JBJS | Dissemination of Wear Particles to the Liver, Spleen, and Abdominal Lymph Nodes of Patients with Hip or Knee Replacement*

The Journal of Bone & Joint Surgery, Volume 82, Issue 4

Articles | April 01, 2000

Dissemination of Wear Particles to the Liver, Spleen, and Abdominal Lymph Nodes of Patients with Hip or Knee Replacement*

Robert M. Urban, †; Joshua J. Jacobs, M.D.†; Michael J. Tomlinson, D.V.M., PH.D.†; John Gavrilovic, PH.D.‡; Jonathan Black, PH.D.§; Michel Peoc'h, M.D.#

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Investigation performed at the Department of Orthopedic Surgery, The Rush Arthritis and Orthopedic Institute, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois
*One or more of the authors has received or will receive benefits for personal or professional use from a commercial party related directly or indirectly to the subject of this article. In addition, benefits have been or will be directed to a research fund, foundation, educational institution, or other nonprofit organization with which one or more of the authors is associated. Funds were received in total or partial support of the research or clinical study presented in this article. The funding sources were National Institutes of Health Grant AR39310, the Crown Family Chair in Orthopedic Surgery, and Zimmer USA.
†Department of Orthopedic Surgery, Rush-Presbyterian-St. Luke's Medical Center, 1653 West Congress Parkway, Chicago, Illinois 60612. E-mail address for R. M. Urban: rurban@rush.edu.
‡McCrone Associates, 850 Pasquinelli Drive, Westmont, Illinois 60559.
§IMN Biomaterials, 409 Dorothy Drive, King of Prussia, Pennsylvania 19406.
#Service D'Anatomie Pathologique, Centre Hospitalier Regional et Universitaire, 38043 Grenoble, France.

The Journal of Bone & Joint Surgery. 2000; 82:457-457

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Abstract

Background: The importance of particles generated by wear and corrosion of joint replacement prostheses has been understood primarily in the context of the local effects of particle-induced periprosthetic osteolysis and aseptic loosening. We studied dissemination of wear particles in patients with total hip and knee replacement to determine the prevalence of and the histopathological response to prosthetic wear debris in the liver, spleen, and abdominal para-aortic lymph nodes.

Methods: Postmortem specimens from twenty-nine patients and biopsy specimens from two living patients with a failed replacement were analyzed. Specimens of tissue obtained from the cadavera of fifteen patients who had not had a joint replacement served as controls. The concentration of particles and the associated tissue response were characterized with the use of light microscopy of stained histological sections. Metallic particles were identified by electron microprobe analysis. Polyethylene particles were studied with the use of oil-red-O stain and polarized light microscopy. The composition of polyethylene particles was confirmed in selected cases by Fourier transform infrared spectroscopy and hot-stage thermal analysis.

Twenty-one of the patients studied post mortem had had a primary total joint replacement. Eleven of them had had a hip prosthesis for a mean of sixty-nine months (range, forty-three to 171 months), and ten had had a knee replacement for a mean of eighty-four months (range, thirty-one to 179 months). The other eight patients studied post mortem had had a hip replacement in which one or more components had loosened and had been revised. The mean time between the initial arthroplasty and the time of death was 174 months (range, forty-seven to 292 months), and the mean time between the last revision procedure and the time of death was seventy-one months (range, one to 130 months).

Results: Metallic wear particles in the liver or spleen were more prevalent in patients who had had a failed hip arthroplasty (seven of eight) than in patients who had had a primary hip (two of eleven) or knee replacement (two of ten). The principal source of wear particles in the majority of these patients involved secondary nonbearing surfaces rather than wear between the two primary bearing surfaces as intended. In one living patient, dissemination of titanium alloy particles from a hip prosthesis with mechanical failure was associated with a visceral granulomatous reaction and hepatosplenomegaly, which required operative and medical treatment.

Metallic wear particles were detected in the para-aortic lymph nodes in 68 percent (nineteen) of the twenty-eight patients with an implant from whom lymph nodes were available for study. In 38 percent (eleven) of all twenty-nine patients with an implant who were studied post mortem, metallic particles had been further disseminated to the liver or spleen, where they were usually found within small aggregates of macrophages occurring as infiltrates without apparent pathological importance. Polyethylene particles elicited a similar response. They were identified in the para-aortic lymph nodes of 68 percent (nineteen) of the twenty-eight patients and the liver or spleen of 14 percent (four) of the twenty-nine patients. The majority of the disseminated wear particles were less than one micrometer in size. Currently available methods lack the sensitivity and specificity necessary to detect very low concentrations of submicrometer polyethylene particles and probably underestimated the prevalence of polyethylene wear debris in the liver and spleen.

Conclusions: In this study, systemic distribution of metallic and polyethylene wear particles was a common finding, both in patients with a previously failed implant and in those with a primary total joint prosthesis. The prevalence of particles in the liver or spleen was greater after reconstructions with mechanical failure. In the majority of patients, the concentration of wear particles in these organs was relatively low and without apparent pathological importance. However, in one rare case, granulomas formed in the liver, spleen, and abdominal lymph nodes in response to heavy accumulation of wear debris from a hip prosthesis with mechanical failure and compromised hepatic function.

Clinical Relevance: These findings underscore the necessity of minimizing the production of particulate debris by joint replacement devices and the need for the surgeon to consider expeditious revision in patients in whom large amounts of particulate debris may be generated. Serum and urine trace-metal analyses may provide early confirmation of failure and aid in the timing of a revision operation in a patient with a symptomatic or failed device.

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Introduction

Introduction | Materials and Methods | Results | Discussion | References

The nature and ultimate fate of wear and corrosion products generated by joint replacement prostheses and the implications of long-term systemic exposure to these products are among the least understood aspects of arthroplasty of the hip or knee. Elevated levels of the metallic elements from which implants are made have been reported in distant organs and body fluids of patients with joint replacement^{3,26,29,31,33-36,49,55,56,69}; however, the chemical form of these elements and their location within the organs have not been identified, to our knowledge. Moreover, efforts to define the fraction of the metal burden that can be attributed to implanted metallic devices must take into account the fact that concentrations of certain elements, particularly iron, titanium, and aluminum, due at least in part to environmental sources, have been shown to vary widely in the organs of patients without joint replacement⁷¹. To the best of our knowledge, there are no published data regarding polyethylene or polymethylmethacrylate in remote organs, largely because of the difficulty of identifying low concentrations of degradation products of these materials in biological specimens⁴⁴.

Particulate debris makes up a substantial portion of the corrosion and wear products generated by the normal use and function of prosthetic joints. Polyethylene particles are recognized as a major factor in the survival of joint prostheses^18,22,79, and metallic particulate species can also play an important role^2,32,75,80. Although there have been numerous studies of the effects of these particles on the periprosthetic tissues - particularly with regard to particle-induced, macrophage-mediated osteolysis^{28,39,46,63,73} - relatively little is known concerning the dissemination of wear debris beyond the local tissues^{1,4,5,7,9,23,30,52,64,65}. Indeed, particles that were thought to be generated by a prosthetic device have been previously reported in distant organs of only a few patients with a hip or knee replacement11,15,37,57. Identification of orthopaedic wear debris can be complicated, even in regional lymph nodes, by the coexistence of particles from other sources^6,47. Inhaled particles in the lungs of control subjects have been characterized^54,67, but baseline data on particles in other organs are lacking.

The purpose of this study was to determine the prevalence of and the histopathological response to prosthetic wear debris in specimens of liver, spleen, and distant lymph nodes obtained post mortem from patients who had had a hip or knee replacement and from subjects who had not had an orthopaedic implant. In addition, biopsy specimens from two living patients with failed implants were studied.

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Fig. 1:: Case 31. Anteroposterior radiograph of the left hip of one of the living patients, made 115 months after revision of the acetabular component. The center of the femoral head is designed to be eccentrically located in the inferior aspect of the custom titanium-alloy acetabular component. Note that there has been gross superior migration of the femoral head, suggesting wear-through, fracture, or disassembly of the polyethylene liner. The broken screw in the pelvis and a fragment of a cerclage wire are from previous surgeries.

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Fig. 2:: Case 29. Polarized light micrograph of a specimen of an abdominal para-aortic lymph node from a patient who had had multiple revisions of a hip replacement, demonstrating the abundance and morphology of birefringent particles within macrophages. These particles were identified as polyethylene by Fourier transform infrared spectroscopy and hot-stage thermal analysis (hematoxylin and eosin, 160).

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Fig. 3-A:: Figs. 3-A and 3-B: Case 21. This patient had had a well functioning, bilateral primary total knee replacement for almost fifteen years.
Fig. 3-A: Partially polarized light micrograph of several macrophages (left) adjacent to a bile duct (upper right) within a portal tract of the liver. The macrophages contained translucent birefringent particles, some of which proved to be polyethylene (UHMWPE) on microanalysis. Silicates of environmental origin, which also show birefringence, were detected as well (hematoxylin and eosin, 1500).

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Fig. 3-B:: The laser Raman microprobe spectrum of polyethylene particles extracted from a section of the liver was nearly identical to the spectrum of an unimplanted ultra-high molecular weight polyethylene standard. The specimens were excited with the use of a 782-nanometer diode laser.

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Fig. 4:: Case 21. Light micrograph showing approximately one dozen pale-staining, vacuolated macrophages accompanied by lymphocytes (top center and left) in a portal tract of the liver. Although not visible at this magnification, numerous submicrometer particles of cobalt-chromium-molybdenum alloy within these macrophages were demonstrated with use of electron microprobe analysis (hematoxylin and eosin, 160).

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Fig. 5-A:: Figs. 5-A and 5-B: Case 31. A liver biopsy from one of the living patients, a fifty-three-year-old woman with a history of developmental dysplasia of the hips and multiple joint replacement procedures, revealed the highest concentration of metallic wear particles but only a mild chronic portal inflammation and a very mild nonspecific lobular hepatitis, findings also compatible with her history of chronic hepatitis-C infection. The titanium-alloy particles were thought to have been generated from contact of the metal femoral head with the concave surface of the metal acetabular shell on the basis of findings at revision surgery (see Fig. 1).
Fig. 5-A: Light micrograph showing that more than 500 particles per high-power field were present within the mobile macrophages of a portal tract. In this field, the macrophages are seen surrounding a lymphoid follicle (hematoxylin and eosin, 125).

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Fig. 5-B:: Light micrograph of a specimen of the liver parenchyma, showing particles of titanium-aluminum-vanadium alloy in the fixed macrophages or Kupffer cells lining the hepatic sinusoids, suggesting hematogenous dissemination as well (hematoxylin and eosin, 281).

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Fig. 6-A:: Figs. 6-A and 6-B: Case 24. One of the living patients, a sixty-one-year-old man, had a loosened titanium-alloy prosthesis and an unusual systemic granulomatous reaction to particles identified as titanium-aluminum-vanadium alloy. The granulomas consisted predominantly of epithelioid macrophages and multinucleated giant cells with a moderate mononuclear cell infiltrate.
Fig. 6-A: Light micrograph of a specimen of the spleen, showing the granulomas distributed throughout the splenic parenchyma (hematoxylin and eosin, 16).

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Fig. 6-B:: Light micrograph of a specimen of the liver, showing the granulomas primarily in the portal tracts, where there was mild bile-duct hyperplasia and moderate fibrosis (hematoxylin and eosin, 40).

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: TABLE IClinical Data and Material Composition of the Joint Replacement Prostheses

*The Harris, Harris-Galante (H-G), BIAS, AML, and Mallory-Head stems had a modular head made of cobalt-chromium-molybdenum alloy. The Butel stem had a modular ceramic head.†Harris hip score21 or The Hospital for Special Surgery knee score24; NR = not recorded.‡Co-Cr-Mo = cobalt-chromium-molybdenum alloy, Ti = commercially pure titanium, Ti-6-Al-4-V = titanium-6 percent aluminum-4 percent vanadium alloy, Fe-Cr-Ni = stainless-steel alloy, UHMWPE = ultra-high molecular weight polyethylene, and Co-Cr-Ni-W = cobalt-chromium-nickel-tungsten alloy.

