While proximal humerus fractures are relatively infrequent and the majority are amenable to non-operative treatment, open reduction with internal fixation remains a surgical mainstay [1,2]. With the advent of locking fixation, the majority of proximal humerus fractures requiring surgery are treated with locking plates. Biomechanical studies have demonstrated that locked plating is superior to intramedullary fixation, conventional or blade plating in two and three part proximal humerus fractures [3,4]. Despite the increased stability and use of locking fixation, loss of reduction remains a post-operative problem in osteoporotic bone with comminuted fractures [5]. Presently we hypothesized that: 1) Medial comminution of the calcar region is a determinant of fracture and fixation stability; and 2) Greater stability and increased resistance to varus deformity is gained through use of locking screws that cross the inferior surgical neck and penetrate the humeral head, i.e., the calcar region of the humerus.

Accurately quantifying the compressive stiffness of whole human vertebrae is important in the development of new treatment regimes for osteoporotic fracture repair and vertebral height restoration. Historically, whole bone stiffness has been measured from in vitro load-deformation behavior of isolated vertebrae using two different methods: 1) maximum slope of the load-deflection curve over a 0.2% strain window (“Method #1) [1, 2], and 2) slope of the best-fit line to the load-deflection curve over a specified loading range (most commonly 100–250 lbs, “Method #2”) [3, 4]. Because the whole bone load-displacement response is non-linear, these two measurement systems may yield different stiffness values for the same set of experimental data. Furthermore, both measurement systems are arbitrary, and there has been no investigation of the sensitivity of the whole bone stiffness metric to its method of measurement. The goal of this study is to develop and validate a standard method for calculating whole bone stiffness based on basic principles. In developing this method, we will also evaluate the robustness of existing stiffness calculation methods.

Osteoporosis is an age-related skeletal condition characterized by low bone mineral density and deterioration of the trabecular architecture leading to increased susceptibility to fracture [1]. Wolff hypothesized that trabecular architecture adapts to have its principal material axes aligned with the principal loading directions. Regions of experimentally labeled trabecular microdamage correspond to areas of high stress and strain calculated from FEA [2]. Studying the morphology of numerically predicted regions of tissue level yielding might provide insight into the role of trabecular architecture in the strength of trabecular bone.

Understanding the biomechanics of periprosthetic fractures is especially important in today’s aging population. As the prevalence of osteoporosis continues to climb, fracture risk, especially in proximity of an orthopaedic implant, is of great concern. In a study designed to investigate the mechanism of such fractures, the authors have chosen to test human cadaveric specimens implanted with short Synthes Titanium Trochanteric Fixation Nails. However, the exact loading conditions that elicit fracture are not known.

Osteoporosis, induced by aging and long-term disuse, often occurs together with muscle loss. Musculoskeletal disuse causes severe physiologic changes and it has been proposed the synergistic effects of muscle function and bone adaptation. Bone fluid flow has been shown to be induced during mechanical loading, and is proposed to be a critical mediator of bone adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Thus, muscular stimulation is proposed to be used to simultaneously treat both muscle and bone loss, but the optimal parameters required for such treatment is unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. Our preliminary research has indicated that dynamic muscle contractions within an optimal frequency range can significantly recover disuse induced bone loss. However, the optimal rest periods required to prevent muscle fatigue during stimulations are not clear. The overall objective of this study was to evaluate optimized dynamic muscle stimulations at relatively high frequency, e.g., 20 Hz, and to test the role of varying the rest duration on muscle mass and bone morphology in a functional hind limb disuse mouse model.

Osteoporosis is a bone disease which manifests itself in the perforation and subsequent resorption of individual trabeculae [1]. Bone mass is consequently reduced leading to a mechanically weakened structure which is prone to fractures. These fractures have serious health and social implications for sufferers of osteoporosis.

Rigid polyurethane (PU) foam is widely used as a test medium for mimicking human cancellous bone e.g. for investigating fixation of bone screws [1,2]. Whilst the solid and higher density PU foams are used as standard test materials [3], very little work has been carried out to date on modelling human osteoporotic bone. Osteoporosis (OP) is a bone disease in which bone resorption exceeds bone deposition, resulting in bone loss. Various low density, open cell rigid PU foams are available for use as OP bone models, but none of these has been standardised or universally accepted as a test material. In this study the objective was to determine whether low density PU foam might be suitable for mimicking human osteoporotic bone.

