CARTILAGE最新文献

PurposeTo clarify and standardize sagittal tibial tubercle-trochlear groove (sTTTG) numerical values in the literature.ResultsSagittal tibial tubercle-trochlear groove distance has been recently popularized as a quantitative marker of patellofemoral contact forces and correlated to patellofemoral chondral lesion incidence, size, and osteoarthritis. There remains controversy over the precise definition of sTTTG.ConclusionThe current erratum clarifies that a relatively anterior tibial tubercle compared to the trochlear groove is quantified as a positive sTTTG, whereas a relatively posterior tibial tubercle compared to the trochlear groove is quantified as a negative sTTTG.

BackgroundKnee bursae are potential sources of anterior, medial, lateral, and posterior knee pain, yet many remain under-recognized in clinical practice. Emerging biological therapies offer promising, minimally invasive options for resistant bursitis, but high-level evidence is limited for several bursal types.PurposeTo systematically review the anatomy, clinical presentation, imaging characteristics, treatment strategies, and outcomes of 11 distinct knee bursae, with emphasis on the role of biologic therapies.MethodsThis systematic review followed PRISMA guidelines. PubMed and Embase were searched (2000-2024) for studies addressing anatomy, diagnosis, imaging, treatment (conservative, injection-based, biologic, or surgical), and outcomes of knee bursae. Studies involving human subjects, published in English, and reporting clinical, imaging, or therapeutic data were included. Levels of Evidence (LOE) were assigned using Oxford criteria.ResultsA total of 76 studies were included. Several randomized controlled trials (LOE I) focused on pes anserine and OA-related bursitis, while additional Level II studies assessed PRP and corticosteroids. Data on rare bursae (e.g., LCL, deep infrapatellar) were primarily derived from imaging reviews and case series (LOE III-IV). Corticosteroid injections showed recurrence rates of 20% to 40%. PRP and PRP+HA demonstrated improved pain relief and reduced recurrence in selected bursae, although protocols remain heterogeneous.ConclusionConservative management remains first-line for most bursae. PRP-based therapies, especially in pes anserine and OA-related bursitis, offer promising alternatives in refractory cases. Although several Level I-II studies support their efficacy, additional high-quality RCTs are warranted-particularly for understudied bursae.

ObjectiveThis study investigates the molecular mechanism by which leucine (Leu) ameliorates collagenase-induced osteoarthritis (CIOA) through macrophage polarization regulation.MethodsA CIOA mouse model was established and evaluated by micro-computed tomography (micro-CT) and histopathological analysis. Leu intervention was administered, and its therapeutic effects on cartilage degeneration and osteophyte formation were assessed. Integrated multi-omics analyses and mechanistic assays were performed to explore the role of the mTORC1/LXRα pathway in synovial macrophage reprogramming and its regulation of the Rspo2/β-catenin axis in chondroprogenitors. Functional validation was conducted using the LXRα inhibitor GSK2033.ResultsLeu intervention demonstrated significant therapeutic effects, reducing cartilage degeneration by 42% (Osteoarthritis Research Society International [OARSI] score) and osteophyte formation by 58% (volume reduction). Integrated multi-omics and mechanistic assays indicated that Leu activated mTORC1/LXRα to reprogram synovial macrophages toward an M2-like state, suppressed Rspo2, and attenuated β-catenin signaling in chondroprogenitors, thereby improving cartilage function. Functional validation using LXRα inhibitor GSK2033 confirmed pathway specificity, reversing Leu-mediated cartilage protection and reactivating osteogenic differentiation.ConclusionThese findings establish a novel "metabolism-immunity-cartilage" axis in which Leu coordinates mTORC1/LXRα-driven macrophage reprogramming with Rspo2/β-catenin axis suppression, offering dual-target therapeutic potential for osteoarthritis. The study redefines nutritional amino acids as immunometabolic modulators in degenerative joint diseases, proposing Leu supplementation as a viable strategy for interrupting the inflammation-bone remodeling cycle in traumatic arthritis. No clinical trials were involved in this preclinical investigation.

