Inflammatory Periprosthetic Bone Loss

Total hip arthroplasty [THA] is one of the most successful and effective procedures developed for the treatment of pain and lack of mobility associated with end-stage arthritis such as osteoarthritis and rheumatoid arthritis. Approximately 1.5 million joint arthroplastic operations are performed annually worldwide. THA, although considered an excellent surgical procedure, can be complicated by periprosthetic osteolysis. Periprosthetic osteolysis (also called ‘Particle disease’) is initiated by wear debris derived from the implant. In most long-term studies on hip arthroplasty, osteolysis related loosening, bone loss or periprosthetic fractures are the most frequent causes for revision surgeries (Talmo et al., 2006). Osteolysis is a particle-induced biologic process at the metal–bone or cement–bone interface of prosthetic implants, manifesting radiographically as scalloped focal or linear endosteal radiolucencies due to bone loss and resulting in the loosening of implants. In the early days of hip arthroplasty, radiolucencies around implants were noticed and were thought to be related to curing of acrylic cement, infection or neoplastic process. These were first described by Charnley in association with Teflon cups, though later were also observed in patients with stable implants (Charnley, 1966). In 1977, Willert and Semlitsch demonstrated the presence of macrophages in response to wear debris and concluded that the particles accumulate macrophages in pericapsular lymph drainage, leading to a foreign body response and eventual loosening of the implant (Willert, 1977). Goldring et al. described the synovial-like character of the interfacial membrane found and demonstrated the presence of prostaglandin E2 [PGE2] and collagenase secretion from the associated cells (Goldring et al., 1983). The early observations of osteolysis in cemented implants led to a general belief that osteolysis was related to the acrylic cement and the term ‘Cement disease’ was introduced. However, after the demonstration of lytic lesions in cementless implants, osteolysis is now considered to be a ‘Particle disease’, suggesting that wear-generated particulate debris is the main cause of periprosthetic osteolysis (Harris, 1995). Biologic responses to implant debris, the basis of periprosthetic tissue destruction, are due to a wide variety of complex events. Aseptic failure occurs later as a secondary issue to the chronic granulomatous and inflammatory response, which is stimulated and maintained by