+publisher:"Cornell University" +contributor:("Hernandez, Christopher J.")

Cornell University

1. Ehlert, Katherine. Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power.

Degree: M.S., Mechanical Engineering, Mechanical Engineering, 2013, Cornell University

URL: http://hdl.handle.net/1813/34293

► Microscopic tissue damage can occur in bone as a result of an isolated overload leading to reduces bone strength under subsequent loads. In addition, microscopic… (more)

Subjects/Keywords: Microdamage; Statistical simulation; Cancellous Bone

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APA (6^th Edition):

Ehlert, K. (2013). Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power. (Masters Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/34293

Chicago Manual of Style (16^th Edition):

Ehlert, Katherine. “Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power.” 2013. Masters Thesis, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/34293.

MLA Handbook (7^th Edition):

Ehlert, Katherine. “Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power.” 2013. Web. 22 Jan 2021.

Vancouver:

Ehlert K. Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power. [Internet] [Masters thesis]. Cornell University; 2013. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/34293.

Council of Science Editors:

Ehlert K. Methods Of Measuring Microscopic Tissue Damage In Cancellous Bone: Sampling And Statistical Power. [Masters Thesis]. Cornell University; 2013. Available from: http://hdl.handle.net/1813/34293

Cornell University

2. Walk, Remy Elisabeth. Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep.

Degree: M.S., Mechanical Engineering, Mechanical Engineering, 2017, Cornell University

URL: http://hdl.handle.net/1813/56951

► Bone mass and mechanical properties are known to influence risk of fragility fracture. Clinical measures of bone mineral density (BMD) are used to evaluate fracture… (more)

▼ Bone mass and mechanical properties are known to influence risk of fragility fracture. Clinical measures of bone mineral density (BMD) are used to evaluate fracture risk, but patients with obesity have greater risk of fracture than would be expected from BMD. Obesity is a common component of metabolic syndrome. Metabolic syndrome may contribute to the increased risk of fracture associated with obesity. Patients with osteoporosis have low bone mass and increased risk of fracture. Parathyroid hormone (PTH) treatment can be used to reverse the effects of osteoporosis. Here, we looked at mechanical properties of bone in an animal model of metabolic syndrome and an animal model of osteoporosis treated with parathyroid hormone. First, we characterized the cortical bone phenotype of the toll-like receptor 5 deficient mouse (TLR5KO). The TLR5KO mouse is a model of metabolic syndrome with mild levels of adiposity. Metabolic syndrome in TLR5KO mice is caused by alterations to the gut microbiome. Male and female mice 10-55 weeks of age (n = 5-19/ group) were used in this study. Cortical bone geometry and mechanical properties of the mid-diaphysis of the femur were analyzed to characterize the cortical bone phenotype. The femurs were tested in three-point bending to obtain peak moment, bending rigidity and post yield displacement. Peak moment was related to geometry to infer the effect of genotype on tissue material properties. We found that metabolic syndrome was associated with impaired cortical bone tissue material properties in both male and female mice in most ages studied. In summary, metabolic syndrome with only mild adiposity was associated with alterations to bone strength that could not be explained by bone geometry and density, suggesting altered bone tissue material properties. Secondly, we determined the mechanical properties of cancellous bone from osteopenic sheep treated with PTH. Osteopenia was induced in 6-7 year-old sheep through a combination of ovariectomy (OVX) and a diet to induce metabolic acidosis (MA). A year after OVX, the sheep were treated with either vehicle (n = 6) or PTH (n = 7) for a year. Cancellous bone cores were taken from the medial caudal quadrant of the right distal femur for mechanical testing. We found no detectable effect of PTH treatment on mechanical properties of cancellous bone in uniaxial compression. Advisors/Committee Members: Hernandez, Christopher J. (chair), van der Meulen, Marjolein (committee member).

Subjects/Keywords: Biomechanics

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APA (6^th Edition):

Walk, R. E. (2017). Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep. (Masters Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/56951

Chicago Manual of Style (16^th Edition):

Walk, Remy Elisabeth. “Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep.” 2017. Masters Thesis, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/56951.

MLA Handbook (7^th Edition):

Walk, Remy Elisabeth. “Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep.” 2017. Web. 22 Jan 2021.

Vancouver:

Walk RE. Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep. [Internet] [Masters thesis]. Cornell University; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/56951.

Council of Science Editors:

Walk RE. Bone Phenotype of Toll-like Receptor 5 Deficient (TLR5KO) Mice and PTH Treated Osteopenic Sheep. [Masters Thesis]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/56951

Cornell University

3. Zhang, Chi. Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle.

Degree: PhD, Mechanical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/36065

► Aging of skeletal muscle, characterized by involuntary loss of muscle mass and strength during aging, has become one of extraordinary concerns for the increasing elderly… (more)

▼ Aging of skeletal muscle, characterized by involuntary loss of muscle mass and strength during aging, has become one of extraordinary concerns for the increasing elderly population. The reduction of muscle strength is partially caused by decreased skeletal muscle cross-sectional area (CSA) with ageing; however, muscle force is lost to a greater extent than the loss of muscle mass, suggesting that other factors are involved. Changes in ATPase activity, metabolite levels, or myosin isoforms cannot fully explain the loss of specific force in aged muscles. These findings suggest that the force transmission pathway from myofibers to the tendon in aged muscles might be impaired, therefore, lead to the loss of skeletal muscle strength. The aim of this study is to characterize the effects of aging on force transmission in skeletal muscle and determine the underlying mechanisms. In current study, firstly, we studied the mechanism of lateral transmission of force in skeletal muscle by a finite element model of single muscle fiber. We found that most of the force generated in myofibers is transmitted near the end of the myofiber through shear stress to the surrounding ECM. Force transmitted to the end is affected by mechanical and geometrical properties of ECM. Secondly, effect of aging on lateral transmission was determined by isometric contractile tests on the extensor longus muscle with series of tenotomy and myotomy on young and old rats. Significant drop in force with myotomy was observed in old rats, indicating the impaired lateral transmission pathway with aging, which could be partly due to increased thickness of the ECM. Possible mechanisms of the age-related change in force transmission were further explored through combining the transmembrane proteins into finite element analysis. We found that force transmitted in the muscle is sensitive to the amount of proteins; more force could be transmitted in model with more transmembrane proteins. However, the force transmission is not sensitive to the stiffness of transmembrane proteins. The thesis was concluded by a discussion of study and possible future work. Advisors/Committee Members: Gao, Yingxin (chair), Earls, Christopher J (committee member), Hernandez, Christopher J. (committee member).

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APA (6^th Edition):

Zhang, C. (2014). Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36065

Chicago Manual of Style (16^th Edition):

Zhang, Chi. “Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle.” 2014. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/36065.

MLA Handbook (7^th Edition):

Zhang, Chi. “Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle.” 2014. Web. 22 Jan 2021.

Vancouver:

Zhang C. Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/36065.

