The relative contribution of bone microarchitecture and matrix composition to implant fixation strength in rats

Abstract

Bone microarchitectural parameters significantly contribute to implant fixation strength but the role of bone matrix composition is not well understood. To determine the relative contribution of microarchitecture and bone matrix composition to implant fixation strength, we placed titanium implants in 12‐week‐old intact Sprague–Dawley rats, ovariectomized‐Sprague–Dawley rats, and Zucker diabetic fatty rats. We assessed bone microarchitecture by microcomputed tomography, bone matrix composition by Raman spectroscopy, and implant fixation strength at 2, 6, and 10 weeks postimplantation. A stepwise linear regression model accounted for 83.3% of the variance in implant fixation strength with osteointegration volume/total volume (50.4%), peri‐implant trabecular bone volume fraction (14.2%), cortical thickness (9.3%), peri‐implant trabecular crystallinity (6.7%), and cortical area (2.8%) as the independent variables. Group comparisons indicated that osseointegration volume/total volume was significantly reduced in the ovariectomy group at Week 2 (~28%) and Week 10 (~21%) as well as in the diabetic group at Week 10 (~34%) as compared with the age matched Sprague–Dawley group. The crystallinity of the trabecular bone was significantly elevated in the ovariectomy group at Week 2 (~4%) but decreased in the diabetic group at Week 10 (~3%) with respect to the Sprague–Dawley group. Our study is the first to show that bone microarchitecture explains most of the variance in implant fixation strength, but that matrix composition is also a contributing factor. Therefore, treatment strategies aimed at improving bone‐implant contact and peri‐implant bone volume without compromising matrix quality should be prioritized.

Zucker Diabetic‐Sprague Dawley Rats Have Impaired Peri‐Implant Bone Formation, Matrix Composition, and Implant Fixation Strength

“…We have previously used this intramedullary rat model to evaluate the skeletal response to implant placement, (31) the pathogenesis of particle-induced loss of implant fixation strength, (48,49) and the efficacy of various anabolic treatments to promote implant osseointegration. (50)(51)(52) Similar to our previous study using the Zucker Diabetic Fatty rat model of T2DM, (13) we found no differences in osseointegration at 2 weeks post-implantation. Unlike the ZDF model, the current study did not find a significant difference in osseointegration 10 weeks post-implant placement.…”

“…After implant placement, animals were then randomly divided into two groups for postsurgical euthanization: 2 weeks and 10 weeks. The postsurgical time points were selected based on our previous study with the ZDF rat, ( 13 ) which showed increasing osseointegration and fixation strength in these two time points, and a study describing the longitudinal remodeling rates after intramedullary implant placement in the rat model that noted gradually increasing bone formation and resorption rates from implant placement to 8‐week postsurgery and a trend toward declining rates at 12‐week postsurgical placement. ( 31 ) The anticipated sample size of 8 per group was selected based on prior experiments demonstrating significant differences in the fixation strength between Sprague Dawley and ZDF.…”

“…( 31 ) The anticipated sample size of 8 per group was selected based on prior experiments demonstrating significant differences in the fixation strength between Sprague Dawley and ZDF. ( 13 ) Two animals in the SPD group were excluded because of poor placement of the titanium rods, resulting in a final sample size of 7 and 8 for SPD and ZDSD rats at each postsurgical euthanization time, respectively. At study termination, right femurs were removed, wrapped in saline‐soaked gauze, and frozen at −20°C until further processing was performed.…”

“…(12) A variety of factors contribute to implant fixation, including osseointegration, or the direct contact between bone and the implant material, bone structure, and matrix composition. (13,14) Importantly, each of these parameters can be directly influenced by T2DM pathophysiology. For instance, bone remodeling rates appear to be suppressed in patients with T2DM (15) and cortical porosity is elevated in patients with T2DM, (16) particularly in those with a history of skeletal fractures.…”

“…(22) A previous study from our laboratory reported that osseointegration is the single most important factor in determining implant fixation strength in normoglycemic and diabetic rats receiving intramedullary implants. (13) Despite the clear deleterious effects of T2DM on implant fixation, our previous study was not designed to examine the potential contributions of T2DM disease-related factors, such as glycemic control, suppressed bone remodeling, (23,24) and systemic inflammation, (25) to implant fixation. Further, our previous study utilized the Zucker Diabetic Fatty (ZDF) rat as a model of T2DM.…”