Abstract

Femoroacetabular impingement (FAI) is a frequent cause of hip pain and may lead to secondary osteoarthritis yet little is known about the molecular events linking mechanical hip impingement and articular cartilage degeneration. The purpose of this study is to compare the cell activity and histological appearance of articular chondrocytes harvested from patients with FAI and examine the relationship of patient age. Cartilage biopsies were obtained from 26 donors with FAI who underwent hip arthroscopy for debridement of cam lesions. Quantitative real-time polymerase chain reaction [qRT-PCR] was performed to assess gene expression of markers for extracellular matrix (ECM) synthesis, inflammation, and cellular senescence. Specimens were separated into the senescent or active cell activity groups based on positive red staining by using safranin O/ fast green staining. The age of the donors were then compared and divided into 2 groups: above and below 40 year olds. Student t test was used to compare between the two groups. P < 0.05 was considered significant. Standard deviation was used to indicate the variation within groups. Chondrocytes derived from FAI cartilage in donors younger than 40 years old (mean=32.3 years old, SD = 7.0 years) had significantly less cell activity (p= 0.005) than donors greater than age 40 (mean = 42.1 years old, SD = 10.8). Red positive staining of safranin O was seen in the extracellular matrix or surrounding the cells of the active group. There was no significant difference between the alpha angles of the two groups (p=0.4). Cartilage in cam-type FAI is molecularly and morphologically different between age groups above and below 40 years old. Specimens with primarily active cells were from donors greater than 40 years old and donors younger than 40 years old had senescent cells. There was no significant difference based on alpha angle and gender. Greater understanding of the molecular differences between cartilage in younger and older patients with FAI may improve their surgical management for the future development of novel treatment that attenuate disease progression to OA.

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