Kim HK, Moran ME, Salter RB. The potential for regeneration of articular cartilage in defects created by chondral shaving and subchondral abrasion: an experimental investigation in rabbits

Division of Orthopaedic Surgery, Hospital for Sick Children, University of Toronto, Ontario, Canada.
The Journal of Bone and Joint Surgery (Impact Factor: 4.31). 11/1991; 73(9):1301-15.
Source: PubMed

ABSTRACT Animal models for chondral shaving and subchondral abrasion were created to resolve the controversy about the nature of the repair tissue after these procedures and to determine the effect of continuous passive motion on the quality of the repair tissue. Chondral shaving was performed on the patella in forty adolescent rabbits, and subchondral abrasion was performed on the patella in another forty rabbits. In both procedures, a three-millimeter-diameter defect was created. After the operation, twenty animals from each group were allowed intermittent active motion; the remainder were treated by continuous passive motion for two weeks, followed by intermittent active motion. Half of the animals from each group were killed at four weeks and the other half, at twelve weeks. There was no evidence of repair tissue in the defects at either four or twelve weeks after chondral shaving, regardless of the postoperative treatment. The remaining underlying cartilage, however, had degenerated. After abrasion of subchondral bone, the defects in animals that were treated with only intermittent active motion healed at twelve weeks, although the quality of the repair tissue varied. All ten of the animals that were treated with continuous passive motion, however, had mature, hyaline-like cartilage as the predominant repair tissue at twelve weeks, compared with six of the ten animals that were treated with intermittent active motion (p less than 0.05). We concluded that, in this model, partial-thickness defects created by chondral shaving do not heal; rather, the remaining underlying cartilage degenerates. Full-thickness defects created by subchondral abrasion can heal by regeneration of hyaline-like cartilage. Such healing is enhanced by continuous passive motion for two weeks postoperatively.

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    • "Articular cartilage has limited reparative abilities and purely chondral defects do not heal spontaneously. Progress of degenerated tissue of the surrounding cartilage may lead to osteoarthritis (OA) [1]. However, articular cartilage injuries that penetrate the subchondral bone can undergo spontaneous repair through the formation of fibrocartilage [2]. "
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    ABSTRACT: A major challenge in cartilage repair is the lack of chondrogenic cells migrating from healthy tissue into damaged areas and strategies to promote this should be developed. The aim of this study was to evaluate the effect of peripheral blood derived mononuclear cell (PBMC) stimulation on mesenchymal stromal cells (MSCs) derived from the infrapatellar fat pad of human OA knee. Cell migration was measured using an xCELLigence electronic migration chamber system in combination with scratch assays. Gene expression was quantified with stem cell PCR arrays and validated using quantitative real-time PCR (rtPCR). In both migration assays PBMCs increased MSC migration by comparison to control. In scratch assay the wound closure was 55% higher after 3 hours in the PBMC stimulated test group (), migration rate was 9 times faster (), and total MSC migration was 25 times higher after 24 hours (). Analysis of MSCs by PCR array demonstrated that PBMCs induced the upregulation of genes associated with chondrogenic differentiation over 15-fold. In conclusion, PBMCs increase both MSC migration and differentiation suggesting that they are an ideal candidate for inclusion in regenerative medicine therapies aimed at cartilage repair.
    Stem cell International 01/2015; Article ID 323454. DOI:10.1155/2015/323454 · 2.81 Impact Factor
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    • "In vivo studies have shown that cartilage from young and adolescent animals can regenerate partial-thickness defects to produce almost normal hyaline cartilage [1] [2], whereas self-repair is not seen in similarly created defects in articular cartilage of adult animals [3]-[7] or in clinical observations of defects in human articular cartilage [8]-[11]. "
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    ABSTRACT: Explants are excellent systems for studying homeostasis in cartilage. The systems are very useful in pharmacological studies involving OA-treatment and in studies of repair mechanisms during injury to hyaline cartilage. The purpose of this study was to evaluate the reparative processes oc-curring in a young age porcine cartilage explant model examining tissue by Light (LM) and Trans-mission Electron Microscopy (TEM). Explants of articular cartilage were dissected from the fe-moral condyles of immature one-year-old pigs and cultured in DMEM/F12 medium with FCS (sti-mulated explant) or in medium without FCS (control explant) for up to 4 weeks. After 1 -4 weeks of culture with FCS, LM showed migration and proliferation of chondrocytes in cartilage close to the injured surface differentiating two areas: proliferative zone and necrotic zone. The chondro-cytes present in the necrotic zone showed a polarization towards the injured surface. After bud-ding through the injured surface, the chondrocytes formed repair tissue in an interface repair zone and in outer repair tissue. TEM showed chondrocytes in expanded lacunae involving the pro-liferative zone. The pericellular matrix of the expanded lacunae was partly dissolved, indicating release of matrix-degrading enzymes during proliferation and remodeling. Migratory chondro-cytes were identified in oval lacunae close to the injured surface. The pericellular matrix of these oval lacunae was significantly dissolved and immunohistochemistry demonstrated strong staining with a polyclonale collagenase antibody around these units, suggesting release of matrix-degrad-ing collagenase contributing to chondrocyte mobility. We describe an explant model comprising two different repair systems in immature articular cartilage. This model provides us with new reference points that are important in understanding the repair mechanisms.
    Microscopy Research 10/2014; 2(2):67-80. DOI:10.4236/mr.2014.24009
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    • "It has long been known that the way in which cartilage is repaired depends on its depth. No appreciable repair occurs in partial-thickness defects that are confined to the cartilage itself (Kim et al. 1991). Since the bone marrow is the reservoir of mesenchymal stem cells (MSCs), the chondrogenic progenitor cells are available only when the cartilage defect is in contact with the marrow space (Yoo et al. 1998). "
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    ABSTRACT: Despite the well-known effect of type-I collagen in promoting cartilage repair, the mechanism still remains unknown. In this study we investigated this mechanism using a rabbit model of cartilage defects. 5-mm-diameter full-thickness defects were created on both patellar grooves of 53 Japanese white rabbits (approximately 13 weeks old). The left defect was filled with collagen gel and the right defect was left empty. The rabbits were killed and examined morphometrically until the twenty-fourth postoperative week, by (1) evaluation of matrix production, (2) enumeration of the total number of cells engaged in cartilage repair, (3) enumeration of the proliferating cells, (4) localization of mesenchymal stem cells, and (v) localization of apoptotic cells. We found that type-I collagen enhances cell recruitment, and thereby increases the number of proliferating cells. A considerable proportion of the proliferating cells were identified as bone marrow-derived mesenchymal stem cells. However, type-I collagen does not prevent the chondrocyte precursors from undergoing apoptotic disengagement from the chondrogenic lineage. Type-I collagen promotes cartilage repair by enhancing recruitment of bone marrow-derived mesenchymal stem cells. Additional use of agent(s) that sustain mesenchymal stem cells along the chondrogenic path of differentiation may constitute an appropriate environment for cartilage repair.
    Acta Orthopaedica 01/2008; 78(6):845-55. DOI:10.1080/17453670710014653 · 2.45 Impact Factor
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