Background: Osteochondral defects mostly occur as a result of trauma or articular degeneration. The poor regenerative ability of articular cartilage remains osteochondral defects are a tricky problem to deal with. The modern treatment strategies mainly focus on cartilage tissue engineering with bioactive materials. In this study, we aimed to develop icariin conditioned serum (ICS) together with hyaluronic acid (HA) and determine their ability in reparing osteochondral tissue in a critical-sized defect in rabbit knees. Methods: Primary chondrocytes were incubated with serum conditioned with icariin at different concentrations, then cell proliferation rates and glycosaminoglycan (GAG) secretion were detected. Rabbits were treated with intra-articular injection of 0.5 mL normal saline (NS), ICS, HA and ICS + HA in the right knee joint, respectively. ICRS scores were used to assess the macroscopic cartilage regeneration. Histological and immunohistochemical analysis including H&E, Safranin O, toluidine blue and collagen II staining were used to determine the repair of cartilage and the regeneration of chondrocytes. Results: Icariin at a low dose of 0.94 g/kg was identified to have significantly promoted the proliferation of chondrocytes and enhance the secretion of GAG. Femoral condyle from rabbits treated by ICS together with HA was observed to be integrated with native cartilage and more subchondral bone regeneration. ICS together with HA could promote repair of the cartilage defect and increase the neoformation of cartilage. Conclusions: These results demonstrated the potential of ICS combined with HA to promote reparative response in cartilage defects and the possible application in bioactive material based cartilage regeneration therapies.

Objective: To compare the effects of repairing and not repairing the lateral ulnar collateral ligament (LUCL) when surgically treating elbow varus posteromedial rotatory instability (PMRI).Methods: In this retrospective study spanning June 2014 to February 2019, 24 patients with elbow PMRI who were treated surgically were assigned to group RL (Repair LUCL) or group NL (Non‐repair LUCL) depending on whether the LUCL was repaired. Hospitalization time, operation time, intraoperative blood loss, and related complications were reviewed. The elbow range of motion (ROM), the visual analog scale (VAS), the Mayo elbow performance score (MEPS), and the disabilities of the arm, shoulder, and hand (DASH) score were used for functional assessment.Results: Among the 24 patients with PMRI, 15 were assigned to group RL and nine were assigned to group NL. The mean blood loss (184.66 ± 20.3 vs 207.33 ± 19.447, P < 0.001), the operation time (98.88 ± 12.693 min vs 184.66 ± 20.3 min, P < 0.001) were significantly lower in group RL compared to group NL. There were no significant differences between the two groups in time until surgery and follow‐up time (6.66 ± 1.838 vs 6.11 ± 1.900 days, 25.53 ± 2.099 vs 26.11 ± 2.891 months, P = 0.577, P = 0.486). All of the patients achieved bone union. The elbow flexion‐extension ROM (122.00° ± 3.162°vs 121.11° ± 3.333° at 12 months, P = 0.520) and pronation‐supination ROM (154.53° ± 3.335° vs 155.55° ± 4.639° at 12 months, P = 0.537). Both groups achieved similar results in MEPS score (90.53 ± 2.695 vs 89.77 ± 3.865, P = 0.578) and DASH (9.77 ± 1.897 vs 9.99 ± 1.550, P = 0.772) score at the final follow‐up. And the MEPS score revealed excellent results (87% in group RL, 89% in group NL).The VAS scores decreased significantly in group RL (from 6.13 ± 0.990 to 1.93 ± 0.593) and group NL (from 5.77 ± 1.481 to 1.88 ± 0.781), and no significant differences in preoperative or final follow‐up were observed between the two groups (P = 0.487, P = 0.876). Complications observed in group NL with one patient occurred cubital tunnel syndrome 3 months after the operation, the patient underwent ulnar nerve simple neurolysis and the symptoms were relieved after 3 weeks.Conclusion: For patients with elbow PMRI, satisfactory functional outcomes can be yielded with non‐repair of the LUCL as long as the stable elbow joint is performed during operation.

Background Osteoarthritis (OA) is a common degenerative joint disease and costly public health problem. Current treatments for OA provide only limited symptomatic benefits. The onset of OA can be a long-term silent process and the articular cartilage will likely have been damaged before the onset of typical symptoms. Therefore, better diagnostic and treatment methods are needed. Objective Chromatin regulators (CRs) are a class of regulators of epigenetics and play an important role in OA. However, the mechanisms of CRs in OA are unclear. Identifying and validating signature CRs in OA will assist in the diagnosis and treatment of OA. And it is essential to further explore the potential mechanisms by which CRs intervene in OA. Methods Firstly, the publicly available Gene Expression Omnibus database was used to download the OA-related chip data sets GSE55235 and GSE55457. Afterward, we extracted the expression matrix of chromatin regulator-related genes (CRRGs) in the OA-related data sets and screened for differentially expressed CRRGs (DECRRGs). GO and KEGG enrichment analyses were performed on the DECRRGs. Subsequently, we constructed the PPI network and screened for the key cluster network. We used three machine-learning methods to screen for potential biomarkers. Two additional OA datasets (GSE12021 and GSE1919) were used to validate the diagnostic value of these biomarkers. Then we performed an immune cell infiltration analysis. Finally, we explore the potential mechanisms through which these biomarkers intervene in OA in the context of the relevant literature published in PubMed over the last five years. Results We obtained the expression matrix for 717 CRRGs. Through differentially expressed analysis, we obtained 85 DECRRGs. By three machine-learning methods, we screened four potential biomarkers. The diagnostic value of these potential biomarkers was evaluated by two additional OA datasets (GSE12021 and GSE1919). Finally, we obtained three biomarkers (BRD4, CHD1, and KDM7A). Through immune cell infiltration analysis, we found that all these biomarkers were significantly associated with mast cells. Through reviewing the relevant literature published in PubMed in the last five years, we have initially revealed the potential mechanisms by which these biomarkers intervene in OA. Conclusion BRD4, CHD1, and KMD7A are potential biomarkers of OA. BRD4 may play an important role in the inflammatory response to OA. CHD1 and KDM7A may contribute to altered epigenetic markers in OA by affecting histone modifications. Our study laid the foundation for further studies to follow.