133 - Mineral Apposition Rate and Systemic Inflammation Affect Osseointegration in a Rat Implant Model

Poster Board Number: 133
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Abstract Body : The prevalence of type 2 diabetes (T2DM) and total joint replacements (TJRs) are expected to rise to 39 million and 4 million annual cases, respectfully, by 2030. T2DM can increase the risk for adverse outcomes in TJR, including late-stage loss of implant fixation. However, the mechanisms contributing to the increased loss of fixation in T2DM patients remains unclear. Various conditions associated with T2DM may well have direct or indirect negative consequences for TJR, including hyperglycemia, altered bone remodeling, and systemic inflammation. Specifically, these factors could affect osseointegration, an important determinant of implant fixation. To determine how variance in serum glucose, bone remodeling, and systemic inflammation affects variance in osseointegration and implant fixation, we fed 15 week old Sprague-Dawley and Zucker Diabetic Sprague-Dawley rats a high fat diet for three weeks and then surgically implanted titanium rods into the femoral canals. The animals had weekly serum draws to measure blood glucose. Rats were sacrificed at 2 or 10 weeks post operatively, at which times bone remodeling endpoints were assessed using dynamic histomorphometry, systemic inflammation markers, monocyte chemoattractant protein-1 (MCP-1) and interleukin 10 (IL-10) were assessed by Luminex, and osseointegration was assessed using high resolution micro-computed tomography. We hypothesized that glycemic status, bone remodeling, and inflammatory markers would all independently contribute to osseointegration and implant fixation. To test our hypothesis, we utilized stepwise linear regression models with the extent of osseointegration or implant fixation as the dependent variable. For osseointegration the most significant variables determined by our model were trabecular mineral apposition rate (Tb. MAR) and MCP-1 which explained 32% and 15.6% of the variance in osseointegration, respectfully. In total our model was able to predict 47.6% of the variance in osseointegration. For implant fixation the most significant variable determined by our model was cortical thickness (Ct.Th) which explained 25.4% of the variance. Our hypothesis was partially supported by the analyses, which demonstrated that bone remodeling and inflammation independently contribute to osseointegration. Our study demonstrates that bone remodeling explains the majority of the variance in osseointegration but also that inflammation around the time of surgery is a contributing factor. Interestingly, hyperglycemia was not an independent predictor of osseointegration, suggesting that data showing reduced osseointegration in diabetic models may be mediated through inflammation rather than because of uncontrolled glucose levels.