Council of Science Editors:

Zhang C. Effect Of Aging On The Lateral Transmission Of Force In Skeletal Muscle. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36065

4. Hunt, Heather Brittany. Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus.

Degree: PhD, Materials Science and Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/64889

► People with type 2 diabetes mellitus (T2DM) have normal to high bone mineral densities, but counterintuitively have greater fracture risks than people without T2DM, even… (more)

▼ People with type 2 diabetes mellitus (T2DM) have normal to high bone mineral densities, but counterintuitively have greater fracture risks than people without T2DM, even after accounting for potential confounders like BMI and falls. Therefore, T2DM may alter aspects of the quality of bone, independently of bone mass, through metabolic or biochemical mechanisms as a result of a T2DM disease state. The main objective of this research was to elucidate the material factors that increase fragility in T2DM by characterizing the material properties, microarchitecture, and mechanics of bone from subjects with and without T2DM. The tissue material properties of bone from two clinical populations and from a rodent model of T2DM were evaluated, and the microarchitecture and and mechanics were evaluated for one of the clinical populations. In the rodent model of T2DM, mice with T2DM had more mineralized tissue, more mature collagen, and less heterogenous mineral properties compared to non-DM littermate controls, all of which are consistent with an older tissue that has undergone less remodeling. Tissue properties of the iliac crest from post-menopausal women varied with different stages of glycemic control, from normal glucose tolerance, impaired glucose tolerance, and overt T2DM. Glycemic derangement was associated with increased mineralization, decreased collagen maturity, and atypical mineral maturation, all of which can alter the mechanics of bone. Finally, femoral neck cancellous bone from men with T2DM had increased mineralization, a less mature mineral, more numerous trabeculae, and greater accumulation of non-enzymatically-formed collagen crosslinks compared to men without T2DM. The mechanical properties of the T2DM specimens reflected these alterations: stiffness and strength were greater in the T2DM specimens because of the greater mineral content and improved microarchitecture. Regression modeling of post-yield toughness demonstrated a significant deleterious impact of mineral maturity and non-enzymatic crosslinks once the improvement in microarchitecture was mathematically accounted for. Together, these results indicate a beneficial effect of T2DM on cancellous microarchitecture, but a deleterious effect of T2DM on the collagen matrix and mineral maturation. In conclusion, this work aids in the understanding of how bone becomes more fragile with T2DM, and this work is clinically relevant because it demonstrates that different populations of T2DM patients may have distinctly different bone fragilities as a result of varying tissue composition and microarchitecture. Advisors/Committee Members: Donnelly, Eve Lorraine (chair), Hernandez, Christopher J. (committee member), Estroff, Lara A. (committee member).

Subjects/Keywords: advanced glycation endproducts; translational; type 2 diabetes mellitus; Materials Science; bone; Biomechanics; Biochemistry; Collagen

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APA (6^th Edition):

Hunt, H. B. (2018). Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/64889

Chicago Manual of Style (16^th Edition):

Hunt, Heather Brittany. “Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus.” 2018. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/64889.

MLA Handbook (7^th Edition):

Hunt, Heather Brittany. “Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus.” 2018. Web. 22 Jan 2021.

Vancouver:

Hunt HB. Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/64889.

Council of Science Editors:

Hunt HB. Characterization of Material Properties, Microarchitecture, and Mechanics of Bone from Subjects with Type 2 Diabetes Mellitus. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64889

Cornell University

5. Slyfield, Craig. The Biomechanics Of Bone Turnover.

Degree: PhD, Mechanical Engineering, 2012, Cornell University

URL: http://hdl.handle.net/1813/29266

► Osteoporosis is a disease characterized by low bone mass and increased fracture risk. In adults, bone mass is primarily modified through bone remodeling. Bone remodeling… (more)

▼ Osteoporosis is a disease characterized by low bone mass and increased fracture risk. In adults, bone mass is primarily modified through bone remodeling. Bone remodeling is the coordinated activity of osteoclasts resorbing bone and osteoblasts forming new bone. Bone remodeling occurs at discrete locations on bone surfaces. The number and size of individual remodeling events influence the total amount of bone turnover in the body. Bone turnover is associated with increased fracture risk independent of bone mass. It is therefore believed that the number and size of individual remodeling events are important factors related to bone fragility and fracture risk. Precisely how metabolic bone disease alters individual remodeling events is not known. As a result, the mechanisms behind how metabolic bone disease alters bone biomechanics to increase bone fragility and fracture risk have not been determined. In the current dissertation, a sub-micron resolution three-dimensional imaging technique was developed to visualize individual remodeling events. The ability to measure individual remodeling events provides a means to understand how alterations in bone biology result in changes in bone turnover and fracture risk. This capability also allows for interpretation of individual remodeling events in terms of basic cell functions (proliferation, differentiation, motility, etc.). Using an animal model of postmenopausal osteoporosis, the serial milling approach was then applied to study how estrogen depletion alters bone remodeling at the level of individual remodeling events. Finally, the serial milling approach was used to determine how bone remodeling is related to bone biomechanics. The techniques developed in the current dissertation provide a means of understanding how metabolic bone disease increases fracture risk by altering individual remodeling event number and size. The current dissertation suggests that estrogen depletion primarily influences osteoclast proliferation and differentiation. Therefore, the increase in bone turnover in postmenopausal osteoporosis is attributed to an increase the number of resorption cavities and, potentially, in the number of stress concentrations. Furthermore, the current dissertation also shows that resorption cavities are preferential sites of microscopic tissue damage formation in cancellous bone. Together, these results suggest a potential mechanism behind increased fracture risk associated with increased bone turnover. Advisors/Committee Members: Hernandez, Christopher J. (chair), van der Meulen, Marjolein (committee member), Bonassar, Lawrence (committee member).

Subjects/Keywords: Bone; Medial Imaging; Biomechanics

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APA (6^th Edition):

Slyfield, C. (2012). The Biomechanics Of Bone Turnover. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/29266

Chicago Manual of Style (16^th Edition):

Slyfield, Craig. “The Biomechanics Of Bone Turnover.” 2012. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/29266.

MLA Handbook (7^th Edition):

Slyfield, Craig. “The Biomechanics Of Bone Turnover.” 2012. Web. 22 Jan 2021.

Vancouver:

Slyfield C. The Biomechanics Of Bone Turnover. [Internet] [Doctoral dissertation]. Cornell University; 2012. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/29266.

