Effects of Osteopontin Deficiency and Aging on Nanomechanics of Mouse Bone
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Effects of Osteopontin Deficiency and Aging on Nanomechanics of Mouse Bone B. Kavukcuoglu1, C. West2, D.T. Denhardt3, A. B. Mann1, 2 Department of Ceramic and Materials Engineering, 2 Department of Biomedical Engineering, 3 Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 1
ABSTRACT Osteopontin (OPN), a phosphorylated glycoprotein, is among the most abundant noncollageneous bone matrix proteins produced by osteoblasts and osteoclasts. OPN has been implicated in bone formation, resorption and remodeling. However, previous studies have presented contradictory results regarding the effect of OPN on the mechanics and microstructure of bone. This study has used nanoindentation to identify local variations in elastic modulus and hardness of OPN deficient (OPN -/-) and wild-type control (OPN+/+) mouse bones. Specifically, the study has looked at changes in the mechanical properties of OPN-/- and OPN+/+ mouse bones with the mouse’s age. Cortical sections of femurs from different age groups ranging from 3 weeks to 58 weeks were tested and compared. The results suggest that there are large, abrupt variations in mechanical properties across the femur’s radial section for 3-week-old mouse bone. The hardness (H) drops significantly towards the inner and outer sections so the cortical bone has a mean H=3.66 GPa with a standard deviation of 2.44 GPa. In contrast, the hardness of the 58week-old mouse bone had a standard deviation of 0.35 GPa and a mean H=1.45 GPa. The hardness across the radial axis of the 58-week-old bone was found to be quite uniform. The elastic modulus showed similar variations to the hardness with respect to age and position on the bone. We conclude that the mechanical properties of the mouse bones decrease substantially with maturity, and statistically the hardness and elastic modulus are more uniform in mature bones than young ones. Surprisingly we found a similar variation in both OPN-/- and OPN+/+ bones, with no statistically significant difference in the mechanical properties of the OPN -/- and OPN+/+ bones. The results for OPN-/- and OPN+/+ mouse bones are particularly important as control of OPN activity has been postulated as a potential treatment for bone pathologies that exhibit a change in the bone mineralization, such as osteoporosis, osteopetrosis and Paget's disease. Understanding the effects of OPN on bone mechanics is a vital step in the development of these new treatments. INTRODUCTION Osteoporosis means ‘porous bone’. It is a disease characterized by low bone mass, microarchitectural deterioration of bone tissue leading to enhanced bone fragility, and a consequent increase in fracture risk [1]. Increase in osteoclastic bone resorption causes loss of bone mineral in postmenopausal osteoporotic patients The osteoclastic bone resorption occurs as a result of attachment of osteoclasts to bone, forming a sealing zone. Once the sealing zone is formed, osteoclasts secrete hydrogen ions, creating an acidic environment causing the dissolution of bone mine
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