CARTILAGE最新文献

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.

ObjectiveThis study aimed to compare short-term arthroscopic and clinical outcomes between microfractures with (treatment group) and without (control group) acellular particulated costal allocartilage in patients undergoing concurrent high tibial osteotomy (HTO).DesignThis retrospective cohort study enrolled 19 and 21 patients in the treatment and control groups, respectively, and reviewed them at a minimum 2-year follow-up after HTO. Cartilage regeneration status was evaluated according to the International Cartilage Repair Society-Cartilage Repair Assessment (ICRS-CRA) grading and Koshino's macroscopic staging systems during medial locked plate removal. Patient-reported measures, including the visual analog scale pain score, Knee Injury and Osteoarthritis Outcome Score, and International Knee Documentation Committee score, assessed clinical outcomes.ResultsThe total points of the ICRS-CRA grading system were significantly higher in the treatment group than in the control group (7.7 ± 3.8 vs 4.2 ± 3.0, respectively; P = 0.007). Likewise, the cartilage status according to Koshino's macroscopic staging system was better in the treatment group (P = 0.022). Patient-reported functional outcomes significantly improved postoperatively but were equivalent between the study groups at the final follow-up.ConclusionsMicrofractures augmented with acellular particulated costal allocartilage resulted in better repair quality than microfractures alone at a minimum 2-year follow-up after HTO, but functional outcomes improved similarly for both treatment approaches.

ObjectiveTo investigate the effect of higher cumulative defined daily dose per year (cDDD/y) compared with lower cDDD/y of statin use in the incidence of any joint osteoarthritis (OA).DesignIn this population-based retrospective cohort study, patients who were aged ≥40 years were newly initiated on statin therapy between 2002 and 2011, and had a statin prescription for ≥90 days in the first year of treatment were identified from the 2000 Longitudinal Generation Tracking Database. All patients were separated into groups with higher cDDD/y (>120 cDDD/y) and lower cDDD/y (≤120 cDDD/y; as an active comparator) values. Propensity score matching was performed to balance potential confounders. All recruited patients were followed up for 8 years. Marginal Cox proportional hazard models were used to estimate time-to-event outcomes of OA.ResultsCompared with lower cDDD/y use, higher cDDD/y use did not reduce the risk of any joint OA (adjusted hazard ratio, 1.07; 95% confidence interval, 0.99-1.14). Dose-related analysis did not reveal any dose-dependent association. A series of sensitivity analyses showed similar results. Joint-specific analyses revealed that statin did not reduce the incidence of knee, hand, hip, and weight-bearing (knee or hip) OA.ConclusionsHigher cDDD/y statin use did not reduce the risk of OA in this Taiwanese nationwide cohort study. The complexity of OA pathogenesis might contribute to the ineffectiveness of statin. Repurposing statin with its anti-inflammation properties might be ineffective for OA development, and balancing the catabolism and anabolism of cartilage might be a major strategy for OA prevention.

ObjectiveOur study was performed to investigate whether micro-223 promotes diabetic Osteoarthritis (OA) progression by regulating cartilage degeneration and subchondral bone remodeling.MethodsThe expression of miR-223 in human normal cartilage, OA cartilage, and subchondral bone tissue with or without DM was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-223 mimic or inhibitor was transfected into chondrocytes. Cell viability and apoptosis were assessed by 3-(4,5)-dimethylthiahiazo(-2)-3,5-diphenyltetrazolium bromide (MTT) and Terminal Deoxynucleotidyl Transferase(TdT)-mediated dUTP nick end labeling (TUNEL) assay, respectively.ResultsmiR-223 was significantly higher in human diabetic OA cartilage and subchondral bone compared with normal OA and healthy control. Overexpression of miR-223 accelerated cartilage degeneration and subchondral bone sclerosis in diabetic OA mice, whereas miR-223 inhibition had the opposite effect. In vitro upregulation of miR-223 decreased proliferation and enhanced apoptosis of chondrocytes. Meanwhile, downregulation of miR-223 promoted glycosaminoglycan (GAG) production in chondrocytes.ConclusionmiR-223 promotes diabetic OA progression by regulating cartilage degeneration and subchondral bone remodeling both in vitro and in vivo.

ObjectiveThe use of porcine animal models for cartilage injury has increased recently due to their similarity with humans with regard to cartilage thickness, limited intrinsic healing of chondral defects, and joint loading biomechanics. However, variations in the mechanical and biochemical properties of porcine hip articular cartilage among various tissue ages and weightbearing (WB) regions are still unknown. This study's aim was to characterize the mechanical and biochemical properties of porcine hip articular cartilage across various ages and WB regions.MethodsArticular cartilage explants were harvested from WB and non-weightbearing (NWB) surfaces of the femoral head and acetabulum of domesticated pigs (Sus scrofa domesticus) at fetal (gestational age: 80 days), juvenile (6 months), and adult (2 years) ages. Explants underwent compressive stress-relaxation mechanical testing, biochemical analysis for total collagen and glycosaminoglycan (GAG) content, and histological staining.ResultsJuvenile animals consistently had the highest mechanical properties, with 2.2- to 7.6-time increases in relaxation modulus, 1.3- to 2.3-time increases in instantaneous modulus, and 4.1- to 14.2-time increases in viscosity compared with fetal cartilage. Mechanical properties did not significantly differ between the WB and NWB regions. Collagen content was highest in the NWB regions of the juvenile acetabulum (65.3%/dry weight [DW]) and femoral head (75.4%/DW) cartilages. GAG content was highest in the WB region of the juvenile acetabulum (23.7%/DW) and the WB region of the fetal femoral head (27.5%/DW) cartilages. Histological staining for GAG and total collagen content followed the trends from the quantitative biochemical assays.ConclusionThis study provides a benchmark for the development and validation of preclinical porcine models for hip cartilage pathologies.

ObjectiveThe superficial zone (SZ) of articular cartilage is responsible for distributing shear forces for optimal cartilage loading and contributes to joint lubrication through the production of proteoglycan 4 (PRG4). PRG4 plays a critical role in joint homeostasis and is chondroprotective. Normal PRG4 production is affected by inflammation and irregular mechanical loading in post-traumatic osteoarthritis (PTOA). THe SZ chondrocyte (SZC) phenotype, including PRG4 expression, is regulated by the actin cytoskeleton in vitro. There remains a limited understanding of the regulation of PRG4 by the actin cytoskeleton in native articular chondrocytes. The filamentous (F)-actin cytoskeleton is a potential node in crosstalk between mechanical stimulation and cytokine activation and the regulation of PRG4 in SZCs, therefore developing insights in the regulation of PRG4 by actin may identify molecular targets for novel PTOA therapies.Materials and methodsA comprehensive literature search on PRG4 and the regulation of the SZC phenotype by actin organization was performed.ResultsPRG4 is strongly regulated by the actin cytoskeleton in isolated SZCs in vitro. Biochemical and mechanical stimuli have been characterized to regulate PRG4 and may converge upon actin cytoskeleton signaling.ConclusionActin-based regulation of PRG4 in native SZCs is not fully understood and requires further elucidation. Understanding the regulation of PRG4 by actin in SZCs requires an in vivo context to further potential of leveraging actin arrangement to arthritic therapeutics.