ObjectiveCurrently, there is a wide range of therapeutics that can be used to treat ankle osteoarthritis (OA), but none of them are able to fully restore the function of the ankle joint long-term. In this narrative review, we aim to summarize the current progress of using bone marrow aspirate concentrate (BMAC) for treating ankle OA.DesignPubMed was searched for publications that were published from 1990 until September 1, 2025 (moment of search). Key search terms were bone marrow aspirate concentrate and ankle OA. This yielded 17 hits, of which 10 were included in this narrative review.ResultsBMAC may enhance cartilage repair in ankle injuries and OA, especially when it is used in combination with other surgical techniques and biological treatments. However, the body of supporting evidence remains largely composed of Level II to IV studies (case-control and retrospective series). In addition, the independent role of BMAC remains unclear due to the lack of studies evaluating BMAC as a stand-alone treatment, as well as the unclear role that it plays as an adjuvant therapy.ConclusionsIn conclusion, the existing literature investigating BMAC for ankle OA is encouraging but remains inconclusive. High-quality randomized controlled trials with standardized protocols, longer follow-up, and head-to-head comparison against other treatment options are needed to establish both efficacy and cost-effectiveness. Establishing minimal reporting standards for BMAC composition is also critical to improve consistency across studies.

ObjectiveTo review the history of chondrocyte transplantation, new approaches to treatment of human chondral and osteochondral defects, animal experiments, the choice of chondrocytes for transplantation, immunological features of human and animal chondrocytes and factors which could influence results of chondrocyte transplantation.DesignAs the material for review served numerous papers collected during our many years' chondrocyte studies supplemented by PubMed search.ResultsAutologous chondrocytes, expanded in culture, were successfully used to repair damaged human articular cartilage. Numerous modifications of the original procedure benefited from a better understanding of factors influencing chondrocyte differentiation. Immunological studies suggested that survival of allogeneic transplants of bioengineered human neocartilage may depend on both passive and active mechanisms of immune evasion. Human chondrocytes with deleted expression of MHC class I molecules produced cartilage which, after transplantation into monkey articular cartilage was attacked by NK cells.ConclusionsImmune response against human chondrocytes requires further investigation. It is already established that allogeneic chondrocytes are safe for treating chondral defects but not for healing osteochondral defects. Full reconstruction of cartilage defects by restoring anatomically identical hyaline cartilage seems not feasible.

ObjectiveOsteoarthritis (OA) is a prevalent age-related degenerative joint disease characterized by cartilage degeneration, joint pain, and reduced mobility, with aging as the primary risk factor. This study aimed to investigate the role and mechanism of FK506 binding protein 38 (FKBP38) in chondrocyte senescence and OA progression.MethodsFKBP38 expression was detected in articular cartilage from natural aging and OA mouse models. Mice with FKBP38 conditional knockout (FKBP38-cKO) and inducible conditional knockout (FKBP38-iKO) were generated for these models. An adeno-associated virus (AAV) vector overexpressing FKBP38 was injected into wild-type mouse joints. Joint damage was assessed at 8 and 18 months for natural aging or 4 and 8 weeks after DMM surgery by histology.ResultsFKBP38 expression was downregulated in cartilage from both natural aging and OA mice. FKBP38 overexpression protected against H2O2-induced senescence in chondrocytes. Addition of rapamycin to inhibit mTORC1 signaling rescued the enhanced senescence and catabolism caused by FKBP38 knockdown in chondrocytes. Conditional deletion of FKBP38 in chondrocytes significantly accelerated senescence and aggravated both natural aging and OA progression by activating mTORC1 signaling, whereas overexpression of FKBP38 delayed these processes.ConclusionThese results indicate that FKBP38 protects against chondrocyte senescence and cartilage degradation to alleviate OA progression by inhibiting mTORC1 signaling.

ObjectiveOsteochondral lesions of the tibial plafond (OLTP) are considered rare, and to date the treatment for these lesions has solely focused on operative management. The aim of this study was to prospectively assess the 2-year patient-reported outcomes, radiological outcomes, and adverse outcomes for the non-operative treatment of patients with a symptomatic OLTP.DesignEighteen patients with a symptomatic OLTP who underwent non-operative treatment were prospectively assessed. The primary outcome concerned the numeric rating scale (NRS) for pain during weightbearing from baseline to 2-year follow-up. Secondarily, the patient-reported outcomes (PROMs) NRS during rest, running, and stairclimbing, as well as the Foot and Ankle Outcome Score (FAOS) and short-form-36 (SF-36) questionnaires were assessed. CT scans at median 2 years (IQR: 1.5-2) follow-up were reviewed for changes in lesion volume or signs of lesion healing. Return to sports and work rates were evaluated. The conversion to surgery rate and any complications were assessed.ResultsThe NRS during weightbearing improved (non-significantly) from a median of 5 (IQR: 3-7) out of 10 at baseline to 2 (IQR: 1-6) out of 10 at 2-year follow-up, P = 0.06. The other NRS subscales, FAOS subscales, and SF-36 did not significantly improve at final follow-up. The follow-up CT-evaluation showed that lesion volume did not change (219 [IQR: 79-890] mm³) compared to baseline (226 [IQR: 79-890] mm³), P = 0.2. In 10 (77%) out of 13 cases, signs of lesion filling or no change was observed. At final follow-up, 93% (13/14) of patients returned to any level of sports, 54% (7/13) of patients returned to preinjury level of sports, and 94% (15/16) of patients returned to work. No adverse events were observed, and 1 (6%) case converted to surgery.ConclusionsNon-operative management for OLTP resulted in minor improvements of patient-reported pain and functional outcomes up to 2-year follow-up. The conversion to surgery rate was 6%. Radiologically, lesion size and filling were found to remain stable at CT follow-up. Moreover, on average 9 out of 10 patients were able to participate in sport and could return to, or remain at, their preinjury work activities.

