Vascular injury of immature epiphyses impair stem cell engraftment in cartilage defects.

The purpose of our study was to investigate if vascular injury in immature epiphyses affects cartilage repair outcomes of matrix-associated stem cell implants (MASI). Porcine bone marrow mesenchymal stromal stem cells (BMSCs) suspended in a fibrin glue scaffold were implanted into 24 full-thickness cartilage defects (5 mm ø) of the bilateral distal femur of six Göttingen minipigs (n = 12 defects in 6 knee joints of 3 immature pigs; age 3.5-4 months; n = 12 defects in 6 knee joints of 3 mature control pigs; age, 21-28 months). All pigs underwent magnetic resonance imaging (MRI) at 2, 4, 12 (n = 24 defects), and 24 weeks (n = 12 defects). After the last imaging study, pigs were sacrificed, joints explanted and evaluated with VEGF, H&E, van Gieson, Mallory, and Safranin O stains. Results of mature and immature cartilage groups were compared using the Wilcoxon signed-rank test. Quantitative scores for subchondral edema at 2 weeks were correlated with quantitative scores for cartilage repair (MOCART score and ICRS score) at 12 weeks as well as Pineda scores at end of the study, using linear regression analysis. On serial MRIs, mature joints demonstrated progressive healing of cartilage defects while immature joints demonstrated incomplete healing and damage of the subchondral bone. The MOCART score at 12 weeks was significantly higher for mature joints (79.583 ± 7.216) compared to immature joints (30.416 ± 10.543, p = 0.002). Immature cartilage demonstrated abundant microvessels while mature cartilage did not contain microvessels. Accordingly, cartilage defects in immature joints showed a significantly higher number of disrupted microvessels, subchondral edema, and angiogenesis compared to mature cartilage. Quantitative scores for subchondral edema at 2 weeks were negatively correlated with MOCART scores (r = - 0.861) and ICRS scores (r = - 0.901) at 12 weeks and positively correlated with Pineda scores at the end of the study (r = 0.782). Injury of epiphyseal blood vessels in immature joints leads to subchondral bone defects and limits cartilage repair after MASI.

Treatment strategies for meniscal lesions: from past to prospective therapeutics.

Menisci play an important role in the biomechanics of knee joint function, including loading transmission, joint lubrication, prevention of soft tissue impingement during motion and joint stability. Meniscal repair presents a challenge due to a lack of vascularization that limits the healing capacity of meniscal tissue. In this review, the authors aimed to untangle the available treatment options for repairing meniscal tears. Various surgical procedures have been developed to treat meniscal tears; however, clinical outcomes are limited. Consequently, numerous researchers have focused on different treatments such as the application of exogenous and/or autologous growth factors, scaffolds including tissue-derived matrix, cell-based therapy and miRNA-210. The authors present current and prospective treatment strategies for meniscal lesions.

One of the most common knee injuries, especially in athletes, is a meniscal tear. There are two wedge-shaped pieces of fibrocartilage that act as shock absorbers between the thighbone and shinbone (menisci). The menisci help to transmit weight from one bone to another and play an important role in knee stability. The challenge for researchers and clinicians is to repair meniscal injuries, despite the lack of vascularization. The authors discuss the available approaches for repairing meniscal tears. Non surgical and surgical procedures are reviewed, clarifying their clinical outcomes. Other approaches to tissue engineering are also discussed. Using the patient's cells may be a potential strategy to repair meniscal injuries and improve the durability of the knee joint.