Council of Science Editors:

Slyfield C. The Biomechanics Of Bone Turnover. [Doctoral Dissertation]. Cornell University; 2012. Available from: http://hdl.handle.net/1813/29266

Cornell University

6. Melville, Katherine. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading.

Degree: PhD, Biomedical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/38857

► Decreased bioavailable estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both… (more)

▼ Decreased bioavailable estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both sexes. Estrogen signaling in bone occurs mainly through estrogen receptors ER[alpha] and ER[beta]. ER[alpha] in particular is important in regulating bone mass and bone's response to mechanical loading, but its particular role in each bone cell type and its cross-talk with BMP signaling are not well studied. ` Osteoblast-specific ER[alpha] knockout (pOC-ER[alpha]KO) and littermate control (LC) were bred by crossing Osteocalcin-Cre and ER[alpha]fl/fl mice. The effects of removing ER[alpha] in osteoblasts and osteocytes on bone mass, bone strength, and bone's response to mechanical loading were studied in 10-week-old animals. In general, cancellous and cortical bone mass were both reduced in pOC-ER[alpha]KO female mice, while bone mass was increased in pOC-ER[alpha]KO male mice compared to their sex-matched LC, measured by microCT in the proximal and midshaft tibia, femur, and L5 vertebra. These bone mass changes correlated with decreased vertebral compressive strength in female knockout mice and increased femoral bending strength in male knockout mice. After two weeks of in vivo tibial compression, female pOC-ER[alpha]KO mice showed a greater increase in bone mass in the proximal tibia, where baseline bone mass was decreased, and at the tibial midshaft, where baseline bone mass was similar to LC. Male pOC-ER[alpha]KO mice exhibited a normal response to mechanical loading. Next, 10-week-old female pOC-ER[alpha]KO and LC mice were administered either RAP-661, a BMPR1a inhibitor, or placebo, and all mice were subjected to daily in vivo tibial compression for two weeks. RAP-661 markedly increased bone mass in the L5 vertebra and cancellous tibial metaphysis of both genotypes, but not at the femoral midshaft, tibial midshaft, or tibial metaphyseal cortex. In the vertebra, the drug-induced increase in bone mass was less in pOC-ER[alpha]KO mice than LC. Animals treated with RAP-661 responded less to mechanical loading in the tibial metaphysis than placebo animals, but similarly at the tibial midshaft. This is the first evidence to indicate that BMPR1a may mediate bone's response to mechanical loading and interact with ER[alpha] in osteoblasts in vivo. Advisors/Committee Members: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Schimenti, John C. (committee member).

Subjects/Keywords: estrogen receptor alpha; bone; loading

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APA (6^th Edition):

Melville, K. (2014). Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/38857

Chicago Manual of Style (16^th Edition):

Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading.” 2014. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/38857.

MLA Handbook (7^th Edition):

Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading.” 2014. Web. 22 Jan 2021.

Vancouver:

Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/38857.

Council of Science Editors:

Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/38857

Cornell University

7. Guss, Jason Daniel. The Role of the Gut Microbiome In Bone and Joint.

Degree: PhD, Biomedical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/64961

► Osteoporosis and osteoarthritis affect millions of people worldwide every year. Osteoporosis related fractures totaled 8.9 million worldwide annually and osteoarthritis affects over 30 million people… (more)

▼ Osteoporosis and osteoarthritis affect millions of people worldwide every year. Osteoporosis related fractures totaled 8.9 million worldwide annually and osteoarthritis affects over 30 million people in the US alone. Recently, the gut microbiome has been identified as a factor that can influence chronic conditions associated with bone and joint disease such as obesity, diabetes, metabolic syndrome, inflammatory bowel diseases, and malnutrition. Though the gut microbiome is studied extensively in relation to metabolic diseases and disorders, the role of the gut microbiome in the development and progression of bone and joint disease is largely unexplored. Recent evidence suggests that the gut microbiome can influence bone mass, however no studies have determined if the mechanical performance of the bone is influenced by the gut microbiome. Therefore, first, we characterize how alterations to the gut microbiome can influence whole bone mechanical performance at skeletal maturity. We evaluate alterations in the gut microbiome caused by genotypic alteration and chronic treatment with antibiotics. Our results demonstrate that disruption of the gut microbiome with antibiotics is associated with reductions in cortical bone mass and whole bone strength, as well as drastic shifts in the composition of the gut microbiome. Furthermore, the changes in whole bone strength are greater than can be explained by the associated changes in bone mass and geometry, suggesting impaired bone tissue material properties in mice with an altered gut microbiome due to genotypic alteration and chronic antibiotic treatment. Next, we evaluate the changes in bone tissue composition caused by alterations in the gut microbiome. Additionally, we investigate how the functional profile of the gut microbiome can influence bone tissue material properties through several potential pathways: 1) regulation of nutrient and vitamin absorption/synthesis; 2) regulation of the immune system; 3) translocation of bacterial products. Our results demonstrate that disruption of the gut microbiome with antibiotics causes changes in bone mineral crystallinity, and that the effect is different per mouse genotype. Furthermore, we show that the functional capacity of the gut microbiome is dramatically altered in mice treated with antibiotics. A pathway involving vitamin K, a factor important for bone health, and associated with fracture risk, is suspected as changes in microbial gene pathways for vitamin K synthesis are disrupted leading to reduced vitamin K levels in organs. Last, we evaluate how alterations in the gut microbiome may influence the development and severity of load-induced osteoarthritis. Here we investigate obesity and metabolic syndrome, two conditions associated with an altered gut microbiome and an increased risk of developing osteoarthritis (OA). We use a mouse model of metabolic syndrome dependent on the gut microbiome, a mouse model of severe obesity/diabetes, and an in vivo non-invasive loading model to induce osteoarthritis-like pathology.… Advisors/Committee Members: Hernandez, Christopher J. (chair), van der Meulen, Marjolein (committee member), Goldring, Steven Reyburn (committee member).

Subjects/Keywords: Biomechanics; bone; Biomedical engineering; Bone Quality; Gut Microbiome; Ostoeporosis

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APA (6^th Edition):

Guss, J. D. (2018). The Role of the Gut Microbiome In Bone and Joint. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/64961

Chicago Manual of Style (16^th Edition):

Guss, Jason Daniel. “The Role of the Gut Microbiome In Bone and Joint.” 2018. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/64961.

MLA Handbook (7^th Edition):

Guss, Jason Daniel. “The Role of the Gut Microbiome In Bone and Joint.” 2018. Web. 22 Jan 2021.

Vancouver:

Guss JD. The Role of the Gut Microbiome In Bone and Joint. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/64961.

Council of Science Editors:

Guss JD. The Role of the Gut Microbiome In Bone and Joint. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64961

Cornell University

8. Torres, Ashley Marie. FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS.

Degree: PhD, Biomedical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/59531

► During daily activities, bone is exposed to repetitive loading, and over time, this can lead to failure. Cancellous bone is the primary load-bearing structure of… (more)

