title: Biochemical and biomechanical properties of lesion and adjacent articular cartilage after chondral defect repair in an equine model.
abstract: BACKGROUND
  Chondral defects may lead to degradative changes in the surrounding cartilage, predisposing patients to developing osteoarthritis.
  
  
  OBJECTIVE
  To quantify changes in the biomechanical and biochemical properties of the articular cartilage adjacent to chondral defects after experimental defect repair.
  
  
  METHODS
  Controlled laboratory study.
  
  
  METHODS
  Specimens were harvested from tissue within (lesion), immediately adjacent to, and at a distance from (remote area) a full-thickness cartilage defect 8 months after cartilage repair with genetically modified chondrocytes expressing insulin-like growth factor-I or unmodified, control chondrocytes. Biomechanical properties, including instantaneous Young's and equilibrium aggregate moduli, were determined by confined compression testing. Biochemical properties, such as water and proteoglycan content, were also measured.
  
  
  RESULTS
  The instantaneous Young's modulus, equilibrium modulus, and proteoglycan content increased, whereas water content decreased with increasing distance from the repaired lesion. The instantaneous Young's and equilibrium moduli of the adjacent articular cartilage were 80% and 50% that of remote area samples, respectively, whereas water content increased 0.9% and proteoglycan content was decreased by 35%. No significant changes in biomechanical and biochemical properties were found either in the lesion tissue or in adjacent cartilage with genetic modification of the chondrocytes.
  
  
  CONCLUSIONS
  Articular cartilage adjacent to repaired chondral defects showed significant remodeling 8 months after chondral defect repair, regardless of whether genetically modified or unmodified cells were implanted.
  
  
  CONCLUSIONS
  Changes in the biochemical and biomechanical properties of articular cartilage adjacent to repaired chondral defects may represent remodeling as part of an adaptive process or degeneration secondary to an altered distribution of joint forces. Quantification of these changes could provide important parameters for assessing progress after operative chondral defect repair.
authors.affiliation: Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York, New York 10021, USA. ejs2002@med.cornell.edu
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Strauss
authors.forename: Laurie R
authors.initials: LR
authors.lastname: Goodrich
authors.forename: Chih-Tung
authors.initials: CT
authors.lastname: Chen
authors.forename: Chisa
authors.initials: C
authors.lastname: Hidaka
authors.forename: Alan J
authors.initials: AJ
authors.lastname: Nixon
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D001857:Bone Matrix / Q000473:pathology; D002358:Cartilage, Articular / Q000737:chemistry* / Q000473:pathology* / Q000601:surgery; D019902:Chondrocytes / Q000502:physiology* / Q000637:transplantation*; D015316:Genetic Therapy; D006736:Horses; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D010003:Osteoarthritis / Q000209:etiology* / Q000517:prevention & control
chemical_list: D007334:Insulin-Like Growth Factor I