CARTILAGE最新文献

ObjectiveIn this study, we investigated whether interleukin (IL)-37 ameliorates experimental osteoarthritis (OA).MethodsThe effects of IL-37 were investigated in collagenase-induced OA (CiOA) and destabilization of the medial meniscus (DMM). Human IL-37-adenovirus (ad-IL-37) was injected into the affected knee joint 4 and 18 days after the induction of OA. Luciferase-adenovirus was injected as control. Mice were sacrificed for histology at early and late stage of OA development. Interleukin-37 protein expression was confirmed by immunohistochemistry. Cartilage damage, osteophyte size and joint capsule thickness were measured. The effectiveness of ad-IL-37 was confirmed in vitro in human OA fibroblasts using real-time qualitative polymerase chain reaction (RT-qPCR) and Western blotting.ResultsInterleukin-37 protein expression was visible for at least 7 days after injection. At day 28, 10 days after the second injection, no clear synovial IL-37 staining was found any more, in both models. At day 28 of CiOA, ad-IL-37 significantly reduced articular cartilage damage and this was still reduced, although not significantly, at the late time point (day 42). In the DMM model, significant beneficial effect of IL-37 on cartilage damage was found at the late time point. In both OA models ad-IL-37 injections reduced the size of osteophytes.ConclusionInterleukin-37 ameliorated OA-induced articular cartilage damage and osteophyte formation in both models.

ObjectiveTo assess the efficacy of arthroscopic debridement combined with platelet-rich plasma (PRP) therapy in treating advanced ankle osteoarthritis (OA).DesignThe data of 34 advanced ankle OA patients were retrospectively analyzed, with 17 patients undergoing arthroscopic debridement alone (No-PRP group) and 17 receiving debridement with PRP therapy (PRP group). The Self-Administered Foot Evaluation Questionnaire (SAFE-Q) was evaluated preoperatively and at 3, 6, and 12 months postoperatively. The complications were assessed throughout the follow-up period.ResultsIn the PRP group, all SAFE-Q subscales significantly improved at 6- and 12-month post-treatment compared with baseline (P < 0.05), whereas improvements in the No-PRP group were limited. For severe ankle OA patients, only the pain-related subscale of the SAFE-Q significantly improved from baseline in the No-PRP group (P < 0.05). In contrast, all SAFE-Q subscales demonstrated significant improvement at 12 months postoperatively in the PRP group (P < 0.05). The recurrence rates were 23.5% in the No-PRP group and 11.8% in the PRP group.ConclusionArthroscopic debridement combined with PRP therapy for advanced ankle OA significantly improved all SAFE-Q subscales postoperatively, whereas debridement alone had limited benefits. This combination may offer an effective treatment for advanced ankle OA.