▼ During daily activities, bone is exposed to repetitive loading, and over time, this can lead to failure. Cancellous bone is the primary load-bearing structure of human vertebral bodies, yet most studies of cancellous bone mechanical performance concentrate on uniaxial properties such as Young's modulus and strength. Mechanical properties of cancellous bone are caused by the accumulation of microdamage, local stress and strain, tissue material properties, and local geometry. In this thesis, I examine the mechanisms associated with fatigue failure of cancellous bone. I then apply the findings to the design of novel microarchitectured materials. To examine the mechanical performance of cancellous bone under fatigue, we submitted human vertebral cancellous bone to cyclic compressive loading to induce microdamage. We found that fatigue failure is caused primarily by the initial sites of microdamage accumulation. In cancellous bone, microdamage formed preferentially in the interior regions of trabeculae, distant from trabecular surfaces. The location of microdamage coincided with locations of greater concentrations of Advanced Glycation Products (AGEs), suggesting the interior regions of trabeculae are more brittle and susceptible to microdamage accumulation. Because local geometry influences failure of cancellous bone, we examined the microarchitectual features of cancellous bone that are associated with damage accumulation. We found that microdamage accumulation in cancellous bone was reduced in specimens with thicker transverse rod-like trabeculae. Early in fatigue life, disproportionately more rod-like trabeculae failed, suggesting the importance of transverse rod-like trabeculae in resisting fatigue failure. To further test the idea that rod-like trabeculae influenced fatigue failure, models of cancellous bone were generated using three-dimensional printing in which transverse rod thickness was increased in a controlled manner. The specimens were submitted to cyclic compressive loading. Increasing the thickness of transverse rod-like trabeculae substantially extended fatigue life. Next, we designed a repeating cellular solid that also demonstrates enhanced fatigue life due to alterations in transverse struts. In summary, both tissue material properties and microarchitecture of cancellous bone influence fatigue failure. Our findings suggest a previously unidentified design strategy of open cell foams in which the strut thickness transverse to loads determines fatigue life. The resulting low-density cellular structure has potential application in a variety of lightweight structures. Advisors/Committee Members: Hernandez, Christopher J. (chair), van der Meulen, Marjolein (committee member), Hayashi, Kei (committee member).

Subjects/Keywords: microarchitectured materials; Mechanical engineering; Biomedical engineering; Biomechanics; Cancellous Bone; Microdamage; cellular solid; cyclic loading; fatigue life

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APA (6^th Edition):

Torres, A. M. (2018). FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/59531

Chicago Manual of Style (16^th Edition):

Torres, Ashley Marie. “FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS.” 2018. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/59531.

MLA Handbook (7^th Edition):

Torres, Ashley Marie. “FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS.” 2018. Web. 22 Jan 2021.

Vancouver:

Torres AM. FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/59531.

Council of Science Editors:

Torres AM. FATIGUE BEHAVIOR OF CANCELLOUS BONE, MICRODAMAGE ACCUMULATION, AND BIOLOGICALLY INSPIRED CELLULAR SOLIDS. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/59531

Cornell University

9. Patel, Radhika. Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics.

Degree: PhD, Mechanical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/37119

► Glenoid component loosening is the primary reason for failure after a total shoulder arthroplasty (TSA) accounting for 32% of complications post-surgery. The design of the… (more)

▼ Glenoid component loosening is the primary reason for failure after a total shoulder arthroplasty (TSA) accounting for 32% of complications post-surgery. The design of the glenoid implant, specifically the degree of conformity or radial mismatch between the bearing surface of the glenoid and humeral components, allows for posterior translation and has been shown to affect glenoid loosening. Existing theories for the failure mechanism are conflicting, suggesting that failure occurs in the bone, cement, or interface, with no agreement on the mechanism that causes glenoid loosening. The focus of this thesis is to obtain a fundamental understanding of glenohumeral joint translations and load transfer in the bone-implant system after a TSA. First, we studied the posterior glenohumeral translations observed clinically using a six degree of freedom computational model of the shoulder. We found that posterior translation increased as a function of radial mismatch, and the increase in posterior translation was explained by the increase in force in the infraspinatus muscle. Secondly, using a finite element model of the healthy scapula, we determined that after a cemented TSA, stress shielding was possible because load bypassed the cancellous bone region and was transferred directly to the stiff cortical bone when the implant pegs were present. Additionally, the cement was more likely to failure during eccentric and high magnitude loading. Finally, using finite element models of an osteoarthritic scapula, we showed that stress shielding and cement failure was more likely in the corrected osteoarthritic glenoid compared to the healthy and retroverted osteoarthritic glenoids during eccentric loading. These findings question the common surgical practice of correcting for glenoid retroversion prior to reconstruction. Furthermore, the reconstructed osteoarthritic glenoid was less sensitive to peg length than the healthy glenoid demonstrating that shorter pegs, requiring less bone resection, may be used in osteoarthritic patients. Advisors/Committee Members: Gao, Yingxin (chair), Wright, Timothy M. (committee member), Hernandez, Christopher J. (committee member).

Subjects/Keywords: Total shoulder arthroplasty; Glenoid loosening; Load Transfer

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APA (6^th Edition):

Patel, R. (2014). Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/37119

Chicago Manual of Style (16^th Edition):

Patel, Radhika. “Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics.” 2014. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/37119.

MLA Handbook (7^th Edition):

Patel, Radhika. “Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics.” 2014. Web. 22 Jan 2021.

Vancouver:

Patel R. Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/37119.

Council of Science Editors:

Patel R. Effects Of Total Shoulder Arthroplasty On Glenohumeral Kinematics And Mechanics. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/37119

Cornell University

10. Matheny, Jonathan Bradford. INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE.

Degree: PhD, Biomedical Engineering, 2017, Cornell University

URL: http://hdl.handle.net/1813/56759

► Increases in bone remodeling impair the mechanical performance of cancellous bone and are associated with the progression of post-menopausal osteoporosis. Bone remodeling is expected to… (more)

▼ Increases in bone remodeling impair the mechanical performance of cancellous bone and are associated with the progression of post-menopausal osteoporosis. Bone remodeling is expected to modify cancellous bone strength by changing both bone quantity and bone quality. Bone quality refers to factors that influence the mechanical performance of bone that are not well explained by bone mass. Here, I investigate how bone quality is changed by altering bone remodeling through pharmaceutical treatment and how aspects of bone quality affect the accumulation of tissue damage (microdamage) in cancellous bone. Finally, I investigate how bone remodeling responds to microdamage in a rabbit model of bone marrow lesions (BMLs). First, we examine how treatment with anti-resorptive agents influences the size of individual resorption cavities. We find that anti-resorptive treatment is associated with reductions in the size of resorption cavities in rat vertebral cancellous bone. A reduction in resorption cavity size is hypothesized to decrease stress concentrations generated by the cavity during loading and thereby reduce the likelihood that damage will form nearby. Next, we determine how treatment with sclerostin antibody modifies the trabecular morphology (shape and orientation of individual trabeculae) in a cynomolgus monkey model. We find that sclerostin antibody increases bone formation leading to a conversion of rod-like trabeculae into plate-like trabeculae and increases thickness of both rods-like and plate-like trabeculae leading to an increase in apparent stiffness, as predicted using finite element models. Although microarchitecture was modified, the improvements in apparent stiffness were well explained by changes in bone mass suggesting that treatment changes bone mass and not bone quality. We then examine how resorption cavities and tissue composition influence where microdamage forms and propagates in cancellous bone submitted to cyclic mechanical loading. We find that microdamage formed preferentially in the interior regions of cancellous bone and distant from trabecular surfaces and resorption cavities. The interior regions of trabeculae experience lower stresses but are composed of more brittle tissue. Finally, we investigate the bone remodeling response to microdamage in an in vivo loading model. We find an increase in bone resorption in response to load-induced microdamage. Cancellous bone from within the bone marrow lesion displayed microdamage and increased bone resorption. In summary, tissue composition of cancellous bone influences cancellous bone mechanics. Resorption cavities, while clearly generating stress concentrations do not influence microdamage accumulation. However, when microdamage does form within cancellous bone there is a focal increase in bone resorption. Advisors/Committee Members: Hernandez, Christopher J. (chair), Donnelly, Eve Lorraine (committee member), Hayashi, Kei (committee member).

