The interfacial membrane between implant and host-bone in aseptically loose total hip arthroplasties has a potential role in the etiology of local bone resorption and loosening of the prosthetic component. Inflammatory/potential "bone-resorbing" agents (cytokines/mediators) released by the cells of the interfacial membranes of loosened uncemented and cemented total hip arthroplasties were measured. Synovial tissues from patients with acute femoral neck fractures, patients with osteoarthritis, and cadavers without joint disorders were used as control subjects. Control synovial tissue from osteoarthritic patients secreted the highest levels of prostaglandin E2, interleukin-8, and tumor necrosis factor alpha. Interleukin-1 alpha was the only cytokine whose levels were elevated as much as 4-fold around uncemented implants compared with cemented implants, and up to 16-fold compared with control synovial tissue. An apparent inverse relation between interleukin-1 alpha and interleukin-6 interfacial membranes of total hip arthroplasties compared with control synovial tissues suggests a complex cellular mechanism through a cytokine/prostaglandin cascade; this may regulate the observed bone resorption in aseptic loosening.