Clinical RelevanceIn recent years, an increased posterior tibial slope has been identified as a nonmodifiable risk factor for anterior cruciate ligament (ACL) injury and increased failure rates after ACL reconstruction (ACLR). To date, the literature consists of clinical case series on slope reducing high tibial osteotomies and reports promising clinical results. However, higher case numbers are still lacking. The goal of the present series of anterior-closed-wedge high tibial osteotomies (ACW-HTO) was to analyze patient-reported outcome measures (PROMs) at a minimum of 2 years. It was hypothesized that an ACW-HTO with secondary ACLR after failed ACL surgery improves clinical outcome as compared with the pre-osteotomy state or can even give sufficient stability to avoid the need for revision ACLR.Material and methodsOne hundred consecutive cases with an ACW-HTO operated between February 2019 and December 2022 were included in 2 surgical centers (57 cases radiographic/51 cases with PROMs Sozialstiftung Bamberg and 43 cases radiographic/35 cases with PROMs Sporthopaedicum Berlin, Germany). The pre-injury (before first injury), the preoperative (before ACW-HTO), and the final postoperative conditions were documented using PROMs.ResultsThe mean follow-up was 36 months (SD ±11, range 24-82), the follow-up rate for the PROMs was 85%. The mean preoperative slope of 14.6° (SD ±2.4°; range 11°-28°), measured according to the method of Dejour and Bonnin, was corrected to a mean of 6.8° (SD ±2.0°; range 0°-12°), P < 0.0001. No relevant complications were noted and no recurrent ACL graft failure was reported within the full follow-up period. Twenty-one patients had not received a revision ACLR after ACW-HTO at final follow-up due to sufficient stability. Prior to the first ACL injury, the mean Tegner activity scale was 7.3 points (SD ±1.7; 3-10) and mean Lysholm score revealed 98 points (SD ±4; range 79-100). Prior to ACW-HTO Tegner Scale was significantly reduced to 3.3 points (SD ±1.8; range 0-9) (P < 0.0001) and Lysholm score revealed 57 points (SD ±28; range 14-94) (P < 0.0001) as compared with the pre-injury level. At final follow-up, mean Tegner activity scale changed to 4.8 points (SD ±1.9; range 0-9), which significantly improved as compared with the pre-osteotomy stage (P < 0.0001). Of 85 patients, 18 achieved their pre-injury Tegner activity level, 2 even reached a level higher than the preoperative level. So the return to pre-injury activity level is 21%. The Lysholm score significantly improved to 83 points. (SD ±18; range 24-100) (P < 0.0001) as compared with the pre-osteotomy stage.ConclusionThe present case series presents the largest published series after ACW-HTO and secondary ACLR. Clinical and radiographic results underline that this procedure is safe and significantly increases the patient's ability to participate in light sports and activities of daily living due to an improved stability. An impor

ObjectiveTo determine the association between socioeconomic deprivation and short-term patient-reported clinical outcomes following autologous chondrocyte implantation (ACI).DesignAll patients receiving knee ACI between 1996 and 2020 in our center were identified. Socioeconomic deprivation of their residential area was quantified using the Index of Multiple Deprivation (IMD). Patient-reported 1-year Lysholm and Intermittent and Constant Osteoarthritis Pain (ICOAP) scores were used as outcome measures in the analyses. After transformation to ensure normal distributions (where required), linear multivariable regression was used to analyze the relationship between IMD and 1-year Lysholm score, adjusting for demographic characteristics (age, sex, body mass index [BMI], and smoking) and baseline Lysholm.ResultsThree hundred and ninety-one patients with a mean age of 50 years (range = 16-84; 266 male) were identified. Median BMI was 27 (17-47), with 138 patients overweight and 105 obese. Seventy-seven patients lived in upper and 41 in lower quintile deprivation areas. The mean baseline Lysholm score was 49.8 ± 17.3 SD, improving to 66.5 ± 21.3 SD at 1 year. Mean 1-year Lysholm scores were significantly lower with increasing area deprivation scores, adjusted for demographic factors. Specifically, areas with high unemployment levels, being female, or having a lower baseline Lysholm were associated with poorer outcomes, but age, BMI, smoking, or higher income deprivation were not.ConclusionThis study demonstrates poorer functional outcomes following ACI in patients from more deprived areas, indicating future studies should consider neighborhood deprivation as a confounding factor. Furthermore, targeting patients from areas with higher deprivation with additional interventions/community support may improve their outcomes.

ObjectiveMicroRNAs (miRNAs) play a key role in the differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) into chondrocytes. Our previous study found that novel-miR-81 can relieve osteoarthritis, but its role in chondrogenic differentiation of BMSCs remains unclear. The purpose of this study was to explore the role of novel-miR-81 in chondrogenic differentiation of BMSCs.MethodsWe used a model in which transforming growth factor (TGF)-β3-induced BMSCs differentiation into chondrocytes. We detected the expression Sox9, Collagen Ⅱ, Aggrecan, novel-miR-81, and Rac2 by real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blot was performed to detect the expression of Sox9, Collagen Ⅱ, and Rac2. Dual-luciferase reporter gene assay confirmed that the association between novel-miR-81 and Rac2. In addition, the ectopic chondrocyte differentiation of BMSCs was performed subcutaneously in nude mice. The effect of novel-miR-81 and Rac2 on ectopic chondrogenic differentiation of BMSCs was determined by immunohistochemical staining.ResultsNovel-miR-81 upregulated in chondrogenic differentiation of BMSCs. Rac2 was a key target of novel-miR-81. Mimic novel-miR-81 and siRac2 upregulated the expression of Sox9, Collagen Ⅱ, and Aggrecan.ConclusionNovel-miR-81 promotes the chondrocytes differentiation of BMSCs by inhibiting the expression of target gene Rac2, which provides potential targets for BMSCs transplantation to repair cartilage defects.

