Parathyroid Hormone and Bone Biomechanics

Parathyroid hormone (PTH) treatment, either in the form of teriparatide or recombinant human PTH(1-34), reduces the fracture risk of osteoporotic women by enhancing both structural and material biomechanical properties. Cortical bone thickness and cross-sectional moment of inertia increase because of new bone formation on periosteal and endocortical surfaces. Intracortical porosity is increased yet preferential localization near the endocortical surface limits any negative biomechanical effects. Greater trabecular bone volume results from a positive basic multicellular unit bone balance and renewed modeling. Initial increases in trabecular thickness are eventually reduced as a result of trabecular tunneling, increasing trabecular number, and connectivity. These geometrical and architectural alterations are the predominant mechanism by which PTH increases structural strength, stiffness, and energy absorption. PTH also positively alters material-level strength, modulus, and toughness. These changes are counterintuitive based on known effects of decreasing average tissue mineralization and increasing tissue heterogeneity. This combination of enhanced structural and material biomechanical properties makes PTH an effective treatment for reducing fracture risk despite smaller gains in bone mineral density compared to other osteoporosis agents.