A case report of pigmented villous nodular synovitis accelerating the progression of femoral head necrosis

Background Avascular necrosis of the femoral head (ONFH) is a debilitating condition in which disruption of the femoral head’s blood supply results in collapse of the articular surface and rapid joint destruction. When osteolysis progresses over weeks or months—sometimes termed rapidly progressive osteonecrosis of the femoral head (R‑ONFH) or rapidly destructive hip disease—the pathogenesis is poorly understood. Pigmented villonodular synovitis (PVNS) is a benign but locally aggressive synovial tumour characterised by villous hyperplasia, hemosiderin deposition and abundant macrophages. However, in certain cases—particularly in the context of R-ONFH—this may accelerate the progression of avascular necrosis of the femoral head.PVNS can erode bone and produce inflammatory mediators, yet its role in R‑ONFH has not been defined. Case presentation: We report a case of bilateral ONFH initially diagnosed as idiopathic stage IV disease on the right and stage I disease on the left. Pre‑operative assessment combined anteroposterior and lateral radiographs with axial and coronal computed tomography to stage the necrosis. The patient underwent total hip arthroplasty (THA) via a posterolateral approach. Intra‑operatively, villonodular synovial proliferation, joint effusion and destruction of the femoral head were observed. All abnormal tissue was excised and sent for histology. Post‑operative radiographs assessed prosthetic position and early outcome. Conclusion This case illustrates that PVNS may not simply coexist with ONFH but can accelerate femoral head necrosis through inflammatory, mechanical and enzymatic mechanisms. Pro‑inflammatory cytokines such as tumour necrosis factor‑α, interleukin‑1β and interleukin‑6 can stimulate fibroblast‑like synoviocytes to secrete matrix metalloproteinases, activate osteoclasts and suppress osteoblasts. Villous synovium may mechanically compress the medial and lateral femoral circumflex arteries and directly erode subchondral bone. Recognising PVNS as a potential driver of R‑ONFH is crucial because misdiagnosis as idiopathic necrosis could lead to insufficient treatment; early magnetic resonance imaging (MRI) and complete synovectomy combined with THA or head‑preserving procedures should be considered. Future studies should systematically evaluate the prevalence of PVNS in R‑ONFH and explore targeted anti‑inflammatory therapies.