Subjects/Keywords: Biomedical engineering; osteoporosis; Biomechanics; Cancellous Bone; Bone Histomorphometry; Bone Remodeling; Microdamage

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APA (6^th Edition):

Matheny, J. B. (2017). INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/56759

Chicago Manual of Style (16^th Edition):

Matheny, Jonathan Bradford. “INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE.” 2017. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/56759.

MLA Handbook (7^th Edition):

Matheny, Jonathan Bradford. “INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE.” 2017. Web. 22 Jan 2021.

Vancouver:

Matheny JB. INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/56759.

Council of Science Editors:

Matheny JB. INTERACTIONS BETWEEN BONE REMODELING AND MICRODAMAGE IN CANCELLOUS BONE. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/56759

Cornell University

11. Goff, Matthew. The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone.

Degree: PhD, Biomedical Engineering, 2015, Cornell University

URL: http://hdl.handle.net/1813/41131

► Bone fractures affect over 1.5 million people a year in the United States and can lead to a decrease in life expectancy and quality of… (more)

▼ Bone fractures affect over 1.5 million people a year in the United States and can lead to a decrease in life expectancy and quality of life. While some fractures occur due to a single overloading event such as a fall, many fractures develop over time. Insufficiency fractures are one type of fracture that develop over time and typically occur in regions of the skeleton dominated by cancellous bone. In cancellous bone, the accumulation of microdamage results in a loss of biomechanical performance and is believed to contribute to fracture incidence. However, relatively little is known about the how microdamage accumulates in cancellous bone and the aspects of cancellous bone structure that influence the development of microdamage. While the development of microdamage is driven by stresses and strains at the tissue-level, the complex microarchitecture of cancellous bone prevents the direct measurement of tissue-level stresses/strains. Additionally, naturally forming stress concentrations called resorption cavities form on the surface of cancellous bone. Finite element models can be used to calculate the tissue-level stress/strain in cancellous bone. According to finite element models, the largest stresses/strains will occur at the surface of cancellous bone and the stresses around resorption cavities will be higher than other surfaces of the bone. However, finite element models are created from three-dimensional images of the bone and the images are not typically obtained at resolutions capable of examining resorption cavities. Additionally, the material properties of cancellous bone are not homogeneous and may influence the location of microdamage formation. The oldest and stiffest tissue is found near the center of trabeculae away from the locations that experience the highest stresses. Therefore, first, we characterized the size and location of resorption cavities. Next, we explored the spatial relationship between microdamage and resorption cavities by developing three-dimensional spatial correlation techniques and determining the spatial relationship between microdamage and resorption cavities. Finally, we examined how well tissue-level strains measured from finite element models predicted the location of microdamage The size and location of resorption cavities suggest that they can generate large stress concentrations in cancellous bone. However, microdamage preferentially formed away from resorption cavities, and the majority of microdamage was located distant from the surface of trabeculae. Additionally, reductions in biomechanical performance during fatigue loading were explained primarily by the largest microdamage sites. Hence, only microdamage sites larger than a certain size appear to influence the mechanical performance of cancellous bone following cyclic loading. Furthermore, when using finite element models, regions of cancellous bone displaying the greatest principal tissue strains were able to predict the location of the largest and most biomechanically relevant microdamage sites. Together, the current… Advisors/Committee Members: Hernandez,Christopher J. (chair), van der Meulen,Marjolein (committee member), Todhunter,Rory James (committee member).

Subjects/Keywords: Bone; Microdamage; Microarchitecture

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APA (6^th Edition):

Goff, M. (2015). The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/41131

Chicago Manual of Style (16^th Edition):

Goff, Matthew. “The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone.” 2015. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/41131.

MLA Handbook (7^th Edition):

Goff, Matthew. “The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone.” 2015. Web. 22 Jan 2021.

Vancouver:

Goff M. The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone. [Internet] [Doctoral dissertation]. Cornell University; 2015. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/41131.

Council of Science Editors:

Goff M. The Role Of Micro And Ultra-Structure In Microdamage Accumulation In Cancellous Bone. [Doctoral Dissertation]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/41131

Cornell University

12. Leineweber, Matthew. Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury.

Degree: PhD, Mechanical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/38881

► Skeletal muscle injuries are frequent in sports and exercise, accounting for between 2055% of all sports injuries, with the vast majority of these injuries being… (more)

▼ Skeletal muscle injuries are frequent in sports and exercise, accounting for between 2055% of all sports injuries, with the vast majority of these injuries being muscle strains or contusions. Although muscle injuries are primarily diagnosed through symptomatology and examination of the injury mechanism, medical imaging techniques such as magnetic resonance imaging (MRI) and ultrasound imaging (US) are gaining popularity for assistance with both diagnoses and prognoses. These imaging techniques provide valuable structural and physiological information that is provides more insight into the nature and extent of the damage to guide image treatment. Currently, MRI is the gold standard for use with musculoskeletal applications, but US is becoming more widespread due to its affordability, portability, and real-time imaging capabilities. Ultrasound elastography (USE) is a family of techniques that are used to allow the visual analysis and quantification of the mechanical properties of soft tissue. Injury induced changes in muscle structure affect the mechanical properties of the tissue, and can be detected using USE. Since the echogenicity of a tissue is not directly related to its mechanical properties, ultrasound elastography can extract important information about tissue stiffness and deformability that might not otherwise be attainable. Such mechanical information is especially useful in distinguishing between fibrotic tissue and fatty infiltration. The goal of this thesis is to develop USE as an affordable, fast, and readily available alternative to MRI for early stage diagnosis of acute muscle injury. In pursuit of this goal, we first developed a technique to obtain repeatable and reproducible strain images using USE. We found that a simple averaging procedure performed on 4-8 repeated USE compression cycles significantly improved both the reproducibility and repeatability of the resulting strain images compared to strain images generated using an automated USE system. We then showed that USE combined with principal component analysis can be used to quantify and locate muscle injury in a finite element model, and can feasibly be applied to strain images generated using USE. Finally, we attempted to use the procedures developed in the first two studies to detect and monitor contusion injury in a rat model. However, due to equipment limitations, the results of this study were inconclusive. This thesis is concluded by a summary of the overall findings and discussion of future work. Advisors/Committee Members: Gao, Yingxin (chair), Hernandez, Christopher J. (committee member), Reeves, Anthony P (committee member).

Subjects/Keywords: ultrasound; elastography; skeletal muscle

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APA (6^th Edition):

Leineweber, M. (2014). Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/38881

Chicago Manual of Style (16^th Edition):

Leineweber, Matthew. “Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury.” 2014. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/38881.

MLA Handbook (7^th Edition):

Leineweber, Matthew. “Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury.” 2014. Web. 22 Jan 2021.

Vancouver:

Leineweber M. Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/38881.

