CARTILAGE最新文献

Objective: To determine if mesenchymal stromal cells (MSCs) derived from human umbilical cords (hUC) could reduce degeneration developing when injected into the knee of a large animal model of osteoarthritis (OA).

Design: Ten million culture-expanded UC-MSCs (pooled from 3 human donors) were injected in 50 μL of tissue culture medium into the left stifle joints of 7 sheep whose medial meniscus was transected 4 weeks previously. Seven other sheep had only 50 μL of medium injected as the no treatment "control" group. After 8 weeks the sheep underwent euthanasia, the joints were excised and examined macroscopically, via x-ray and magnetic resonance imaging (MRI), both via histology for degenerative and inflammatory changes and immunohistochemically to identify any human cells within the joint tissues. Activity monitoring both before meniscus transection and euthanasia was also undertaken.

Results: There was a significant reduction in the Kellgren-Lawrence x-ray score for joints injected with hUC-MSCs compared with the control joints. Likewise, macroscopic, MRI, synovitis and OARSI histology scores were all lower (better) in the joints injected with hUC-MSCs than in the control arm, but not significantly. Activity levels and synovitis scores were similar in both groups of animals.

Conclusions: hUC-MSCs appear to modify and reduce the development of osteoarthritic changes in the ovine stifle joint after meniscal destabilization, an injury which commonly leads to OA in humans. These results are encouraging for the potential benefit of culture expanded UC-MSCs as an allogeneic cell therapy in patients who may have early OA following a meniscal injury of the knee.

Objective: Traditional autologous chondrocyte implantation (ACI) involves arthroscopically harvesting a cartilage biopsy (stage 1), followed by arthrotomy 3 to 4 weeks later to apply a periosteal patch and implant culture-expanded chondrocytes underneath (stage 2). This study aimed to determine if patch application during stage 1 rather than stage 2 improved clinical outcome.

Design: A randomized controlled trial was conducted from 1998 to 2001. Patients were randomized to receive either traditional ACI (control/late) or ACI with "early" patch during stage 1 (intervention/early). Clinical outcome (Lysholm score) was assessed pre-operatively and annually post-operatively.

Results: Seventy-seven patients were recruited, with 40 patients randomized to the early and 37 to the late patch group. The overall mean pre-operative Lysholm score was 51.8 (range 11-89) and significantly improved by 11.1 points (95% confidence interval [CI] = 4.8 to 17.4) at mean 12.7 years (range 1.5-23.7) follow-up. Latest mean Lysholm scores for the early and late groups were 68.4 (95% CI = 19 to 100) versus 56.7 (95% CI = 18 to 98). Adjusted for covariate imbalances, no evidence was found for a difference between the groups (mean difference = 8.5, 95% CI = -5.2 to 22.2, P = 0.22). Twenty-year survival until any re-operation or arthroplasty was 59.6%/82.1% for the early and 56.8%/69.5% for the late group, with no evidence for a difference.

Conclusion: ACI is an effective durable treatment for cartilage defects, with high levels of patient satisfaction and low failure rates. No evidence was found that applying the periosteal patch at the time of chondrocyte harvest improved long-term Lysholm scores or survival until any re-operation or arthroplasty.

Objective: The purpose of this study was to evaluate outcomes following autologous osteochondral transplantation (AOT) for the treatment of osteochondral lesions of the talus (OLT) at a minimum of 10-year follow-up.

Design: Retrospective chart review identified patients who underwent AOT for the treatment of OLT. Pre-operative magnetic resonance imaging (MRI) scans were obtained in all patients. Clinical outcomes assessed included: pre- and post-operative foot and ankle outcome score (FAOS), visual analog scale (VAS), patient satisfaction, complications, failures and secondary surgical procedures.

Results: Thirty-nine patients with a mean lesion size was 122.3 ± 64.1 mm² and mean follow-up time of 138.9 ± 16.9 months were included. The mean FAOS scores improved from a preoperative score of 51.9 ± 16.0 to 75.3 ± 21.9 (P < 0.001). Increasing lesion size was variable associated with inferior FAOS scores (R² = 0.2228). There was statistically significant higher mean T2 relaxation values at the superficial layer at the site of the AOT graft (42.9 ± 5.2 ms) compared to the superficial layer of the adjacent native cartilage (35.8 ± 3.8 ms) (P < 0.001). Seventeen complications (43.6%) were observed, the most common of which was anterior ankle impingement (25.6%). There were 2 failures (5.1%), both of which had a history of prior bone marrow stimulation via microfracture and post-operative cysts identified on MRI.

Conclusion: This retrospective review found that AOT for the treatment of large OLTs produced a 94.9% survival rate at a minimum of 10-year follow-up. Increasing lesion size was associated with inferior clinical outcomes. The findings of this study indicates that AOT is a viable long-term surgical strategy for the treatment of large OLTs.

Objective: This study investigates how the inflammatory response of ATDC5 murine chondrogenic cells influences the activity of C6 (rat) and GL261 (mouse) glial cell lines. Prior research suggested nitric oxide (NO) involvement in cartilage-immune crosstalk. The current study explores whether NO, produced by inflamed chondrocytes, mediates signaling between chondrocytes and glial cells.

Design: Pre-challenged ATDC5 cells with 250 ng/ml of lipopolysaccharide (LPS) were cocultured with GL261 or C6 glioma cells for 24 h with a transwell culture system. Cell viability was assessed using MTT assay. Gene and protein expression were evaluated by qRT-PCR and WB, respectively.

