Circular RNAs (circRNAs) are involved in the development of various diseases, but there is little knowledge of circRNAs in osteoarthritis (OA). The aim of study was to identify circRNA expression in articular cartilage and to explore the function of chondrocyte extracellular matrix (ECM)-related circRNAs (circRNA-CER) in cartilage. To identify circRNAs that are specifically expressed in cartilage, we compared the expression of circRNAs in OA cartilage with that in normal cartilage. Bioinformatics was employed to predict the interaction of circRNAs and mRNAs in cartilage. Loss-of-function and rescue experiments for circRNA-CER were performed in vitro. A total of 71 circRNAs were differentially expressed in OA and normal cartilage. CircRNA-CER expression increased with interleukin-1 and tumor necrosis factor levels in chondrocytes. Silencing of circRNA-CER using small interfering RNA suppressed MMP13 expression and increased ECM formation. CircRNA-CER could compete for miR-136 with MMP13. Our results demonstrated that circRNA-CER regulated MMP13 expression by functioning as a competing endogenous RNA (ceRNA) and participated in the process of chondrocyte ECM degradation. We propose that circRNA-CER could be used as a potential target in OA therapy.

Objective: Long noncoding RNAs (lncRNAs) play crucial regulatory roles in diverse biologic processes, but knowledge of lncRNAs in osteoarthritis (OA) is limited. The aim of this study was to identify lncRNA expression in articular cartilage and to explore the function of cartilage injury–related lncRNAs (lncRNA‐CIR) in OA.Methods: To identify lncRNAs specifically expressed in OA cartilage, we compared the expression of lncRNAs in OA cartilage with that in normal cartilage using microarray and quantitative polymerase chain reaction (qPCR) analyses. In OA cartilage, lncRNA‐CIR was specifically, differentially, and highly expressed. The function of lncRNA‐CIR was determined by silencing and overexpression in vitro. Extracellular matrix (ECM)–related molecules were detected by qPCR, Western blot, and immunofluorescence analyses.Results: Up to 152 lncRNAs were found to be differentially expressed (>8‐fold) in OA and normal cartilage (82 lncRNAs more highly expressed and 70 less highly expressed in OA cartilage than in normal cartilage). A specific differentially expressed lncRNA‐CIR was selected according to the results of the higher expression in OA cartilage and OA chondrocytes. The expression of lncRNA‐CIR increased in chondrocytes with in vitro treatment with interleukin‐1β and tumor necrosis factor α. Silencing of lncRNA‐CIR by small interfering RNA promoted the formation of collagen and aggrecan and reduced the expression of matrix‐degrading enzymes, such as MMP13 and ADAMTS5. The expression of collagen and aggrecan was reduced, whereas the expression of matrix‐degrading enzymes was increased, after overexpression of lncRNA‐CIR.Conclusion: The results indicate that lncRNA‐CIR contributes to ECM degradation and plays a key role in the pathogenesis of OA. We propose that lncRNA‐CIR could be used as a potential target in OA therapy.

Circular RNAs (circRNAs) are involved in the development of various diseases; however, knowledge on circRNAs in osteoarthritis (OA) is limited. This study aims to identify circRNA expression in different regions affected by OA and to explore the function of mechanical stress-related circRNAs (circRNAs-MSR) in cartilage. Bioinformatics was employed to predict the interaction of circRNAs and mRNAs in the cartilage. Loss-of-function experiments for circRNAs-MSR were performed in vitro. A total of 104 circRNAs were differentially expressed in damaged versus intact cartilage. Of these circRNAs, 44 and 60 were upregulated and downregulated, respectively, in the damaged tissue. circRNA-MSR expression increased under mechanical stress in chondrocytes. circRNAs-MSR were silenced using small interfering RNA, and knockdown of circRNAs-MSR could suppress tumor necrosis factor alpha (TNF-α) expression and increase extracellular matrix (ECM) formation. Our results demonstrated that circRNAs-MSR regulated TNF-α expression and participated in the chondrocyte ECM degradation process. We propose that the inhibition of circRNAs-MSR could inhibit the degradation of chondrocyte ECM and knockdown of circRNAs-MSR could be a potential therapeutic target for OA.

