SSSara E. Sacher

Sara E. Sacher

*This is an algorithmically generated author record based on publicly available information.

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Sara E. Sacher has a total of 30 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Arthrofibrosis Severity in Knees With Failed Total Knee Arthroplasties Differs With Magnetic Resonance Imaging Synovial Classification

    by Sara E. Sacher, Yu-Fen Chiu, Hollis G. Potter, Thomas P. Sculco, Peter K. Sculco, Timothy M. Wright, Matthew F. Koff


  • Association of Total Hip Arthroplasty Flexural Rigidity with Magnetic Resonance Imaging and Histological Findings

    by Sara E. Sacher, Elexis C. Baral, Timothy Wright, Thomas W. Bauer, Qian Li, Douglas Padgett, Hollis G. Potter, Matthew F. Koff


  • The role of advanced metal artifact reduction MRI in the diagnosis of periprosthetic joint infection

    by Sara E. Sacher, Matthew F. Koff, Ek T. Tan, Alissa Burge, Hollis G. Potter

    Identification and diagnosis of periprosthetic joint infection (PJI) are challenging, requiring a multi-disciplinary approach involving clinical evaluation, laboratory tests, and imaging studies. MRI is advantageous to alternative imaging techniques due to superior soft tissue contrast and absence of ionizing radiation. However, the presence of metallic implants can cause signal loss and artifacts. Metal artifact suppression (MARS) MRI techniques have been developed that mitigate metal artifacts and improve periprosthetic soft tissue visualization. This paper provides a review of the various MARS MRI techniques, their clinical applicability and accuracy in PJI diagnosis and evaluation, and current challenges and future perspectives.


  • Characterization of Ultralow‐Density Cellular Solids: Lessons from 30 years of Bone Biomechanics Research

    by Sara Sacher, Christopher J Hernandez, Eve Donnelly

    Advances in additive manufacturing techniques have enabled the development of microarchitectured materials displaying a combination of low‐density and lightweight structures with high specific strength and toughness. The mechanical performance of microarchitectured materials can be assessed using standard techniques; however, when studying low‐ and ultralow‐density microarchitectured materials, standard characterization techniques can be subject to experimental artifacts. In addition, quantitative assessment and comparisons of microarchitectures with distinct lattice patterns are not always straightforward. Cancellous bone is a natural, ultralow‐density (porosity often exceeding 90%), irregular, cellular solid that has been thoroughly characterized in terms of microarchitecture and mechanical performance over the past 30 years. However, most of the literature on cancellous bone mechanical properties and microstructure–function relationships is in the medical literature and is not immediately accessible to materials designers. Herein, a brief review of state‐of‐the‐art approaches for characterizing the microarchitecture and mechanical performance of ultralow‐density cancellous bone is provided, including methods of addressing experimental artifacts during mechanical characterization of ultralow‐density cellular solids, methods of quantifying microarchitecture, and currently understood structure–function relationships.


  • Open Access

    Increased Advanced Glycation Endproducts, Stiffness, and Hardness in Iliac Crest Bone From Postmenopausal Women With Type 2 Diabetes Mellitus on Insulin

    by Sashank Lekkala, Sara E Sacher, Erik A Taylor, Rebecca M Williams, Kendall F Moseley, Eve Donnelly

