Haixiao Liu

Background: Nocturnal pain is a common symptom in patients with subacromial bursitis (SAB), yet its underlying determinants and optimal management remain unclear. Purpose: To evaluate the impact of bursal pathological and morphological features on nocturnal pain and the effectiveness of arthroscopic bursectomy. Study Design: Cohort Study; Level of evidence, 2. Methods: A total of 130 patients were initially enrolled for arthroscopic surgery between January and July 2025. Five patients were lost to follow-up, leaving 125 patients for analysis. Preoperative baseline characteristics and intraoperative bursal features—including morphological classifications (filamentous, reticular, septate, and fullness type) and pathological types (hyperemic and fibrofatty)—were recorded. Nocturnal pain was assessed using the visual analog scale preoperatively and at 4 and 12 weeks postoperatively. Data were analyzed using Friedman and Gamma regression tests. Results: Nocturnal pain declined substantially after arthroscopic bursectomy, with clear improvements from preoperative assessment to 4 and 12 weeks postoperatively. Fullness-type bursal morphology was associated with significantly greater pain burden, showing a 22% increase compared with the filamentous reference type, whereas reticular and septate morphologies did not differ significantly. Pathological findings were strongly related to symptom severity. Compared with patients exhibiting no pathological features, those with “both positive” pathology reported 29% higher pain scores, followed by fibrofatty (16% higher) and hyperemic pathology (13% higher). No meaningful associations were observed for patient age, sex, or body mass index. Conclusion: Hyperemic, fibrofatty, and “both positive” pathological features, as well as fullness-type bursal morphology, are strongly associated with higher nocturnal pain in patients with SAB. Arthroscopic bursectomy yields rapid and sustained symptom relief, supporting its role as an effective treatment option for patients who do not respond to conservative management.

Background: Glucocorticoids (GCs) overuse is associated with decreased bone mass and osseous vasculature destruction, leading to severe osteoporosis. Platelet lysates (PL) as a pool of growth factors (GFs) were widely used in local bone repair by its potent pro-regeneration and pro-angiogenesis. However, it is still seldom applied for treating systemic osteopathia due to the lack of a suitable delivery strategy. The non-targeted distribution of GFs might cause tumorigenesis in other organs.Results: In this study, PL-derived exosomes (PL-exo) were isolated to enrich the platelet-derived GFs, followed by conjugating with alendronate (ALN) grafted PEGylated phospholipid (DSPE-PEG-ALN) to establish a bone-targeting PL-exo (PL-exo-ALN). The in vitro hydroxyapatite binding affinity and in vivo bone targeting aggregation of PL-exo were significantly enhanced after ALN modification. Besides directly modulating the osteogenic and angiogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and endothelial progenitor cells (EPCs), respectively, PL-exo-ALN also facilitate their coupling under GCs’ stimulation. Additionally, intravenous injection of PL-exo-ALN could successfully rescue GCs induced osteoporosis (GIOP) in vivo.Conclusions: PL-exo-ALN may be utilized as a novel nanoplatform for precise infusion of GFs to bone sites and exerts promising therapeutic potential for GIOP.Graphical

The random-pattern skin flap is a crucial technique in reconstructive surgery and flap necrosis caused by ischemia/reperfusion injury is a major postoperative complication. Herein, we investigated the mechanism of mitophagy induced by Melatonin (ML) and its effect on the survival of skin flaps. Our results demonstrated that ML could activate mitophagy, ameliorate oxidative stress and alleviate apoptosis in Tert-Butyl hydroperoxide solution (TBHP)-stimulated human umbilical vein endothelial cells in vitro. Inhibiting ML-induced mitophagy considerably abolished its protective effects. Moreover, knockdown of Parkin by siRNA inhibited ML-induced mitophagy, and subsequently exacerbated oxidative stress and apoptosis. Further study demonstrated that inhibition of AMPK reversed these protective effects of ML and downregulated the expression of TFEB. In the vivo study, ML effectively promoted flap survival by activating mitophagy and subsequently ameliorating oxidative stress and mitigating apoptosis. These results established that ML is a potent agent capable for increasing random-pattern skin flap survival by activating Parkin-dependent mitophagy through the AMPK-TFEB signaling pathway.

Background: No evaluation has been done on the relationship of the acromion–greater tuberosity impingement index (ATI) with retear after arthroscopic rotator cuff repair (ARCR). Our purpose was to evaluate whether a higher ATI is associated with retear after ARCR. Methods: 132 patients received ARCR and underwent MRI scan at a one year follow-up to assess tendon healing, and the findings were graded no retear (NR), partial-thickness retear (PR) or full-thickness retear (FR). The ATI, the critical shoulder angle (CSA), acromion index (AI) and lateral acromial angle (LAA) were measured with postoperative radiographs. Functional scores were obtained preoperatively and at a one year follow-up. Results: Postoperative Constant scores and ASES scores were significantly different between groups with inferior outcomes in the FR group ( p < 0.05 for all). The UCLA score was significantly better in the NR group compared with the PR and FR groups ( p < 0.05), and in the PR group compared with the FR group ( p < 0.05). For ATI and CSA, the values of the PR and FR groups were larger than the NR group ( p < 0.05 for all), but there were no significant differences between the PR and FR groups ( p > 0.05 for all). No significant differences were observed with regard to the AI and LAA ( p > 0.05, respectively). The repair integrity was positively related to the ATI (0.304, p < 0.05) and CSA (0.252, p < 0.05), but not related to the AI or LAA ( p > 0.05 for both). ATI was not related to any functional scores ( p > 0.05 for all). Conclusion: This study revealed that the ATI was positively related to rotator cuff retear. Patients with retears had significantly greater ATIs after ARCR. Level of Evidence: III, case–control study.

Osteoarthritis (OA) is one of the most common degenerative diseases, ultimately leading to long-term joint pain and severe articular malformation. Controlling local chronic inflammation is a crucial strategy for delaying OA development. Linarin is a natural flavonoid glycoside that is widely available in Compositae, Chrysanthemum indicum and Dendrocalamus and processes protective effects in several animal models. The purpose of our work was to study the protective effect of Linarin for OA. Cellular experiments data showed that Linarin suppressed lipopolysaccharide (LPS)-caused the overproduction of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) in chondrocyte. In addition, LPS-stimulated expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide nitrate (iNOS) was decreased by Linarin pre-treatment. Together, Linarin prevented the catabiosis of extracellular matrix caused by LPS. For mechanism, Linarin inhibited the formation of Toll-like receptor 4 (TLR4) / myeloid differentiation protein-2 (MD-2) dipolymer complex and subsequently intervened NF-κB activation. Our mouse DMM model further clarified the protection of Linarin in vivo. In summary, our results suggested that Linarin may be a potential effective agent for OA.

Oxidative stress-mediated excessive apoptosis and senescence of chondrocytes are the main pathological alterations in the osteoarthritis (OA) development. The protective effects of theaflavin (TF), a common group of polyphenols in black tea, against many degenerative diseases by attenuating oxidative stress are well reported. Nevertheless, its role in the OA treatment is still scantily understood. In the current research, by applying enzyme-linked immunosorbent assay (ELISA) kits and immunofluorescent staining, TF treatment was found to inhibit tert-Butyl hydroperoxide (TBHP)-induced imbalance of anabolism and catabolism in primary mouse chondrocytes. Then, according to western blot, live-dead staining, and SA-β-gal staining, the dramatically increased level of apoptosis and senescence of chondrocytes in response to TBHP was also found to be reduced by TF administration. With regard to upstream signaling investigation, the in vitro molecular binding analysis indicated that the beneficial effects of TF might be related to the regulation of the Keap1/Nrf2/HO-1 axis. Furthermore, the Silencing of Nrf2 resulted in the abolishment of the anti-apoptosis and anti-senescence effects of TF. In addition, the oral administration of TF was demonstrated to ameliorate osteoarthritis development in a surgically induced mouse OA model. Taken together, these results suggest that TF might be a promising therapeutic option for the treatment of OA.

The imbalance between the anabolism and catabolism of the extracellular matrix (ECM) is of great importance to osteoarthritis (OA) development. Aberrant inflammatory responses and hypertrophic changes of chondrocytes are the main contributors to these metabolic disorders. In the present study, we found that Oroxylin A (ORA), a flavonoid compound derived from Oroxylum indicum, maintained ECM hemostasis of chondrocytes by Interleukin-1β (IL-1β) stimulation. Besides, it was demonstrated that IL-1β induced over-production of inflammatory mediators was attenuated by ORA treatment. Moreover, ORA could rescue IL-1β mediated hypertrophic alterations of chondrocytes. Mechanistically, ORA's protective effects were found to be associated with both NF-κB and Wnt/β-catenin signaling inhibition. Meanwhile, molecular docking analysis revealed that ORA could strongly bind to the inhibitor kappa B kinaseβ (IKKβ) and dishevelled, Dsh Homolog 2 (Dvl2), the upstream molecules of the NF-κB axis and β-catenin axis, respectively. In addition, ORA driven chondroprotective effects were also affirmed in a surgically induced OA mouse model. Taken together, the current study suggested that ORA might be a promising therapeutic option for the treatment of OA.

Obesity is related to osteoarthritis (OA). Aberrant lipid metabolism results in increased levels of free fatty acids, such as palmitate (PA), leading to inflammatory responses and excess catabolism of chondrocytes. Asiatic acid (AA), a plant anti-inflammatory compound, has been reported to exert protective effects for several diseases, but its effect on obesity-related OA is still unclear. The aim of this study is to evaluate the chondro-protective effect of AA on PA-induced human chondrocytes and a high fat diet (HFD)-fed mouse cartilage degeneration model. In vitro, the levels of the inflammatory and extracellular matrix (ECM) markers of chondrocytes after being treated with PA (500 μM) and AA (2.5–10 μM) were determined using western blotting and immunofluorescence enzyme-linked immunosorbent assay (ELISA). In vivo, after the oral administration of HFD and AA, X-ray examination, safranin O staining, and ELISA assay were conducted to evaluate cartilage calcification and degeneration and cytokine and adipokine levels in the serum of mice. AA treatment eliminated the inflammation caused by PA and extracellular matrix degradation. Mechanistically, AA blocked the stimulation of the NF-κB pathway. Analysis with co-immunoprecipitation and molecular docking indicated that the MD-2/TLR4 complex was a target of AA. In vivo, AA treatment not only prevented HFD-induced OA changes but also reduced proinflammatory cytokine and adipokine production in obese mice. AA exerted a chondroprotective effect by inhibiting the TLR4/MD-2 axis, thus showing promise for treating obesity-related OA.