Analysis of retrieved hip resurfacing arthroplasties reveals the interrelationship between interface hyperosteoidosis and demineralization of viable bone trabeculaeStefan Breer Matthias Krause Björn Busse Michael Hahn Wolfgang Rüther Michael M. Morlock Michael Amling Jozef Zustin
Retrieved hip resurfacing arthroplasties (HRA) revised for causes other than osteonecrosis enable further insights into bone–cement interactions within the interface with only minimal biomechanical stresses. Our primary objective was to investigate the mineralization changes at the trabecular bone interface in retrieved hips using bright field and polarized light microscopy and by quantitative backscattered electron imaging. Because superficial seams of non‐mineralized bone tissue varied substantially, we defined hyperosteoidosis as an osteoid seam of more than 20 µm thickness. We hypothesized that interface hyperosteoidosis might be caused by the demineralization of previously mineralized bone tissue. One hundred and thirty‐one retrieved HRAs with viable bone remnant tissue were analyzed. Bone mineral density distribution obtained from backscattered signal intensities of the trabecular bone at the bone–cement interface was assessed in cases with and without interface hyperosteoidosis. In cases with interface hyperosteoidosis, the degree of trabecular mineralization was also analyzed in deeper areas of the femoral remnants. Thirty‐four cases showed hyperosteoidosis at the bone–cement interface, mostly in female patients. Bone trabeculae with hyperosteoidosis displayed a mineral density distribution pattern suggestive of the demineralization of a previously mineralized bone matrix. Our results demonstrate the localized disorder of the mineralization pattern of bone trabeculae at the bone–cement interface in a group of retrieved HRAs. In previously well‐fixed femoral components, potential adverse effects on the load‐bearing bone due to a decreased degree of mineralization at the bone–cement interface may affect the durability of the implant’s function.