IntroductionCell therapy is a rapidly growing area of research for the treatment of osteoarthritis (OA). This work is aimed to investigate the efficacy of intra-articular adipose-derived stromal cell (ASC) injection in the healing process on cartilage, synovial membrane and menisci in an experimental rabbit model.MethodsThe induction of OA was performed surgically through bilateral anterior cruciate ligament transection (ACLT) to achieve eight weeks from ACLT a mild grade of OA. A total of 2 × 106 and 6 × 106 autologous ASCs isolated from inguinal fat, expanded in vitro and suspended in 4% rabbit serum albumin (RSA) were delivered in the hind limbs; 4% RSA was used as the control. Local bio-distribution of the cells was verified by injecting chloro-methyl-benzamido-1,1'-dioctadecyl-3,3,3'3'-tetra-methyl-indo-carbocyanine per-chlorate (CM-Dil) labeled ASCs in the hind limbs. Cartilage and synovial histological sections were scored by Laverty's scoring system to assess the severity of the pathology. Protein expression of some extracellular matrix molecules (collagen I and II), catabolic (metalloproteinase-1 and -3) and inflammatory (tumor necrosis factor- α) markers were detected by immunohistochemistry. Assessments were carried out at 16 and 24 weeks.ResultsLabeled-ASCs were detected unexpectedly in the synovial membrane and medial meniscus but not in cartilage tissue at 3 and 20 days from ASC-treatment. Intra-articular ASC administration decreases OA progression and exerts a healing contribution in the treated animals in comparison to OA and 4% RSA groups.ConclusionsOur data reveal a healing capacity of ASCs in promoting cartilage and menisci repair and attenuating inflammatory events in synovial membrane inhibiting OA progression. On the basis of the local bio-distribution findings, the benefits obtained by ASC treatment could be due to a trophic mechanism of action by the release of growth factors and cytokines.
The transplantation of BMC-HA provided the best effects in supporting regenerative processes in cartilage, meniscus, and synovium and at less extent in bone. On the whole, both MSC and BMC combined with HA reduced inflammation and contributed to switch off fibrotic and hypertrophic processes. The observed regenerative potential by BMC-HA on meniscus could open new perspectives, suggesting its use not only for OA care but also for the treatment of meniscal lesions, even if further analyses are necessary to confirm its healing potential at long-term follow-up.
Purpose: We are developing the cell therapy, especially using hBMSCs, for cartilage defect. The result of this therapy would be better if we could get the cells, having more chondrogenic capacity, enough to target the cartilage defect. The cell-sheet would be a good candidate of the applications to get better result. Our colleagues have reported the Abstracts / Osteoarthritis and Cartilage 22 (2014) S57-S489 S487
cartilage degeneration. Knee joints from the mice at 4 and 8 weeks post surgery (n¼4 in each group) were collected for morphological analysis. Results: 1) We did not find the initiation and acceleration of articular cartilage degeneration by the genetic inactivation of Tgfbr2 in knee joints of mice at the age of 9 months or older. We also did not find hypertrophic chondrocytes in the articular cartilage of the mice. 2) We found that intra-articular injection of neutralizing TGF-b1 antibody into the knee joints of Col11a1þ/-mice delayed articular cartilage degeneration approximately 3 months, compared to that in Col11a1þ/-mice without the injection of the antibody. It takes about 15 months for Col11a1þ/-mice to form OA knee joints. 3) We found that treatment with Losartan delayed articular cartilage degeneration, induced by DMM, compared to that in control littermates. 4) We found that removal of Tgfbr2 in articular cartilage of knee joints delayed articular cartilage degeneration, induced by DMM, at least 6 weeks, compared to that in wild-type littermates. It takes about 16 weeks for mice with DMM to develop OA knee joints. Conclusion: Inhibition of Tgf-b1 signaling attenuated articular cartilage degeneration in mature knee joints of mouse models of OA. Therefore, inhibition activity of TGF-b1, not application of TGF-b1, may be considered in treatment of OA in mature joints.
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