I.-Ming Jou

Aims: Tendinopathy is a pathological condition characterized by pain and significant dysfunction, with its pathogenesis involving various factors including chronic inflammation, cellular senescence, and apoptosis. Previous research indicates that blocking CD44 signalling exacerbates apoptosis and inflammation in tendinopathic tenocytes. Furthermore, microRNA-146a (miR-146a) has been shown to counteract interleukin-1β (IL)-1β-induced senescence in these cells, and is upregulated by CD44 in knee osteoarthritis. Therefore, this study aimed to investigate the CD44-miR-146a signalling axis in regulating apoptosis in tendinopathy. Methods: Lentiviral vectors (LVs) were used to overexpress CD44 cDNA (LVCD44) and miR-146a precursor (LVmiR-146a) in rat primary tendinopathic tenocytes and tendons. Apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining. To dissect the CD44-AKT-miR-146a signalling pathway, the PI3K/AKT inhibitor LY294002 and the CD44 antagonizing antibody OX-50 were used. In situ hybridization (ISH) and immunohistochemistry (IHC) were performed to examine the pathway’s effect on Smad4 expression in tendinopathic tenocytes and tendons. Results: Overexpression of CD44 and miR-146a in tendinopathic tenocytes resulted in significantly reduced apoptosis compared to controls. The CD44-AKT-miR-146a signalling axis was found to mitigate apoptosis in IL-1β-stimulated tenocytes and in a rat model of collagenase-induced Achilles tendinopathy, primarily by suppressing Smad4 expression. Conclusion: This study highlights the protective role of the CD44-AKT-miR-146a axis in tendinopathy. By modulating the AKT/miR-146a/Smad4 signalling pathway, CD44 and miR-146a effectively reduce apoptosis in tendinopathic tenocytes and tendons. Cite this article: Bone Joint Res 2026;15(1):88–97.

Background: de Quervain’s disease is a well-recognized tendon disorder affecting the wrist, yet its pathogenesis remains poorly understood. Some research indicates that the disease may stem from intrinsic degeneration, while others suggest an inflammatory component. Autophagy, often initiated by oxidative stress, plays a critical role in both degenerative and inflammatory conditions and could be a significant factor in de Quervain’s disease. However, the role of autophagy in this disease has not been previously explored. This study aims to investigate the involvement of oxidative stress in de Quervain’s disease. Methods: Specimens from the first dorsal retinaculum were collected from 45 patients diagnosed with de Quervain’s disease for analysis. These specimens were classifed into mild, moderate, and severe groups based on disease severity. Results: The analysis revealed that levels of IL-6, LC-3, beclin-1, and Malondialdehyde (MDA) in the retinaculum specimens correlated positively with the severity of de Quervain’s disease. Furthermore, nitric oxide and lipid peroxidation levels were significantly elevated in the severe group compared to the moderate and mild groups. Conclusion: The results suggest that autophagy-related to oxidative stress may be a key factor in the pathogenesis and progression of de Quervain’s disease. Therefore, antioxidants could be potentially useful in managing and preventing the progression of de Quervain’s disease.Cite this article as: Chiu Y, Hsieh T, Ma C, Jou I, Wu C. Oxidative stress-associated autophagy correlates to the disease severity of de Quervain’s disease.Eur J Rheumatol. 2025, 12(3), 0053, doi:10.5152/eurjrheum.2025.24053.

Aims: This study aimed to evaluate the effects of Nd:YAG laser treatment on fracture healing in a rat model. We hypothesized that laser therapy would accelerate healing by stimulating early neovascularization and osteoblast recruitment.Methods: A total of 54 male Sprague-Dawley rats received intramedullary Kirschner wire (K-wire) osteosynthesis following femoral osteotomy, and were randomly divided into two groups (n = 27 each): the control group, and the laser group that received daily pulsed Nd:YAG laser for ten days immediately after osteotomy. Fracture sites were assessed using micro-CT (μCT; n = 8 at each timepoint), histology (n = 4), and three-point bending tests (n = 4) at week 2, week 4, and week 6, respectively. At week 2, an additional three rats per group were selected for the western blot tests.Results: Compared to controls, the laser group showed higher vascular endothelial growth factor (VEGF), CD31, and Runx2 protein expression, and significantly higher neovascular area density and osteoblast density (p = 0.025 and p = 0.008, respectively) at week 2. At week 4, the laser treatment led to higher histological fracture healing scale and flexural modulus, and less strain (p = 0.001, p = 0.020, and p = 0.004, respectively). Macroscopically, the laser group showed higher mature bone volume fraction and radiological union score at weeks 4 and 6 (volume fraction: p = 0.017 and p = 0.001; union score: p = 0.001 and p = 0.024, respectively).Conclusion: Pulsed Nd:YAG laser therapy accelerates multiple quantitative indicators of fracture healing within six weeks in a rat femoral osteotomy model, which was associated with enhanced angiogenesis and osteogenesis during the early healing phase.Cite this article: Bone Joint Res 2025;14(5):376–388.

Joint Diseases and Related Surgery (JDRS), the official journal of the Turkish Joint Diseases Foundation, is an international, peer-reviewed, immediate open access journal. All published articles in JDRS has been free for everyone, without embargo, since 1990.

Background: This study aimed to evaluate the outcome of using an External Joint Stabilizer – Elbow (EJS-E) for persistent elbow instability based on biomechanical experiments and analysis of clinical results. Methods: An EJS-E was used in 17 elbow instability patients. The median follow-up was 26 months (range, 12–42 months). We evaluated the flexion–extension and pronation-supination movement arcs, visual analog scale (VAS) score, Mayo Elbow Performance Score (MEPS), Broberg and Morrey classification system, and occurrence of complications in these patients. Moreover, construct stiffness and maximum strength tests were performed to evaluate the strength of the fixation techniques. Results: The final median range of the extension-to-flexion and pronation-to-supination arc of the elbow was 135° (range, 110°–150°) and 165° (range, 125°–180°), respectively. The VAS pain scores were > 3 in two patients. The median MEPS was 90 (range, 80–100 points). Five patients showed signs of grade I post-traumatic osteoarthritis according to the Broberg and Morrey radiographic classification system, while grade II changes were observed in three patients. Complications included axis pin loosening with pin-tract infection in two patients, transient ulnar nerve symptoms in two patients, heterotopic ossification in two patients, and suture anchors infection in one patient. Based on the biomechanical testing results, the EJS-E exhibited higher stiffness and resisting force in varus loading. It was 0.5 (N/mm) stiffer and 1.8 (N·m) stronger than the internal joint stabilizer (IJS) by difference of medians (p < 0.05). Conclusions: Biomechanical and clinical outcomes show that EJS-E via the posterior approach can restore mobility and stability in all patients, thus serving as a valuable alternative option for the treatment of persistent instability of the elbow.

Delayed-onset muscle soreness (DOMS) is associated with exercise-induced muscle damage and inflammation, which is mainly caused by prolonged eccentric exercise in humans. Triptolide, an extract from the Chinese herb Tripterygium wilfordii Hook F, has been used for treating autoimmune and inflammatory diseases in clinical practice. However, whether triptolide attenuates acute muscle damage is still unclear. Here, we examined the effect of triptolide on carrageenan-induced DOMS in rats. Rats were injected with 3% of carrageenan into their muscles to induce acute left gastrocnemius muscular damage, and triptolide treatment attenuated carrageenan-induced acute muscular damage without affecting hepatic function. Triptolide can significantly decrease lipid hydroperoxide and nitric oxide (NO) levels, proinflammatory cytokine production, and the activation of nuclear factor (NF)-ĸB, as well as increase a reduced form of glutathione levels in carrageenan-treated rat muscles. At the enzyme levels, triptolide reduced the inducible nitric oxide synthase (iNOS) expression and muscular myeloperoxidase (MPO) activity in carrageenan-treated DOMS rats. In conclusion, we show that triptolide can attenuate muscular damage by inhibiting muscular oxidative stress and inflammation in a carrageenan-induced rat DOMS model.

We read with great interest the study by Lin et al [1] investigating the potential effect of gallstone disease (GSD) on the long-term risk of subsequent hip fracture. Lin et al [1] provided valuabl...

Letter for the article The Risk of Gout in Patients with Psoriasis: A Population-Based Cohort Study in Taiwan