EP9.27 Distinct Synovial Gene Expression Profiles in Femoroacetabular Impingement and Pre-Collapse Avascular Necrosis of the Hip

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ID: 331321
2026
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Abstract
Abstract Background Femoroacetabular impingement (FAI) and avascular necrosis (AVN) are two major causes of pain in the pre-arthritic hip, both capable of progressing to joint deterioration and arthritis. The synovium plays an important role in joint homeostasis through production of cytokines, proteases, and signaling mediators that regulate cartilage metabolism and inflammatory activity. However, synovial molecular activity in these conditions remains poorly characterized. The purpose of this study was to characterize synovial gene expression in patients undergoing arthroscopic treatment for FAI and arthroscopic-assisted core decompression for pre-collapse AVN. Methods Synovial tissue was collected arthroscopically from the anterolateral capsulolabral recess in six FAI patients (mean age 39 years; 5 males) and six pre-collapse AVN patients (mean age 37 years; 4 males). RNA was extracted using the Zymo Research Direct-Zol RNA Mini Kit, and cDNA was synthesized with SuperScript IV VILO Master Mix. Gene expression was profiled across 88 key genes involved in cartilage breakdown and repair using the GeneQuery Human Osteoarthritis and Cartilage Repair qPCR Array (ScienCell Research Laboratories). Data were normalized to five housekeeping genes (ACTB, GAPDH, LDHA, NONO, PPIH), and a quantification cycle (Cq) of >35 was excluded from downstream analysis. Differential expression was assessed using a two-tailed unequal-variance t-test (p <0.05). Expression fold change of AVN samples relative to FAI samples was calculated using the equation: fold change = 2^-(Mean ΔCq AVN - Mean ΔCq FAI). Results Both groups demonstrated high synovial gene expression (ΔCq<1) of mediators involved in early cartilage degradation and osteoarthritis, including COL1A1, COL1A2, COL3A1, COL5A1, HMGB1, MMP2, HTRA1, ASPN, CILP, CTNNB1, and FN1. Eleven genes exhibited significantly higher expression in pre-collapse AVN compared with FAI: ACAN (7.7x, p = 0.02), MAPK8 (3.4x, p = 0.04), MATN3 (6.7x, p = 0.01), WNT4 (7.1x, p = 0.01), NOS2 (6.3x, p = 0.04), SMAD9 (2.6x, p = 0.02), CCR7 (5.8x, p <0.01), RUNX2 (1.8x, p <0.01), TNFRSF11A (4.4x, p = 0.04), TGFB1 (5.5x, p = 0.04), and BMP2 (3.3x, p = 0.01). Discussion This study demonstrates distinct synovial gene expression profiles in hip FAI and pre-collapse AVN. Compared with FAI, pre-collapse AVN demonstrated increased expression of MAPK8, NOS2, CCR7, RUNX2, TNFRSF11A, and BMP2, which may represent molecular drivers of progressive joint destruction and subchondral collapse. In contrast, increased expression of ACAN, MATN3, WNT4, and TGFB1 may reflect a compensatory reparative response through pro-chondrogenic signaling and extracellular matrix stabilization. These preliminary findings provide a foundation for future investigations into the pathogenesis and potential therapeutic targets for both conditions.
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Authors Kory B. Dylan Pasko, Melanie Oakes, Tanin Jouyan, Marlena Ramanis, Brian J. Gallagher, Amanda Marinko, James Learned, Melissa S. Albersheim, Dean Wang
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Journal Journal of hip preservation surgery
Year 2026
DOI
10.1093/jhps/hnag043.507
URL
https://doi.org/10.1093/jhps/hnag043.507
Keywords Keywords not found

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