title: Inflammation and Degeneration in Cartilage Samples from Patients with Femoroacetabular Impingement.
abstract: BACKGROUND
  Femoroacetabular impingement (FAI) has been reported as a cause of hip pain in young patients and is suggested as the trigger for hip osteoarthritis (OA). The goal of this study was to quantify the metabolic profiles of articular tissues (cartilage, synovium, and labrum) harvested from patients with FAI and with end-stage OA. In addition, we sought to investigate the development of secondary OA in hips with FAI.
  
  
  METHODS
  Tissue samples were obtained from thirty hips undergoing arthroscopic surgery for FAI with or without labral tear and thirty hips undergoing total hip arthroplasty for OA. Quantitative real-time polymerase chain reaction (PCR) was performed to determine the gene expression of inflammatory cytokines and metabolic (anabolic and catabolic) enzymes. The differences in gene expression in articular tissues from the patients with FAI were also evaluated on the basis of clinical parameters (age range and alpha angle).
  
  
  RESULTS
  The messenger RNA (mRNA) expression of the inflammatory cytokines interleukin-1 beta (IL-1β) and IL-8 and of matrix metalloproteinase (MMP)-3 (a catabolic gene) in both the synovium and the labrum, and the expression of collagen type I alpha 1 (an anabolic gene) in the labrum, was higher in the samples from hips with OA than in those from hips with FAI (p < 0.05). In cartilage, however, the mRNA expression of the inflammatory cytokines and the catabolic genes MMP-13 and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs-4) was higher in the FAI samples compared with the OA samples (p < 0.01). When the expression of inflammatory cytokines was evaluated among the three types of tissues within each disease group, the expression levels were the highest in cartilage within the FAI samples (p < 0.01). In FAI cartilage, we found higher gene expression of aggrecan (ACAN) and ADAMTS-4 in the samples from patients with larger alpha angles (≥60°) (p < 0.01).
  
  
  CONCLUSIONS
  Our results indicate that the metabolic conditions of articular cartilage in FAI and OA are different and that the expression of genes associated with inflammation is greater in the articular cartilage of patients with FAI compared with the synovium and the labrum. The metabolic changes were heightened by mechanical impingement.
  
  
  CONCLUSIONS
  The articular cartilage from the impingement lesion in patients with FAI showed biologically higher inflammation and degeneration, supporting the concept that FAI may be a trigger for joint degeneration.
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan n_chinzei@yahoo.co.jp.
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Chinzei
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan shingo1023@theia.ocn.ne.jp.
authors.forename: Shingo
authors.initials: S
authors.lastname: Hashimoto
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan taka2446@yg8.so-net.ne.jp.
authors.forename: Takaaki
authors.initials: T
authors.lastname: Fujishiro
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan s11793290@yahoo.co.jp.
authors.forename: Shinya
authors.initials: S
authors.lastname: Hayashi
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan noriyukikanzaki@hotmail.co.jp.
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Kanzaki
authors.affiliation: Department of Orthopaedic Surgery, Wakamatsu Hospital for University of Occupational and Environmental Health, Wakamatsu-ku, Kitakyushu, Japan soushi@med.uoeh-u.ac.jp.
authors.forename: Soshi
authors.initials: S
authors.lastname: Uchida
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan kurodar@med.kobe-u.ac.jp.
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Kuroda
authors.affiliation: Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan kurosaka@med.kobe-u.ac.jp.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kurosaka
mesh_terms: D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D019644:Arthroplasty, Replacement, Hip / Q000379:methods; D001182:Arthroscopy / Q000379:methods; D002358:Cartilage, Articular / Q000378:metabolism / Q000473:pathology*; D000090602:Collagen Type I, alpha 1 Chain; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D018450:Disease Progression; D005260:Female; D057925:Femoracetabular Impingement / Q000473:pathology* / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D015207:Osteoarthritis, Hip / Q000473:pathology* / Q000601:surgery; D010007:Osteochondritis / Q000473:pathology* / Q000601:surgery; D011379:Prognosis; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D018570:Risk Assessment; D012494:Sampling Studies; D018709:Statistics, Nonparametric; D055815:Young Adult
chemical_list: C000716127:COL1A1 protein, human; D000090602:Collagen Type I, alpha 1 Chain; D016207:Cytokines; D012333:RNA, Messenger