Background:The clinical efficacy of reverse shoulder arthroplasty (RSA), hemiarthroplasty (HA), and non-surgical management in the treatment of proximal humeral fractures (PHFs) is inconclusive. This systematic review and meta-analysis compared the clinical outcomes of arthroplasty and non-surgical management of PHFs. Methods:The databases of PubMed, Embase, Web of Science, and Cochrane Library were searched on 5 May 2023 for studies comparing arthroplasty and non-surgical treatment of PHFs. Both randomized controlled trials (RCTs) and non-randomized controlled trials (nRCTs), were included. Standard methodological quality assessments were conducted for both types of studies. The primary outcome was the Constant-Murley Score (CMS) after surgical or non-surgical treatment. Secondary study outcomes included the visual analog scale (VAS), range of motion, and complications. All functional scores and complications were subjected to subgroup and sensitivity analyses. Results:A total of four RCTs and six nRCTs were included in this study, which provided 508 patients in total for meta-analysis: 238 treated with arthroplasty and 270 treated non-surgically, of which 83 were treated with HA and 155 with RSA. All relevant information was collected, including functional scores, VAS, range of motion, and complications. The study found no significant difference in functional outcomes (mean difference, 2.82; 95% confidence interval, -0.49 to 6.14; P = 0.10; I 2 = 77%) and complications (mean difference, 1.08; 95% confidence interval, 0.51-2.25; P = 0.85; I 2 = 47%) between arthroplasty and non-surgical treatment. Both RCTs and nRCTs showed the same results. However, VAS scores were significantly lower in surgical treatment compared to non-surgical treatment. Subgroup and sensitivity analyses showed that RSA could achieve better functional scores than non-surgical treatment (mean difference, 6.00; 95% confidence interval, 1.97-10.03; P = 0.004; I 2 = 0%), while the results for HA were not significant (P > 0.05). Conclusion:There were no significant differences in complications between arthroplasty and non-surgical treatment for PHFs. RSA could achieve better functional results than non-surgical treatment, while HA could only achieve better forward flexion.

目的:探讨岭南伤科验方联合椎旁封闭治疗骨质疏松性中位胸椎骨折PVP术后残余痛的临床疗效.方法:选取2021年1月至2022年1月我院收治的40例骨质疏松性中位胸椎骨折PVP术后残余痛患者,按照随机数字法,分为对照组与治疗组各30例.治疗组采用岭南伤科验方口服,配合椎旁封闭.对照组采用龙血竭胶囊口服,配合病变椎体两侧膀胱经的穴位针刺,疗程14天.比较治疗前后胸背痛视觉模拟评分法(VAS)、卧床下地时间、Oswestry功能障碍指数(ODI).结果:与治疗前相比,两组VAS评分、卧床下地时间、ODI明显下降,比较有显著性差异(P<0.05),且治疗组比对照组改善明显(P<0.05).结论:岭南伤科验方联合椎旁封闭治疗骨质疏松性中位胸椎骨折PVP术后残余痛的疗效优越,且安全性良好.

Osteoporosis, which typically affects postmenopausal women, is an osteolytic disease due to over-activation of osteoclasts. However, current drugs targeting osteoclast inhibition face various side effects, making natural compounds with great interest as alternative treatment options. Cycloastragenol (CAG) is a triterpenoid with multiple biological activities. Previously, CAG's activity against aging-related osteoporosis was reported, but the mechanisms of actions for the activities were not understood. This study demonstrated that CAG dose-dependently inhibited osteoclast formation in receptor activator of nuclear factor-κB ligand (RANKL)-stimulated bone marrow macrophage (BMMs). Mechanism studies showed that CAG inhibited NF-κB, calcium, and nuclear factor of activated T cells 1 (NFATc1) pathways. Additionally, CAG also promoted the nuclear factor-erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1)/anti-oxidative response element (ARE) pathway that scavenges reactive oxygen species (ROS). Furthermore, CAG was also found to prevent bone loss of postmenopausal osteoporosis (PMO) in a preclinical model of ovariectomized (OVX) mice. Collectively, our research confirms that CAG inhibits the formation and function of osteoclasts by regulating RANKL-induced intracellular signaling pathways, which may represent a promising alternative for the therapy of osteoclast-related disease.

Aims: Tert-butylhydroquinone (tBHQ) has been identified as an inhibitor of oxidative stress-induced injury and apoptosis in human neural stem cells. However, the role of tBHQ in osteoarthritis (OA) is unclear. This study was carried out to investigate the role of tBHQ in OA. Methods: OA animal model was induced by destabilization of the medial meniscus (DMM). Different concentrations of tBHQ (25 and 50 mg/kg) were intraperitoneally injected in ten-week-old female mice. Chondrocytes were isolated from articular cartilage of mice and treated with 5 ng/ml lipopolysaccharide (LPS) or 10 ng/ml interleukin 1 beta (IL-1β) for 24 hours, and then treated with different concentrations of tBHQ (10, 20, and 40 μM) for 12 hours. The expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in blood were measured. The expression levels of interleukin 6 (IL-6), IL-1β, and tumour necrosis factor alpha (TNF-α) leptin in plasma were measured using enzyme-linked immunoabsorbent assay (ELISA) kits. The expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathway proteins, and macrophage repolarization-related markers, were detected by western blot. Results: Tert-butylhydroquinone significantly attenuated cartilage destruction in DMM-induced mice in vivo. It demonstrated clear evidence of inhibiting IL-1β-induced chondrocyte apoptosis, inflammation, and differentiation defect in vitro. Meanwhile, tBHQ inhibited LPS-induced activation of NF-κB and MAPK signalling pathways, and also inhibited LPS-induced reactive oxygen species production and macrophages repolarization in vitro. Conclusion: Taken together, tBHQ might be a potential therapeutic strategy for protecting against OA development. Cite this article: Bone Joint Res 2021;10(11):704–713.