Case	Gender, Age at Death(yrs.)	Cause of Death	Joint	Year of Operation	Type of Prosthesis*	Time Since Initial Arthroplasty(mos.)	Hip or Knee Score at Most Recent Examination†(points)	Materials‡
Cement	Femoral Component	Acetabular or Tibial Component	Other Implants
Primary hip replacement
1	F, 65	Pancreatic carcinoma	R hip	1989	Harris stem, H-G cup	43	100	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
2	M, 91	Pneumonia	R hip	1988	Harris stem, H-G cup	44	62	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
3	F, 86	Metastatic breast carcinoma	R hip	1987	Harris stem, H-G cup	46	95	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
4	M, 74	Mycosis fungoides	R hip	1990	Harris stem, H-G cup	48	69	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			L hip	1990	Harris stem, H-G cup	48	70	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
5	F, 83	Congestive heart failure	R hip	1988	Harris stem, H-G cup	54	79	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
6	M, 71	Metastatic lung carcinoma	L hip	1987	BIAS porous-coated stem, H-G cup	54	83	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
7	M, 71	Cerebrovascular accident	R hip	1987	Harris stem, H-G cup	57	91	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
8	M, 54	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	78	98	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
9	M, 59	Myocardial infarction	R hip	1986	H-G porous-coated stem, H-G cup	89	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
10	M, 71	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	99	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
11	F, 86	Cardiorespiratory arrest	R hip	1983	6-Ti-32 stem, cemented cup	171	NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni hip nail
Primary knee replacement
12	F, 83	Metastatic colon carcinoma	L knee	1995	Miller-Galante II	31	NR	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
13	M, 18	Metastatic osteosarcoma	L knee	1993	Kinematic II rotating hinge with porous-coated modular distal femoral replacement	34	NR	Yes	Co-Cr-Mo	Co-Cr-Mo, UHMWPE
14	F, 64	Congestive heart failure	L knee	1993	Miller-Galante II	51	99	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
15	F, 70	Ovarian carcinoma	R knee	1991	Miller-Galante II with tibial stem	48	95	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1990	Miller-Galante II with tibial stem	60	92	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
16	F, 94	Metastatic carcinoma, primary unknown	R knee	1991	Miller-Galante II	54	85	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1989	Insall-Burstein II posterior stabilized with tibial stem and wedge	61	87	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Co-Cr-Mo intramed. rod
17	M, 75	Dissecting aortic aneurysm	L knee	1989	Miller-Galante II	74	98	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
18	M, 89	Cardiac arrhythmia	R knee	1990	Miller-Galante II	81	100	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Shoulder hemiarth.
19	F, 93	Congestive heart failure	L knee	1980	Miller-Galante II with tibial stem	85	91	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
20	F, 61	Septicemia	L knee	1988	Miller-Galante	113	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
			R knee	1988	Miller-Galante	124	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
21	F, 80	Metastatic lung carcinoma	R knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
			L knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
Revision hip replacement
22	M, 62	Pancreatic carcinoma	R hip	1988	Harris stem, H-G cup	47		Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1989	Periprosthetic femoral fracture treated with long Harris stem			Yes	Co-Cr-Mo		Fe-Cr-Ni plate
			R hip	1990	Allograft-prosthesis composite with Harris stem		79	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
23	F, 62	Central nervous system carcinoma	R hip	1988	Osteonics bipolar	65		Yes	Ti-6-Al-4-V, Ti
			R hip	1991	Harris stem, H-G cup			Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1991	Periprosthetic femoral fracture treated with allograft						Fe-Cr-Ni plate, Co-Cr-Ni-W cables
			R hip	1991	AML porous-coated stem			No	Co-Cr-Mo
			R hip	1992	Allograft-prosthesis composite with Harris stem		59	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
24	M, -	-	R hip	1987	Butel isoelastic stem and cup	96	NR	Yes	Ti-6-Al-4-V	Ti, UHMWPE
			R hip	1995	Revision of femoral stem
25	M, 74	Myocardial infarction	R hip	1981	Austin Moore hemiarthroplasty	156		Yes	Co-Cr-Mo
			R hip	1982	Clayton stem, Müller cup			Yes	Co-Cr-Mo	UHMWPE	Fe-Cr-Ni wires
			R hip	1984	Gustilo-Kyle porous-coated stem and allograft, H-G cup		68	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
26	F, 86	Myocardial infarction	R hip	1986	Charnley	96	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1980	Austin Moore hemiarthroplasty	164		Yes	Co-Cr-Mo
			L hip	1982	6-Ti-32 stem, Müller-type cup		NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni wires
27	F, 67	Pancreatic carcinoma	R hip	1978	Charnley-Müller	198		Yes	Co-Cr-Mo	UHMWPE
			R hip	1988	BIAS porous-coated stem and allograft, H-G cup		93	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
28	M, 76	Acute leukemia	L hip	1978	Müller	204		Yes	Co-Cr-Mo	UHMWPE
			L hip	1987	BIAS porous-coated stem and allograft, H-G cup		89	No	Ti-6-Al-4-V, Ti
29	F, 85	Cardiomyopathy	R hip	1973	Unknown hip replacement	284		Unknown	Unknown	Unknown
			R hip	1981	Townley Total Hip			Yes	Co-Cr-Mo	UHMWPE
			R hip	1986	BIAS porous-coated stem and allograft, H-G cup		73	No	Ti-6-Al-4-V	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires, Ti staples
30	F, 66	Myocardial infarction	R hip	1972	Charnley-type	232	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1967	Charnley-type	292		Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1968	Revision of polyethylene cup			Yes		UHMWPE
			L hip	1991	H-G cup with allograft, repair of trochanteric fixation		NR	No	Fe-Cr-Ni	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires
31	F, -	-	R hip	1971	Unknown hip replacement	336		Yes	Unknown	Unknown
			R hip	1978	Unknown hip replacement			Yes	Unknown	Unknown
			R hip	1984	Unknown hip replacement			No	Unknown	Unknown
			R hip	1996	Solution System cup		NR	No	Ti-6-Al-4-V, UHMWPE
			L hip	1972	Unknown hip replacement	329		Yes	Unknown	Unknown
			L hip	1980	Unknown hip replacement			Yes	Unknown	Unknown
			L hip	1987	Mallory-Head femoral, Biogroove acetabular cup and allograft			No	Ti-6-Al-4-V, UHMWPE	Ti-6-Al-4-V
			L hip	1990	Custom cementless cup and allograft		NR	No	Ti-6-Al-4-V, UHMWPE		Co-Cr-Ni-W cables

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: TABLE IClinical Data and Material Composition of the Joint Replacement Prostheses

Case	Gender, Age at Death(yrs.)	Cause of Death	Joint	Year of Operation	Type of Prosthesis*	Time Since Initial Arthroplasty(mos.)	Hip or Knee Score at Most Recent Examination†(points)	Materials‡
Cement	Femoral Component	Acetabular or Tibial Component	Other Implants
Primary hip replacement
1	F, 65	Pancreatic carcinoma	R hip	1989	Harris stem, H-G cup	43	100	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
2	M, 91	Pneumonia	R hip	1988	Harris stem, H-G cup	44	62	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
3	F, 86	Metastatic breast carcinoma	R hip	1987	Harris stem, H-G cup	46	95	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
4	M, 74	Mycosis fungoides	R hip	1990	Harris stem, H-G cup	48	69	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			L hip	1990	Harris stem, H-G cup	48	70	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
5	F, 83	Congestive heart failure	R hip	1988	Harris stem, H-G cup	54	79	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
6	M, 71	Metastatic lung carcinoma	L hip	1987	BIAS porous-coated stem, H-G cup	54	83	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
7	M, 71	Cerebrovascular accident	R hip	1987	Harris stem, H-G cup	57	91	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
8	M, 54	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	78	98	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
9	M, 59	Myocardial infarction	R hip	1986	H-G porous-coated stem, H-G cup	89	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
10	M, 71	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	99	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
11	F, 86	Cardiorespiratory arrest	R hip	1983	6-Ti-32 stem, cemented cup	171	NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni hip nail
Primary knee replacement
12	F, 83	Metastatic colon carcinoma	L knee	1995	Miller-Galante II	31	NR	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
13	M, 18	Metastatic osteosarcoma	L knee	1993	Kinematic II rotating hinge with porous-coated modular distal femoral replacement	34	NR	Yes	Co-Cr-Mo	Co-Cr-Mo, UHMWPE
14	F, 64	Congestive heart failure	L knee	1993	Miller-Galante II	51	99	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
15	F, 70	Ovarian carcinoma	R knee	1991	Miller-Galante II with tibial stem	48	95	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1990	Miller-Galante II with tibial stem	60	92	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
16	F, 94	Metastatic carcinoma, primary unknown	R knee	1991	Miller-Galante II	54	85	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1989	Insall-Burstein II posterior stabilized with tibial stem and wedge	61	87	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Co-Cr-Mo intramed. rod
17	M, 75	Dissecting aortic aneurysm	L knee	1989	Miller-Galante II	74	98	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
18	M, 89	Cardiac arrhythmia	R knee	1990	Miller-Galante II	81	100	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Shoulder hemiarth.
19	F, 93	Congestive heart failure	L knee	1980	Miller-Galante II with tibial stem	85	91	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
20	F, 61	Septicemia	L knee	1988	Miller-Galante	113	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
			R knee	1988	Miller-Galante	124	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
21	F, 80	Metastatic lung carcinoma	R knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
			L knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
Revision hip replacement
22	M, 62	Pancreatic carcinoma	R hip	1988	Harris stem, H-G cup	47		Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1989	Periprosthetic femoral fracture treated with long Harris stem			Yes	Co-Cr-Mo		Fe-Cr-Ni plate
			R hip	1990	Allograft-prosthesis composite with Harris stem		79	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
23	F, 62	Central nervous system carcinoma	R hip	1988	Osteonics bipolar	65		Yes	Ti-6-Al-4-V, Ti
			R hip	1991	Harris stem, H-G cup			Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1991	Periprosthetic femoral fracture treated with allograft						Fe-Cr-Ni plate, Co-Cr-Ni-W cables
			R hip	1991	AML porous-coated stem			No	Co-Cr-Mo
			R hip	1992	Allograft-prosthesis composite with Harris stem		59	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
24	M, -	-	R hip	1987	Butel isoelastic stem and cup	96	NR	Yes	Ti-6-Al-4-V	Ti, UHMWPE
			R hip	1995	Revision of femoral stem
25	M, 74	Myocardial infarction	R hip	1981	Austin Moore hemiarthroplasty	156		Yes	Co-Cr-Mo
			R hip	1982	Clayton stem, Müller cup			Yes	Co-Cr-Mo	UHMWPE	Fe-Cr-Ni wires
			R hip	1984	Gustilo-Kyle porous-coated stem and allograft, H-G cup		68	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
26	F, 86	Myocardial infarction	R hip	1986	Charnley	96	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1980	Austin Moore hemiarthroplasty	164		Yes	Co-Cr-Mo
			L hip	1982	6-Ti-32 stem, Müller-type cup		NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni wires
27	F, 67	Pancreatic carcinoma	R hip	1978	Charnley-Müller	198		Yes	Co-Cr-Mo	UHMWPE
			R hip	1988	BIAS porous-coated stem and allograft, H-G cup		93	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
28	M, 76	Acute leukemia	L hip	1978	Müller	204		Yes	Co-Cr-Mo	UHMWPE
			L hip	1987	BIAS porous-coated stem and allograft, H-G cup		89	No	Ti-6-Al-4-V, Ti
29	F, 85	Cardiomyopathy	R hip	1973	Unknown hip replacement	284		Unknown	Unknown	Unknown
			R hip	1981	Townley Total Hip			Yes	Co-Cr-Mo	UHMWPE
			R hip	1986	BIAS porous-coated stem and allograft, H-G cup		73	No	Ti-6-Al-4-V	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires, Ti staples
30	F, 66	Myocardial infarction	R hip	1972	Charnley-type	232	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1967	Charnley-type	292		Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1968	Revision of polyethylene cup			Yes		UHMWPE
			L hip	1991	H-G cup with allograft, repair of trochanteric fixation		NR	No	Fe-Cr-Ni	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires
31	F, -	-	R hip	1971	Unknown hip replacement	336		Yes	Unknown	Unknown
			R hip	1978	Unknown hip replacement			Yes	Unknown	Unknown
			R hip	1984	Unknown hip replacement			No	Unknown	Unknown
			R hip	1996	Solution System cup		NR	No	Ti-6-Al-4-V, UHMWPE
			L hip	1972	Unknown hip replacement	329		Yes	Unknown	Unknown
			L hip	1980	Unknown hip replacement			Yes	Unknown	Unknown
			L hip	1987	Mallory-Head femoral, Biogroove acetabular cup and allograft			No	Ti-6-Al-4-V, UHMWPE	Ti-6-Al-4-V
			L hip	1990	Custom cementless cup and allograft		NR	No	Ti-6-Al-4-V, UHMWPE		Co-Cr-Ni-W cables

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: TABLE IIHistological Grading System for Opaque or Translucent Birefringent Particles

Grade	Particles per High-Power Field
0+	0-0
1+	1-9
2+	10-19
3+	20-49
4+	50-499
5+	Â³500

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: TABLE IIHistological Grading System for Opaque or Translucent Birefringent Particles

Grade	Particles per High-Power Field
0+	0-0
1+	1-9
2+	10-19
3+	20-49
4+	50-499
5+	Â³500

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: TABLE IIIHistological Grades of Particle Concentration and Composition of Wear Particles*

*NA = not available, and ND = no particles of prosthetic origin were detected.†Histological grade of all opaque, refractile particles.‡Histological grade of all translucent, colorless, birefringent particles.§PE = polyethylene, Ti = commercially pure titanium, Ti-6-Al-4-V = titanium-6 percent aluminum-4 percent vanadium alloy, Co-Cr-Mo = cobalt-chromium-molybdenum alloy, Cr-PO4 = chromium phosphate corrosion product, Co-Cr-Ni-W = cobalt-chromium-nickel-tungsten alloy, Cr-Fe = chromium-iron corrosion product, and Fe-Cr-Ni = stainless-steel alloy.

