title: Autologous chondrocyte implantation drives early chondrogenesis and organized repair in extensive full- and partial-thickness cartilage defects in an equine model.
abstract: Autologous chondrocyte implantation (ACI) has been used clinically for over 15 years and yet definitive evidence of chondrocyte persistence and direct impact on cartilage repair in full-thickness lesions is scant and no data are available on ACI in partial-thickness defects in any animal model. This study assessed the effect of chondrocytes secured using periosteal overlay in partial- and full-thickness cartilage defects in the equine model. Paired cartilage defects 15 mm in diameter were made in the patellofemoral joint of 16 horse and repaired with ACI or periosteal flap alone. Response was assessed at 8 weeks by clinical, microradiographic, and histologic appearance, and by collagen type II immunohistochemistry, and proteoglycan and DNA quantification. ACI improved histologic scores in partial- and full-thickness cartilage defects, including defect filling, attachment to the underlying subchondral bone, and presence of residual chondrocyte accumulations. For partial-thickness defects chondrocyte predominance, collagen type II content, and toluidine stained matrix were enhanced, and attachment to the surrounding cartilage improved. DNA and PG content of grafted partial-thickness defects was improved by chondrocyte implantation. Periosteal patches alone did not induce cartilage repair. This study indicated implantation of chondrocytes to cartilage defects improved healing with a combination of persisting chondrocyte regions, enhanced collagen type II formation, and better overall cartilage healing scores. Use of ACI in the more challenging partial-thickness defects also improved histologic indices and biochemical content. The equine model of cartilage healing closely resembles cartilage repair in man, and results of this study confirm cell persistence and improved early cartilage healing events after ACI.
authors.affiliation: Comparative Orthopaedics Laboratory, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA. ajn1@cornell.edu
authors.forename: Alan J
authors.initials: AJ
authors.lastname: Nixon
authors.forename: Laila
authors.initials: L
authors.lastname: Begum
authors.forename: Hussni O
authors.initials: HO
authors.lastname: Mohammed
authors.forename: Barbara
authors.initials: B
authors.lastname: Huibregtse
authors.forename: Michael M
authors.initials: MM
authors.lastname: O'Callaghan
authors.forename: Gloria L
authors.initials: GL
authors.lastname: Matthews
mesh_terms: D000818:Animals; D001706:Biopsy; D002114:Calcinosis / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D002358:Cartilage, Articular / Q000293:injuries* / Q000473:pathology / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D019902:Chondrocytes / Q000473:pathology / Q000637:transplantation*; D020219:Chondrogenesis / Q000502:physiology*; D024043:Collagen Type II / Q000378:metabolism; D004195:Disease Models, Animal; D006085:Graft Survival / Q000502:physiology; D006736:Horses; D013582:Synovial Fluid / Q000502:physiology; D014945:Wound Healing / Q000502:physiology*
chemical_list: D024043:Collagen Type II