title: Inflammatory changes in ruptured canine cranial and human anterior cruciate ligaments.
abstract: OBJECTIVE
  To compare expression of tartrate-resistant acid phosphatase (TRAP) and cathepsin K and histologic changes in canine cranial cruciate ligaments (CCLs) and human anterior cruciate ligaments (ACLs).
  
  
  METHODS
  Sections of cruciate ligaments from 15 dogs with ruptured CCLs, 8 aged dogs with intact CCLs, 14 human beings with ruptured ACLs, and 11 aged human beings with intact ACLs.
  
  
  METHODS
  The CCLs and ACLs were evaluated histologically, and cells containing TRAP and cathepsin K were identified histochemically and immunohistochemically, respectively.
  
  
  RESULTS
  The proportion of ruptured CCLs that contained TRAP+ cells was significantly higher than the proportion of intact ACLs that did but similar to proportions of intact CCLs and ruptured ACLs that did. The proportion of ruptured CCLs that contained cathepsin K+ cells was significantly increased, compared with all other groups. Numbers of TRAP+ and cathepsin K+ cells were significantly increased in ruptured CCLs, compared with intact ACLs. The presence of TRAP+ cells was correlated with inflammatory changes, which were most prominent in ruptured CCLs.
  
  
  CONCLUSIONS
  Results suggest that synovial macrophage-like cells that produce TRAP are an important feature of the inflammation associated with CCL rupture in dogs. Identification of TRAP and cathepsin K in intact CCLs and ACLs from aged dogs suggests that these enzymes have a functional role in cruciate ligament remodeling and repair. We hypothesize that recruitment and activation of TRAP+ macrophage-like cells into the stifle joint synovium and CCL epiligament are critical features of the inflammatory arthritis that promotes progressive degradation and eventual rupture of the CCL in dogs.
authors.affiliation: Comparative Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706, USA.
authors.forename: Jennifer G
authors.initials: JG
authors.lastname: Barrett
authors.forename: Zhengling
authors.initials: Z
authors.lastname: Hao
authors.forename: Benjamin K
authors.initials: BK
authors.lastname: Graf
authors.forename: Lee D
authors.initials: LD
authors.lastname: Kaplan
authors.forename: John P
authors.initials: JP
authors.lastname: Heiner
authors.forename: Peter
authors.initials: P
authors.lastname: Muir
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D016118:Anterior Cruciate Ligament / Q000378:metabolism* / Q000473:pathology; D000070598:Anterior Cruciate Ligament Injuries; D056657:Cathepsin K; D002403:Cathepsins / Q000378:metabolism*; D004285:Dogs / Q000293:injuries; D006801:Humans; D007150:Immunohistochemistry / Q000662:veterinary; D007527:Isoenzymes / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism*; D013583:Synovial Membrane / Q000166:cytology* / Q000378:metabolism; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D002403:Cathepsins; C534130:CTSK protein, human; D056657:Cathepsin K