BackgroundShort-stem humeral replacements achieve fixation by anchoring to the metaphyseal trabecular bone. Fixing the implant in high-density bone can provide strong fixation and reduce the risk of loosening. However, there is a lack of data mapping the bone density distribution in the proximal humerus. The aim of the study was to investigate the bone density in proximal humerus.MethodsEight computed tomography scans of healthy cadaveric humeri were used to map bone density distribution in the humeral head. The proximal humeral head was divided into 12 slices parallel to the humeral anatomic neck. Each slice was then divided into 4 concentric circles. The slices below the anatomic neck, where short-stem implants have their fixation features, were further divided into radial sectors. The average bone density for each of these regions was calculated, and regions of interest were compared using a repeated-measures analysis of variance with significance set at P < .05.ResultsAverage apparent bone density was found to decrease from proximal to distal regions, with the majority of higher bone density proximal to the anatomic neck of the humerus (P < .05). Below the anatomic neck, bone density increases from central to peripheral regions, where cortical bone eventually occupies the space (P < .05). In distal slices below the anatomic neck, a higher bone density distribution in the medial calcar region was also observed.ConclusionThis study indicates that it is advantageous with respect to implant fixation to preserve some bone above the anatomic neck and epiphyseal plate and to use the denser bone at the periphery.
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.
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 5×10 to 1×10 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.
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