Case	Type of Arthroplasty	Site	Para-Aortic Lymph Nodes			Spleen			Liver
Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§
1	Primary	Hip	2+	4+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	4+	1+	ND	1+	1+	ND
2	Primary	Hip	2+	1+	PE, Ti, Ti-6-Al-4-V	1+	0+	Ti, Ti-6-Al-4-V	1+	1+	ND
3	Primary	Hip	1+	4+	PE	4+	2+	ND	1+	0+	ND
4	Primary	Hip	1+	5+	PE, Co-Cr-Mo	1+	2+	ND	1+	1+	Ti, Ti-6-Al-4-V
5	Primary	Hip	2+	1+	PE, Ti	1+	1+	PE	2+	1+	PE
6	Primary	Hip	1+	1+	PE, Ti, Ti-6-Al-4-V	2+	1+	ND	1+	1+	ND
7	Primary	Hip	1+	1+	PE	1+	1+	ND	1+	0+	ND
8	Primary	Hip	1+	5+	PE, Ti, Cr-PO4	1+	1+	ND	1+	0+	ND
9	Primary	Hip	1+	3+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	1+	1+	ND	1+	0+	ND
10	Primary	Hip	1+	1+	PE	3+	2+	ND	1+	1+	ND
11	Primary	Hip	2+	4+	PE, Ti-6-Al-4-V	1+	0+	ND	0+	0+	ND
12	Primary	Knee	2+	1+	Ti-6-Al-4-V	1+	0+	ND	1+	0+	ND
13	Primary	Knee	2+	1+	ND	1+	1+	PE	0+	0+	ND
14	Primary	Knee	NA	NA	NA	3+	2+	ND	1+	0+	ND
15	Primary	Knee	5+	0	ND	4+	1+	ND	3+	1+	ND
16	Primary	Knee	1+	1+	PE	2+	2+	ND	1+	1+	ND
17	Primary	Knee	2+	2+	PE, Ti-6-Al-4-V	1+	1+	ND	1+	1+	ND
18	Primary	Knee	1+	1+	PE	2+	1+	ND	1+	0+	ND
19	Primary	Knee	1+	1+	ND	2+	0+	ND	1+	1+	ND
20	Primary	Knee	4+	1+	Ti-6-Al-4-V	4+	1+	Ti-6-Al-4-V	3+	1+	Ti-6-Al-4-V
21	Primary	Knee	3+	3+	PE, Co-Cr-Mo	3+	1+	Co-Cr-Mo	3+	2+	PE, Co-Cr-Mo
22	Revision	Hip	5+	1+	Ti	4+	1+	Ti	3+	1+	Ti
23	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Co-Cr-Ni-W, Cr-Fe	2+	2+	ND	1+	1+	Co-Cr-Mo
24	Revision	Hip	3+	1+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V
25	Revision	Hip	1+	1+	Ti-6-Al-4-V	1+	1+	Ti, Ti-6-Al-4-V	1+	0+	Ti
26	Revision	Hip	2+	1+	PE, Fe-Cr-Ni	1+	1+	Ti-6-Al-4-V	1+	1+	ND
27	Revision	Hip	5+	3+	PE, Ti, Ti-6-A1-4-V	2+	1+	PE	2+	1+	PE, Ti, Ti-6-Al-4-V
28	Revision	Hip	1+	1+	ND	1+	1+	ND	1+	1+	ND
29	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Ti	2+	1+	Ti	1+	1+	Ti
30	Revision	Hip	1+	1+	Fe-Cr-Ni	3+	2+	Fe-Cr-Ni	1+	0+	ND
31	Revision	Hip	NA	NA	NA	NA	NA	NA	5+	1+	Ti-6-Al-4-V
32	None	Control	2+	1+	ND	2+	1+	ND	1+	1+	ND
33	None	Control	NA	NA	NA	2+	1+	ND	2+	1+	ND
34	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
35	None	Control	4+	1+	ND	4+	3+	ND	2+	1+	ND
36	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
37	None	Control	1+	1+	ND	1+	1+	ND	0+	0+	ND
38	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
39	None	Control	2+	1+	ND	4+	1+	ND	3+	1+	ND
40	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
41	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
42	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
43	None	Control	1+	0	ND	1+	1+	ND	1+	0+	ND
44	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
45	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
46	None	Control	1+	1+	ND	1+	1+	ND	1+	0+	ND

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: TABLE IIIHistological Grades of Particle Concentration and Composition of Wear Particles*

Case	Type of Arthroplasty	Site	Para-Aortic Lymph Nodes			Spleen			Liver
Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§
1	Primary	Hip	2+	4+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	4+	1+	ND	1+	1+	ND
2	Primary	Hip	2+	1+	PE, Ti, Ti-6-Al-4-V	1+	0+	Ti, Ti-6-Al-4-V	1+	1+	ND
3	Primary	Hip	1+	4+	PE	4+	2+	ND	1+	0+	ND
4	Primary	Hip	1+	5+	PE, Co-Cr-Mo	1+	2+	ND	1+	1+	Ti, Ti-6-Al-4-V
5	Primary	Hip	2+	1+	PE, Ti	1+	1+	PE	2+	1+	PE
6	Primary	Hip	1+	1+	PE, Ti, Ti-6-Al-4-V	2+	1+	ND	1+	1+	ND
7	Primary	Hip	1+	1+	PE	1+	1+	ND	1+	0+	ND
8	Primary	Hip	1+	5+	PE, Ti, Cr-PO4	1+	1+	ND	1+	0+	ND
9	Primary	Hip	1+	3+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	1+	1+	ND	1+	0+	ND
10	Primary	Hip	1+	1+	PE	3+	2+	ND	1+	1+	ND
11	Primary	Hip	2+	4+	PE, Ti-6-Al-4-V	1+	0+	ND	0+	0+	ND
12	Primary	Knee	2+	1+	Ti-6-Al-4-V	1+	0+	ND	1+	0+	ND
13	Primary	Knee	2+	1+	ND	1+	1+	PE	0+	0+	ND
14	Primary	Knee	NA	NA	NA	3+	2+	ND	1+	0+	ND
15	Primary	Knee	5+	0	ND	4+	1+	ND	3+	1+	ND
16	Primary	Knee	1+	1+	PE	2+	2+	ND	1+	1+	ND
17	Primary	Knee	2+	2+	PE, Ti-6-Al-4-V	1+	1+	ND	1+	1+	ND
18	Primary	Knee	1+	1+	PE	2+	1+	ND	1+	0+	ND
19	Primary	Knee	1+	1+	ND	2+	0+	ND	1+	1+	ND
20	Primary	Knee	4+	1+	Ti-6-Al-4-V	4+	1+	Ti-6-Al-4-V	3+	1+	Ti-6-Al-4-V
21	Primary	Knee	3+	3+	PE, Co-Cr-Mo	3+	1+	Co-Cr-Mo	3+	2+	PE, Co-Cr-Mo
22	Revision	Hip	5+	1+	Ti	4+	1+	Ti	3+	1+	Ti
23	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Co-Cr-Ni-W, Cr-Fe	2+	2+	ND	1+	1+	Co-Cr-Mo
24	Revision	Hip	3+	1+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V
25	Revision	Hip	1+	1+	Ti-6-Al-4-V	1+	1+	Ti, Ti-6-Al-4-V	1+	0+	Ti
26	Revision	Hip	2+	1+	PE, Fe-Cr-Ni	1+	1+	Ti-6-Al-4-V	1+	1+	ND
27	Revision	Hip	5+	3+	PE, Ti, Ti-6-A1-4-V	2+	1+	PE	2+	1+	PE, Ti, Ti-6-Al-4-V
28	Revision	Hip	1+	1+	ND	1+	1+	ND	1+	1+	ND
29	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Ti	2+	1+	Ti	1+	1+	Ti
30	Revision	Hip	1+	1+	Fe-Cr-Ni	3+	2+	Fe-Cr-Ni	1+	0+	ND
31	Revision	Hip	NA	NA	NA	NA	NA	NA	5+	1+	Ti-6-Al-4-V
32	None	Control	2+	1+	ND	2+	1+	ND	1+	1+	ND
33	None	Control	NA	NA	NA	2+	1+	ND	2+	1+	ND
34	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
35	None	Control	4+	1+	ND	4+	3+	ND	2+	1+	ND
36	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
37	None	Control	1+	1+	ND	1+	1+	ND	0+	0+	ND
38	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
39	None	Control	2+	1+	ND	4+	1+	ND	3+	1+	ND
40	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
41	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
42	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
43	None	Control	1+	0	ND	1+	1+	ND	1+	0+	ND
44	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
45	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
46	None	Control	1+	1+	ND	1+	1+	ND	1+	0+	ND

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: TABLE IVPrincipal Wear Modes in Patients with Wear Particles in the Liver or Spleen

*Co-Cr-Mo = cobalt-chromium-molybdenum alloy, and Ti-6-Al-4-V = titanium-6 percent aluminum-4 percent vanadium alloy.†The wear modes of McKellop et al.45 are mode 1, wear between two primary bearing surfaces as intended; mode 2, wear from primary bearing surface rubbing against a secondary surface in an unintended manner; mode 3, wear between two primary bearing surfaces with a third body interposed; and mode 4, wear from secondary, nonbearing surfaces rubbing together.

Case	Joint	Type of Arthroplasty	Observed Damage*	Principal Wear Mode†
2	Hip	Primary	Fretting of acetabular fixation screws	4
4	Hip	Primary	Fretting of acetabular fixation screws	4
5	Hip	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
13	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
20	Knee	Primary	Metal-metal wear due to failed patellar component	2
21	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing with embedded cement	3
22	Hip	Revision	Metal-metal wear due to recurrent dislocation	2
23	Hip	Revision	Fretting of loose femoral stem	4
24	Hip	Revision	Wear at ceramic and metal head-neck junction; loose femoral stem	4
25	Hip	Revision	Fretting of loose femoral stem	4
26	Hip	Revision	Wear of Ti-6-Al-4-V and polyethylene bearing with embedded cement	3
27	Hip	Revision	Fretting of loose femoral and acetabular components	4
29	Hip	Revision	Fretting of loose femoral stem	4
30	Hip	Revision	Fretting of stainless-steel trochanteric fixation wires	4
31	Hip	Revision	Metal-metal wear due to failed socket liner	2

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: TABLE IVPrincipal Wear Modes in Patients with Wear Particles in the Liver or Spleen

Case	Joint	Type of Arthroplasty	Observed Damage*	Principal Wear Mode†
2	Hip	Primary	Fretting of acetabular fixation screws	4
4	Hip	Primary	Fretting of acetabular fixation screws	4
5	Hip	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
13	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
20	Knee	Primary	Metal-metal wear due to failed patellar component	2
21	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing with embedded cement	3
22	Hip	Revision	Metal-metal wear due to recurrent dislocation	2
23	Hip	Revision	Fretting of loose femoral stem	4
24	Hip	Revision	Wear at ceramic and metal head-neck junction; loose femoral stem	4
25	Hip	Revision	Fretting of loose femoral stem	4
26	Hip	Revision	Wear of Ti-6-Al-4-V and polyethylene bearing with embedded cement	3
27	Hip	Revision	Fretting of loose femoral and acetabular components	4
29	Hip	Revision	Fretting of loose femoral stem	4
30	Hip	Revision	Fretting of stainless-steel trochanteric fixation wires	4
31	Hip	Revision	Metal-metal wear due to failed socket liner	2

Materials and Methods

Introduction | Materials and Methods | Results | Discussion | References

Microscopic particles were investigated in the liver, spleen, and abdominal para-aortic lymph nodes from forty-six patients. The specimens were obtained post mortem from forty-four patients from our hospital. In addition, we studied biopsy specimens, sent to our laboratory for analysis, from two living patients who had been treated at other institutions. Thirty-one of the patients had had a total hip or knee replacement (Table I). The other fifteen, who had not had insertion of an orthopaedic implant, served as controls. The prosthetic components and periprosthetic tissues from all of the dead patients with joint replacement were available for study. The type and material composition of the prostheses and the Harris hip score²¹ or The Hospital for Special Surgery knee score²⁴ from the latest examination were recorded (Table I). Clinical data obtained from hospital records, office notes, and clinical radiographs were also reviewed.

