title: Inflammatory cytokine profiles associated with chondral damage in the anterior cruciate ligament-deficient knee.
abstract: OBJECTIVE
  Patients with chronic anterior cruciate ligament (ACL) deficiency are at high risk of articular cartilage damage and the development of osteoarthritis (OA). It has been hypothesized that biochemical factors, such as cytokines, contribute to the process. The purpose of our study was to determine the concentrations of potentially chondrodestructive and chondroprotective cytokines in the chronic ACL-deficient knee, and to determine if the cytokine profile or other factors correlated with the amount of chondral damage present in the knee.
  
  
  METHODS
  A consecutive series of patients who consented to the Institutional Review Board-approved study.
  
  
  METHODS
  Synovial fluid lavages were obtained from 31 patients with ACL-deficient knees. Four patients had lavages aspirated from their contralateral normal knee. These lavages were analyzed for interleukin (IL)-1alpha, IL-1beta, IL-1ra, and tumor necrosis factor (TNF)-alpha. At arthroscopy, the amount of chondral damage was graded based on the Outerbridge classification.
  
  
  RESULTS
  Concentrations of chondrodestructive IL-1beta and TNF-alpha were significantly higher in patients with ACL ruptures than in the contralateral normal knees. The more severe the chondral damage, the higher the concentration of IL-1beta and TNF-alpha. Chondroprotective cytokine concentrations decreased with increasing grades of chondral damage. We found a linear correlation between the severity of chondral damage and the time from injury (r2 = .954).
  
  
  CONCLUSIONS
  A difference was seen in the cytokine profiles between the normal and injured knees. This difference varied based on the severity of chondral damage, which was associated with time from injury.
  
  
  CONCLUSIONS
  Cytokine levels are associated with chondral damage.
authors.affiliation: Department of Orthopaedic Surgery, University of Toronto, Orthopaedic and Arthritic Institute, Toronto, Ontario, Canada.
authors.forename: Paul H
authors.initials: PH
authors.lastname: Marks
authors.forename: Michelle L Cameron
authors.initials: ML
authors.lastname: Donaldson
mesh_terms: D000293:Adolescent; D000328:Adult; D016118:Anterior Cruciate Ligament / Q000601:surgery*; D000070598:Anterior Cruciate Ligament Injuries; D001182:Arthroscopy; D002358:Cartilage, Articular / Q000473:pathology*; D016207:Cytokines / Q000032:analysis*; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000209:etiology / Q000503:physiopathology; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology; D011184:Postoperative Period; D012421:Rupture; D012720:Severity of Illness Index; D012795:Sialoglycoproteins / Q000032:analysis; D013582:Synovial Fluid / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha