title: The acute structural changes of loaded articular cartilage following meniscectomy or ACL-transection.
abstract: OBJECTIVE
  Meniscectomy and anterior cruciate ligament (ACL) rupture have been identified as precursors of osteoarthrosis (OA) in clinical reviews and animal experiments. In this study, the acute effects of these injuries on articular cartilage matrix deformation, preserved in a loaded state using a cryopreservation technique, were studied by scanning electron microscopy (SEM).
  
  
  METHODS
  Whole knee joints from adult White New Zealand rabbits (N=87) were loaded ex vivo, using a simulated quadriceps pull under static and cyclic loading conditions, following medial meniscectomy or transection of the ACL. Specimens were plunge-frozen while under load, or following a recovery period, and prepared for SEM by cryofixation. Using SEM and photographic images, the medial tibial plateau cartilage was assessed both qualitatively and quantitatively.
  
  
  RESULTS
  After meniscectomy, significantly increased bending and crimping of radial collagen fibers occurred with static loading. Compared to intact knees, the area of tibial cartilage showing an indentation was increased by 80% (P< 0.05), the articular cartilage thickness was significantly more reduced when under load (for high force long duration static loading, intact joints had 53%+/-3 reduction in cartilage thickness compared to 39%+/-4 after meniscectomy, P< 0.05), and it took nearly twice as long for the cartilage thickness to recover following loading. These post-meniscectomy differences were either not present or were minimal when the joint was allowed to extend when loaded. ACL-transection slightly increased collagen deformation in the deeper zones, but only with cyclic loading.
  
  
  CONCLUSIONS
  The findings indicate that, with static loading, significantly increased deformation of articular cartilage collagen structure can occur following meniscectomy, but is minimized by joint motion. This increased deformation may be relevant to the etiology and progression of joint degeneration.
authors.affiliation: AO/ASIF Research Institute, Davos, Switzerland. max.kaeaeb@charite.de
authors.forename: M J
authors.initials: MJ
authors.lastname: Kääb
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: J M
authors.initials: JM
authors.lastname: Clark
authors.forename: H P
authors.initials: HP
authors.lastname: Nötzli
mesh_terms: D000818:Animals; D000070598:Anterior Cruciate Ligament Injuries; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure*; D003094:Collagen / Q000648:ultrastructure; D015925:Cryopreservation; D005260:Female; D008592:Menisci, Tibial / Q000601:surgery*; D008855:Microscopy, Electron, Scanning; D010003:Osteoarthritis / Q000473:pathology* / Q000503:physiopathology; D011183:Postoperative Complications / Q000473:pathology* / Q000503:physiopathology; D011817:Rabbits; D013314:Stress, Mechanical
chemical_list: D003094:Collagen