ObjectiveOsteoarthritis (OA) is a degenerative joint disease. A growing number of studies have shown that microRNAs (miRNAs) play an important role in the pathogenesis of OA. However, the specific function of miR-322 in OA is unknown. This study was aimed to explore the ability of miR-322 in the cartilage matrix degradation and the mechanism in OA.MethodsQuantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to detect miR-322 expression in cartilage and OA-associated gene expression in chondrocytes treated with miR-322 mimics/inhibitors or interleukin (IL)-1β, respectively. The targets of miR-322 were analyzed using software and the luciferase reporter experiment. In vivo, intra-articular injection of miR-322 mimics was administered at the knee of DMM mice. After 12 weeks, the knee joints of mice were collected for histological analysis.ResultsThe expression of miR-322 was decreased in knee cartilage of DMM mice and was significantly reduced by IL-1β. miR-322 mimics inhibited IL-1β-induced extracellular matrix degradation, as evidenced by higher expression of Col2α1 and Aggrecan, and lower expression of Adamts5, MMP3, and MMP13. In contrast, miR-322 inhibitor promoted extracellular matrix degradation of chondrocytes. TRAF3 was the predicted target of miR-322 from databases. Luciferase reporter assay verified the targeting relationship between miR-322 and TRAF3. The effect of miR-322 on extracellular matrix degradation was partially reversed by overexpression of TRAF3. In addition, H&E and Safranin-O fast green staining assays in OA mouse models showed that miR-322 mimics attenuated the progression of OA in vivo.ConclusionsmiR-322 suppressed chondrocytes matrix degradation and alleviated OA cartilage injury via inhibition of the TRAF3.

ObjectiveThe purpose of this study is to analyze how the largest insurance companies support their medical necessity policies regarding osteochondral allograft transplantation (OCA) and to determine whether the literature they cite in their policies is of a high level of evidence (LOE).DesignThe 10 largest national health insurance companies were identified. Each payer was contacted via phone or email to obtain their coverage policy regarding OCA. For each policy, the medical necessity criteria were recorded, and all cited references were screened. For all references applicable to OCA, the LOE was recorded, and each reference was screened to determine whether they mentioned the specific criteria reported in the policies.ResultsThe medical policies for 6 of the 10 national health insurance companies were identified. These 6 policies cited a collective total of 102 applicable references. Most of these studies were an LOE of IV (n = 58, 56.9%) and an LOE of V (n = 18, 17.6%). There were similarities amongst the medical necessity criteria between different commercial payers; however, most criteria were poorly supported by the cited literature.ConclusionsOur results demonstrate that commercial insurance companies utilize studies that are of a low LOE when justifying their medical necessity criteria. Moreover, these cited studies infrequently support or mention the commercial payers' criteria. Future studies should continue to explore how well-supported insurance policies are with the goal of potentially increasing access and authorization for well-supported treatment modalities.