In total, there were fourteen men and seventeen women who had had total hip or knee replacement and nine men and six women without an implant. The mean age at the time of death was seventy-three years (range, eighteen to ninety-four years) for the patients with joint replacement and sixty-seven years (range, twenty-seven to eighty-four years) for the patients without a prosthesis. The two living patients were fifty-three and sixty-one years old at the time of biopsy.

No death was related to the presence of the joint replacement (Table I). Of the fifteen control patients without a joint replacement, three died of pneumonia; two, of myocardial infarction; two, of congestive heart failure; and one each, of malignant hypertension, cerebrovascular accident, cryptogenic cirrhosis, multiple sclerosis, pulmonary embolism, malignant fibrous histiocytoma, metastatic round-cell carcinoma, and metastatic breast carcinoma.

Eleven of the patients with an implant (Cases 1 through 11) had had a primary total hip replacement for a mean duration of sixty-nine months (range, forty-three to 171 months). A porous-coated hemispherical acetabular component with a modular polyethylene articular liner had been inserted with the use of screws in ten of these patients, and an all-polyethylene component had been implanted with cement in one. Femoral reconstruction had consisted of a stem inserted with cement in seven patients and a porous-coated stem implanted without cement in four (Table I).

Ten patients (Cases 12 through 21) had had a primary total knee replacement for a mean duration of eighty-four months (range, thirty-one to 179 months). In all patients but one (Case 20), acrylic cement had been used as the method of fixation of one or more components. In nine patients, a condylar-type prosthesis had been employed. In eight of them, the tibial component was modular with a metal tray and a polyethylene or polyethylene-graphite-composite articular insert; in one, the tibial component had been fabricated entirely from polyethylene. A rotating hinged knee and modular distal femoral replacement had been implanted in another patient. The patellar components, one of which had a metal backing, were made of polyethylene.

The remaining eight patients (Cases 22, 23, and 25 through 30) with an implant who were studied post mortem had had a total hip replacement in which one or more of the components had been implanted in a revision operation. Six of these patients had had a complicated history of failure of the arthroplasties and multiple revision procedures (Table I). The mean time between the initial arthroplasty and the time of death was 174 months (range, forty-seven to 292 months), and the mean time between the last revision procedure and the time of death was seventy-one months (range, one to 130 months). The reason for revision had been loosening of cemented components without infection in seven patients and loosening with infection in one. The revision procedures had involved both the femoral and the acetabular component in five patients, only the femoral stem in two, and only the acetabular component in one. Two patients had sustained a periprosthetic fracture and had ultimately required reconstruction with use of a femoral prosthesis-allograft composite.

The two living patients also had undergone revision of one or more components of a hip replacement. Operative biopsy specimens of the liver, spleen, abdominal lymph nodes, and periprosthetic tissues from the first patient (Case 24) were submitted to us from another hospital for microanalysis of particulate debris associated with granulomatous hepatitis. This patient was a sixty-one-year-old man who presented with an aseptically loosened titanium-alloy femoral stem and unexplained weight loss, fatigue, and hepatosplenomegaly eight years after a primary total hip replacement. Clinical and laboratory tests had ruled out infectious hepatitis, sarcoidosis, prior hepatic or biliary disease, vasculitis, inflammatory colitis, drug-induced hepatitis, and effects of occupational or environmental toxins⁵⁷. The patient recovered following revision of the loosened component, splenectomy, and a course of steroid therapy. At the operation to revise the loosened femoral prosthesis, severe wear at the tapered junction between the ceramic modular head and the neck of the titanium-alloy femoral stem, with extensive black-staining of the periprosthetic tissues, was observed.

The second living patient (Case 31) was a fifty-three-year-old woman with a history of congenital dysplasia of the hips and multiple joint replacement procedures. Primary hip arthroplasty procedures in 1971 (right) and 1972 (left) were followed by three revision procedures on the right (1978, 1984, and 1996) and the left (1980, 1987, and 1990). In 1990, the left acetabular component was revised to a custom titanium-alloy cementless device with an eccentric acetabular component (so-called double bubble). In 1994, the patient was diagnosed with non-A, non-B viral hepatitis, and contemporary serological testing confirmed the presence of antibodies to the hepatitis-C virus in 1999. In preparation for participation in a research trial on interferon treatment for chronic hepatitis C, the patient underwent a liver biopsy at an outside institution. Because of the appearance of particulate debris in the histological sections of the liver, the patient and the pathological specimens were referred to our institution. On presentation, the patient reported a several-month history of discomfort, grinding, and instability of the left hip. She had no systemic symptoms of malaise, jaundice, or fatigue. Physical examination revealed a short-limb, Trendelenburg gait on the left side, with pain on passive motion of the left hip. Crepitation was found during range-of-motion maneuvers. Radiographs of the hip revealed gross superior migration of the femoral head, suggesting wear-through, fracture, or disassembly of the acetabular polyethylene liner (Fig. 1). The patient underwent venipuncture for serum titanium analysis with use of previously published protocols^26,33. In addition, a panel of routine serum liver-function tests was obtained. After serum specimens were obtained, the patient underwent revision surgery, at which time disassembly and wear-through of the polyethylene liner as well as severe wear of the metal-backing of the acetabular component and gross black-staining of the surrounding tissues were noted.

In addition to the hip or knee replacement components, ten patients had other metallic devices (fixation plates and screws, wires, or cables) (Table I). Acrylic cement that had been used in the insertion of the hip and knee replacement components contained granules of contrast medium made of barium sulfate in twenty-five patients and zirconium oxide in one.

Methods of Evaluation

Specimens of liver, spleen, and abdominal para-aortic lymph nodes as well as the implants with surrounding bone and soft tissue were removed and fixed in 10 percent neutral buffered formalin. Lymph nodes were not available from three control patients and one patient with a joint replacement. The soft-tissue specimens were processed and embedded in paraffin. Five-micrometer-thick serial sections were cut on a rotatory microtome. Sections were treated with alcoholic picric acid to remove formalin pigment⁶⁸and stained with hematoxylin and eosin for histopathological evaluation and characterization of particles by light microscopy. Other sections were processed with use of oil-red-O stain (Rowley Biochemical, Danvers, Massachusetts) for histological identification of polyethylene⁶²and Harris's hematoxylin. Positive and negative control specimens were included in each batch of slides stained with oil red O. Additional sections were prepared unstained for microanalytical identification of metallic and polyethylene particles.

The sections stained with hematoxylin and eosin were examined under conventional and polarized light for particulate debris and associated cellular infiltration, fibrosis, and necrosis. Two types of particles were studied: metal-like particles, which were opaque and refractile, and polyethylene-like particles, which were translucent, colorless, and birefringent. A modification of the system of Mirra et al.⁵⁰ was used to describe the concentrations of these two types of particles in the lymph nodes, spleen, and liver. At a magnification of 500 times, the maximum concentration of particles in at least five microscopic fields was counted, averaged, and classified as grade 0 to grade 5+ (Table II). The concentrations of metal-like particles and polyethylene-like particles were graded separately. The locations of the particulate debris were marked on composite photomicrographs of the sections to aid in relating observations made with light microscopy of the stained sections to the findings of the microanalytical studies.

The sections stained with oil red O were used to detect macrophages containing primarily submicrometer particles of polyethylene, as might be expected in remote organs. A specimen was considered positive for polyethylene when the cytoplasm of macrophages was stained by oil red O and birefringent particles were observed in the corresponding hematoxylin and eosin-stained sections.

Microanalysis for polyethylene in the lymph nodes was performed on specimens from ten patients in which the concentration of polyethylene-like particles was twenty or more per high-power field (Table III). Aggregates of macrophages were excised from the unstained sections with use of techniques previously described by Teetsov⁷⁰, and the tissue was digested in sodium hypochlorite. The extracted particles and samples of the corresponding polyethylene components were analyzed, and their spectra were compared with use of a Fourier transform infrared microprobe spectrometer (IRS; Spectra-Tech, Stamford, Connecticut). In addition, a computer-controlled hot-stage thermal analysis system (model FP52; Mettler Corporation, Hightown, New Jersey) was used in conjunction with a polarizing microscope to determine the melting point of the samples, which was defined as the temperature at which the birefringent particles became isotropic.

Fourier transform infrared spectroscopy or hot-stage thermal analysis could not be performed on sections of liver or spleen due to the low concentration and small size of polyethylene-like particles. However, in one cadaver (Case 21), an experimental method was employed in which particles extracted from ten portal tracts from one section of the liver were pooled and analyzed with use of a laser Raman microprobe spectrometer (Ramascope System 1000; Renishaw, Gloucestershire, United Kingdom).

Microanalysis of metallic particles was conducted on unstained sections mounted directly onto pyrolytic graphite planchets (Ernest Fullam, Latham, New York). Electron microprobe analysis of particles ranging in size from fifty micrometers to as small as 0.1 micrometer was performed on specific sites in the organs and lymph nodes from all patients and on selected periprosthetic membranes. Backscattered electron imaging was used to locate the particles, and electron microprobe with energy-dispersive and wavelength-dispersive x-ray analysis (model 8900RL; JEOL, Peabody, Massachusetts) was used to determine the composition of individual particles. This system allowed the detection of elements with an atomic number equal to or greater than that of carbon. The size, elemental composition, and anatomical location of the particles were recorded. Particles analyzed with use of the electron microprobe were classified on the basis of their x-ray spectra as (1) consistent with one of the metallic materials from which the prostheses had been fabricated, (2) background particulates of environmental, occupational, or iatrogenic origin other than the joint replacement components, or (3) endogenous, including iron-oxide-like and calcium-rich particles. Particles of cobalt-chromium and stainless-steel alloys were evident by their distinctive spectra. Particles of metallic titanium, consistent with commercially pure titanium from the prosthetic components, had a characteristic spectrum with low oxygen content, in contrast to the spectrum of titanium dioxide, a potential environmental particulate. The presence of vanadium in particles of titanium alloy was confirmed by wavelength-dispersive x-ray analysis.

The primary source of the specific particles of prosthetic origin found in the spleen or liver of each patient was determined by examination of parts of the prostheses composed of the same material for evidence of surface damage and by identification of particles of the same material in the periprosthetic tissues. The components and the surrounding bone and soft tissues were studied with light microscopy of undecalcified, plastic-embedded sections stained with basic fuchsin and toluidine blue^58,74. Metallic particles in the periprosthetic membranes adjacent to the sites of observed damage were identified with use of energy-dispersive x-ray analysis. The bearing surfaces were examined with light microscopy at magnifications of ten to seventy-five times. The reconstructions were categorized for four different wear modes with use of the classification system of McKellop et al.⁴⁵ (Table IV).

The prevalence of metallic and polyethylene particles in the liver, spleen, and para-aortic lymph nodes was determined for the twenty-nine patients with implants who were studied post mortem. The two living patients were excluded from the calculations because these cases were biased by prior knowledge of particulate debris in the organs. The histopathological response to and the apparent source of wear particles in the organs were studied in all thirty-one patients.

Results

Introduction | Materials and Methods | Results | Discussion | References

Postmortem gross and radiographic examinations of the joint replacement specimens demonstrated that all of the primary hip and knee components were well fixed. Of the ten patients who had a revision hip replacement (eight dead and two living), five (Cases 23, 24, 25, 27, and 29) had one or more aseptically loose components.

