Commentary: ALVAL & Metal-on-Metal Joint Replacements

March 27, 2005

(The following is a Commentary & Perpective review of the article on Aseptic Lymphocyte-dominated Vasculitis-Associated Lesions (ALVAL) and Metal-on-Metal Joint Replacements written by Craig Rineer, MD of the Brigham and Women’s Hospital on 01/27/2005)

by Joshua J. Jacobs, MD*,
Rush Medical College, Chicago, Illinois

Metal-on-metal hip arthroplasty is gaining popularity in the United States and abroad. Therefore, the study by Willert et al. concerning the phenomenon of hypersensitivity associated with failed metal-on-metal bearings is particularly timely. The concern about metal hypersensitivity leading to implant failure is not new—there were many studies published in the McKee-Farrar era during the 1970s that suggested this association1. In the current era of “second-generation” metal-on-metal devices, there have been substantial improvements in metallurgy, manufacturing, and design; however, the concern about metal hypersensitivity as a mode of failure persists. The authors of the present study add to this growing body of literature by performing a careful histomorphological study on nineteen patients who underwent revision of a metal-on-metal hip replacement. The authors make a strong case for the role of hypersensitivity in implant failure; however, it must be recognized that the evidence presented is largely circumstantial because cause and effect have not been proven.

One of the more interesting aspects of the authors’ observations is that the delayed-type hypersensitivity-like reactions (which the authors term “aseptic lymphocyte-dominated vasculitis-associated lesion”) that were observed on histological analysis were associated with periprosthetic osteolysis—the very problem that metal-on-metal bearings were presumed to solve—in seven of the nineteen cases. The authors proposed a mechanism whereby the continuous release of metal ions facilitates and/or accelerates sensitization, resulting in an immunological response that leads to periprosthetic bone loss. This proposed mechanism should be seriously considered because the lead author is widely credited as being the first to propose that the cellular response to particulate wear debris was the cause of osteolysis and aseptic loosening. This was suggested more than twenty-five years ago2 and is now generally accepted as the most plausible mechanism for this prevalent failure mode.

It is important to view the authors’ current findings with certain caveats. The observations were gathered from a small number of retrievals from an unknown population of patients undergoing total hip arthroplasty with metal-on-metal bearings. Thus, the true prevalence of implant failure attributable to Aseptic Lymphocyte-dominated Vasculitis-Associated Lesions (ALVAL) cannot be ascertained from the study. The authors suggest that implant failure due to this phenomenon is likely to be a low-probability event.

Another point worthy of note is that the analysis of the particles present in the periprosthetic tissue was limited to light microscopy. Recently, it has been recognized that most of the debris generated from metal-on-metal bearings is in the nanometer size range, which is well beyond the limit of resolution light microscopy3. A true accounting of the particulate debris in the periprosthetic environment would require techniques such as transmission electron microscopy. This fact may explain why the authors did not observe a correlation between the amount of particulate debris and the histological response. Another possibility is that the biologically active degradation products are metal-protein complexes4, which cannot be imaged even by electron microscopic techniques.

If hypersensitivity to metal degradation products is in fact a mechanism of failure in a small percentage of patients undergoing metal-on-metal hip replacement, is there a method by which individuals can be screened preoperatively to determine if they are at risk for the development of osteolysis? This is obviously a very important question, but one that cannot be answered definitively at this time. Both patch testing and the in vitro lymphocyte transformation testing have been described as ways to determine the presence of metal hypersensitivity1. However, both methodologies have their drawbacks, including the fact that the specificity and sensitivity have not been defined for either technique. The development of preoperative screening tests as well as postoperative diagnostic tests for metal hypersensitivity is highly desirable and is an area under study. This requires prospective evaluation of large numbers of patients undergoing total joint arthroplasty, with use of currently available hypersensitivity testing methodology in correlation with clinical and radiographic outcomes.

This is an exciting era for the adult reconstructive surgeon who now has several bearing surface options that all promise to improve implant survivorship. Unfortunately, each bearing couple has potential drawbacks. The “Achilles’ heel” of metal-on-metal arthroplasty appears to be the biological reaction to metal degradation products, which can include the development of metal hypersensitivity. Metal hypersensitivity is likely to be more prevalent in patients with metal-on-metal bearings due to the fact that it has been well documented that systemic metal transport is greater in patients with well-functioning metal-on-metal total hip replacements than metal-on-polyethylene total hip replacements5. Further intermediate and long-term multicenter studies of patients with metal-on-metal bearings are required to establish the prevalence of this complication.

References

1. Hallab N, Merritt K, Jacobs JJ. Metal sensitivity in patients with orthopaedic implants. J Bone Joint Surg Am. 2001;83:428-36.
2. Willert HG. Reactions of the articular capsule to wear products of artificial joint prostheses. J Biomed Mater Res. 1977;11:157-64.
3. Doorn PF, Campbell PA, Worrall J, Benya PD, McKellop HA, Amstutz HC. Metal wear particle characterization from metal on metal total hip replacements: transmission electron microscopy study of periprosthetic tissues and isolated particles. J Biomed Mater Res. 1998;42:103-11.
4. Hallab NJ, Jacobs JJ, Skipor A, Black J, Mickecz K, Galante JO. Systemic metal-protein binding associated with total joint replacement arthroplasty. J Biomed Mater Res. 2000;49:353-61.
5. Jacobs JJ, Hallab NJ, Skipor AK, Urban RM. Metal degradation products: a cause for concern in metal-metal bearings? Clin Orthop. 2003;417:139-47.

DePuy Hip Implant Attorney

If you or a loved one have been injured as the result of a DePuy Orthopaedics – Johnson & Johnson hip replacement implant product, talk to a DePuy Hip Implant Attorney at the Willis Law Firm for legal advice about a potential DePuy hip replacement lawsuit. Please fill out the Free Case Evaluation at the right or call us toll-free at 1-800-883-9858.

IMPORTANT NOTE: If you are required to have a revision replacement surgery to remove and replace a faulty DePuy Hip Implant, notify your doctors that you want the hip implant to be preserved as evidence and NOT shipped or returned to the manufacturer, as it is critical evidence in a potential product liability lawsuit against DePuy and Johnson & Johnson.

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