The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 88, Issue suppl 2

Workshop Articles | April 01, 2006

Wear Particles

Joshua J. Jacobs, MD; Nadim J. Hallab, PhD; Robert M. Urban; Markus A. Wimmer, PhD

In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding from Zimmer Inc., Wright Medical, Medtronics, the National Institutes of Health (the National Institute of Arthritis and Musculoskeletal and Skin Diseases), DePuy, and Smith and Nephew. In addition, one or more of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity (Zimmer Inc., Wright Medical, Medtronics, Archus Orthopaedics, DePuy, and Smith and Nephew). Also, a commercial entity (Zimmer Inc., Wright Medical, Medtronics, and DePuy) paid or directed, or agreed to pay or direct, benefits to a research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

The Journal of Bone and Joint Surgery, Incorporated

J Bone Joint Surg Am, 2006 Apr 01;88(suppl 2):99-102. doi: 10.2106/JBJS.F.00102

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Abstract

Particulate and ionic debris resulting from in vivo degradation of total joint replacement components are recognized as major factors limiting the longevity of the joint reconstruction and the overall success of the procedure. Particulate and ionic wear and corrosion debris have been associated with a locally aggressive biologic response that can lead to synovitis, periprosthetic bone loss, and aseptic loosening of the implants. Furthermore, concerns exist regarding the systemic dissemination of prosthetic debris, including potential effects resulting from end-organ retention. The long-term success of total disc arthroplasty may well depend, at least in part, on the ability to minimize implant debris generation and the subsequent local and systemic response.

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Total joint arthroplasty has emerged as one of the most successful and cost-effective interventions in health care, with high success rates at ten to fifteen-year follow-up intervals. Despite the excellent results achieved by this procedure, however, the generation of particulate wear and corrosion debris and the subsequent biologic response continue to pose major problems that may limit the durability of the joint reconstruction and the success of the procedure. As spine surgeons consider motion-preserving surgery for degenerative disc disease, hopefully the application of many of the lessons learned about wear and corrosion in total hip and total knee arthroplasty will result in total disc replacement reconstructions that are not compromised by wear, corrosion, and their sequelae. This review will address the mechanisms of debris generation in total joint arthroplasty and the local and systemic consequences of this debris.

Basic Considerations

Particulate debris after total joint arthroplasty can be generated by wear or corrosion. Wear involves the loss of prosthetic material and results from either adhesion, abrasion, or fatigue¹. Abrasive wear occurs when asperities in one surface plow grooves in a softer surface. Adhesive wear occurs when minute shards of a surface are pulled off by the motion of a contacting surface to which a bond had formed. Fatigue wear occurs in the setting of cyclic surface stresses that lead to the formation of subsurface cracks, which coalesce and result in delamination of portions of the surface. An additional mechanism, third-body wear, occurs when fine particles such as cement, hydroxyapatite, and/or metal are entrapped in an articulation and cause abrasive wear of one or both surfaces.

McKellop defined four modes of wear according to the mechanical condition under which the debris generation occurs¹. Mode-1 wear refers to the generation of wear debris that occurs with motion between the two bearing surfaces as intended by the designers. Mode-2 wear refers to a primary bearing surface rubbing against a secondary surface in a manner not intended by the designers (e.g., complete wear-through of a polyethylene liner resulting in a femoral head articulating with an acetabular shell). Mode-3 wear is wear of two primary bearing surfaces with interposed third-body particles (i.e., bone, cement, or metal). Mode-4 wear refers to two nonbearing surfaces rubbing together (such as back-sided acetabular liner wear, fretting of the Morse taper, or stem-cement fretting). Although several modes of wear often occur simultaneously, mode-1 wear accounts for the majority of wear in a well-functioning hip or knee replacement.

Because of its complexity, there are no equations of state that can accurately predict the magnitude of wear in an articulating couple of interest. The Archard equation ?=k (WV/H) (where ? = wear rate, k = constant, W = applied load, V = sliding velocity, and H = hardness) has been used in some analytic models², but it is applicable only to adhesive wear. In fact, the most reliable way to predict wear in a given tribosystem is to simulate the motion, loads, lubricants, and operating conditions as closely as possible in in vitro testing apparatuses. Refinements in such simulations, based on observed damage patterns in retrieved devices, are currently helpful in predicting wear in total hip arthroplasty. Simulations in total knee arthroplasty are still being refined; typically, the correlation between the damage pattern on retrieved devices and devices tested in knee simulators is suboptimal. The science of wear simulation in spinal arthroplasty devices is in its infancy, limiting the predictive value of such in vitro tests.

Corrosion involves the release of metal ions from metal surfaces that occurs as a result of a thermodynamically driven electrochemical process. Corrosion products (metal ions and/or their precipitates) can be generated at any metal surface but occur most commonly at the metal-metal modular interfaces of either similar or dissimilar articulations³. A well-described particulate corrosion product implicated in implant failure is chromium orthophosphate, which has been identified in the membrane around failed implants and at sites distant from the implant³.