Light microscopy of the stained sections revealed opaque refractile particles as well as translucent birefringent particles in the liver, spleen, or lymph nodes whether or not a patient had had a prosthesis (Table III); this finding indicated a background of environmental particulates, as expected. The patients who had had a prosthesis generally had greater concentrations of particles than the control patients did, especially in the lymph nodes, because both prosthetic wear debris and the particles of environmental origin were present. The most prevalent particles of prosthetic origin included polyethylene, which was followed by commercially pure titanium, titanium-aluminum-vanadium and cobalt-chromium-molybdenum alloys, barium sulfate, stainless-steel alloy, cobalt-chromium-nickel-tungsten alloy from a cable-grip system, zirconium oxide, and corrosion products of cobalt-chromium and stainless-steel alloys. Particles of similar composition were not found in the lymph nodes or organs of the fifteen control patients without implants, with the exception of barium sulfate.

Metallic Wear Particles

Electron microprobe analysis indicated that metallic wear particles were present in the para-aortic lymph nodes of 68 percent (nineteen) of the twenty-eight patients with a hip or knee replacement from whom lymph nodes were available for study and that they had further disseminated to the liver or spleen in 38 percent (eleven) of all twenty-nine patients with a replacement who were studied post mortem (Table III). Most disseminated metallic particles were less than one micrometer in size, but the range of particle sizes differed by material composition. Particles of commercially pure titanium and titanium-aluminum-vanadium alloy ranged from 0.1 micrometer to as large as fifty micrometers in the lymph nodes and as large as ten micrometers in the liver and spleen. In contrast, although the smallest particles of cobalt-chromium and stainless-steel alloys were also 0.1 micrometer, the largest rarely exceeded three micrometers.

Particles associated with corrosion were identified in the para-aortic lymph nodes of two patients. In one of the patients (Case 23), particles rich in chromium, phosphorous, and iron had originated from corrosion of a stainless-steel fixation plate⁸². In another patient (Case 8), corrosion at the modular head-neck junction of the femoral component was the source of chromium orthophosphate hydrate-rich particles^29,75.

Metallic wear particles were detected in both the spleen and the liver in five patients, in the spleen alone in three patients, and in the liver alone in three patients who were studied post mortem (Table III). These particles were more common in patients who had had a failed arthroplasty. They were found in the liver or spleen in seven of the eight patients in whom a hip replacement component had been revised, but they were detected in only two of the eleven patients with primary hip replacement and in two of the ten patients with primary knee replacement.

Polyethylene Wear Particles

Sections processed by the oil-red-O staining technique for polyethylene demonstrated positive cytoplasmic staining of macrophages in the para-aortic lymph nodes of 68 percent (nineteen) of the twenty-eight patients with a prosthesis from whom lymph nodes were available for study. Examination of the corresponding hematoxylin and eosin-stained sections under polarized light revealed birefringent particles ranging in size from less than one to thirty micrometers (Fig. 2). The smaller particles were granular, needle-like, or plate-like, and the larger particles consisted of long filamentous or shredded fibers. A few scattered macrophages in the lymph nodes of three control patients (Cases 32, 34, and 46) also demonstrated staining by oil red O.

Fourier transform infrared spectra of polyethylene particles that were extracted from the lymph nodes closely matched the spectra of samples from the corresponding polyethylene components. The melting-point measurements ranged from 134 to 137 degrees Celsius, both for the particles and for the samples from the retrieved components. These temperatures were consistent with the melting point of ultra-high molecular weight polyethylene^43,78.

Sections of liver and spleen processed with use of the oil-red-O technique were positive for polyethylene in 10 percent (three) of the twenty-nine patients who had had a prosthesis and in none of the control patients (Table III). Sections from another five patients with an implant (Cases 21, 22, 26, 28, and 29) showed low concentrations of minute birefringent particles in sections stained by hematoxylin and eosin (Fig. 3-A) and only faint cytoplasmic staining in the corresponding sections processed by the oil-red-O technique. Laser Raman microprobe spectroscopy of particles isolated from the liver of one of these patients (Case 21) identified the particles as polyethylene (Fig. 3-B) despite the equivocal finding with use of oil-red-O stain. Thus, a total of 14 percent (four) of the twenty-nine patients with implants who were studied post mortem had polyethylene in the liver or spleen.

Particles of Bone-Cement Contrast Material

Particles of barium sulfate, 0.2 to two micrometers in size, were present in the liver or spleen of five patients and in the lymph nodes of five patients in the group of twenty-five patients in whom bone cement containing this material had been employed. Similarly sized particles of barium sulfate, possibly representing residual material from diagnostic radiographic studies, were detected in the liver, spleen, and lymph nodes of a control subject (Case 46) and in the lymph nodes of another control subject (Case 34). Abundant particles of zirconium oxide were detected in the lymph nodes of the one patient in whom this material had been used as a contrast agent in bone cement.

Histopathological Findings

In the lymph nodes, metallic and polyethylene particles were contained in macrophages and rare multinucleated giant cells within the medullary sinus. The number of particles and the cellular response ranged from a few scattered cells to extensive infiltrates of macrophages. Granulomatous inflammation was present in the lymph nodes of seventeen patients, and fibrosis was present in ten. In several patients with a revised hip replacement, the para-aortic lymph node chain was grossly stained black due to the heavy concentration of metallic particles. Lymph node necrosis was observed in one of these patients (Case 22). In another patient (Case 29), who had undergone multiple revisions of a hip reconstruction, the number of polyethylene particles was so great that macrophages laden with polyethylene (and less numerous metallic particles) nearly replaced the lymph nodes (Fig. 2).

In the liver and spleen, polyethylene and metallic wear particles were usually found within pale-staining, often vacuolated macrophages that were seen as infiltrates in portal tracts (Fig. 4) and near the splenic trabeculae. The infiltrates consisted of macrophages occurring singly or as small aggregates without apparent pathological importance. Multinucleated giant cells containing wear debris were not observed. Neither fibrosis nor necrosis was found in conjunction with wear debris in these specimens.

The highest concentration of metal particles was observed in the liver biopsy specimen from one of the living patients (Case 31), in whom 500 or more titanium-alloy particles per high-power field were present within macrophages in the portal tracts (Fig. 5-A). Metallic particles were also apparent in Kupffer cells lining the hepatic sinusoids (Fig. 5-B). In this patient, there was only mild chronic portal inflammation and very mild nonspecific lobular hepatitis, findings also compatible with the history of chronic hepatitis-C infection. Neither fibrosis nor piecemeal necrosis, findings associated with hepatitis-C infection, was present.

The other living patient (Case 24), who had systemic granulomatous disease, presented with different histological features. In this patient, epithelioid granulomas consisting predominantly of epithelioid macrophages and multinucleated giant cells with mild-to-moderate small mononuclear cell infiltrates were present in the lymph nodes, liver, and spleen. The granulomas effaced the normal nodal architecture. In the liver and spleen, the granulomas were found primarily in portal tracts and were distributed throughout the splenic parenchyma (Fig. 6-A). In the liver, there was mild bile-duct hyperplasia and moderate fibrosis (Fig. 6-B). Abundant particles of titanium-aluminum-vanadium alloy were demonstrated in the granulomas in the liver, spleen, and lymph nodes, as were birefringent calcium-oxalate crystals⁶⁰.

Serum Analysis

The concentration of titanium in the serum from the patient with the greatest concentration of particles in the liver (Case 31) was 1203 nanograms per milliliter (parts per billion). Normal values for our laboratory for individuals without titanium implants is less than two parts per billion³³. For patients with a well functioning unilateral total hip replacement, at thirty-six months postoperatively the mean serum titanium value is 4.1 parts per billion (range, 1.1 to 11.2 parts per billion)³³, and for patients with a failed titanium-containing total hip replacement the mean serum titanium value is 8.1 parts per billion (range, less than 2.1 to 17.2 parts per billion)²⁶. All serum liver-function markers (including total protein, albumin, gamma glutamyl transpeptidase, total bilirubin, alkaline phosphatase, lactic dehydrogenase, glutamic-oxaloacetic transaminase, and glutamic-pyruvate transaminase levels) were within normal limits, with the exception of the level of serum albumin, which was just below the normal range (value in our patient, thirty-three grams per liter; normal, thirty-five to fifty grams per liter).

Sources of Wear Particles in the Liver and Spleen

Examination of the prosthetic components and periprosthetic tissues from the fifteen patients with dissemination of polyethylene or metallic wear particles to the liver or spleen (Table III) revealed that the principal wear modes in these reconstructions were secondary nonbearing surfaces rubbing together (eight patients), a primary bearing surface rubbing against a secondary surface (three patients), and wear between two primary bearing surfaces as intended (two patients) and with a third body interposed (two patients) (Table IV). These determinations were based on the identification of particles in the organs and in the periprosthetic tissues that were of the same elemental composition as the parts of the components observed to have surface damage.

Background Particulates

The majority of background particles were found, on electron microprobe analysis, to have originated from environmental sources. Most particles were less than one micrometer in size, with energy-dispersive x-ray spectra of silica and aluminum or magnesium silicates. Many of these particles contained variable amounts of titanium, and some had traces of chromium. These particles were frequently strongly birefringent. A lesser fraction of the environmental particles were aluminum-oxide-like and titanium-oxide-like particles, which were invariably smaller than one micrometer. The greatest concentrations of particles in the control subjects consisted of particles rich in antimony (Case 35) and aluminum silicates (Case 39).

Gold particles, alone or intermixed with wear debris, were found in three patients (Cases 15, 20, and 21) who had received chronic intramuscular gold therapy prior to having bilateral knee replacement for rheumatoid arthritis. These particles appeared as aggregates of opaque granules, approximately 0.1 to 0.2 micrometer in diameter, within infiltrates of macrophages in the liver, spleen, and lymph nodes.

Discussion

Introduction | Materials and Methods | Results | Discussion | References

This study demonstrated that dissemination of wear particles to the liver, spleen, or abdominal lymph nodes is a common occurrence in patients who have a total hip or knee replacement. Metallic or polyethylene wear particles were present in the para-aortic lymph nodes of 89 percent (twenty-five) of twenty-eight patients with a joint replacement prosthesis from whom lymph nodes were available for study. Metallic or polyethylene wear particles in the liver or spleen were more prevalent in patients who had had a previously failed reconstruction (seven of eight) than in patients who had had a primary hip (three of eleven) or knee (three of ten) arthroplasty. In the majority of patients, the concentration of wear particles in the liver or spleen was relatively low and without apparent pathological importance. However, biopsy specimens from two living patients (Cases 24 and 31) demonstrated that very high concentrations of particles in the liver and spleen can result when large amounts of wear debris are generated from the mechanical failure of a device.

In most patients, the wear debris disseminated to the liver and spleen had been generated by wear modes other than wear of the intended primary bearing surfaces. This determination was based on the identification of particles in the organs and in the periprosthetic tissues that were of the same elemental composition as the parts of the components with observed surface damage. The highest concentrations of metallic wear particles were generated by wear of loose metallic components against bone or cement, by wear at the tapered junction between a ceramic modular head and the neck of a femoral stem, or by wear of the metallic bearing surface against an unintended secondary metal surface because of wear-through of the polyethylene or instability of the prosthetic head in the socket. The highest concentration of polyethylene in the liver or spleen was associated with wear of polyethylene and cobalt-chromium-molybdenum bearing surfaces with interposed cement and was in a patient (Case 21) who had had a well fixed, well functioning, bilateral primary total knee prosthesis for almost fifteen years. The modular design of contemporary hip and knee replacement components, screw-component interfaces, and wire-and-cable systems for trochanteric fixation also contributed to the systemic burden of wear and corrosion products in this study.

In one living patient (Case 31), a comparison could be made between the serum titanium concentration and the histological findings on a liver biopsy, which was performed for reasons unrelated to the failed arthroplasty. This patient had the most extensive particulate infiltration in the liver, consistent with the finding that she had the highest serum titanium value reported by our laboratory to date^{26,29,30,33,34}. The serum concentration was three orders of magnitude higher than that of individuals who do not have an implant containing titanium³³. In other reports, our laboratory has shown that elevated serum or urine titanium, cobalt, and chromium concentrations can be associated with mechanical dysfunction of a device^{26,29,30,31,33,34} such as wear-through of a metal-backed patellar component, fretting corrosion of modular femoral total hip replacement components, and accelerated wear of metal-on-metal total hip replacements. The findings in this patient also suggest that serum metal levels may reflect the extent of deposition of metal degradation products in remote tissues. Thus, serum metal levels may prove to be a useful diagnostic adjunct to aid in the evaluation of a patient with a joint replacement device and in the determination of the timing of revision surgery in a patient with a symptomatic or failed device.