Osteoporosis is an age-related disease characterized by low bone mass and architectural deterioration. Other than bone volume fraction (BV/TV), microarchitecture of trabecular bone, such as trabecular type (rods or plates), connectivity, and orientation of the trabecular network is also believed to be important in governing the mechanical properties of trabecular bone. A recent study [1] showed that the microarchitecture alone affects elastic moduli of trabecular bone and, further, that trabecular plates make a far greater contribution than rods. In human vertebral trabecular bone, the roles of transverse vs. vertical rods in conferring mechanical properties of trabecular bone have been debated [2, 3]. It has been suggested that the role of transverse trabecular rod is critical in determining elastic modulus of vertebral trabecular bone. However, without explicit classifications of trabecular type, or orientation assessment at an individual trabecula level, it is not possible yet to test this hypothesis in human trabecular bone samples despite the development of three-dimensional (3D) micro computed tomography (μCT) and μCT based finite element (FE) models of human trabecular bone. With the newly developed technique of complete volumetric decomposition and individual trabecula based orientation analyses [4], now it is possible to quantitatively examine the contributions of trabecular rods of various orientations in the elastic properties of vertebral trabecular bone.

The Wnt/β-Catenin signaling pathway is a key regulator in bone development and bone homeostasis. Inactivating mutations in the Wnt co-receptor Low density lipoprotein Receptor related Protein 5 (LRP5) results in osteoporosis while “activating” mutations in LRP5 results in high bone mass. Dickkopf-1 ( Dkk1 ) is a secreted Wnt inhibitor that binds to LRP5 and LRP6 reducing their availability to form a complex with Wnt and Frizzled and resulting in unrestrained Wnt signaling. It is expected that a decrease in Dkk1 will result in an increase in Wnt activity and ultimately a high bone mass phenotype. An allelic series of Dkk1 mutant mice were generated to examine the affects of reduced Dkk1 levels on bone density, morphology, and mechanical properties.

Endplate subsidence and vertebral body (VB) fracture are potential complications following lumbar total disc replacement (TDR) [1]. Early clinical evidence suggests that these events can be ameliorated in patients with osteopenia and osteoporosis by vertebral augmentation performed at the time of TDR [2]. However, the biomechanical basis to support vertebral augmentation of TDR has not been established. The objective of this study was to quantify the effects of vertebral augmentation with Cortoss on VB mechanics under compression by a TDR implant. We hypothesize that augmentation with Cortoss will improve the mechanical behavior in compression.

Three-dimensional structure of trabecular bone can be modeled by 2D or 3D Voronoi structure. The effect of missing cell walls on the mechanical properties of 2D honeycombs is a first step towards understanding the effect of local bone resorption due to osteoporosis. In patients with osteoporosis, bone mass is lost first by thinning and then by resorption of the trabeculae [1]. Furthermore, creep response is important to analyze in cellular solids when the temperature is high relative to the melting temperature. For trabecular bone, as body temperature (38 °C) is close to the denaturation temperature of collagen (52 °C), trabecular bone creeps [1]. Over the half of the osteoporotic vertebral fractures that occur in the elderly, are the result of the creep and fatigue loading associated with the activities of daily living [2]. The objective of this work is to understand the effect of missing walls and filled cells on elastic-plastic behavior of both regular hexagonal and non-periodic Voronoi structures using finite element analysis. The results show that the missing walls have a significant effect on overall elastic properties of the cellular structure. For both regular hexagonal and Voronoi materials, the yield strength of the structure decreased by more than 60% by introducing 10% missing walls. In contrast, the results indicate that filled cells have much less effect on the mechanical properties of both regular hexagonal and Voronoi materials.

Osteoporosis is a critical challenge in orthopedic surgery. Osteoporotic patients have an increased risk of loosening and failure of implant constructs due to a weaker bone-implant interface than with healthy bone. Pullout strength of pedicle screws is enhanced by increased screw insertion depth. However, more knowledge is needed to define optimal pedicle screw insertion depth in relation to screw-bone interface biomechanics and the resulting loosening risk. This study evaluates the effects of screw length on loosening risk in the osteoporotic lumbar spine.

Optimization of pedicle screw insertion depth for ideal fixation and fusion remains a clinical challenge. Improved screw purchase may improve fixation strength 1 , which is especially critical in an osteoporotic patient population. Extended screw insertion depths, up to and through the anterior cortex, have yet to be compared to more commonly used shorter pedicle screws in a laboratory controlled series of experiments. The purpose of this study is to evaluate screw purchase in the osteoporotic lumbar spine as a function of insertion depth, which may be used to optimize pedicle screw-rod constructs.

Kyphoplasty/vertebroplasty procedures traditionally use PMMA to treat the fractured vertebrae due to its mechanical properties. However, with time the bone erodes around the cement due to osteoporosis and inhibited bone remodeling due to the cyotoxicity of PMMA (1). The exothermic reaction of PMMA is also responsible for thermal necrosis and can cause complications in cases of extravasation (1; 2; 3). Lastly, PMMA is not bioactive and will not be reabsorbed (1; 2; 3). Thus, alternative cements with similar mechanical strengths are being explored. Calcium phosphate cements (CaP) have been explored due to their bioactive and non-thermal properties (3; 4). Despite these advantages, there are reservations of traditional CaP cements due to deficiencies in mechanical properties (1; 4). We evaluated new polymerized calcium phosphate (pCaP) cement which is not brittle like traditional CaP cements. Mechanical properties of vertebral bodies augmented with either PMMA or pCaP after fracture were determined.

