A mechanochemical hypothesis for bone remodeling induced by mechanical stress.

Abstract

A new mechanism is presented to explain how increased or decreased mechanical stresses applied to bone are translated into osteoblastic and/or osteoclastic activity. A mechano-chemical hypothesis for bone remodeling induced by mechanical stress is presented in an attempt to explain this phenomenon. Bone responds to mechanical stress by differential growth so as to resist the applied stress; therefore mechanically induced bone remodeling is probably regulated by a negative feedback system. The hypothesis is that a change in the loading of bone results in an altered straining of the hydroxyapatite crystals in bone. This in turn alters the solubility of the crystals, providing the required negative feedback message to the bone cells in the form of a mechanically induced chemical change. The cells then take appropriate action to compensate for the alteration in the localized calcium activity either by building up bone to redistribute an increased stress, or by removing bone which is surplus to the structural needs imposed by a reduced stress. In order to test the hypothesis, synthetic hydroxyapatite crystals were stressed and changes in calcium ion activity were recorded from a divalent cation activity electrode. The results show that a mechanochemical effect can be detected in hydroxyapatite crystals which, when stressed, generate a calcium activity of 9×10−5 moles/l compared to 7×10−5 moles/l when unstressed. The experimental results in this study and evidence from cellular physiology are consistent with the mechanochemical hypothesis proposed here.