Background Hydroxyapatite is widely used as a coating on metallic implants to promote bioactivity. The coating is typically produced using a high temperature, resulting in phase heterogeneity and coating delamination, which may lead to failure of the coating clinically. Development of a simple and low-temperature hydroxyapatite coating technique may improve the bone bonding ability of implants. Objectives To investigate responses to hydroxyapatite-coated titanium produced by a newly developed sol–gel by osteoblasts in vitro and bone in vivo. Methods Osteoblast proliferation was characterized using a methyl thiazolyl tetrazolium assay and cell calcification with an Alizarin red S assay, and the results were compared with those of uncoated titanium. Uncoated and coated screws were inserted into the trabecular bone of New Zealand white rabbit legs. These implants were evaluated mechanically and histologically after 7, 12, and 24 weeks. Results Hydroxyapatite-coated titanium showed a significantly greater cell proliferation and mineralization than uncoated titanium. Extraction torques for the coated screws increased with time of implantation and were significantly greater than those of uncoated screws. We observed bone fragments attached to the surface of all coated screws after removal, but none on uncoated screws. Hematoxylin and eosin-stained bone showed no active inflammatory responses to implantation at any time examined. Bone surrounding either uncoated or coated screws followed typical remodeling stages, but maturation of bone healing was faster with coated screws. Conclusions The sol–gel-derived hydroxyapatite coating showed bioactivity, indicating its potential application as an alternative coating technique to improve the bone bonding ability of implants.
Background: Adjacent segment disease (ASD) is a major complication following spinal instrumentation and fusion. The search for of the rod flexibility factors responsible for junctional degeneration is still ongoing. Objective: Determine the rod stiffness and ASD following posterior instrumentation and fusion for lumbar spine and find the proper rod diameter for adult spinal instrumentation for fusion. Subject and methods: Retrospective evaluation of all patients requiring spinal instrumentation to determine the different rod diameter that predispose toward junctional degeneration was completed. All patients requiring spinal instrumentation over a one-year period were studied retrospectively. One-hundred eight-seven patients (mean age 61.6 years) who had undergone decompression and fusion with pedicle screw instrumentation were evaluated. The average follow-up was 4.2 years. The average number of levels fused was 2.9 segments (range: 1-8). Adjacent spinal level pre- and post-operatively was determined on the plain X-rays. Junctional degeneration was defined as new episode of degeneration of the adjacent level on radiologic finding. Asymptomatic patients did not demonstrate junctional degeneration on the routine post-operative X-rays. Results: ASD developed in 15 (8.0%) out of 187 patients, including compression fractures (n=2), spinal stenosis (n=6), and symptomatic disc collapse (n=7). There was a close correlation between the posterior instrument stiffness and the development of ASD (p=0.011). For fusion and fixation with 5.5 mm and 6.0 mm rod diameter, ASD occurred in four (3.7%) out of 108 patients and in 11 (13.9 %) out of 79 patients, resepectively. The incidences of ASD were greater when the posterior instrument used were stiffer in lumbar spine fusion. The pre-operative age, gender, and indication for surgery were not associated with the development of ASD. Conclusion: The prevalence of symptomatic ASD relatively increased with increasing stiffness of spinal implant. The diameter of the longitudinal rod strongly affected the fixator loads, and influenced the stresses in the vertebral endplates. The rod diameter had influence on the stresses in the adjacent spinal motion segment.
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