Abstract

STUDY DESIGN. An ex vivo histologic study in rabbits. OBJECTIVE. To evaluate the early histologic effects of polymethylmethacrylate (PMMA) injection on bone and intraosseous neural tissue following vertebroplasty in rabbit lumbar vertebrae. SUMMARY OF BACKGROUND DATA. Vertebroplasty with PMMA is performed to treat painful osteoporotic vertebral fractures. Early pain relief has been consistently documented, but its mechanism has not been elucidated. Among the mechanisms of pain relief may be the immediate stabilizing effects of the cement, and the exothermic reaction during curing, which may lead to intraosseous neural ablation. It has been well established that PMMA can induce thermal osteonecrosis after arthroplasty, but the potential for osteonecrosis after vertebroplasty has not been established. Previous studies have suggested that temperature elevations during cement curing may induce thermal bone necrosis. However, this cause-and-effect relationship has not yet been histologically studied in an animal model. METHODS. Vertebroplasty with PMMA was performed at 2 levels in 12 New Zealand rabbits (24 levels); trochar insertion without PMMA injection was performed at 3 levels each of 2 control animals (6 levels). Sacrifice was performed 24 hours after the procedure. Histologic examination was performed to evaluate the presence of bone or intraosseous neural tissue necrosis. RESULTS. Half of the levels with PMMA showed evidence of necrosis at the bone-cement interface. Almost all (11 of 12) showed only focal necrosis, with only 1 specimen showing necrosis along the entire periphery of the PMMA. The other 12 specimens and all control levels displayed no bone necrosis. There was no evidence of intraosseous neural tissue necrosis in control or PMMA-injected specimens. CONCLUSION. Injection of PMMA in rabbit lumbar vertebral bodies produces early, focal bone necrosis in only half of cases, suggesting that competency of the cement-bone interface is reasonable in most cases. No evidence of intraosseous neural tissue damage was found. © 2008 Lippincott Williams & Wilkins, Inc.