April 29, 2008
Chromium, Cobalt and Titanium Metallosis Involving a Nottingham Shoulder Replacement
By Khan, W S Agarwal, M; Malik, A A; Cox, A G; Denton, J; Holt, E M
Metallosis after shoulder replacement has not previously been described in the literature. We report a patient who developed extensive metallosis after implantation of an uncemented Nottingham shoulder replacement. He underwent a revision procedure. Examination of the retrieved prosthesis showed that the titanium porous coating was separating from the humeral stem and becoming embedded in the ultra-high-molecular-weight polyethylene glenoid component, resulting in abrasive wear of the humeral component. There was metallosis despite exchange of the modular humeral head. Both components had to be exchanged to resolve the problem.Merallosis is the accumulation of metal wear debris in the peri- prosthetic tissues which results in a cellular reaction characterised by a macrophagic response with formation of giant cells and fibrosis. Few cases have been reported in the literature and mostly after hip replacement.1 We describe a patient who developed extensive metallosis after implantation of an uncemented shoulder replacement. Extensive metallosis after shoulder replacement has not previously been described.
A 55-year-old right-handed man underwent uncemented Nottingham shoulder replacement (Biomet, Bridgend, United Kingdom) for destructive rheumatoid arthritis. The humeral stem and head were made from cast cobalt-chromium-molybdenum alloy. The proximal part of the humeral stem had an argon plasmasprayed titanium coating to encourage osteointegration. The glenoid component was made of ultra- high-molecular-weight polyethylene (UHMWPE) and was attached by a snap-fit mechanism to a glenoid tray secured to the bone by two screws. The glenoid tray and screws were made from titanium alloy.
a) Ante ro poste ri o r and b) lateral view radiographs of the right shoulder one week before the initial exploration procedure with the uncemented Nottingham shoulder replacement in situ.
He complained of persistent pain and underwent exploration 28 months after implantation. Radiographs taken one week before the exploration (Fig. 1) showed no radiolucent lines, osteolysis or vertical or horizontal migration of the components. They did, however, show that one of the titanium screws used to attach the glenoid tray was broken. The bubble sign,2 the outlining of the joint cavity by metallic debris, was not noted on the radiographs. At operation blackening was found involving intra-articular and extraarticular tissues and the subchondral bone. There was no evidence of osteolysis involving the humerus or glenoid, loosening of the components or tear of the rotator cuff. The findings did not suggest infection and microbiological samples taken at the time of surgery confirmed this. Other than obtaining material for biopsy, no further surgery was undertaken.
a) Photomicrograph showing the ablation area through the intracellular metal particles and b) graph showing spectroscopic determination of their composition.
Table I. Urine analysis was performed 30 months after the initial procedure to identify the concentration ([mu]/l) of metals present in alloys used in the components. Raised levels are highlighted in bold
Histology showed a profound macrophage response to the debris with some giant-cell formation (Fig. 2). The macrophages and giant cells contained numerous black intracellular particles mostly beween 1 [mu]m and 5 [mu]m in size. Spectrometry using a single-line Microprobe Laser Ablation-Inductively Coupled Plasma-Mass Spectrometer system indicated that the intracellular particles contained the elements chromium, cobalt and molybdenum. These three elements were in the same relative proportions as those in the prosthetic humeral head. Occasional large extracellular particles 200 [mu]m in size were identified as titanium with an identical elemental signature as the osteointegration layer on the humeral component. No UHMWPF, particles were identified. Urine analysis 30 months after the initial procedure showed elevated levels of the essential trace elements cohalt and chromium and of the non- essential trace elements titanium and aluminium (Table ().
In view of the continuing pain and the histological diagnosis of metallosis he underwent further debridement and exchange of the modular 22 mm humeral head to one of 20 mm, 30 months after the initial operation. Once again there was no evidence of osteolysis or loosening intraoperatively. Macroscopic examination of the retrieved humeral head showed numerous radial scratches on the head consistent with abrasive wear (Fig. 3), raising concerns regarding ongoing metallosis and the potential of cobalt and chromium toxicity. The pain continued and it was decided to revise the implant to a cemented Biomodular total shoulder replacement (Biomet UK) 38 months after the original operation. Although macroscopic analysis of the titanium porous coating of the removed stem indicated some signs of osteo-integration, it also showed that the coating had started to delaminate and disintegrate peripherally (Fig. 4). Plasma-mass spectrometry analysis of the particles embedded in the glenoid component had the same elemental composition as those in the coating layer of the humeral component and those in the larger peri- prosthetic particles. Three years after the revision, he remains free from pain.