Council of Science Editors:

Leineweber M. Applying Ultrasound Elastography To Detecting Skeletal Muscle Injury. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/38881

Cornell University

13. Ko, Frank. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.

Degree: PhD, Mechanical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/37056

► Osteoarthritis (OA) is the leading cause of disability among the elderly population, affecting approximately 27 millions Americans and costing $60 billion in related-health care costs.… (more)

▼ Osteoarthritis (OA) is the leading cause of disability among the elderly population, affecting approximately 27 millions Americans and costing $60 billion in related-health care costs. Mouse models of OA have been developed to study the mechanisms of OA and therapeutic interventions. However, traditional animal models induce OA pathology through traumatic surgeries, which only represent 10% of human OA patients. Thus, in this thesis, a novel noninvasive OA mouse model was developed, characterized, and applied to transgenic mice. The changes in articular cartilage and subchondral bone were analyzed by histology, immunohistochemistry, and microcomputed tomography. To develop a noninvasive OA mouse model, an in vivo tibial loading model was used to investigate the adaptive responses of cartilage and bone to mechanical loading and to assess the influence of load level and duration. Peak cyclic compression of 4.5 and 9.0N was applied to the left tibia via the knee joint of adult (26-week-old) male mice for 1, 2, and 6 weeks at 1200 cycles/day. In addition, 9.0N loading was utilized in young (10-week-old) mice. Loading promoted cartilage damage, cartilage thinning, and subchondral cortical bone thickening in both age groups. Both age groups developed periarticular osteophytes at the tibial plateau in response to the 9.0N load, but no osteophyte formation occurred in adult mice subjected to 4.5N load. Development of a novel noninvasive loading model was followed by investigating the traumatic vs. nontraumatic nature of cyclic loading of the mouse knee joint. To differentiate traumatic tissue damage versus cell-mediated processes in the development of OA pathology, a single nondestructive 5-minute loading session was applied to the left tibia of adult (26-weekold) mice at a peak load of 9.0N. Knee joints were subsequently analyzed at 0, 1 and 2 weeks after loading. At T = 0, no change was evident in cartilage or subchondral bone. However, cartilage pathology demonstrated by localized thinning, proteoglycan loss, and inhibition of chondrocyte autophagy occurred at 1 and 2 weeks after the single session of loading. Transient cancellous bone loss was evident at 1 week, associated with increased osteoclast number, reversed at 2 weeks. Finally, the in vivo tibial loading model was implemented to study the role of Dickkopf1, an inhibitor of the Wnt pathway, in the development of load-induced OA. To identify the role of Dickkopf-1 protein in OA, novel viable mice with Dickkopf-1 knockout and Wnt3 knockdown (Dkk1-/-;Wnt3+/-) were used. The left tibia of 10-week-old Dkk1-/-;Wnt3+/- and respective control groups, littermate control (Dkk1+/+;Wnt3+/+) and Wnt3 knockdown (Dkk1+/+;Wnt3+/-) mice, underwent cyclic compression at a peak load of 9.0N for 2 weeks. As a result of loading, both Dkk1-/-;Wnt3+/- and Dkk1+/+;Wnt3+/+ mice demonstrated cartilage erosion, subchondral cancellous bone loss, and osteophyte formation. However, Dkk1+/+;Wnt3+/- mice did not undergo cartilage degeneration and showed limited osteophyte formation, indicating… Advisors/Committee Members: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Farnum, Cornelia E (committee member), Wright, Timothy M. (committee member).

Subjects/Keywords: Osteoarthritis; Mouse model; Mechanical loading

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APA (6^th Edition):

Ko, F. (2014). In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/37056

Chicago Manual of Style (16^th Edition):

Ko, Frank. “In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.” 2014. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/37056.

MLA Handbook (7^th Edition):

Ko, Frank. “In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.” 2014. Web. 22 Jan 2021.

Vancouver:

Ko F. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/37056.

Council of Science Editors:

Ko F. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/37056

Cornell University

14. Brock, Garry. Changes In Bone Tissue Properties With Osteoporosis Treatment.

Degree: PhD, Mechanical Engineering, 2015, Cornell University

URL: http://hdl.handle.net/1813/39339

► Osteoporosis is a disease characterized by low bone mass leading to an increased risk of fracture. Bisphosphonate therapies are commonly prescribed medications that reduce the… (more)

▼ Osteoporosis is a disease characterized by low bone mass leading to an increased risk of fracture. Bisphosphonate therapies are commonly prescribed medications that reduce the risk of osteoporotic fractures through reduced bone turnover. Recently, a rise in atypical femoral fractures (AFF) has occurred in patients taking long-term bisphosphonate treatments. These fractures have features similar to a fatigue failure; however, the mechanisms through which these fractures initiate are unknown. Knowledge of material property changes with bisphosphonates has been limited to monotonic tests and measures above the scale of bone structures. The purpose of this thesis was to examine the fatigue and nanoscale properties of bisphosphonatetreated cortical bone tissue. To examine these properties an osteoporosis model was used in sheep followed by osteoporosis treatment: bisphosphonate (alendronate or zoledronate), SERM (raloxifene), PTH (teriparatide) or vehicle. Beams of known geometry were created from the cortical bone tissue and tested in four-point bend fatigue to failure. Differences in fatigue life occurred including a loss of fatigue life with alendronate and a rise in fatigue life with PTH treatment when compared to the grand mean. The lack of fatigue life change with zoledronate treatment indicates that factors such as dosage, method of administration, or chemical structure are affecting material properties, and not solely the class of drug. Increased fatigue life with PTH may indicate effectiveness for AFF treatment. Fatigue loading induces microdamage in cortical bone tissue that is well characterized using microscale techniques. Bisphosphonate treatments are likely inducing changes to tissue properties at the nanoscale, below levels typically viewed with bone measure techniques. To examine nanoscale tissue damage, methods were developed and implemented using transmission-ray microscopy with synchrotron radiation to gain nanoscale imaging of fatigue damaged bone tissue. Heavy metal staining of microdamage was used, in conjunction with transmission x-ray tomography (TXM), to determine where damage initiates and forms at the nanoscale. Fatigue loaded samples had more staining present within the lacunar-canalicular network as compared to monotonic loaded samples. Damage may, therefore, be occurring within the bone structures themselves and not through surrounding tissue. The lacunar-canalicular network may be altered through bisphosphonate treatments, leading to development of novel imaging networks to examine these questions. Trabeculae were examined with TXM, and tomographies were created to compare nanoscale porosity. Results indicated porosity differences throughout trabeculae with the majority of the lacunar-canalicular network forming near the surface. The TXM methods are among the first studies to view bone at the nanoscale in three dimensions. Overall, results indicated differences in fatigue life of bone tissue given an osteoporosis treatment, with novel methods developed to help examine the origin of this… Advisors/Committee Members: van der Meulen, Marjolein (chair), Baker, Shefford P. (committee member), Hernandez, Christopher J. (committee member), Ingraffea, Anthony R (committee member).

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APA (6^th Edition):

Brock, G. (2015). Changes In Bone Tissue Properties With Osteoporosis Treatment. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/39339

Chicago Manual of Style (16^th Edition):

Brock, Garry. “Changes In Bone Tissue Properties With Osteoporosis Treatment.” 2015. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/39339.

