Long-term effects of high or low Ca intakes and of lack of parathyroid function on rat femur biomechanics.

In order to assess the repercussion of chronically affected parathyroid function on bone biomechanics, 3-point flexion tests were carried out with fresh, whole femurs of young, intact rats fed diets with low, normal, or high Ca contents, and thyroparathyroidectomized (TPTX) rats fed normal Ca diet. Ca-restriction reduced, and TPTX augmented, inertial parameters and load-resistance of the whole femurs, not affecting the bending stress or the modulus of elasticity of the bone material, suggesting that parathyroid status affected bone mass and architecture without biomechanical alteration of bone tissue. High-Ca feeding enhanced tissue strength and stiffness as a direct effect, not altering bone geometry. The relationships between the energy-absorbing capacity of the whole bones or of the bone tissue, and the moment of inertia of the fracture sections in weight-paired animals showed that (1) in intact rats under normocalcic diet, the inertia of the section was unrelated to the whole-bone biomechanical performance, while bone section architecture depended on bone tissue biomechanical quality; and (2) in the absence of the parathyroids, or in chronically-induced hyperparathyroidism, this last relationship did not apply, but section architecture had a major influence on the whole-bone biomechanics, independently of physiological stresses. The evidence obtained can be interpreted to indicate that architectural changes brought about by the parathyroids contribute to the regulation of bone biomechanics by adapting organ inertial parameters to tissue quality.