Research Papers

Do Capsular Pressure and Implant Motion Interact to Cause High Pressure in the Periprosthetic Bone in Total Hip Replacement?

[+] Author and Article Information
Hamidreza Alidousti, Mark Taylor

School of Engineering Sciences,  University of Southampton, Highfield, Southampton, UK, SO17 1BJ

Neil W. Bressloff1

School of Engineering Sciences,  University of Southampton, Highfield, Southampton, UK, SO17 1BJN.W.Bressloff@soton.ac.uk


Corresponding author.

J Biomech Eng 133(12), 121001 (Dec 21, 2011) (10 pages) doi:10.1115/1.4005455 History: Received May 17, 2011; Revised November 10, 2011; Published December 21, 2011; Online December 21, 2011

When there is a debonding at the 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. To explain this phenomenon, 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 can play a defining role in inducing periprosthetic flow. In order to obtain a better understanding of the main influences on periprosthetic flows and the development of osteolysis, steady state and transient 2D computational fluid dynamic simulations were performed for the joint capsule of the lateral side of a stem-femur system, and a gap in communication with the capsule and the surrounding bone. It was shown 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, gap micromotion of only very long and narrow gaps generated significant velocity spikes in the bone at the bottom of the gaps.

Copyright © 2011 by American Society of Mechanical Engineers
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Figure 1

Cross-sectional cut of the 3D geometry that was employed to generate the 2D model

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Figure 2

The meshed geometry for a 5 mm length and 30 μm width gap to demonstrate an example of a meshed geometry. Models with different lengths and widths are meshed in the same manner. It can be seen that mesh resolution is much higher in the gap region and its surrounding bone where there are large flow gradients in the model.

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Figure 3

Transitional velocity and displacement of the implant in the x direction as a result of the angular motion around the tip of the gap for 300 μm opening. It can be seen that when velocity reaches zero, the gap is open to its maximum displacement and closes as the velocity turns negative.

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Figure 4

Schematic of the implant angular motion around the pivot point at the bottom of the gap (not to scale). The displacement and the size of the gap are exaggerated for demonstration purposes. l and w are the gap length and width, respectively, d is the amount of gap opening at the entrance, and ω is the angular velocity of the implant. Bone, gap, and top-gap are the profile lines, where the velocity and pressure measurements are taken.

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Figure 5

Pressure (left) and velocity (right) contour for steady state solution of the 80 L-500 W-0D model at 60 kPa pressure. The extension of high capsular pressure down the gap and the flow of fluid to the gap region can be seen.

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Figure 6

Pressure measurement along the bone profile line. Pressure drops up to five times from the capsular level for the longest and narrowest gap (80 L-30 W-0D) while it stays unchanged for all other models. Only four models are demonstrated here.

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Figure 7

y velocity measured for different gap dimensions at gap profile line at steady state. It can be seen that changing gap dimension can induce over 16 times increase in fluid velocity in to the gap.

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Figure 11

Velocity of fluid in the gap for the longest and narrowest gap with smallest displacement (80 L-30 W-30D) at different times during one cycle. It can be seen that even at t = 0.15 when the gap is closing the velocity value is still negative meaning the fluid still flow down the gap.

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Figure 10

Velocity plot at bone profile line. It can be seen that 80 L-30 W-30D model shows suction of fluid from the bone to the gap as the spike is in the positive direction.

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Figure 9

Very large velocity spikes caused by gap displacement in the 80 L-30 W-30D and 80 L-30 W-300D models. All other models show no significant change in the velocity spike.

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Figure 8

Gap displacement usually has no effect on the fluid pressure experienced by the bone adjacent to the gap. However, for the longest and narrowest gap even a small displacement as shown in this figure can cause pressure fluctuation up to 80 kPa.



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