Long-Term Survival of Chondrocytes in an Osteochondral Articular Cartilage Allograft. A Case Report*

Fr, Convery; Wh, Akeson; Amiel, David; Mh, Meyers; Monosov, Anna Z.

doi:10.2106/00004623-199607000-00013

Cited by 84 publications

(27 citation statements)

References 10 publications

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“…The high incidence of OA is due in part to the minimal intrinsic healing capacity of injured articular cartilage. Despite this, there has been significant progress in improving cartilage repair through transfer of allogenous or autogenous tissues, and through free cell transplantation procedures [4,6,9,23,40,50,52,57]. Cartilage resurfacing by transplantation of autogenous or allogenous chondrocytes, or through the use of mesen-*Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

Chondrocytic differentiation of mesenchymal stem cells sequentially exposed to transforming growth factor‐β1 in monolayer and insulin‐like growth factor‐I in a three‐dimensional matrix

Worster

Brower-Toland

Fortier

et al. 2001

Journal Orthopaedic Research

256

171

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This study evaluated chondrogenesis of mesenchymal progenitor stem cells (MSCs) cultured initially under pre-confluent monolayer conditions exposed to transforming growth factor-81 (TGF-Pl ), and subsequently in three-dimensional cultures containing insulin-like growth factor I (IGF-I). Bone marrow aspirates and chondrocytes were obtained from horses and cultured in monolayer with 0 or 5 ng of TGF-P1 per ml of medium for 6 days. TGIF-81 treated and untreated cultures were distributed to threedimensional fibrin disks containing 0 or 100 ng of IGF-I per ml of medium to establish four treatment groups. After 13 days, cultures were assessed by toluidine blue staining, collagen types I and I1 in situ hybridization and immunohistochemistry, proteoglycan production by [35S]-s~ilfate incorporation, and disk DNA content by fluorometry. Mesenchymal cells in monolayer cultures treated with TGF-81 actively proliferated for the first 4 days, developed cellular rounding, and formed cell clusters. Treated MSC cultures had a two-fold increase in medium proteoglycan content. Pretreatment of MSCs with TGF-81 followed by exposure of cells to IGF-I in three-dimensional culture significantly increased the formation of markers of chondrocytic flmction including disk proteoglycan content and procollagen type I1 mRNA production. However, proteoglycan and procollagen type I1 production by MSC's remained lower than parallel chondrocyte cultures. MSC pretreatment with TGF-P1 without sequential IGF-I was less effective in initiating expression of markers of chondrogenesis. This study indicates that although MSC differentiation was less than complete when compared to mature chondrocytes, chondrogenesis was observed in IGF-I supplemented cultures, particularly when used in concert with TGF-81 pretreatment. 0 9001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.

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Section: Introductionmentioning

confidence: 99%

Chondrocytic differentiation of mesenchymal stem cells sequentially exposed to transforming growth factor‐β1 in monolayer and insulin‐like growth factor‐I in a three‐dimensional matrix

Worster

Brower-Toland

Fortier

et al. 2001

Journal Orthopaedic Research

256

171

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“…chondrocyte viability, and retrieved grafts have contained viable chondrocytes up to twenty-nine years after implantation [1][2][3][4][5] . In contrast, frozen osteochondral allografts, used for massive oncologic joint reconstructions, have low chondrocyte viability at implantation, and grafts retrieved at approximately one to five years contain acellular and often degenerate cartilage 6,7 .…”

mentioning

confidence: 99%

Treatment of Articular Cartilage Defects in the Goat with Frozen Versus Fresh Osteochondral Allografts: Effects on Cartilage Stiffness, Zonal Composition, and Structure at Six Months

Pallante

Görtz

Chen

et al. 2012

Journal of Bone and Joint Surgery

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“…Bleeding from the subchondral bone promotes wound healing and results in a hyaline-like but more cellular tissue at the defect site of the cartilage (Mainil-Varlet et al, 2003). During recent years, intensive efforts have been made to develop cell therapies for cartilage repair, such as the autologous transplantation of chondrocytes (Brittberg et al, 1994;Convery et al, 1996;Ghazavi et al, 1997). Large quantities of healthy cells from limited source are required in such cell-based therapies.…”

mentioning

confidence: 99%

Differential effect of ECM molecules on re‐expression of cartilaginous markers in near quiescent human chondrocytes

Chiu

Chen

et al. 2011

Journal Cellular Physiology

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The limited source of healthy primary chondrocytes restricts the clinical application of tissue engineering for cartilage repair. Therefore, method to maintain or restore the chondrocyte phenotype during in vitro expansion is essential. The objective of this study is to establish the beneficial effect of ECM molecules on restoring the re-expression of cartilaginous markers in primary human chondrocytes after extensive monolayer expansion. During the course of chondrocyte serial expansion, COL2A1, SOX9, and AGN mRNA expression levels, and GAG accumulation level were reduced significantly in serially passaged cells. Exogenous type II collagen dose-dependently elevated GAG level and induced the re-expression of cartilaginous marker mRNAs in P7 chondrocytes. Chondroitin sulfate did not show significant effect on P7 chondrocytes, while hyaluronic acid inhibited the expression of SOX9 and AGN mRNAs. Upon treatment with type II collagen, FAK, ERK1/2, and JNK were activated via phosphorylation in P7 chondrocytes within 15 min. Furthermore, GFOGER integrin blocking peptide, MEK inhibitor and JNK inhibitor, not p38 inhibitor, significantly reduced the type II collagen-induced GAG deposition level. Finally, in the presence of TGF-β1 and IGF-I, P7 chondrocytes cultured in 3D type II collagen matrix exhibited better cartilaginous features than those cells cultured in the type I collagen matrix. In conclusion, type II collagen alone can effectively restore cartilaginous features of expanded P7 human chondrocytes. It is probably mediated via the activation of FAK-ERK1/2 and FAK-JNK signaling pathways. The potential application of type II collagen in expanding a scarcity of healthy chondrocytes in vitro for further tissue engineering is implicated.

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Long-Term Survival of Chondrocytes in an Osteochondral Articular Cartilage Allograft. A Case Report*

Cited by 84 publications

References 10 publications

Chondrocytic differentiation of mesenchymal stem cells sequentially exposed to transforming growth factor‐β1 in monolayer and insulin‐like growth factor‐I in a three‐dimensional matrix

Chondrocytic differentiation of mesenchymal stem cells sequentially exposed to transforming growth factor‐β1 in monolayer and insulin‐like growth factor‐I in a three‐dimensional matrix

Treatment of Articular Cartilage Defects in the Goat with Frozen Versus Fresh Osteochondral Allografts: Effects on Cartilage Stiffness, Zonal Composition, and Structure at Six Months

Differential effect of ECM molecules on re‐expression of cartilaginous markers in near quiescent human chondrocytes

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