    Individuals with type 2 diabetes mellitus (T2DM) have a greater risk of bone fracture compared with those with normal glucose tolerance (NGT). In contrast, individuals with impaired glucose tolerance (IGT) have a lower or similar risk of fracture. Our objective was to understand how progressive glycemic derangement affects advanced glycation endproduct (AGE) content, composition, and mechanical properties of iliac bone from postmenopausal women with NGT (n = 35, age = 65 ± 7 years, HbA1c = 5.8% ± 0.3%), IGT (n = 26, age = 64 ± 5 years, HbA1c = 6.0% ± 0.4%), and T2DM on insulin (n = 25, age = 64 ± 6 years, HbA1c = 9.1% ± 2.2%). AGEs were assessed in all samples using high-performance liquid chromatography to measure pentosidine and in NGT/T2DM samples using multiphoton microscopy to spatially resolve the density of fluorescent AGEs (fAGEs). A subset of samples (n = 14 NGT, n = 14 T2DM) was analyzed with nanoindentation and Raman microscopy. Bone tissue from the T2DM group had greater concentrations of (i) pentosidine versus IGT (cortical +24%, p = 0.087; trabecular +35%, p = 0.007) and versus NGT (cortical +40%, p = 0.003; trabecular +35%, p = 0.004) and (ii) fAGE cross-link density versus NGT (cortical +71%, p < 0.001; trabecular +44%, p < 0.001). Bone pentosidine content in the IGT group was lower than in the T2DM group and did not differ from the NGT group, indicating that the greater AGE content observed in T2DM occurs with progressive diabetes. Individuals with T2DM on metformin had lower cortical bone pentosidine compared with individuals not on metformin (−35%, p = 0.017). Cortical bone from the T2DM group was stiffer (+9%, p = 0.021) and harder (+8%, p = 0.039) versus the NGT group. Bone tissue AGEs, which embrittle bone, increased with worsening glycemic control assessed by HbA1c (Pen: R2 = 0.28, p < 0.001; fAGE density: R2 = 0.30, p < 0.001). These relationships suggest a potential mechanism by which bone fragility may increase despite greater tissue stiffness and hardness in individuals with T2DM; our results suggest that it occurs in the transition from IGT to overt T2DM. © 2022 American Society for Bone and Mineral Research (ASBMR).


  • Open Access

    Distributions of Microdamage Are Altered Between Trabecular Rods and Plates in Cancellous Bone From Men With Type 2 Diabetes Mellitus

    by Sara E. Sacher, Heather B. Hunt, Sashank Lekkala, Kelsie A. Lopez, Jesse Potts, Alison K. Heilbronner, Emily M. Stein, Christopher J. Hernandez, Eve Donnelly

    Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of fragility fracture despite exhibiting normal to high bone mineral density (BMD). Conditions arising from T2DM, such as reduced bone turnover and alterations in microarchitecture, may contribute to skeletal fragility by influencing bone morphology and microdamage accumulation. The objectives of this study were (1) to characterize the effect of T2DM on microdamage quantity and morphology in cancellous bone, and (2) relate the accumulation of microdamage to the cancellous microarchitecture. Cancellous specimens from the femoral neck were collected during total hip arthroplasty (T2DM: n = 22, age = 65 + 9 years, HbA1c = 7.00 + 0.98%; Non-DM: n = 25, age = 61 + 8 years, HbA1c = 5.50 + 0.4%), compressed to 3% strain, stained with lead uranyl acetate to isolate microdamage, and scanned with micro-computed tomography. Individual trabeculae segmentation was used to isolate rod-like and plate-like trabeculae and their orientations with respect to the loading axis. The T2DM group trended toward a greater BV/TV (+27%, p = 0.07) and had a more plate-like trabecular architecture (+8% BVplates, p = 0.046) vs. non-DM specimens. Rods were more damaged relative to their volume compared to plates in the non-DM group (DVrods/BVrods vs. DVplates/BVplates: +49%, p < 0.0001), but this difference was absent in T2DM specimens. Longitudinal rods were more damaged in the non-DM group (DVlongitudinal rods/BVlongitudinal rods: +73% non-DM vs. T2DM, p = 0.027). Total damage accumulation (DV/BV) and morphology (DS/DV) did not differ in T2DM vs. non-DM specimens. These results provide evidence that cancellous microarchitecture does not explain fracture risk in T2DM, pointing to alterations in material matrix properties. In particular, cancellous bone from men with T2DM may have an attenuated ability to mitigate microdamage accumulation through sacrificial rods.