Apparently, the hepatic particulate burden in this patient (Case 31) had been well tolerated up to the time of this study, as evidenced by the patient's normal serum liver-function markers and the histopathological findings that revealed only mild chronic portal inflammation and very mild nonspecific lobular hepatitis, findings also compatible with her history of chronic hepatitis-C infection. As in other patients with particles in the liver or spleen, the primary wear mode was from contact of an articulating surface (the metal femoral head) with an unintended secondary surface (the metal backing of the acetabular shell).

In this study, electron microprobe analysis was employed to characterize metal-like particles in the organs. This technique allowed identification of individual submicrometer metallic wear particles against a background of particles from environmental and other sources. Gold particles, which might have been misinterpreted as wear debris with use of light microscopy, were identified in the organs of three patients who had received chronic gold therapy prior to knee arthroplasty. The composition of the environmental particles was consistent with particulate burdens in the lung that were previously reported for urban populations, although their concentration in the liver and spleen was orders of magnitude lower, as would be expected^54,67. Many environmental particles contained titanium or aluminum, partly explaining the variable concentrations of these elements in the liver and spleen of control patients in previous studies in which bulk analytic techniques were used⁷¹. Overall, the smallest identifiable metallic particle, given the methods employed in the present study, was 0.1 micrometer. Reports that wear debris may well extend into the nanometer range^13,72,74,81 suggest that additional methods of specimen preparation and analytic instrumentation will be required to define the burden of wear particles in remote tissues more fully.

Polyethylene appeared to be a major portion of the disseminated wear debris after both primary and revision reconstructions. However, it must be recognized that currently available techniques for identification of polyethylene particles lack the sensitivity and specificity of the methods employed to identify metallic particles⁶. With use of oil-red-O stain and polarized light, polyethylene particles were found in the para-aortic lymph nodes of 68 percent (nineteen) of the twenty-eight patients who had had a prosthesis. In the lymph nodes of ten of these patients, a sufficient concentration of particulate debris (twenty or more particles per high-power field) allowed definitive identification of polyethylene by Fourier transform infrared spectroscopy and thermal analysis. Scattered oil-red-O staining of macrophages was observed in the lymph nodes of three control patients. The nature of the stained material was not identified, but all three patients had had an abdominal operation, suggesting the presence of other polymeric materials such as sutures. Other long-chain hydrocarbons might also have been responsible⁶².

The presence of polyethylene wear debris in the liver or spleen, which has not been previously reported to our knowledge, presented an even greater technical challenge because of the still smaller size and lower concentration of particles. For these reasons, the prevalence of polyethylene particles in the liver and spleen may have been underestimated. Polyethylene particles were demonstrated in the organs of three patients with use of oil-red-O stain. In another five patients, polyethylene in the liver or spleen was suspected, but the faint cytoplasmic staining of macrophages was not definitive. For one of these patients, an experimental method was employed in which a minute quantity of submicrometer particles extracted from portal tract macrophages was analyzed with use of a laser Raman microprobe spectrometer. Submicrometer particles of polyethylene were definitively identified with this method, despite the equivocal cytoplasmic staining with use of the oil-red-O technique. With additional developments, this method promises to be a valuable tool for future studies.

Lymphatic transport was a major route for dissemination of wear debris. Wear particles may have migrated through perivascular lymph channels as free or phagocytosed particles within macrophages²⁰. Most disseminated particles were smaller than a micrometer, but particles as large as fifty micrometers were identified in abdominal lymph nodes. In the liver and spleen, the maximum size of wear particles was an order of magnitude smaller. These smaller particles typically accumulated in the mobile macrophages of the portal tracts of the liver, most likely by means of lymphatic transport. In the patients with extensive dissemination of debris (Cases 21, 24, and 31), the particles were also found in the fixed macrophages or Kupffer cells lining the hepatic sinusoids, suggesting the possibility of hematogenous dissemination as well. Particulate debris may also be transported to and accumulated in other sites that were not examined in this study. Transport of particles to remote bone marrow by circulating monocytes or by entry of small particles directly into the bloodstream has been hypothesized¹⁵. Contamination of blood by titanium debris has been reported when an intraoperative blood-conservation system was employed during revision of a hip replacement⁶⁶; this finding presents the possibility of infusion of microscopic metallic particles directly into the bloodstream. We were able to rule out this factor in all but one revision operation, which had been performed at another hospital.

Dissemination of large amounts of metallic and polyethylene wear debris to the para-aortic lymph nodes was associated with lymphadenopathy, gross pigmentation due to metallic debris, fibrosis, lymph node necrosis, and histiocytosis, including complete effacement of nodal architecture. Similar findings have been demonstrated by regional and pelvic lymph node biopsies of patients with a replacement arthroplasty^{1,4,5,7,9,23,30,52,64,65}. The inflammatory response to metallic and polymeric debris in lymph nodes has been shown to include immune activation of macrophages and associated production of cytokines²³. Accumulation of such debris in the liver, spleen, and lymph nodes may explain, in part, the observation that circulating peripheral blood monocytes from patients with joint replacements are more reactive to particulate wear debris stimulation than are monocytes from individuals without implants³⁹.

In the liver and spleen, as in the lymph nodes, cells of the mononuclear phagocyte system may accumulate small amounts of a variety of foreign materials without apparent clinical importance, as appeared to be the case for the majority of the patients in the present study. However, it is well established that heavy accumulation of exogenous particles, including debris from implanted devices, can induce granulomas or granulomatoid lesions in the liver and spleen^{8,10,12,14,19,25,38,40-42,51,59,61}. Therefore, it is not surprising that, in the present study, one living patient (Case 24) with heavy accumulation of titanium-alloy wear particles demonstrated granulomatous lesions in the liver and spleen requiring operative and medical treatment⁵⁷. Similar epithelioid granulomas have been reported in association with high concentrations of cobalt-base-alloy particles or titanium and stainless-steel-alloy particles in regional lymph nodes draining the sites of total knee replacement prostheses^11,30.

The fate of wear particles in the liver and spleen is unknown, but the well studied example of thorium dioxide, persistent in the liver twenty to thirty years after its injection into patients as a radiographic contrast material, illustrates the long-term retention of particulate matter by end organs⁴⁰. It has been suggested that certain types of orthopaedic wear debris, presumably polymethylmethacrylate or polyethylene, may be ultimately biodegradable⁶.Degradation of metallic particles, however, implies the slow dissolution of their constituent metal elements, for which the potential metabolic, immunological, and oncogenic effects have yet to be ascertained.

There have been several epidemiological studies of cancer incidence in the first and second decades following total hip replacement. Two of these demonstrated a slight increase in the risk of lymphatic tumors in patients who had a cobalt-alloy total hip replacement and in patients who had a metal-on-metal device^16,76,77. Larger and more recent studies found no significant increase in leukemias or lymphomas; however, they did not include as large a proportion of patients with a metal-on-metal prosthesis^17,48,53. Thus, despite case reports of malignant tumors arising in proximity to joint-replacement prostheses²⁷, no clear epidemiological evidence of an increased risk of a malignant tumor has been identified in the first two decades following implantation of a prosthesis, to our knowledge. Nonetheless, the pervasive distribution of wear particles observed in the liver and spleen of some patients in this study, along with the chronic inflammatory response to particulate debris, should continue to be of concern for patients with evidence of major wear or a prior revision, or both, as well as for patients who may have a well functioning primary joint replacement for several decades.

The findings of this study indicate that wear particles are commonly transported to the liver, spleen, or abdominal lymph nodes of patients with joint replacements. Particles in the liver and spleen were most often found in patients with a failed reconstruction rather than in patients in whom the device had functioned as intended. In most of the patients examined in this study, the concentration of metallic and polyethylene wear particles in the liver and spleen was relatively low and no toxic effects were apparent on histological examination. However, as demonstrated in one rare case, granulomas may form in remote organs in response to heavy accumulation of wear debris and may compromise organ function. The orthopaedic surgeon should be aware of this phenomenon and should consider expeditious revision in patients in whom large amounts of particulate debris may be generated. The finding of marked elevations in serum or urine metal concentration may help to identify those patients whose implants are generating a high volume of debris and may assist in the determination of the timing of revision surgery.

Note: The authors are grateful to Jorge O. Galante, M.D., for his continuous guidance and support of this project and for editing the manuscript; to Pat Campbell, Ph.D., Thomas Bauer, M.D., Shiriam Jakate, M.D., Steven Li, Ph.D., Basile Pasquier, M.D., Coretta Sapienza, M.D., and Anna Teetsov for their cooperation and consultation; to Aivars Berzins, M.D., Paul Sauer, M.D., Craig Silverton, M.D., Alex Starr, M.D., and William Edwards, M.D., for their assistance in the procurement of specimens; and to Charles Engh, M.D., Steven Gitelis, M.D., William Hejna, M.D., Aaron Rosenberg, M.D., Mitchell Sheinkop, M.D., and William Streitz, M.D., for their valuable cooperation.

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Jacobs, J. J.; Urban, R. M.; Gilbert,J. L.; Skipor, A. K.; Black, J.; Jasty, M.; and Galante, J. O.: Localand distant products from modularity. Clin. Orthop., 319: 94-105,1995.

Jacobs, J. J.; Urban, R. M.; Wall,J.; Black, J.; Reid, J. D.; and Veneman, L.: Unusual foreign-bodyreaction to a failed total knee replacement: simulation of a sarcomaclinically and a sarcoid histologically. A case report. J. Boneand Joint Surg., 77-A: 444-451, March 1995.

Jacobs, J. J.; Skipor, A. K.; Doorn,P. F.; Campbell, P.; Schmalzried, T. P.; Black, J.; and Amstutz,H. C.: Cobalt and chromium concentrations in patients with metalon metal total hip replacements. Clin. Orthop., 329S: S256-S263,1996.

Jacobs, J. J.; Gilbert, J. L.; andUrban, R. M.: Current concepts review. Corrosion of metal orthopaedicimplants. J Bone Joint Surg, 80-A: 268-282, Feb. 1998.

Jacobs, J. J.; Skipor, A. K.; Patterson,L. M.; Hallab, N. J.; Paprosky, W. G.; Black, J.; and Galante, J.O.: Metal release in patients who have had a primary total hip arthroplasty.A prospective, controlled, longitudinal study. J Bone Joint Surg,80-A: 1447-1458, Oct. 1998.

Jacobs, J. J.; Silverton, C.; Hallab,N. J.; Skipor, A. K.; Patterson, L.; Black, J.; and Galante, J. O.:Metal release and excretion from cementless titanium alloy totalknee replacements. Clin. Orthop., 358: 173-180, 1999.