MLA Handbook (7^th Edition):

Brock, Garry. “Changes In Bone Tissue Properties With Osteoporosis Treatment.” 2015. Web. 22 Jan 2021.

Vancouver:

Brock G. Changes In Bone Tissue Properties With Osteoporosis Treatment. [Internet] [Doctoral dissertation]. Cornell University; 2015. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/39339.

Council of Science Editors:

Brock G. Changes In Bone Tissue Properties With Osteoporosis Treatment. [Doctoral Dissertation]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/39339

15. Wong, Yu-Chern. Stress Analysis of Bacteria Submitted to Extrusion Loading.

Degree: M.S., Mechanical Engineering, Mechanical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/64910

► Bacteria are known to sense and respond to mechanical signals. To examine bacterial mechanics and their relation to biological responses, we used a microfluidic device… (more)

▼ Bacteria are known to sense and respond to mechanical signals. To examine bacterial mechanics and their relation to biological responses, we used a microfluidic device to apply a mechanical loading condition we refer to as extrusion loading to individual Escherichia coli. Extrusion loading was generated by flowing bacteria in liquid media into tapered constrictions. A difference in fluid pressure across the bacteria and the frictional and normal forces from the channel walls generate loads and deformations on the bacteria. The recent experimental findings in our group suggests that extrusion loading can influence growth rates and the performance of cell membrane proteins involved in the resistance to toxins. Mechanical models of bacteria under extrusion loading were developed to determine the stress state and Young’s modulus of the cell envelope. Here I used analytical and finite element models to characterize the stresses in the cell envelope of bacteria submitted to extrusion loading. The analytical model was derived based on a force balance and transversely isotropic constitutive laws. An axisymmetric nonlinear finite element model was developed using solid elements with transversely isotropic material properties. As many aspects of bacteria material properties are not known, a parametric analysis was performed to determine the combinations of material properties that yielded finite element simulations consistent with experimental results. We found that extrusion loading led to increases in tensile axial stress, shear stress, and compressive radial stress, and decreases in tensile hoop stress. Besides, the internal pressure on bacteria (the “turgor pressure”) increased during extrusion loading. Additionally we used a series of analytical and finite element models to determine the cell envelope Young’s modulus. The analytical model provided a closed form solution for Young’s modulus. An axisymmetric nonlinear finite element model was developed using solid elements with isotropic material properties to identify the cell envelope Young’s moduli that were consistent with experimental observations. The analytical analysis was extremely sensitive to experimental measurements suggesting that small errors in measurement would have large effects on the predicted Young’s modulus. The parametric finite element analysis showed resulting deformations insensitive to the tested range of Young’s moduli, preventing us from iteratively determining a Young’s modulus. Proposed future approaches to determine the cell envelope Young’s modulus are discussed. Advisors/Committee Members: Hernandez, Christopher J. (chair), Hui, Chung-Yuen (committee member).

Subjects/Keywords: Cell mechanics; Mechanical modeling; Microfluidic device; Elasticity; Mechanical engineering; Biomechanics; Finite element method; Continuum mechanics

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APA (6^th Edition):

Wong, Y. (2018). Stress Analysis of Bacteria Submitted to Extrusion Loading. (Masters Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/64910

Chicago Manual of Style (16^th Edition):

Wong, Yu-Chern. “Stress Analysis of Bacteria Submitted to Extrusion Loading.” 2018. Masters Thesis, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/64910.

MLA Handbook (7^th Edition):

Wong, Yu-Chern. “Stress Analysis of Bacteria Submitted to Extrusion Loading.” 2018. Web. 22 Jan 2021.

Vancouver:

Wong Y. Stress Analysis of Bacteria Submitted to Extrusion Loading. [Internet] [Masters thesis]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/64910.

Council of Science Editors:

Wong Y. Stress Analysis of Bacteria Submitted to Extrusion Loading. [Masters Thesis]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64910

16. Holyoak, Derek. Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis.

Degree: PhD, Biomedical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/64868

► Osteoarthritis (OA) is a degenerative joint disease that affects millions of people worldwide and is the leading cause of disability in the elderly population. To… (more)

▼ Osteoarthritis (OA) is a degenerative joint disease that affects millions of people worldwide and is the leading cause of disability in the elderly population. To date, no cure exists for OA, and the exact cause is not clearly understood. Mechanical loading at high magnitudes, however, is a primary risk factor for the disease. To better understand the role of mechanical loading in OA, we used an in vivo model that applies cyclic axial compression to the knee joints of mice. First, we used the model to study the role of abnormal cartilage matrix properties in load-induced OA. Next, we characterized a novel hydrogel-based drug delivery system and tested the hydrogel’s therapeutic efficacy for intra-articular treatment of load-induced OA. Finally, we applied low-level mechanical forces to attenuate OA-like changes after joint injury. We first sought to understand the effects of an abnormal cartilage matrix on the onset and progression of load-induced OA. The cho/+ mouse has abnormal collagen fibrils in its cartilage matrix due to a Col11a1 haploinsufficiency. We hypothesized that cho/+ mice would develop more severe load-induced OA pathology compared to wildtype (WT) littermates with normal cartilage. Contrary to our hypothesis, cho/+ mice had less severe load-induced cartilage damage. Cho/+ mice also had thinner, less dense cortical bone and thicker cartilage. Both characteristics may have played a role in attenuating load-induced OA pathology in cho/+ mice. The next goal was to characterize an on-demand hydrogel-based drug delivery system for intra-articular OA treatment. Synthetic hydrogels were made of cross-linked 4-arm maleimide functionalized polyethylene glycol, and we analyzed their mechanical integrity and on-demand release in vitro. The hydrogels maintained their mechanical properties after 10,000 cycles of cyclic compression at 80% strain. In addition, they released particles in response to collagenase exposure, highlighting their on-demand release characteristics in the OA joint environment. In vivo, hydrogel injections reduced load-induced cartilage damage and osteophyte size. Further work is needed to determine the most effective drugs to combine with the hydrogel system. Finally, we sought to determine whether low-level loads could attenuate post-traumatic OA. Mice underwent the destabilization of the medial meniscus (DMM) surgery to mimic an injury in the knee joint. These DMM joints were then loaded with low-level cyclic axial compression. The loading regimen attenuated DMM-induced cartilage degradation, osteophyte formation, and subchondral bone sclerosis. Thus, low-level axial loading may be used to slow post-traumatic OA progression. In summary, in vivo cyclic tibial compression allowed us to better understand the role of mechanical loading in the pathology, treatment, and prevention of OA. Our results show that both cartilage and bone are involved in OA progression, and both tissues must be considered when predicting disease severity. Furthermore, synthetic hydrogel systems combined with… Advisors/Committee Members: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Goldring, Mary (committee member).

Subjects/Keywords: Mechanical engineering; bone; mechanobiology; Biomedical engineering; Biomechanics; Animal models; Cartilage; Osteoarthritis

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APA (6^th Edition):

Holyoak, D. (2018). Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/64868

Chicago Manual of Style (16^th Edition):

Holyoak, Derek. “Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis.” 2018. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/64868.