Results: Real-time reverse transcription-polymerase chain reaction (RT-qPCR) indicated statistically significant upregulation of LCN2, IL-6, TNF-α, IL-1β, and GFAP in glial cells following 24-h coculture with challenged ATDC5 cells. Suppression of LPS-induced NO production by aminoguanidine decreased LPS-mediated LCN2 and IL-6 expression in glioma cells. We identified also the involvement of the ERK1/2 and AKT signaling pathways in the glial neuroinflammatory response.

Conclusions: This study demonstrates, for the first time, that NO produced by inflamed murine chondrocytes mediated pro-inflammatory responses in glial cells via ERK1/2 and AKT signaling, highlighting a potential mechanism linking cartilage NO to neuroinflammation and chronic pain in osteoarthritis.

Objective: This 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).

Design: This 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.

Results: The 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.

Conclusions: Microfractures 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.

Objective: To assess whether change of semiquantitatively magnetic resonance imaging (MRI)-defined bone marrow lesions (BMLs) and inflammatory markers is associated with change in quantitatively-assessed cartilage loss in the femorotibial joint (FTJ) in knees with radiographic osteoarthritis (OA) over 24 months.

Design: Participants were included from the IMI-APPROACH and the Osteoarthritis Initiative FNIH studies. Semiquantitative MRI assessment was performed for BMLs, Hoffa- and effusion-synovitis. Quantitative cartilage thickness measurements were performed manually. Definitions of change included number of subregions with BMLs, change in sum and change in maximum increase in size. Change in Hoffa-synovitis and effusion-synovitis was categorized in addition. Between-group comparisons regarding cartilage loss in the FTJ, medial and lateral compartments were performed using analysis of variance (ANOVA).

Results: A total of 629 participants were included. Knees without any BMLs at baseline (BL) and follow-up (FU) had significantly less cartilage loss compared to the other subgroups. Change in both directions in the sum score of BMLs was associated with increased rates of cartilage loss. Maximum increase in size of BMLs was associated with increased rates of cartilage loss (FTJ increase by 2 grades -0.183 mm, 95% CI [-0.335, -0.031], by 3 grades -0.306 mm, [-0.511, -0.101]). Worsening of Hoffa-synovitis was associated with increased rates of cartilage loss.

Conclusion: Knees without BMLs at BL and FU showed lowest rates of cartilage loss. Knees with an increase in BML size showed increased rates of concurrent cartilage loss. Approaches with the aim to inhibit BML development, avoidance of increase in size and avoidance of Hoffa-synovitis worsening may have beneficial effects on cartilage loss.

Purpose: This study aimed to comprehensively analyze the landscape of osteoarthritis (OA) biomarker research through the citation analysis of top-cited articles, identifying trends and gaps in this field.

Methods: The Web of Science Core Collection was utilized to retrieve the top 50 cited articles on OA biomarkers. Data extraction included publication characteristics, citation metrics, and biomarker categorization. Statistical analyses were conducted to discern correlations and assess significance.

Results: The top 50 cited articles spanned the years 1999 to 2020, and collectively cited 4849 articles, accumulating a total of 6177 citations, resulting in an average of 123.5 citations per document. Citations per article varied between 78 and 359, with a citation density ranging from 3.9 to 23.93. Analysis of the top 50 cited articles revealed comparable impact between recent and older publications. Predominant trends included cartilage-related and blood-based biomarkers, while inflammation-related, radiomics, and multi-omics emerged as potential future research directions. In BIPEDS classification, gaps were identified in biomarkers evaluating intervention efficacy and safety.

Conclusion: Despite significant advancements, there is no universally acknowledged biomarker for OA. Addressing gaps in biomarker exploration is crucial for enhancing OA management strategies. This study provides insights into prevailing trends and future research directions in OA biomarkers, guiding future investigations and therapeutic development.

Objective: The 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.

Design: The 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.

Results: This 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.

Conclusions: This 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.

Objective: The purpose of the study was to determine average tensile forces resulting in suture failure while tying a knot during repair of complete radial meniscus tears and to compare the failure tensile force based on meniscus tissue location: the peripheral (red-red) versus inner (white-white).

Design: This study was designed as a cadaveric biomechanical study using 24 menisci harvested from fresh frozen cadaveric knees with midbody radial tears. Tears were repaired using 2-0 nonabsorbable suture in both the inner meniscus and the peripheral meniscus. A force gauge was used to measure the tension of a surgeon's knot until failure of either the suture or the meniscus tissue. Statistical analysis was performed comparing suture failure tensile forces between inner and peripheral sutures using 2-sample t test.

Results: Suture repairs primarily failed due to meniscal tissue cut-out after suture tensioning (96%). There was no statistical difference in failure mode between medial and lateral meniscus for both the inner (100% cut-out) and the peripheral (92% cut-out; P = 0.703) sutures. The peripheral sutures failed as significantly higher loads (54 ± 26 N) than the inner sutures (36 ± 11 N, P = 0.006). The peripheral meniscus tissue tolerated significantly higher tension at failure (36 ± 7 N) than the inner meniscus (26 ± 7 N, P < 0.001).

Conclusion: When tying parallel sutures to repair a radial meniscus tear, suture tensile forces above 30 N may tear through meniscus tissue. Surgeons should not use suture tying forces above 30 N when repairing radial meniscus tears with parallel sutures. The peripheral meniscus can withstand higher knot-tying forces than the inner meniscus, so surgeons should consider tying the peripheral suture before the inner suture.