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: TABLE IClinical Data and Material Composition of the Joint Replacement Prostheses

Case	Gender, Age at Death(yrs.)	Cause of Death	Joint	Year of Operation	Type of Prosthesis*	Time Since Initial Arthroplasty(mos.)	Hip or Knee Score at Most Recent Examination†(points)	Materials‡
Cement	Femoral Component	Acetabular or Tibial Component	Other Implants
Primary hip replacement
1	F, 65	Pancreatic carcinoma	R hip	1989	Harris stem, H-G cup	43	100	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
2	M, 91	Pneumonia	R hip	1988	Harris stem, H-G cup	44	62	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
3	F, 86	Metastatic breast carcinoma	R hip	1987	Harris stem, H-G cup	46	95	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
4	M, 74	Mycosis fungoides	R hip	1990	Harris stem, H-G cup	48	69	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			L hip	1990	Harris stem, H-G cup	48	70	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
5	F, 83	Congestive heart failure	R hip	1988	Harris stem, H-G cup	54	79	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
6	M, 71	Metastatic lung carcinoma	L hip	1987	BIAS porous-coated stem, H-G cup	54	83	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
7	M, 71	Cerebrovascular accident	R hip	1987	Harris stem, H-G cup	57	91	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
8	M, 54	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	78	98	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
9	M, 59	Myocardial infarction	R hip	1986	H-G porous-coated stem, H-G cup	89	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
10	M, 71	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	99	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
11	F, 86	Cardiorespiratory arrest	R hip	1983	6-Ti-32 stem, cemented cup	171	NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni hip nail
Primary knee replacement
12	F, 83	Metastatic colon carcinoma	L knee	1995	Miller-Galante II	31	NR	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
13	M, 18	Metastatic osteosarcoma	L knee	1993	Kinematic II rotating hinge with porous-coated modular distal femoral replacement	34	NR	Yes	Co-Cr-Mo	Co-Cr-Mo, UHMWPE
14	F, 64	Congestive heart failure	L knee	1993	Miller-Galante II	51	99	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
15	F, 70	Ovarian carcinoma	R knee	1991	Miller-Galante II with tibial stem	48	95	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1990	Miller-Galante II with tibial stem	60	92	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
16	F, 94	Metastatic carcinoma, primary unknown	R knee	1991	Miller-Galante II	54	85	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1989	Insall-Burstein II posterior stabilized with tibial stem and wedge	61	87	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Co-Cr-Mo intramed. rod
17	M, 75	Dissecting aortic aneurysm	L knee	1989	Miller-Galante II	74	98	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
18	M, 89	Cardiac arrhythmia	R knee	1990	Miller-Galante II	81	100	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Shoulder hemiarth.
19	F, 93	Congestive heart failure	L knee	1980	Miller-Galante II with tibial stem	85	91	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
20	F, 61	Septicemia	L knee	1988	Miller-Galante	113	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
			R knee	1988	Miller-Galante	124	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
21	F, 80	Metastatic lung carcinoma	R knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
			L knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
Revision hip replacement
22	M, 62	Pancreatic carcinoma	R hip	1988	Harris stem, H-G cup	47		Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1989	Periprosthetic femoral fracture treated with long Harris stem			Yes	Co-Cr-Mo		Fe-Cr-Ni plate
			R hip	1990	Allograft-prosthesis composite with Harris stem		79	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
23	F, 62	Central nervous system carcinoma	R hip	1988	Osteonics bipolar	65		Yes	Ti-6-Al-4-V, Ti
			R hip	1991	Harris stem, H-G cup			Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1991	Periprosthetic femoral fracture treated with allograft						Fe-Cr-Ni plate, Co-Cr-Ni-W cables
			R hip	1991	AML porous-coated stem			No	Co-Cr-Mo
			R hip	1992	Allograft-prosthesis composite with Harris stem		59	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
24	M, -	-	R hip	1987	Butel isoelastic stem and cup	96	NR	Yes	Ti-6-Al-4-V	Ti, UHMWPE
			R hip	1995	Revision of femoral stem
25	M, 74	Myocardial infarction	R hip	1981	Austin Moore hemiarthroplasty	156		Yes	Co-Cr-Mo
			R hip	1982	Clayton stem, Müller cup			Yes	Co-Cr-Mo	UHMWPE	Fe-Cr-Ni wires
			R hip	1984	Gustilo-Kyle porous-coated stem and allograft, H-G cup		68	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
26	F, 86	Myocardial infarction	R hip	1986	Charnley	96	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1980	Austin Moore hemiarthroplasty	164		Yes	Co-Cr-Mo
			L hip	1982	6-Ti-32 stem, Müller-type cup		NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni wires
27	F, 67	Pancreatic carcinoma	R hip	1978	Charnley-Müller	198		Yes	Co-Cr-Mo	UHMWPE
			R hip	1988	BIAS porous-coated stem and allograft, H-G cup		93	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
28	M, 76	Acute leukemia	L hip	1978	Müller	204		Yes	Co-Cr-Mo	UHMWPE
			L hip	1987	BIAS porous-coated stem and allograft, H-G cup		89	No	Ti-6-Al-4-V, Ti
29	F, 85	Cardiomyopathy	R hip	1973	Unknown hip replacement	284		Unknown	Unknown	Unknown
			R hip	1981	Townley Total Hip			Yes	Co-Cr-Mo	UHMWPE
			R hip	1986	BIAS porous-coated stem and allograft, H-G cup		73	No	Ti-6-Al-4-V	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires, Ti staples
30	F, 66	Myocardial infarction	R hip	1972	Charnley-type	232	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1967	Charnley-type	292		Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1968	Revision of polyethylene cup			Yes		UHMWPE
			L hip	1991	H-G cup with allograft, repair of trochanteric fixation		NR	No	Fe-Cr-Ni	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires
31	F, -	-	R hip	1971	Unknown hip replacement	336		Yes	Unknown	Unknown
			R hip	1978	Unknown hip replacement			Yes	Unknown	Unknown
			R hip	1984	Unknown hip replacement			No	Unknown	Unknown
			R hip	1996	Solution System cup		NR	No	Ti-6-Al-4-V, UHMWPE
			L hip	1972	Unknown hip replacement	329		Yes	Unknown	Unknown
			L hip	1980	Unknown hip replacement			Yes	Unknown	Unknown
			L hip	1987	Mallory-Head femoral, Biogroove acetabular cup and allograft			No	Ti-6-Al-4-V, UHMWPE	Ti-6-Al-4-V
			L hip	1990	Custom cementless cup and allograft		NR	No	Ti-6-Al-4-V, UHMWPE		Co-Cr-Ni-W cables

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: TABLE IClinical Data and Material Composition of the Joint Replacement Prostheses

Case	Gender, Age at Death(yrs.)	Cause of Death	Joint	Year of Operation	Type of Prosthesis*	Time Since Initial Arthroplasty(mos.)	Hip or Knee Score at Most Recent Examination†(points)	Materials‡
Cement	Femoral Component	Acetabular or Tibial Component	Other Implants
Primary hip replacement
1	F, 65	Pancreatic carcinoma	R hip	1989	Harris stem, H-G cup	43	100	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
2	M, 91	Pneumonia	R hip	1988	Harris stem, H-G cup	44	62	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
3	F, 86	Metastatic breast carcinoma	R hip	1987	Harris stem, H-G cup	46	95	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
4	M, 74	Mycosis fungoides	R hip	1990	Harris stem, H-G cup	48	69	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			L hip	1990	Harris stem, H-G cup	48	70	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
5	F, 83	Congestive heart failure	R hip	1988	Harris stem, H-G cup	54	79	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
6	M, 71	Metastatic lung carcinoma	L hip	1987	BIAS porous-coated stem, H-G cup	54	83	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
7	M, 71	Cerebrovascular accident	R hip	1987	Harris stem, H-G cup	57	91	Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
8	M, 54	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	78	98	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
9	M, 59	Myocardial infarction	R hip	1986	H-G porous-coated stem, H-G cup	89	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
10	M, 71	Myocardial infarction	R hip	1987	H-G porous-coated stem, H-G cup	99	100	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
11	F, 86	Cardiorespiratory arrest	R hip	1983	6-Ti-32 stem, cemented cup	171	NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni hip nail
Primary knee replacement
12	F, 83	Metastatic colon carcinoma	L knee	1995	Miller-Galante II	31	NR	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
13	M, 18	Metastatic osteosarcoma	L knee	1993	Kinematic II rotating hinge with porous-coated modular distal femoral replacement	34	NR	Yes	Co-Cr-Mo	Co-Cr-Mo, UHMWPE
14	F, 64	Congestive heart failure	L knee	1993	Miller-Galante II	51	99	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
15	F, 70	Ovarian carcinoma	R knee	1991	Miller-Galante II with tibial stem	48	95	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1990	Miller-Galante II with tibial stem	60	92	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
16	F, 94	Metastatic carcinoma, primary unknown	R knee	1991	Miller-Galante II	54	85	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
			L knee	1989	Insall-Burstein II posterior stabilized with tibial stem and wedge	61	87	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Co-Cr-Mo intramed. rod
17	M, 75	Dissecting aortic aneurysm	L knee	1989	Miller-Galante II	74	98	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
18	M, 89	Cardiac arrhythmia	R knee	1990	Miller-Galante II	81	100	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE	Shoulder hemiarth.
19	F, 93	Congestive heart failure	L knee	1980	Miller-Galante II with tibial stem	85	91	Yes	Co-Cr-Mo	Ti-6-Al-4-V, UHMWPE
20	F, 61	Septicemia	L knee	1988	Miller-Galante	113	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
			R knee	1988	Miller-Galante	124	99	No	Ti-6-Al-4-V, Ti	Ti-6-Al-4-V, Ti; Ti-6-Al-4-V screws, UHMWPE-graphite
21	F, 80	Metastatic lung carcinoma	R knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
			L knee	1980	Insall-Burstein total condylar	179	100	Yes	Co-Cr-Mo	UHMWPE
Revision hip replacement
22	M, 62	Pancreatic carcinoma	R hip	1988	Harris stem, H-G cup	47		Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1989	Periprosthetic femoral fracture treated with long Harris stem			Yes	Co-Cr-Mo		Fe-Cr-Ni plate
			R hip	1990	Allograft-prosthesis composite with Harris stem		79	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
23	F, 62	Central nervous system carcinoma	R hip	1988	Osteonics bipolar	65		Yes	Ti-6-Al-4-V, Ti
			R hip	1991	Harris stem, H-G cup			Yes	Co-Cr-Mo	Ti, Ti-6-Al-4-V screws, UHMWPE
			R hip	1991	Periprosthetic femoral fracture treated with allograft						Fe-Cr-Ni plate, Co-Cr-Ni-W cables
			R hip	1991	AML porous-coated stem			No	Co-Cr-Mo
			R hip	1992	Allograft-prosthesis composite with Harris stem		59	Yes	Co-Cr-Mo		Fe-Cr-Ni plate
24	M, -	-	R hip	1987	Butel isoelastic stem and cup	96	NR	Yes	Ti-6-Al-4-V	Ti, UHMWPE
			R hip	1995	Revision of femoral stem
25	M, 74	Myocardial infarction	R hip	1981	Austin Moore hemiarthroplasty	156		Yes	Co-Cr-Mo
			R hip	1982	Clayton stem, Müller cup			Yes	Co-Cr-Mo	UHMWPE	Fe-Cr-Ni wires
			R hip	1984	Gustilo-Kyle porous-coated stem and allograft, H-G cup		68	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
26	F, 86	Myocardial infarction	R hip	1986	Charnley	96	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1980	Austin Moore hemiarthroplasty	164		Yes	Co-Cr-Mo
			L hip	1982	6-Ti-32 stem, Müller-type cup		NR	Yes	Ti-6-Al-4-V	UHMWPE	Fe-Cr-Ni wires
27	F, 67	Pancreatic carcinoma	R hip	1978	Charnley-Müller	198		Yes	Co-Cr-Mo	UHMWPE
			R hip	1988	BIAS porous-coated stem and allograft, H-G cup		93	No	Ti-6-Al-4-V, Ti	Ti, Ti-6-Al-4-V screws, UHMWPE
28	M, 76	Acute leukemia	L hip	1978	Müller	204		Yes	Co-Cr-Mo	UHMWPE
			L hip	1987	BIAS porous-coated stem and allograft, H-G cup		89	No	Ti-6-Al-4-V, Ti
29	F, 85	Cardiomyopathy	R hip	1973	Unknown hip replacement	284		Unknown	Unknown	Unknown
			R hip	1981	Townley Total Hip			Yes	Co-Cr-Mo	UHMWPE
			R hip	1986	BIAS porous-coated stem and allograft, H-G cup		73	No	Ti-6-Al-4-V	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires, Ti staples
30	F, 66	Myocardial infarction	R hip	1972	Charnley-type	232	NR	Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1967	Charnley-type	292		Yes	Fe-Cr-Ni	UHMWPE	Fe-Cr-Ni wires
			L hip	1968	Revision of polyethylene cup			Yes		UHMWPE
			L hip	1991	H-G cup with allograft, repair of trochanteric fixation		NR	No	Fe-Cr-Ni	Ti, Ti-6-Al-4-V screws, UHMWPE	Fe-Cr-Ni wires
31	F, -	-	R hip	1971	Unknown hip replacement	336		Yes	Unknown	Unknown
			R hip	1978	Unknown hip replacement			Yes	Unknown	Unknown
			R hip	1984	Unknown hip replacement			No	Unknown	Unknown
			R hip	1996	Solution System cup		NR	No	Ti-6-Al-4-V, UHMWPE
			L hip	1972	Unknown hip replacement	329		Yes	Unknown	Unknown
			L hip	1980	Unknown hip replacement			Yes	Unknown	Unknown
			L hip	1987	Mallory-Head femoral, Biogroove acetabular cup and allograft			No	Ti-6-Al-4-V, UHMWPE	Ti-6-Al-4-V
			L hip	1990	Custom cementless cup and allograft		NR	No	Ti-6-Al-4-V, UHMWPE		Co-Cr-Ni-W cables

