Research Article: Necrotic and inflammatory changes in metal-on-metal resurfacing hip arthroplasties

Date Published: December 4, 2009

Publisher: Informa Healthcare

Author(s): Gayana Mahendra, Hemant Pandit, Karolina Kliskey, David Murray, Harinderjit Singh Gill, Nick Athanasou.


Background Necrosis and inflammation in peri-implant soft tissues have been described in failed second-generation metal-on-metal (MoM) resurfacing hip arthroplasties and in the pseudotumors associated with these implants. The precise frequency and significance of these tissue changes is unknown.

Partial Text

Second generation metal-on-metal (MoM) hip resurfacing is a recent development in hip arthroplasty. Although early clinical results of second generation MoM hip replacement were encouraging (Amstuz et al. 2004a, Treacy et al. 2005, Back et al. 2005, Pollard et al. 2006, Hing et al. 2007), a number of complications have been reported including thinning of the femoral neck, avascular necrosis, femoral neck fracture, implant loosening, metal ion release and hypersensitivity, and the formation of inflammatory pseudotumors (Capello et al. 1978, Amstuz et al. 2004b, Park et al. 2005, Shimmin et al. 2005, Boardman et al. 2006, Jacobs et al. 2006, Pandit et al. 2008).

Our study included 50 patients (29 females) with a mean age of 55 (25–75) years at the time of revision surgery, which was carried out between 2001 and 2007 (Table). The primary operation was hip resurfacing in all patients. In 2 patients, the revision surgery was performed on both hips. The commonest cause of revision surgery was fracture (21). Other causes included periarticular pseudotumor formation (13), component loosening (9), instability or recurrent dislocation (3), unexplained pain (5), and avascular necrosis (1). The mean time to revision surgery was 20 months (range: 1 week to 75 months). All cases initially underwent arthroplasty for osteoarthritis; none of the cases had microbiological or histological evidence of acute infection and cases of rheumatoid disease were excluded. In 30 cases, samples of periprosthetic soft tissue (including the pseudocapsule and the acetabular and femoral pseudomembrane) and the revised femoral head were examined. In 14 cases only the femoral head was examined and in 8 cases only the periprosthetic tissue was examined.

Our findings indicate that a spectrum of necrotic and inflammatory changes can be seen in peri-implant tissues of MoM arthroplasties and that these changes are most pronounced in cases of component loosening and pseudotumor formation. The pathogenesis of the necrosis and inflammation that occurs as a result of the deposition of Co-Cr wear particles in MoM peri-implant tissues is not certain, but our results suggest that both cytotoxicity and hypersensitivity to metal particles may play a role in inducing these changes.