Peri-Implant Distribution of Polyethylene Debris in Postmortem-Retrieved Knee Arthroplasties: Can Polyethylene Debris Explain Loss of Cement-Bone Interlock in Successful Total Knee Arthroplasties?

Abstract

Background Loss of mechanical interlock between cement and bone with in vivo service has been recently quantified for functioning, non-revised, cemented Total Knee Arthroplasties (TKA). The cause of interlocking trabecular resorption is not known. The goal of this study was to quantify the distribution of PE debris at the cement-bone interface and determine if polyethylene (PE) debris is locally associated with loss of interlock. Methods Fresh, non-revised, postmortem-retrieved TKAs (n=8) were obtained en bloc. Lab-prepared constructs (n=2) served as negative controls. The intact cement-bone interface of each proximal tibia was embedded in Spurr’s resin, sectioned, and imaged under polarized light to identify birefringent PE particles. PE wear particle number density was quantified at the cement-bone interface and distal to the interface, then compared to local loss of cement-bone interlock. Results The average PE particle number density for postmortem retrieved TKAs ranged from 8.6 (1.3) to 24.9 (3.1) particles/mm2 (SE) but was weakly correlated with years in service. The average particle number density was twice as high distal (> 5mm) to the interface compared to at the interface. The local loss of interlock at the interface was not related to presence, absence, or particle density of PE. Conclusions PE debris can migrate extensively along the cement-bone interface of well-fixed tibial components. However, the amount of local bone loss at the cement-bone interface was not correlated with the amount of PE debris at the interface, suggesting that the observed loss of trabecular interlock in these well-fixed TKAs may be due to alternative factors.

Similitude of cement‐bone micromechanics in cemented rat and human knee replacement

“…Large quantities of wear particles from the articulating surface can result in local inflammation, osteoclast accumulation at the implant interface, and impaired osteoblast function 33 . However, in postmortem retrievals, extensive resorption of interdigitated trabecular bone has also been found in the absence of fibrous tissue or debris particles 34 …”

“…33 However, in postmortem retrievals, extensive resorption of interdigitated trabecular bone has also been found in the absence of fibrous tissue or debris particles. 34 Rodent models are often used as an initial preclinical model due to relatively low cost compared to larger animal models and human clinical studies. 35 In the context of scaling from a rat-sized knee (~6 mm) to human knee (~80 mm), the work presented here shows that micromotion and potential induced fluid flow scale appropriately, such that induced fluid shear would be similar in both species.…”

The Neuroimmune Interplay in Joint Pain: The Role of Macrophages

“…Tissue inflammation in response to prosthetic byproducts has been pointed to as the main responsible for AL ( 97 ). Wear particles released from implant devices that accumulate around the bone-implant interface, induce the release of pro-inflammatory mediators by tissue-resident macrophages ( 98 ) ( Figure 2 ). The continuous release of wear particles perpetuates a chronic low-grade inflammation around the implant.…”

Inflammation time-axis in aseptic loosening of total knee arthroplasty: A preliminary study

“…Contemporary biological theory links resident tissue cells [5] to maintaining local tissue homeostasis around TKA contributing to stable and functional TKA for many years [6]. However, the continuous burden of wear particles, liberating from the articulation surfaces of TKA during each step and migrating around bone-implant interface [7], induce release of pro-inflammatory mediators triggering and perpetuating chronic low-grade inflammation around TKA [8]. This chronic inflammatory condition favours secretion of a number of osteoclastogenic mediators, namely the receptor activator of nuclear factor kappa-B (RANK) ligand and others, which in turn promote differentiation of macrophages into osteoclasts and multinucleated giant cells, effecting bone resorption [9–11].…”