Bone is a dynamic organ that constantly undergoes remodeling throughout one’s life. The remodeling process is required to repair damaged bone tissue and more importantly, to regulate calcium and phosphate homeostasis through the osteocytic network in conjunction with the microvascular network within bone marrow. Recently, techniques combining micro computed tomography (μCT) imaging with vascular network perfusion were developed to allow for 3-D visualization of the bone vascular network structure [1]. However, simultaneous visualization of the trabecular and vascular microstructures using standard μCT remains challenging, and thus the precise relationships between blood vessel formation and trabecular remodeling, as well as the impact of these relationships on metabolic bone diseases such as osteoporosis, remain unclear.

Hip fractures are among the most common types of osteoporotic fractures that affect one in three women and one in six men over the age of 50 [1]. It is well known that loss of bone mass, quantified by bone mineral density using Dual-energy X-ray Absorptiometry (DXA), is associated with the increasing risk of bone fractures. However, bone mineral density (BMD) alone cannot fully explain changes in fracture risks [2, 3]. In particular, BMD is not able to predict fracture risks for women with osteopenia, in which a BMD T-score is between −1.0 and −2.5. This suggests additional factors (i.e., bone quality) should be considered in predicting fracture risks [4].

Bone mineral density gained during adolescent years is a significant determinant of bone quality maintained during adult-hood [1]. The ability to enhance the structural integrity of bone at a young age reduces the risk of bone fracture as well as the development of musculoskeletal diseases, such as osteoporosis [1].

Aging shifts bone remodeling toward a negative balance between bone formation and resorption, causing bone loss and increased fracture risk. Anti-resorptive agents are commonly used to inhibit bone resorption and stabilize bone mass. While they are effective to prevent further bone loss, there is also a great need for anabolic agents which can reverse bone deterioration and regain lost skeletal integrity. Intermittent parathyroid hormone (PTH) treatment is the only FDA-approved anabolic treatment for osteoporosis, which greatly stimulates bone formation. Combined therapy of anti-resorptive drugs, such as alendronate (ALN), and PTH have been proposed and are expected to further stimulate bone formation. However, studies show conflicting results regarding the effectiveness of combined treatments: some have reported the addition of ALN to impair PTH function [1, 2], while others suggest an improvement over PTH monotherapy [3, 4]. The first objective of this study is to document the immediate changes of individual trabecular structures due to PTH and combined therapy within 12 days using in vivo micro computed tomography (μCT). As PTH is typically prescribed for 1 to 3 years to osteoporotic patients, a treatment of 12 days for rats (approximately equivalent to one year of human life) may be more clinically relevant than long-term treatment studies on rats. The secondary purpose of this study was to gain insight into the mechanism of combined versus PTH treatments through a bone dynamic imaging strategy to track events over an individual remodeling site. We hypothesized that PTH and combined treatments would immediately enhance bone formation on the trabecular surface.

Rapid bone loss during spaceflight is a well-established and continuing medical issue for astronauts. It has been reported that astronauts have displayed bone loss at rates of up to 2.7%/month in weight-bearing bones, or about 6 times that of post-menopausal women [1]. Rodent models have provided a means to further our understanding of the effects of microgravity on bone quality, both from studies in which rodents have flown aboard space missions and those in which weightlessness is simulated on earth through musculoskeletal unloading [2]. Such studies have the potential to not only further our understanding of the cause of decreased bone integrity in space, but also provide an accelerated model for the study of osteo-degenerative diseases affecting the general public, leading to improved treatment methods for both spaceflight and age or illness related osteoporosis.

The bone mineral density (BMD) in a given fracture site may affect the outcome of fracture fixation. Low BMD values, such as those occurring in osteoporotic bone, can determine the fixation method and the postoperative care. Evaluation of the BMD is either done subjectively during surgery or by a preoperative measurement. The technique most commonly used to measure BMD preoperatively is dual-energy X-ray absorptiometry (DEXA). DEXA scans have been shown to be site specific [1,2] and therefore may be inaccurate in determining local BMD at the fixation site. Furthermore, in trauma cases, patients frequently do not present with a pre-operative DEXA scan; and the ideal method of assessment would be intraoperative. Intraoperative BMD assessment could be used to guide surgical decisions such as the point of entry of a screw for a fracture plating system or use of locking versus non-locking screw-plate contruct.