Although numerous studies describe patterns and magnitudes of wear and corrosion in retrieved total hip and knee devices, very little information is available on such patterns in retrieved spinal arthroplasty devices. One such retrieval study, involving a polyethylene-on-metal disc replacement device, suggested that, in the intermediate term, the patterns of damage may be similar to that observed in polyethylene acetabular components from total hip arthroplasty⁴ (Figs. 1-A, 1-B, and 1-C).

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Figs. 1-A, 1-B, and 1-C: Fig. 1-A Photomicrograph of a retrieved polyethylene component from a total disc replacement two years and eleven months after implantation. This side of the component had evidence of transverse cracks (arrows). Fig. 1-B Microcomputed tomography of the device illustrates a transverse crack in this two-dimensional section. Fig. 1-C A section in a three-dimensional reconstruction illustrates potential pit formation. (Figs. 1-A, 1-B, and 1-C reprinted, from: Kurtz SM, Peloza J, Siskey R, Villarraga ML. Analysis of a retrieved polyethylene total disc replacement component. Spine J. 2005;5:346-7; with permission from Elsevier.)

Local Effects of Debris

Periprosthetic bone loss associated with wear debris has been a concern since Charnley's original reports of metal-on-Teflon total hip replacement. Willert was the first investigator to propose a biologic mechanism for periprosthetic bone loss associated with particulate wear debris⁵. Willert and his colleagues suggested that bearing surface wear debris may overload local afferent transport mechanisms, resulting in accumulation of particulate wear debris in the surrounding tissues (Figs. 2-A and 2-B) and ultimately leading to periprosthetic bone resorption and aseptic loosening of the femoral and/or acetabular components.

The mechanism of periprosthetic bone loss associated with particulate debris has been critically evaluated in in vitro models, animal models, and retrieval studies⁶. Extensive research has revealed that submicrometer and micrometer-sized wear particles are phagocytosed by macrophages, fibroblasts, and osteoblasts, resulting in the release of various proinflammatory factors and chemical mediators from these activated cells. Numerous cellular mediators that are known to be involved in inflammation have been shown to play a major role in osteolysis, including interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a), and prostaglandin E₂ (PGE₂). These cellular mediators act in a paracrine and autocrine fashion, resulting in the differentiation and stimulation of osteoclast precursors and osteoclasts as well as inhibition of osteoblasts. In addition to inflammatory mediators, lysosomal enzymes and matrix metalloproteinases (collagenase, gelatinase, and stromelysins) are released that act directly on bone, causing further resorption. These factors act in concert, resulting in diminished bone stock in the periprosthetic region. As this process progresses, the implant may lose its fixation, leading to the further generation of debris by mode-3 and mode-4 wear.

Another active area of research involves the roles of receptor activator of nuclear factor-?B (RANK), RANK ligand (RANKL), and osteoprotegerin in periprosthetic bone loss. Several investigators have recently shown that RANK:RANKL signaling plays a critical role in periprosthetic bone resorption⁷. RANK and RANKL have been reported to be involved in down-regulation of osteoblast function and, in combination with TNF-a, stimulation of osteoclast precursors to become mature osteoclasts (osteoclastogenesis)⁷.

In vitro and in vivo studies have shown that the major determinants of particle bioreactivity are particle size, composition, shape, and concentration. Several studies have shown that particles of phagocytosable sizes (i.e., micrometer and submicrometer particles) are more stimulatory than larger particles, and that particle bioreactivity shows a dose-dependent response⁶.

Systemic Effects of Debris

In addition to the local effects of wear and corrosion debris, the potential systemic effects of such debris have also been considered³. Numerous studies have documented elevated serum and urine metal levels in patients undergoing total joint replacement, particularly in those patients with metal-on-metal bearing devices. Presumably, these metals are in ionic form, bound to serum proteins. In addition, the analysis of postmortem specimens from patients with primary and revision joint replacements has revealed that systemic distribution of metallic and polyethylene wear particles to para-aortic abdominal lymph nodes was a common finding, with higher levels of metallic particles in the liver and spleen of patients with failed reconstructions⁸. Fortunately, in the majority of cases, the concentration of wear particles in these remote locations was relatively low and without apparent pathologic importance. However, longer-term follow-up is necessary to determine what, if any, detrimental effects could occur from end-organ retention of particulate wear debris.

Despite multiple reports of implant debris in the serum, urine, and end organs, the clinical implications of the systemic distribution of implant debris remain unclear. Large comparative epidemiologic studies will be necessary to clarify the toxicologic effects, if any, of the systemic distribution of implant debris.

Hypersensitivity to Implant Materials

Many investigators have studied the potential association between metallic orthopaedic implants and hypersensitivity reactions such as dermatitis, urticaria, vasculitis, and possibly aseptic loosening and osteolysis^9,10. Although dermal sensitivity to metal is common and has been reported in up to 10% to 15% of the general population⁹, the significance of this response and its role in the pathogenesis of implant failure remains unclear. Furthermore, the mechanisms by which in vivo metal hypersensitivity occurs have not been well characterized. One major difficulty that researchers face in determining the clinical implications of metal hypersensitivity is that, currently, there is no generally accepted test for metal hypersensitivity to implanted devices. A heightened concern exists about the clinical implications of metal hypersensitivity, given that recent articles have reported delayed-type hypersensitivity-like histologic responses as well as osteolysis in patients with metal-on-metal total hip replacements¹⁰.

