Osteolysis and periprosthetic bone loss have been a concern since Charnley’s original reports of metal on Teflon. Willart and Semlitch were the first investigators to propose a biologic mechanism for osteolysis associated with particulate wear debris. Harris in 1976 and Goldring 1983 describe the presence of macrophages and giant cells in the synovial membrane at the bone cement interface in loose THR. Initially it was associated with cement and it was called cement disease. Reports of resorption around cementless implants led to the realization that PE alone was good enough to create bone loss.
Aetiology: Submicron wear particles are phagocytosed by macrophages resulting in release of various cellular mediators from these activated cells.
Cellular mediators playing significant role in osteolysis are IL-1, IL-6, TNF-a, PGE2. These mediators lead to stimulation and differentiation of osteoclasts and inhibition of osteoblasts.
These factors together assist in the dissolution of bone at the interface allowing for micromotion of the prosthesis that leads to further generation of wear debris.
On top of the above there is release of collagenase, stromelysin, gelatinase which further destroy the bone. Another active area of research involves roles at Rank, Rank and osteoprotegerin. Recently there is extensive work done as far as it concerns the role of endotoxin in osteolysis and periprosthetic bone loss. It still remains a controversial issue.
Other researchers have studied the effects of elevated periarticular hydrostatic pressure and fluid access in the development of osteolysis (effective joint space).
Particles bioreactivity: It has been shown that the major determinants of particle bioreactivity are particle size, composition, shape, and concentration. Particles of submicron size are more stimulatory and there is a dose dependent response. Concerning the composition it has been found that UHMWPE, CoCr and stainless steel particles induce more severe reactions than Titanium and alumina ceramic. It also has been found that Al2O3 particles were more easily phagocytosed than UHMWPE at the same size and concentration but TNF-a release was higher with than UHMWPE with Al2O3. Concerning the metal to metal particles it has been found that the volumetric wear is less than M/P with smaller particles and less intensive tissue reaction but Shanbhag reported that bioreactivity of metal wear debris is a function of the total surface area and not the volume of wear debris and casts doubts at the theory that metal to metal wear particles produce a less intense biological response. Concerning the highly crosslinked PE it has been found that wear debris from gamma crossed –linked remelted PE contains very few fibrils after a dose of 5 Mrads and virtually none after 9.5 Mrads.
Clinical Manifestations: The majority of patients with osteolysis are asymptomatic. Pain is caused mainly from a fracture.Ultimately periprosthetic bone loss results in aseptic loosening. Furthermore if the component becomes loose bone loss often progress more rapidly resulting in large bone defects that can lead to catastrophic failure or fracture.
Radiographic manifestations: Characteristic radiographic patterns of osteolysis have been described on both the femoral and acetabular side with cemented and cementless components. Recent studies have suggested that plain radiographs often underestimate the extent of osteolysis and CT or MRI may be necessary to assess the true extent of the bone loss.
