cartilage and tissues around the synovial joint. The key objective of this study was to determine the effect of miR-186-5p administration on the expression of pathogenic signalling in the chondrocytes using a surgical destabilization of the medial meniscus (DMM) model of KOA, and to testify the mechanism of P2X7-mediated regulation of RUNX2/ADAMTS5 axis by miR-186 in the KOA rats. After eight weeks of intra-articular injection of the miR-186-5p and negative control lentivirus samples, the knee cartilage tissues were subjected to histopathological analysis Safranin-O/Fast green staining. Further, the articular chondrocytes were separated and analysed for various proteins including P2X7, cathepsin-K, RUNX2 and ADAMTS5 using Western blotting method. We observed that the protein expressions of P2X7, cathepsin-K/RUNX2/ADAMTS5, and also MMP-13 were upmodulated in the KOA rats, while intra-articular miR-186-5p lentivirus administration prevented these aberrations. Hence, the study concludes that miR-186 orchestrates P2X7 expression and the P2X7-mediated cathepsin-K/RUNX2/ADAMTS5 axis and regulates the pathogenesis of KOA. In light of this evidence, we propose that molecular therapeutic interventions targeting miR-186 activation might attenuate osteoarthritic cartilage degeneration.

Perioperative visual loss (POVL) is an infrequent, devastating complication. Increased recognition and discussion of this complication is reported in recent literature, most notably following spinal and cardiac surgery. The most common causes are ischemic optic neuropathy, central retinal artery occlusion, and cortical blindness. Here, we present a case of a 54 y old female who developed acute visual loss in her eyes after lateral position total hip arthroplasty that might explain this complication.