MLA Handbook (7^th Edition):

Holyoak, Derek. “Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis.” 2018. Web. 22 Jan 2021.

Vancouver:

Holyoak D. Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/64868.

Council of Science Editors:

Holyoak D. Role of in vivo mechanical loading in the pathology, treatment, and prevention of osteoarthritis. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64868

17. Chen, Julia. ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT.

Degree: PhD, Mechanical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/59324

► Osteoporosis, an age-related bone disease characterized by low bone mass, is a potential public health problem responsible for over 8.9 million fractures annually. From an… (more)

▼ Osteoporosis, an age-related bone disease characterized by low bone mass, is a potential public health problem responsible for over 8.9 million fractures annually. From an engineering perspective to understanding the mechanism of increased fragility with osteoporosis, we applied engineering theory to study this complex composite material, bone. Amount of bone, bone distribution, and tissue material properties are determinants of whole bone strength. Parathyroid hormone (PTH, teriparatide, hPTH [1-34]) is a FDA-approved anabolic osteoporosis treatment. PTH has shown to reduce fracture risk by over 50% and increased bone volume fraction. However, the alterations in material properties and mechanical properties with PTH treatment, and the correlations to bone mechanical failure are unknown. The objectives of this research were to 1) examine alterations in microstructure and tissue properties of both cortical and cancellous bone with PTH treatment using an osteopenia sheep model, and 2) investigate the influence of microstructure and anisotropic material properties on crack propagation in a pre-notched cortical beam under bending. To investigate the alterations in tissue properties across different length scales, a large, multi-level experiment was designed for both cortical and cancellous bone in an osteopenia sheep model. The first study focused on cortical bone and the effect of PTH treatment was greater at the micro- and nanoscale than at the whole bone level. There was no difference with whole-bone strength; however, fatigue life has shown to increase compared to other bisphosphonate-treated samples whereas fracture toughness was decreased in PTH-treated group and osteon density was higher. Furthermore, mineralization increased whereas indentation modulus decreased and hardness reduced with PTH treatment. Millimeter and nano-scale material properties were correlated with whole bone strength, but fatigue properties correlated little to bending strength or fracture toughness. In the second study, cancellous bone was examined. There was no difference in monotonic compressive strength with PTH treatment; however, PTH-treated group preserved mechanical properties during cyclic loading compared to vehicle group. Additionally, PTH increased the volume fraction of rod-type trabeculae and decreased mineralization whereas nanoindentaion and hardness were not different. Correlating tissue composition, microstructure, and mechanical performance, energy dissipation was highly correlated with volume fraction of rods and mineralization. In the third study, fracture behavior in a single pre-notched cortical bone tissue was examined with finite element based simulation software (FRANC2D). The role of anisotropy of fracture toughness and of altered microstructure in crack trajectory and the force needed to propagate a crack was investigated. Cortical bone with more osteons located further away from the applied loads to maximize intact material would withstand more load before propagating cracks and fracturing. Advisors/Committee Members: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Warner, Derek H. (committee member).

Subjects/Keywords: Parathyroid Hormone; Sheep Model; osteoporosis; Biomechanics; Biomedical engineering; Engineering; Anisotropic Fracture Toughness; Bone Tissue Properties; Micro-crack Propagation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, J. (2018). ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/59324

Chicago Manual of Style (16^th Edition):

Chen, Julia. “ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT.” 2018. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/59324.

MLA Handbook (7^th Edition):

Chen, Julia. “ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT.” 2018. Web. 22 Jan 2021.

Vancouver:

Chen J. ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/59324.

Council of Science Editors:

Chen J. ALTERATIONS IN BONE TISSUE PROPERTIES WITH PARATHYROID HORMONE TREATMENT. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/59324

18. Cresswell, Erin N. Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone.

Degree: PhD, Mechanical Engineering, 2017, Cornell University

URL: http://hdl.handle.net/1813/51562

► Bone is a vital component of the musculoskeletal system. The morphology and material properties of bone allow our skeletons to support the loads caused from… (more)

▼ Bone is a vital component of the musculoskeletal system. The morphology and material properties of bone allow our skeletons to support the loads caused from daily activity. Fractures occur when loads exceed the mechanical capacity of bone. Physical forces are a powerful anabolic stimulus that regulates bone formation, bone geometry, and bone density. Forces on whole bones cause non-uniform tissue strains throughout bone’s internal structure. Bone formation is hypothesized to occur at locations of greatest tissue strains. In this dissertation, I examined the relationship between locations of bone formation and local tissue strains in cancellous bone. The rat tail loading model was used to stimulate mechanically induced bone formation. Finite element modeling was performed to determine local tissue strains. High-resolution three-dimensional images were collected to identify osteocyte lacunae and locations of bone formation. The number of bone formation sites was greater in loaded animals than unloaded controls. The additional bone formation sites were attributed to bone adaptation at locations of greatest tissue strains. However, tissue stress and strain were only modest predictors of locations of bone formation (32-41%), and the ability to predict locations of bone formation was not improved by including the local osteocyte density. As an example of bones adapted to high intensity loading, I examined bone microstructure in racehorses. Changes in bone morphology have been associated with increased fracture risk in racehorses. I examined the association between bone volume fraction, exercise history, and fracture incidence in the proximal sesamoid bones. Bone morphology was assessed using micro-computed tomography images of the proximal sesamoid bones in racehorses that experienced a proximal sesamoid bone fracture as well as in control racehorses. Greater bone volume fraction was associated with fracture. Additionally, animals with fractures had a history of longer periods of rest interrupted by shorter periods of high speed exercise. The ratio of the total number of weeks with high speed exercise to the number of weeks of rest (work-to-rest ratio) was less in animals that sustained a fracture. In summary, mechanically induced bone formation occurred at regions of trabecular microarchitecture that experienced the greatest tissue strain. Locations of bone formation were regulated by the local tissue strain, independent of local osteocyte lacunar density. Whole bone density was influenced by exercise, and in the case of racehorses, greater amounts of rest was associated with greater bone volume fraction and fracture risk. Therefore, alteration of the training/racing schedule could regulate bone density and decrease fracture risk. Advisors/Committee Members: Hernandez, Christopher J (chair), Bonassar, Lawrence J (committee member), van der Meulen, Marjolein CH (committee member).

Subjects/Keywords: Veterinary science; Fracture; Biomechanics; Cancellous Bone; Finite Element Modeling; Functional Adaptation; In vivo; Mechanotransduction; Engineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cresswell, E. N. (2017). Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/51562

Chicago Manual of Style (16^th Edition):

Cresswell, Erin N. “Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone.” 2017. Doctoral Dissertation, Cornell University. Accessed January 22, 2021. http://hdl.handle.net/1813/51562.

MLA Handbook (7^th Edition):

Cresswell, Erin N. “Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone.” 2017. Web. 22 Jan 2021.

Vancouver:

Cresswell EN. Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1813/51562.

Council of Science Editors:

Cresswell EN. Spatial Regulation of Bone Formation in Functional Adaptation of Cancellous Bone. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/51562

Open Access Theses and Dissertations