Mechanical stress plays a key role in the development of cartilage degradation in osteoarthritis (OA). Nevertheless, the role of long noncoding RNAs in mechanical stress-induced regulation of chondrocytes remains unclear. The aim of this study was to explore the function of mechanical stress-related long noncoding RNAs in cartilage. Tissue samples were collected from 50 patients and chondrocytes were exposed to cyclic tensile strain (CTS). A total of 107 lncRNAs were differentially expressed in damaged cartilage versus intact cartilage. Of these lncRNAs, 51 were upregulated and 56 were downregulated in the damaged tissue. The TMSB4 pseudogene, lncRNA-MSR, was upregulated in the damaged cartilage and was activated in chondrocytes in response to mechanical stress. Furthermore, lncRNA-MSR regulated the expression of TMSB4 by competing with miRNA-152 in chondrocytes. Our results demonstrated that upregulation of lncRNA-MSR initiates pathological changes that lead to cartilage degradation, and the inhibition of lncRNA-MSR could represent a potential therapeutic target for OA.

Mechanical factors play a key role in regulating the development of cartilage degradation in osteoarthritis. This study aimed to identify the influence of mechanical stress in cartilage and chondrocytes. To explore the effects of mechanical stress on cartilage morphology, we observed cartilages in different regions by histological and microscopic examination. Nanoindentation was performed to assess cartilage biomechanics. To investigate the effects of mechanical stress on chondrocytes, cyclic tensile strain (CTS, 0.5 Hz, 10%) was applied to monolayer cultures of human articular chondrocytes by using Flexcell-5000. We quantified the mechanical properties of chondrocytes by atomic force microscopy. Chondrocytes were stained with Toluidine blue and Alcian blue after exposure to CTS. The expression of extracellular matrix (ECM) molecules was detected by qPCR and immunofluorescence analyses in chondrocytes after CTS. Our results demonstrated distinct morphologies and mechanical properties in different cartilage regions. In conclusion, mechanical stress can affect the chondrocyte phenotype, thereby altering the expression of chondrocyte ECM.

Background: Some studies have advocated the use of suture button fixation during Bristow-Latarjet surgery to reduce complications associated with screw fixation. However, data comparing these fixation methods are relatively incomplete. Purpose: To investigate the efficacy of modified arthroscopic Bristow-Latarjet surgery and compare the clinical and radiographic outcomes using screw versus suture button fixation. Study Design: Cohort study; Level of evidence, 3. Methods: We evaluated 136 patients with traumatic anterior shoulder instability who underwent the modified arthroscopic Bristow-Latarjet surgery between June 2015 and February 2018. Of these patients, 117 who met the inclusion criteria were enrolled at a mean follow-up of 3.3 ± 0.7 years. Shoulders were separated into 2 groups based on fixation technique: screw fixation (group A; n = 63) or suture button fixation (group B; n = 54). Computed tomography imaging findings and clinical results were assessed preoperatively; immediately after operation; and postoperatively at 3 months, 6 months, 1 year, and final follow-up. Results: There were no significant differences between the groups in terms of postoperative clinical scores, the level of return to sports, range of motion, graft position, or reoperation rates. Bone healing was observed in 97.4% of the cases overall (114/117), with 98.4% bone union in group A and 96.3% in group B at final follow-up. Bone absorption was more common in group A (n = 30; 47.6%) compared with group B (n = 10; 18.5%) ( P = .003). There were no hardware-related complications in group B, compared with 7.9% of patients in group A ( P = .034). One patient in group B had a recurrent dislocation due to an unexpected event, and there were no recurrent dislocations in group A. Conclusion: After the modified arthroscopic Bristow-Latarjet procedure, both suture button and screw fixation methods demonstrated high bony healing rates and low risk of recurrence. Less coracoid graft resorption and no hardware-related complications were seen with suture button fixation.