Mature and inactive microvessels are prominent in areolar synovium of femoroacetabular impingement and hip osteoarthritis patients.

Objective: To provide insight into the earliest changes in hip osteoarthritis (OA) pathogenesis. Histopathology of synovium was investigated in patients with femoroacetabular impingement (FAI), FAI with early hip osteoarthritis, and advanced hip osteoarthritis.

Methods: Synovium biopsies were collected from ten FAI, fourteen FAI with early osteoarthritis, and twelve advanced osteoarthritis patients. Histopathological grading allowed assessment of osteoarthritis-associated features. Microvessel density and maturity were determined through immunofluorescent labelling of CD31 and α-smooth muscle actin. Immunohistochemical staining was applied to calculate CD105 microvessel density, providing insight into microvessel activity.

Results: In all groups, vascularization was prominent, with a mean [95 ​% confidence interval] of 1.64 [1.40, 1.89]. In all three groups, mature microvessel density was greater than immature microvessel density (82.32 [62.92, 101.71] versus 14.84 [9.86, 19.83] microvessels/mm). Low CD105 microvessel density across all groups (3.14 [0.92, 5.37] microvessels/mm) suggests microvessel inactivity. Inflammatory composite scores were significantly greater in the advanced OA (1.08 [0.84, 1.32]) versus the FAI group (0.47 [0.26, 0.68]), and in the advanced OA versus the FAI with early OA group (0.69 [0.49, 0.89]) (p ​< ​0.017).

Conclusion: Synovium from patients with FAI (with and without hip osteoarthritis) demonstrated synovitis and other OA-associated changes. Mature, inactive microvasculature was prominent in all three groups investigated. Histopathological similarities between FAI and hip OA synovium indicate that disordered synovium appears in FAI patients. These findings highlight a potential role of synovial changes in the progression from FAI to hip OA, underscoring the need for early intervention and further investigation into early disease mechanisms.