We are not aware of previous reports of metallosis following shoulder replacement. In our case it seems likely that the cobalt and chromium particles were from the articulating surface of the humeral head, and detached titanium particles became embedded in the polyethylene surface producing abrasive wear. This would explain why the metallosis continued despite an exchange of the humeral head.
Photograph of the retrieved 22 mm humeral head showing numerous radial scratches on its surface consistent with abrasive wear.
Photograph of the humeral component showing partial detachment of the porous titanium coating.
After hip replacement, metallosis has been reported as being a cause of osteolysis, but the latter was not seen in our case. It has been suggested that osteolysis may be due to the synergistic interaction between metal and polyethylene particles' causing a profound activation of histiocytes. In our case, however, histological analysis revealed only metal particles composed of chromium, cobalt and titanium. Although metallosis can mask the radiological features of osteolysis, there was no radiological or intra-operative evidence to support osteolysis or loosening in our patient.
Titanium particles were identified in the surface of the polyethylene. Since titanium was not used in the bearing surface, it seems probable that the titanium porous coating had detached from the humeral stem. Alternatively, the titanium debris may have originated from the broken screw, but since the screw was covered by the glenoid tray, this seems less likely. Cobalt-chromium alloy is almost twice as hard as titanium," but the embedded particles seem to have been sufficiently hard to produce attrition of the cobaltchromium head as demonstrated by the radial scratches on the humeral head. Previous reports of titanium-induced metallosis have been reported but only in cases in which the softer metal had been used in the bearing surface.6
The possible long-term effects of metal wear debris in orthopaedic patients has recently been reviewed.
Cobalt toxicity is known to cause thyroid dysfunction and cardiomyopathy, and is carcinogenic.8'9 Chromium and vanadium toxicity can cause cardiac and renal dysfunction and psychosis.10 Titanium toxicity can induce pulmonary disease and platelet dysfunction while aluminium produces bone-marrow suppression, renal failure and neurological dysfunction.1 These toxicities result from extremely high circulating concentrations of the elements which are unlikely to occur from degradation of an implant. To date, there is no study which has shown a cause-and-effect relationship between implant devices and toxic levels of metal release. Likewise, no epidemiological evidence is available to suggest that the risk of carcinogenesis is anything more than theoretical.9
Our report supports previously documented evidence13 that radiographs may appear to be normal and cannot always reliably demonstrate the presence of metallosis.
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.
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W. S. Khan, M. Agarwal, A. A. Malik, A. G. Cox, J. Den ton, E. M. Holt
From the University
W. S. Khan, PhD, MRC Clinical Research Fellow Faculty of Life Sciences
J. Denton. MSc, Pathology
University of Manchester,
Oxford Road, Manchester M13
9 PT, UK.
M. Agarwal, FRCS (Orth), Orthopaedic Specialist Register
A- A, Malik, MRCS, Orthopaedic Specialist Reg ist a r
E, M. Holt, FRCS, Consultant
Wythenshawe Hospital, South
Teaching Hospitals NHS Trust,
Southrnoof Road, Manchester
M23 9LT, UK.
* A. G. Cox, MPhil, Centre
Centre of Analytical Sciences,
Dainton Building, University of
Sheffield, Western Bank.
Sheffield S3 7HF. UK.
Correspondence should be sent to Dr W. S. Khan at The Old Bakery, Northaw, Hertfordshire EN6 4NW. UK; e-mail: [email protected]
(c)2008 British Editorial Society of Bone and Joint Surgery
doi:10.1302/0301-620X.90B4. 20302 $2.00
J Bone Joint Surg IBrI 2008:90-8:502-5.
Received 8 October 2007; Accepted 21 November 2007
Copyright British Editorial Society of Bone & Joint Surgery Apr 2008
(c) 2008 Journal of Bone and Joint Surgery; British volume. Provided by ProQuest Information and Learning. All rights Reserved.