ObjectiveTo assess the relation between microbiome and lipopolysaccharide (LPS), in the blood and synovial fluid (SF) with femoral cartilage thickness (FCT) measured by ultrasound (US) in knee osteoarthritis (KOA) patients.MethodsThis cross-sectional study included 40 primary KOA patients recruited between September 2022 and June 2023. Age, gender, and body mass index (BMI) were recorded. Patients underwent full clinical examination, standing plain x-ray of the knee joint and knee US examination to measure medial, intercondylar, and lateral FCT. Microbiomes (specific bacterial phyla) were detected by real-time polymerase chain reaction and LPS levels were measured by enzyme-linked immunosorbent assay kit in the patients' serum and SF.ResultsThe patient's age ranged from 43 to 72 years. Most patients were females (72.5%), with a mean BMI of 35.8 ± 6.21 kg/m². The mean medial, intercondylar, and lateral FCT were less than cut-off values. All 40 (100%) patients showed positive bacterial deoxyribonucleic acid (16S ribosomal RNA) in both blood and SF samples. Firmicutes was the most abundant in patients' blood (48.49%) and SF (63.59%). The mean serum LPS level was significantly higher compared to mean SF LPS (t =4.702, P < 0.001). There was a statistically significant negative correlation between lateral FCT and Firmicutes relative abundance in both patients' blood and SF.ConclusionMicrobiome and LPS are present in the blood and SF of primary KOA patients. Microbiome (Firmicutes) was associated with decreased lateral FCT. This might provide a potential link between both systemic and local microbiomes and cartilage affection in KOA patients.

ObjectiveCartilage degeneration is a key feature of osteoarthritis (OA) and rheumatoid arthritis and is thought to negatively impact patients' quality of life. Diclofenac etalhyaluronate (DEH, SI-613/ONO-5704) is a hyaluronic acid (HA) derivative chemically bound to diclofenac (DF) that has been reported to improve OA symptoms; however, its effect on cartilage degeneration remains unknown. In the present study, we investigated the chondroprotective effect of DEH in rats with collagen-induced arthritis and interleukin-1β-stimulated human chondrocytes.DesignRats with collagen-induced arthritis were administered DEH and HA intra-articularly, and DF orally. Knee joint swelling, histological scores of articular cartilage, and inflammatory (Il1b) and catabolic (Mmp3 and Mmp13) gene expression in the synovial tissue and cartilage were evaluated. In vitro direct effects of DEH on matrix metalloproteinase (MMP)-3 and MMP-13 expression were examined in interleukin-1β-stimulated human chondrocytes.ResultsIn a rat model of collagen-induced arthritis, a single intra-articular dose of DEH inhibited knee joint inflammation and cartilage degeneration. Daily oral administration of DF had similar effects. Conversely, HA administered as a single intra-articular dose had no effect. Only DEH inhibited Mmp3 gene expression in the cartilage, whereas DEH and DF inhibited Mmp3 and Mmp13 mRNA expression in the synovial tissue. In interleukin-1β-stimulated human chondrocytes, DEH and HA inhibited MMP-3 and MMP-13 production, whereas DF had no effect.ConclusionsIn this study, we demonstrated the chondroprotective effect of DEH in rats with collagen-induced arthritis and in interleukin-1β-stimulated human chondrocytes. Thus, DEH may suppress cartilage degeneration in patients with musculoskeletal diseases, such as OA.

ObjectiveThe aim of this study is to both quantify and qualify the way insurance companies justify their coverage policies for autologous chondrocyte implantation (ACI) and determine whether these policies align with recent research on the subject.DesignThe top 11 national commercial health insurance payers for ACI were identified. Coverage policy documents were recovered for 8 payers. These documents were examined, and the type of reference and the level of evidence (LOE) were recorded for each applicable reference. Specific coverage criteria for each individual payer were then extracted and assessed for similarities among commercial payers. Finally, all references cited by each payer were examined to determine whether they mentioned the specific payer criteria.ResultsThis study found that the majority of cited references were primary journal articles (86, 58.1%) and that only 30 (20.2%) references were level I or level II evidence. This study also found significant homogeneity among payer coverage criteria. Cited sources inconsistently mentioned specific payer coverage criteria. In addition, payer criteria tended to be poorly supported by current evidence on ACI.ConclusionsThis study demonstrates that commercial insurance payers' coverage policies for ACI poorly cite references, cite a majority of references with low LOE, and cite references which infrequently mention their specific coverage criteria. In addition, payer coverage policies have a high degree of homogeneity and many of their specific criteria are poorly supported by current research on ACI.