Periprosthetic fluid flow, particle distribution modelling and the implications for osteolysis in cementless total hip replacements

Abstract

When there is debonding at a bone-implant interface, the difference in stiffness between the implant and the bone can result in micromotion, allowing existing gaps to open further or new gaps to be created during physiological loading. It has been suggested that periprosthetic fluid flow and high pressure may play an important role in osteolysis development in the proximity of these gaps. It has also been suggested that the periprosthetic flow may facilitate migration of wear polyethylene particles to the periprosthetic bone, which can also cause osteolysis. To explain these phenomena, the concepts of ’effective joint space’ and ’pumping stem’ have been cited in many studies. However, there is no clear understanding of the factors causing, or contributing to these mechanisms.

It is likely that capsular pressure, gap dimensions and micromotion of the gap during cyclic loading of an implant as well as factors such as biological osteolysis threshold, the rate of wear generation and the degree of particle clogging in the periprosthetic tissue, play defining roles in periprosthetic flow, particle migration and osteolysis generation. In order to obtain a better understanding of the above mechanisms and factors, steady state and transient 2D computational fluid dynamic models of the lateral side of a stem-femur system including the joint capsule, a gap in communication with the capsule and the surrounding bone were studied. First, fluid velocities and pressures in the periprosthetic tissue were investigated. Then, particles were introduced to the continuum fluid at the gap entrance as a discrete phase and their migration to the bone was analysed. Lastly, the models were further refined by introducing algorithms and factors developed to simulate particle clogging and permeability variation caused by the fibrous tissue generation in osteolytic lesion and particle clogging in the periprosthetic tissue throughout postoperative periods.

Simulations without particles showed that high capsular pressure may be the main driving force for high fluid pressure and flow in the bone surrounding the gap, while micromotion of only very long and narrow gaps can cause significant pressure and flow in the bone. At low capsular pressure, micromotion induced large flows in the gap region; however, the flow in the bone tissue was almost unaffected. The results also revealed the existence of high velocity spikes in the bone region at the bottom of the gap. These velocity spikes can exert excessive fluid shear stress on the bone cells and disturb the local biological balance of the surrounding interstitial fluid which can result in osteolysis development. High capsular pressure was observed to be the main cause of these velocity spikes whereas, at low capsular pressure, gapmicromotion of only very long and narrow gaps generated significant velocity spikes in the bone at the bottom of the gaps.

Simulations with particles also showed that capsular pressure is the main driving force for particle migration to periprosthetic tissue. In contrast to common belief, the models showed that implant micromotion pumped out, rather than sucked in the particles to the interfacial gaps, except in long gaps in which, even at low pressure, particles that made it to the bottom region migrate to the bone tissue as a result of micromotion. Particles entered the periprosthetic tissue along the entire length of the gap with higher concentration at proximal and distal regions. However, particles mainly accumulated with an increasing concentration at the bottom of the gap because of the presence of the fluid spikes in this region. Therefore, focal osteolysis is more likely to develop in the gap bottom region, whereas linear osteolysis, which requires less particle concentration, is more likely to develop along the entire gap length. It was also shown that risk of osteolysis development was higher for shorter gaps since they experience higher particle concentration. In addition, the models showed that for osteolysis to develop, a constant supply of particles, as well as an access route to the endosteal bone must be available.

When a particle clogging model was included, it was shown that the depth of particle penetration into the surrounding tissue reduced, leading to increased particle concentrations. Particle clogging and accumulation initially occurred at distal and proximal gap regions in the stem proximity. However, as time elapsed, this accumulation extended along the entire interface. The rate of particle accumulation was a function of particle wear generation. Accumulation of particles at the interface caused changes in the tissue permeability and periprosthetic flows. Partial clogging and particle accumulation in the gap bottom region caused increases in fluid spikes in that region. Once this region was completely clogged, the magnitude of fluid spikes reduced. In addition, there was a complementary relationship between particle concentration and the reduction of permeability; regions with lower permeability tended to experience higher particle accumulation.

Models developed to simulate fibrous tissue generation in osteolytic lesions, presented this tissue by regions with increased permeability. It was showed that, as time elapses, particle concentrations become higher than the osteolytic threshold which leads to increased periprosthetic tissue permeability. In general, for lower osteolysis thresholds, regions with increased permeability progresses faster at the bottom of the gap. This results in increased permeability having a linear pattern along the interface and a focal pattern at the bottom of an interfacial gap. Higher osteolysis thresholds, generally, result in only a linear pattern of increased permeability along the gap except for the cases with high wear generation rates in which a focal pattern at the bottom of the gap can still be seen.

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