Intramembranous bone regeneration is critical to implant fixation. In cementless joint replacement (as opposed to cemented joint replacement), saline irrigation is not typically performed during surgery so that the osteogenic stimulus provided by the marrow is preserved. Several groups are now using the rat marrow ablation model to study intramembranous bone regeneration and implant fixation. In this model, the marrow contents are mechanically disrupted, and debris is often cleared by saline irrigation, a step that appears inconsistent with the clinical situation. Furthermore, in contrast to conventional wisdom, it has been reported that saline irrigation enhanced bone-implant contact and peri-implant bone formation in the rat model (Ishizaka et al. Bone 1996;19:589-594), although mechanical fixation of the implant was not investigated. Accordingly, the present study was performed to determine if saline irrigation leads to enhanced mechanical fixation of implants in the rat model. Forty-eight 400 to 450 g male rats were divided equally into two groups. The treatment group, in contrast to the control group, received saline irrigation in the ablated medullary canal prior to placement of hydroxyapatite/tricalcium phosphate-coated implants. Eight animals in each group were killed at 2, 4, or 8 weeks after implantation, at which time the specimens were analyzed by micro computed tomography to measure bone formation around the implant, followed by a mechanical pull-out test to measure the strength of fixation of the implant. As expected, there was increased fixation strength over time, but there were no significant differences in peri-implant bone volume, bone-implant contact, or implant fixation strength between the two groups. Thus, we found no effect of saline irrigation on bone formation or implant fixation strength in this study in which the implant had an osteoconductive coating.

Implant debris remains the major factor limiting the longevity of total joint replacements. Whether soluble implant debris of Zr and Nb containing implant alloys constitute a greater risk than other implant metals remains unknown. We evaluated the relative effects of soluble forms of Zr+4 and Nb+5 (0.001–10.0 mM) relative to Cr+3, Mo+5, Al+3, Co+2, Ni+2, Fe+3, Cu+2, Mn+2, Mg+2, Na+2, and V+3 chloride solutions on human peri-implant cells (i.e., osteoblast-like MG-63 cells, fibroblasts, and lymphocytes). Metals were ranked using a 50% decrease in proliferation and viability to determine toxic concentrations. Lymphocytes, fibroblasts, and osteoblasts were, generally, similarly affected by metals where the most toxic metals, Co, Ni, Nb, and V required <1.0 mM to induce toxicity. Less toxic metals Al, Cr, Fe, Mo, and Zr generally required >1.0 mM challenge to produce toxicity. Overall, Co and V were the most toxic metals tested, thus Zr and Nb containing implant alloys would not likely be more toxic than traditional implant alloys. Below concentrations of 0.1 mM, neither Zr nor Nb reduced osteoblast, lymphocyte, or fibroblast proliferation. Zr was generally an order of magnitude less toxic than Nb to lymphocytes, fibroblasts, and osteoblasts. Our results indicated that soluble Zr and Nb resulting from implant degradation likely act in a metal- and concentration-specific manner capable of producing adverse local and remote tissue responses to the same degree as metals from traditional implant alloys, e.g., Ti-6Al-4V (ASTM F 138) and Co-Cr-Mo alloys (ASTM F 75).

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Accelerated corrosion of metallic implants in vivo can generate both soluble and insoluble products that can be detected locally and systemically. Retrieved stainless steel implants for trauma fixation or spinal instrumentation demonstrate iron and chromium-containing solid products of corrosion deposited around corroded modular junctions and as phagocytosable particles in the adjacent tissues. In some cases, the resulting adverse local tissue reaction has been associated with pain, inflammation and osteolysis, requiring removal of the implant. In vitro cell and organ culture studies confirm that corrosion products such as particles of chromium phosphate can elicit proinflammatory cytokine secretion from macrophages and promote macrophage-mediated bone resorption. Systemically, soluble corrosion products of chromium can be detected in the serum of selected patients with accelerated corrosion of chromium-containing implants. Metal-protein binding studies indicate that the high molecular weight serum proteins including immunoglobulins have the highest affinity for chromium. These findings stress the importance of the design of modular junctions to minimize corrosion of stainless steels used in orthopaedic appliances.