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.
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).
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).
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.
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.