Pain is one of the primary indicators of a bone fracture and serves both a functional and practical role in guiding recovery. However, fracture pain can persist long after the fracture itself has clinically healed. The neural and molecular mechanisms that drive acute pain postfracture, and how these mechanisms are pathologically usurped to trap patients into persistent, debilitating, and often difficult to treat, chronic pain, are not well understood. The aim of this review is to provide insight into the risk factors for pain persistence after fracture, review the physiological and pathophysiological mechanisms of fracture pain, and critically evaluate the literature around fracture pain assessment techniques/models. Taken together, the concepts covered herein will provide a strong foundation to support the development of more effective treatments to better alleviate postfracture pain.

Bone marrow–derived mesenchymal stem cells (BM‐MSCs) are well established for their osteogenic potential but are prone to senescence with aging or in vitro expansion. Drug treatments that reduce cellular senescence may enhance the regenerative capacity of BM‐MSCs. This study investigates the effects of losartan and fisetin, both separately and in combination, on cellular senescence and osteogenesis. Human BM‐MSCs were exposed to low and high concentrations of each drug for 24 h. Our findings showed that high‐dose losartan exhibited cytotoxicity, focusing subsequent analyses on the low doses. Both low‐dose losartan and fisetin effectively mitigated cellular senescence, with combined treatment showing synergistic effects in reducing senescence markers. From these initial findings, subsequent experiments utilized low doses of both compounds to evaluate their effect on differentiation capacity. Our multimodal approach, incorporating flow cytometry, senescence‐associated heterochromatin foci (SAHF) immunohistochemistry, senescence‐associated secretory phenotype (SASP) quantification, and differentiation potential assays, revealed that the combination of 23.6 μM of losartan and 50 μM of fisetin was optimal for reducing cellular senescence and enhancing osteogenesis in BM‐MSCs. These results support potential therapeutic strategies to counteract age‐related declines in bone health and improve healing. By targeting cellular senescence while promoting osteogenesis, losartan and fisetin offer promising avenues for future research aimed at enhancing the regenerative capacity of BM‐MSCs in the context of musculoskeletal regenerative medicine.

Purpose: To compare intraoperative findings associated with instability and clinical outcomes after hip arthroscopic femoroacetabular impingement syndrome (FAIS) surgery in patients with normal anteversion (NA) and excessive femoral anteversion (EA). Methods: Inclusion criteria were FAIS cases who underwent primary arthroscopic management from January 2016 to December 2019. Patients who met exclusion criteria, such as osteoarthritis (Tonnis grade ≧ 2), and patients with less than a 2‐year follow‐up were excluded. The remaining hips were divided into 2 groups: the NA group (femoral anteversion 10°‐25°) and the EA group (femoral anteversion > 25°). Clinical outcomes were assessed using the International Hip Outcome Tool 12 (iHOT12), hip outcome score activity of daily living scale (HOS‐ADL), hip outcome score activity of sports (HOS‐SP), and modified Harris hip score (mHHS). Achievement rates for the patient acceptable symptomatic state (PASS) and the minimal clinically important difference (MCID) were also evaluated. Intraoperative findings suggestive of instability were analyzed. Results: The NA group included 34 hips, while the EA groups included 16 hips. Anteroinferior labral tears were significantly more prevalent in the EA group (75% vs 29.4%; P = .0051). Postoperative PROMs at 2 years were significantly worse in the EA group for iHOT12 (79.1 vs 95.1, P = .0017), HOS‐ADL (91.2 vs 98.5, P = .0224), HOS‐SP (83.3 vs 100, P = .0049), and mHHS (86.9 vs 96.8, P = .002). Regarding some PROMs, PASS achievement rates were also significantly lower in the EA group (iHot12: 56.2% vs 88.2%; P = .024, HOS‐ADL: 62.5% vs 94.1%; P = .009), while no statistical difference was observed in MCID achievement rates. Three reoperations occurred in patients with EA, with femoral anteversion angles of 29°, 32.5°, and 33.5°. Conclusions: Patients with EA had inferior outcomes of hip arthroscopy and a higher prevalence of anteroinferior labral tears. Level of Evidence: Level III, retrospective comparative case series.

Background/Objectives: Long-standing groin pain is a severe issue for athletes, often associated with the cleft sign on magnetic resonance imaging (MRI) scans, yet its underlying causes are poorly understood. The purpose of this study is to histologically examine the pubic plate structure in cadavers with and without the cleft sign on MRI, shedding light on the pathology behind the cleft sign. Methods: Three fresh human pelvic cadavers underwent 3.0T MRI to detect the cleft sign before histological dissection of pubic plates. Pubic plate tissues were fixed in formalin, decalcified, and processed. Of the two cleft sign-negative specimens, one was cut into sagittal sections, and the other was cut into coronal sections for histology. For the cleft sign positive specimen, a sagittal section was cut. Moreover, 5 µm thick sections were cut at different axial levels for each orientation. Sections were subjected to Safranin O, Alcian blue, and Herovici’s staining or hematoxylin and eosin staining. Results: MRI confirmed that one specimen had a cleft sign in the inferior region on both sides of the pubis and that two specimens had no cleft sign. Both sagittal and coronal sections showed the presence of a cartilage structure continuing from the pubic symphysis to 3 mm laterally within the pubic plate. In the specimen with a positive cleft sign, cartilage damage within the pubic symphysis and pubic plate was identified as revealed by Safranin O staining, Herovici’s staining, and H&E staining. Conclusions: This study elucidated the existence of a cartilage component extending from the pubic symphysis to the pubic plate. The cleft sign in MRI correlated with a disruption in the cartilage component in histology within this specific area.

This study aimed to investigate the associations between hip cartilage lesions and bony morphologic parameters in the hip joints using a computed tomography-based software system. Seventy-nine symptomatic hips that underwent hip arthroscopic labral preservation surgery were enrolled in this study. Bony structural morphologic parameters were subsequently assessed via a computed tomography-based software system. The indices included the femoral neck anteversion (FNA), alpha angle (AA) at each o'clock position of the femoral head, lateral center-edge angle (LCEA), and three-dimensional acetabular coverage (3D-AC). Cartilage damage was confirmed arthroscopically and classified according to the Multicenter Arthroscopy of the Hip Outcome Research Network (MAHORN) classification as well as the International Cartilage Repair Society classification. Of the 79 hips, 41 patients were male, and 38 were female, with a mean age of 39.1 years ​±16.1 years (11-78). The mean LCEA was 27.6° ​± ​8.6° (range 7°-46°), and the mean FNA was 22.9° ​± ​14.4° (range -2°-63°). Grade 4 or 5 MAHORN acetabulum cartilage lesions were observed in 10 hips (13 ​%), while femoral head cartilage lesions with ICRS grade of 3 or 4 were found in 10 hips. Patients with MAHORN grade 4 or 5 cartilage lesions had significantly greater FNA compared with those with MAHORN grade 0 to 3 lesions (32.6° ​± ​10.3° versus 21.4° ​± ​14.4°, p ​= ​0.009). Although patients with MAHORN grade 4 or 5 lesions had greater AA at the entire o'clock of the femoral neck, the difference was not statistically significant. Patients whose FNAs were 26° or larger had a 6.2-fold greater odds ratio (95 ​% confidence interval, 1.2-31.5) of acetabular cartilage damage than those whose FNAs were less than 26° (p ​= ​0.015). The use of computed tomography-based software provided detailed insights into bony abnormalities reinforcing its utility in evaluating hip joint pathologies and their relationship with cartilage lesions. Level III.