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: 5.28). 11/1991; 73(9):1301-15.
Source: PubMed


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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    • "Various cartilage repair techniques have been developed. Resurfacing techniques include abrasion arthroplasty [24], Pridie drilling [36] and microfracture technique (MF) [3, 43]. MF procedures stimulate and recruit mesenchymal cells from the subchondral bone marrow and subsequently form a fibrin clot that eventually turns into a predominantly fibrocartilaginous regenerate with inferior biomechanical characteristics compared to native hyaline articular cartilage [11]. "
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    ABSTRACT: To compare long-term functional and radiological outcome following microfracture technique (MF) versus osteochondral autologous transplantation (OAT) mosaicplasty for treating focal chondral lesions of the knee. Twenty-five patients (mean age 32.3 years, SD 7.7) with a full-thickness (International Cartilage Repair Society grade 3 or 4) chondral lesion of the articulating surface of the femur were randomized to either MF (n = 11) or OAT mosaicplasty (n = 14). At a median follow-up of 9.8 years (range 4.9-11.4), the patients were evaluated using Lysholm score (n = 25), Knee Injury and Osteoarthritis Outcome Score (KOOS, n = 25), isokinetic quadriceps measurement and hamstring strength measurement (n = 22) and standing radiographs (n = 23). There were no significant differences in Lysholm score, KOOS, isokinetic muscle strength or radiographic osteoarthritis between MF-treated patients and OAT mosaicplasty-treated patients at follow-up. Mean Lysholm score at follow-up was 69.7 [95 % confidence interval (CI), 55.1-84.4] for the MF group and 62.6 (95 % CI, 52.6-72.6) for the OAT mosaicplasty group. At long-term follow-up, there were no significant differences between patients treated with MF and patients treated with OAT mosaicplasty in patient-reported outcomes, muscle strength or radiological outcome. Therapeutic study, Level II.
    Knee Surgery Sports Traumatology Arthroscopy 01/2014; 22(6). DOI:10.1007/s00167-014-2843-6 · 3.05 Impact Factor
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