The implication of the osteolysis threshold and interfacial gaps on periprosthetic osteolysis in cementless total hip replacement.

Osteolysis around joint replacements may develop due to migration of wear particles from the joint space into gaps between the interface bone and the implant where they can accumulate in high concentrations to cause tissue damage. Osteolysis may appear in various postoperative times and morphological shapes which can be generalized into linear and focal. However, there are no clear explanations on the causes of such variations. Patients' degree of sensitivity to polyethylene particles (osteolysis thresholds), the local particle concentration and the access route provided by the interface gaps have been described as determining factors. To study their effects, a 2D computational fluid dynamics model of the hip joint capsule in communication with an interfacial gap and the surrounding bone was employed. Particles were presented using a discrete phase model (DPM). High capsular fluid pressure was considered as the driving force for particle migration. Simulations were run for different osteolysis thresholds ranging from 5×108 to 1×1012 particle number per gram of tissue and fibrous tissue generation in osteolytic lesion due to particles was simulated for the equivalent of ten postoperative years. In patients less sensitive to polyethylene particles (higher threshold), osteolysis may be linear and occur along an interfacial gap in less than 5% of the interfacial tissue. Focal osteolysis is more likely to develop in patients with higher sensitivity to polyethylene particles at distal regions to an interfacial gaps where up to 80% of the interfacial tissue may be replaced by fibrous tissue. In these patients, signs of osteolysis may also develop earlier (third postoperative year) than those with less sensitivity who may show very minor signs even after ten years. This study shows the importance of patient sensitivity to wear particles, the role of interfacial gaps in relation to morphology and the onset of osteolysis. Consequently, it may explain the clinically observed variation in osteolysis development.