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Figs. 2-A and 2-B: Photomicrographs of periprosthetic interfascial tissue removed from patients with failed cementless (Fig. 2-A) and cemented (Fig. 2-B) total hip replacements. Numerous submicrometer birefringent particles that are most likely polyethylene (Fig. 2-A) and dark metal particles (Fig. 2-B) are seen within the cells (original magnification, × 50). (Reprinted, with permission, from: Glant TT, Jacobs JJ, Mikecz K, Yao J, Chubinskaja S, Williams JM, Urban RL, Shanbhag AS, Lee SH, Sumner DR. Particulate-induced, prostaglandin- and cytokine-mediated bone resorption in an experimental system and in failed joint replacements. Am J Ther. 1996;3:33.)

Summary

Implant wear and corrosion and the subsequent local and systemic effects remain clinically significant issues in total hip and total knee arthroplasty. These processes should also be of concern in spinal disc arthroplasty. Some degree of wear and corrosion is inevitable in the current generation of joint replacement materials, giving rise to debris that can result in a highly inflammatory biologic response. In turn, this inflammatory response can lead to localized periprosthetic bone loss and aseptic loosening. Little is currently known about the effect of this chronic inflammatory reaction on adjacent neural tissues, which is a consideration unique to spinal disc arthroplasty. In addition, the systemic effects of implant debris following joint arthroplasty warrant further study.

Issues related to wear and corrosion are of primary importance to adult reconstructive orthopaedic surgeons and basic-science researchers. These issues now need appropriate scrutiny in the field of spine surgery. Efforts continue in the development and study of newer materials with greater wear and corrosion resistance and less biologic reactivity than existing materials. In addition, new approaches for pharmacologic modification of the host response to implant debris are emerging from in vitro and animal models of osteolysis. Further elucidation of the cellular and molecular basis of the debris-induced inflammatory response, implant retrieval studies, spinal wear simulation studies, and long-term clinical follow-up studies of patients with disc replacements are required to generate strategies that minimize the clinical impact of wear and corrosion in spinal disc arthroplasty devices. ?

References

Schmalzried TP, Callaghan JJ. Wear in total hip and knee replacements. J Bone Joint Surg Am. 1999;81: 115-36.81115 1999 [PubMed]

Ludema KC. Friction, wear, lubrication: a textbook of tribology. Boca Raton, FL: CRC Press; 1996. p 131.131 1996

Jacobs JJ, Gilbert JL, Urban RM. Corrosion of metal orthopaedic implants. J Bone Joint Surg Am. 1998;80: 268-82.80268 1998 [PubMed]

Kurtz S, Van Ooij A, John P, Ciccarelli L, Zeiger A, Villarraga M. Central core and rim damage in retrieved polyethylene total disc replacement components. Spine J. 2005;5(4 Suppl): 8S-9S.58S 2005 [CrossRef]

Willert HG. Reactions of the articular capsule to wear products of artificial joint prostheses. J Biomed Mater Res. 1977;11: 157-64.11157 1977 [CrossRef]

Archibeck MJ, Jacobs JJ, Roebuck KA, Glant TT. The basic science of periprosthetic osteolysis. J Bone Joint Surg Am. 2000;82: 1478-89.821478 2000

Haynes DR, Crotti TN, Potter AE, Loric M, Atkins GJ, Howie DW, Findlay DM. The osteoclastogenic molecules RANKL and RANK are associated with periprosthetic osteolysis. J Bone Joint Surg Br. 2001;83: 902-11.83902 2001 [CrossRef]

Urban RM, Jacobs JJ, Tomlinson MJ, Gavrilovic J, Black J, Peoc'h M. Dissemination of wear particles to liver, spleen, and abdominal lymph nodes of patients with hip or knee replacement. J Bone Joint Surg Am. 2000;82: 457-76.82457 2000 [PubMed][CrossRef]

Hallab N, Merritt K, Jacobs JJ. Metal sensitivity in patients with orthopaedic implants. J Bone Joint Surg Am. 2001;83: 428-36.83428 2001 [CrossRef]

Willert HG, Buchhorn GH, Fayyazi A, Flury R, Windler M, Koster G, Lohmann CH. Metal-on-metal bearings and hypersensitivity in patients with artificial hip joints. A clinical and histomorphological study. J Bone Joint Surg Am. 2005;87: 28-36.8728 2005 [PubMed][CrossRef]

Topics

hypersensitivity ; aggressive behavior ; bone resorption ; corrosion ; hip joint ; longevity ; metals ; animal model ; osteolysis ; prostheses and implants

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Joshua J. Jacobs, Nadim J. Hallab, Robert M. Urban, Markus A. Wimmer; Wear Particles. The Journal of Bone & Joint Surgery. 2006 Apr;88(suppl_2):99-102.

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