ObjectiveTo compare the effects of equine MSCs and their extracellular vesicles (EV) on stimulated cartilage explants and assess how serum type influences EV production and cartilage inflammation.MethodsEVs were isolated from bone marrow-derived MSCs cultured in equine serum (ES) or fetal bovine serum (FBS) media and concentrated via ultracentrifugation. Cartilage explants were stimulated with IL-1β and TNF-α and treated with MSCs, EVs, or left untreated. Cartilage explants were analyzed for cytokine concentration and examined for gene expression, glycosaminoglycan depletion, and histology.ResultsEVs produced by MSCs cultured in ES or FBS had similar characteristics. Cartilage explants treated with MSCs in ES media had decreased concentrations of IL-1β and increased concentrations of IL-6 in the supernatant compared to cartilage explants alone. Treatment with EVs did not significantly alter supernatant mediators. Cartilage explants cultured in ES had higher levels of IL-1β, IL-6, and TNF-α, while cartilage explants cultured in FBS had higher levels of PGE2. Treatment of stimulated cartilage explants with either MSCs or EVs did not alter gene expression or support extracellular matrix (ECM) degradation.ConclusionEquine MSCs appear to have enhanced immunomodulatory properties compared to EVs when used to treat stimulated cartilage explants. While some beneficial alterations in culture supernatants were detected, ECM degradation was not affected by treatment.

ObjectiveSaline is typically suspended at a certain height to maintain a clear surgical field in arthroscopic surgery. The effects of saline on cartilage have been extensively studied; however, the impact of the pressure generated by saline solution suspended at different heights on injured cartilage is largely unknown. This study investigates suspension-height-dependent cellular responses and tissue damage in traumatized cartilage.MethodsOsteochondral explants were harvested from porcine stifle joints, then were cut perpendicularly before immersed or irrigated for 2 hours with saline at 4 heights (80/105/130/155 cm). The explants were then transferred to and cultured in chondrogenic medium for 5 days. Chondrocytes viability was subsequently assessed with confocal imaging. Cell response was assessed with expression levels of proapoptosis and proinflammatory genes. Tissue damage was evaluated by secretome analysis of proinflammatory cytokines and extracellular matrix and histological test.ResultsIrrigation exacerbated cut-induced chondrocytes death in superficial zone of cartilage, with mild change on 80 cm, 105 cm, 130 cm and severe damage on 155 cm. Similarly, explants that underwent irrigation with heights of 80 cm to 130 cm exhibited relatively slighter change of gene expression of BAX, BCL2, IL-6 and NOS2 and release of GAG, IL-6 and NO to a comparable extent.ConclusionThis study provides evidence of damaging effects of irrigation on injured cartilage surface. Suspension heights of 80 cm to 130 cm led to comparable minor cartilage damage.

PurposeThe mechanobiological response of cartilage redox balance might change in response to altered substrate availability. The purpose of this study is to investigate effects of key metabolic substrates (glucose, glutamine, and oxygen) on the mechanoresponsiveness of cartilage redox balance using a label-free imaging technique that measures autofluorescence from endogenous redox cofactors.FindingsCompared with room oxygen tension, low oxygen tension had higher autofluorescence intensity in green (FAD) channel after a single sub-failure tensile load. Cartilage explants cultured in high glucose medium with glutamine supply had higher autofluorescence intensity in both channels (FAD and NADH/NADPH) compared with low glucose with glutamine group or high glucose without glutamine group, while no difference was observed between the latter 2 groups.ConclusionsLow oxygen tension or high glucose culture medium with glutamine supply increases the mechanoresponsiveness of cartilage redox balance induced by sub-failure mechanical loading. Glutamine appears to partially serve as a glucose substitute in this process.