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: TABLE IIHistological Grading System for Opaque or Translucent Birefringent Particles

Grade	Particles per High-Power Field
0+	0-0
1+	1-9
2+	10-19
3+	20-49
4+	50-499
5+	Â³500

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: TABLE IIHistological Grading System for Opaque or Translucent Birefringent Particles

Grade	Particles per High-Power Field
0+	0-0
1+	1-9
2+	10-19
3+	20-49
4+	50-499
5+	Â³500

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: TABLE IIIHistological Grades of Particle Concentration and Composition of Wear Particles*

Case	Type of Arthroplasty	Site	Para-Aortic Lymph Nodes			Spleen			Liver
Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§
1	Primary	Hip	2+	4+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	4+	1+	ND	1+	1+	ND
2	Primary	Hip	2+	1+	PE, Ti, Ti-6-Al-4-V	1+	0+	Ti, Ti-6-Al-4-V	1+	1+	ND
3	Primary	Hip	1+	4+	PE	4+	2+	ND	1+	0+	ND
4	Primary	Hip	1+	5+	PE, Co-Cr-Mo	1+	2+	ND	1+	1+	Ti, Ti-6-Al-4-V
5	Primary	Hip	2+	1+	PE, Ti	1+	1+	PE	2+	1+	PE
6	Primary	Hip	1+	1+	PE, Ti, Ti-6-Al-4-V	2+	1+	ND	1+	1+	ND
7	Primary	Hip	1+	1+	PE	1+	1+	ND	1+	0+	ND
8	Primary	Hip	1+	5+	PE, Ti, Cr-PO4	1+	1+	ND	1+	0+	ND
9	Primary	Hip	1+	3+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	1+	1+	ND	1+	0+	ND
10	Primary	Hip	1+	1+	PE	3+	2+	ND	1+	1+	ND
11	Primary	Hip	2+	4+	PE, Ti-6-Al-4-V	1+	0+	ND	0+	0+	ND
12	Primary	Knee	2+	1+	Ti-6-Al-4-V	1+	0+	ND	1+	0+	ND
13	Primary	Knee	2+	1+	ND	1+	1+	PE	0+	0+	ND
14	Primary	Knee	NA	NA	NA	3+	2+	ND	1+	0+	ND
15	Primary	Knee	5+	0	ND	4+	1+	ND	3+	1+	ND
16	Primary	Knee	1+	1+	PE	2+	2+	ND	1+	1+	ND
17	Primary	Knee	2+	2+	PE, Ti-6-Al-4-V	1+	1+	ND	1+	1+	ND
18	Primary	Knee	1+	1+	PE	2+	1+	ND	1+	0+	ND
19	Primary	Knee	1+	1+	ND	2+	0+	ND	1+	1+	ND
20	Primary	Knee	4+	1+	Ti-6-Al-4-V	4+	1+	Ti-6-Al-4-V	3+	1+	Ti-6-Al-4-V
21	Primary	Knee	3+	3+	PE, Co-Cr-Mo	3+	1+	Co-Cr-Mo	3+	2+	PE, Co-Cr-Mo
22	Revision	Hip	5+	1+	Ti	4+	1+	Ti	3+	1+	Ti
23	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Co-Cr-Ni-W, Cr-Fe	2+	2+	ND	1+	1+	Co-Cr-Mo
24	Revision	Hip	3+	1+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V
25	Revision	Hip	1+	1+	Ti-6-Al-4-V	1+	1+	Ti, Ti-6-Al-4-V	1+	0+	Ti
26	Revision	Hip	2+	1+	PE, Fe-Cr-Ni	1+	1+	Ti-6-Al-4-V	1+	1+	ND
27	Revision	Hip	5+	3+	PE, Ti, Ti-6-A1-4-V	2+	1+	PE	2+	1+	PE, Ti, Ti-6-Al-4-V
28	Revision	Hip	1+	1+	ND	1+	1+	ND	1+	1+	ND
29	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Ti	2+	1+	Ti	1+	1+	Ti
30	Revision	Hip	1+	1+	Fe-Cr-Ni	3+	2+	Fe-Cr-Ni	1+	0+	ND
31	Revision	Hip	NA	NA	NA	NA	NA	NA	5+	1+	Ti-6-Al-4-V
32	None	Control	2+	1+	ND	2+	1+	ND	1+	1+	ND
33	None	Control	NA	NA	NA	2+	1+	ND	2+	1+	ND
34	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
35	None	Control	4+	1+	ND	4+	3+	ND	2+	1+	ND
36	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
37	None	Control	1+	1+	ND	1+	1+	ND	0+	0+	ND
38	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
39	None	Control	2+	1+	ND	4+	1+	ND	3+	1+	ND
40	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
41	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
42	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
43	None	Control	1+	0	ND	1+	1+	ND	1+	0+	ND
44	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
45	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
46	None	Control	1+	1+	ND	1+	1+	ND	1+	0+	ND

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: TABLE IIIHistological Grades of Particle Concentration and Composition of Wear Particles*

Case	Type of Arthroplasty	Site	Para-Aortic Lymph Nodes			Spleen			Liver
Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§	Metal-Like Particles†	Polyethylene-Like Particles‡	Composition of Wear Particles§
1	Primary	Hip	2+	4+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	4+	1+	ND	1+	1+	ND
2	Primary	Hip	2+	1+	PE, Ti, Ti-6-Al-4-V	1+	0+	Ti, Ti-6-Al-4-V	1+	1+	ND
3	Primary	Hip	1+	4+	PE	4+	2+	ND	1+	0+	ND
4	Primary	Hip	1+	5+	PE, Co-Cr-Mo	1+	2+	ND	1+	1+	Ti, Ti-6-Al-4-V
5	Primary	Hip	2+	1+	PE, Ti	1+	1+	PE	2+	1+	PE
6	Primary	Hip	1+	1+	PE, Ti, Ti-6-Al-4-V	2+	1+	ND	1+	1+	ND
7	Primary	Hip	1+	1+	PE	1+	1+	ND	1+	0+	ND
8	Primary	Hip	1+	5+	PE, Ti, Cr-PO4	1+	1+	ND	1+	0+	ND
9	Primary	Hip	1+	3+	PE, Co-Cr-Mo, Ti, Ti-6-Al-4-V	1+	1+	ND	1+	0+	ND
10	Primary	Hip	1+	1+	PE	3+	2+	ND	1+	1+	ND
11	Primary	Hip	2+	4+	PE, Ti-6-Al-4-V	1+	0+	ND	0+	0+	ND
12	Primary	Knee	2+	1+	Ti-6-Al-4-V	1+	0+	ND	1+	0+	ND
13	Primary	Knee	2+	1+	ND	1+	1+	PE	0+	0+	ND
14	Primary	Knee	NA	NA	NA	3+	2+	ND	1+	0+	ND
15	Primary	Knee	5+	0	ND	4+	1+	ND	3+	1+	ND
16	Primary	Knee	1+	1+	PE	2+	2+	ND	1+	1+	ND
17	Primary	Knee	2+	2+	PE, Ti-6-Al-4-V	1+	1+	ND	1+	1+	ND
18	Primary	Knee	1+	1+	PE	2+	1+	ND	1+	0+	ND
19	Primary	Knee	1+	1+	ND	2+	0+	ND	1+	1+	ND
20	Primary	Knee	4+	1+	Ti-6-Al-4-V	4+	1+	Ti-6-Al-4-V	3+	1+	Ti-6-Al-4-V
21	Primary	Knee	3+	3+	PE, Co-Cr-Mo	3+	1+	Co-Cr-Mo	3+	2+	PE, Co-Cr-Mo
22	Revision	Hip	5+	1+	Ti	4+	1+	Ti	3+	1+	Ti
23	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Co-Cr-Ni-W, Cr-Fe	2+	2+	ND	1+	1+	Co-Cr-Mo
24	Revision	Hip	3+	1+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V	4+	2+	Ti-6-Al-4-V
25	Revision	Hip	1+	1+	Ti-6-Al-4-V	1+	1+	Ti, Ti-6-Al-4-V	1+	0+	Ti
26	Revision	Hip	2+	1+	PE, Fe-Cr-Ni	1+	1+	Ti-6-Al-4-V	1+	1+	ND
27	Revision	Hip	5+	3+	PE, Ti, Ti-6-A1-4-V	2+	1+	PE	2+	1+	PE, Ti, Ti-6-Al-4-V
28	Revision	Hip	1+	1+	ND	1+	1+	ND	1+	1+	ND
29	Revision	Hip	4+	5+	PE, Co-Cr-Mo, Ti	2+	1+	Ti	1+	1+	Ti
30	Revision	Hip	1+	1+	Fe-Cr-Ni	3+	2+	Fe-Cr-Ni	1+	0+	ND
31	Revision	Hip	NA	NA	NA	NA	NA	NA	5+	1+	Ti-6-Al-4-V
32	None	Control	2+	1+	ND	2+	1+	ND	1+	1+	ND
33	None	Control	NA	NA	NA	2+	1+	ND	2+	1+	ND
34	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
35	None	Control	4+	1+	ND	4+	3+	ND	2+	1+	ND
36	None	Control	2+	1+	ND	1+	1+	ND	1+	0+	ND
37	None	Control	1+	1+	ND	1+	1+	ND	0+	0+	ND
38	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
39	None	Control	2+	1+	ND	4+	1+	ND	3+	1+	ND
40	None	Control	NA	NA	NA	1+	1+	ND	1+	1+	ND
41	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
42	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
43	None	Control	1+	0	ND	1+	1+	ND	1+	0+	ND
44	None	Control	1+	1+	ND	1+	0+	ND	0+	0+	ND
45	None	Control	2+	1+	ND	1+	1+	ND	1+	1+	ND
46	None	Control	1+	1+	ND	1+	1+	ND	1+	0+	ND

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: TABLE IVPrincipal Wear Modes in Patients with Wear Particles in the Liver or Spleen

Case	Joint	Type of Arthroplasty	Observed Damage*	Principal Wear Mode†
2	Hip	Primary	Fretting of acetabular fixation screws	4
4	Hip	Primary	Fretting of acetabular fixation screws	4
5	Hip	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
13	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
20	Knee	Primary	Metal-metal wear due to failed patellar component	2
21	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing with embedded cement	3
22	Hip	Revision	Metal-metal wear due to recurrent dislocation	2
23	Hip	Revision	Fretting of loose femoral stem	4
24	Hip	Revision	Wear at ceramic and metal head-neck junction; loose femoral stem	4
25	Hip	Revision	Fretting of loose femoral stem	4
26	Hip	Revision	Wear of Ti-6-Al-4-V and polyethylene bearing with embedded cement	3
27	Hip	Revision	Fretting of loose femoral and acetabular components	4
29	Hip	Revision	Fretting of loose femoral stem	4
30	Hip	Revision	Fretting of stainless-steel trochanteric fixation wires	4
31	Hip	Revision	Metal-metal wear due to failed socket liner	2

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: TABLE IVPrincipal Wear Modes in Patients with Wear Particles in the Liver or Spleen

Case	Joint	Type of Arthroplasty	Observed Damage*	Principal Wear Mode†
2	Hip	Primary	Fretting of acetabular fixation screws	4
4	Hip	Primary	Fretting of acetabular fixation screws	4
5	Hip	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
13	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing	1
20	Knee	Primary	Metal-metal wear due to failed patellar component	2
21	Knee	Primary	Wear between Co-Cr-Mo and polyethylene bearing with embedded cement	3
22	Hip	Revision	Metal-metal wear due to recurrent dislocation	2
23	Hip	Revision	Fretting of loose femoral stem	4
24	Hip	Revision	Wear at ceramic and metal head-neck junction; loose femoral stem	4
25	Hip	Revision	Fretting of loose femoral stem	4
26	Hip	Revision	Wear of Ti-6-Al-4-V and polyethylene bearing with embedded cement	3
27	Hip	Revision	Fretting of loose femoral and acetabular components	4
29	Hip	Revision	Fretting of loose femoral stem	4
30	Hip	Revision	Fretting of stainless-steel trochanteric fixation wires	4
31	Hip	Revision	Metal-metal wear due to failed socket liner	2