Mechanobiological regulation of the remodelling cycle in trabecular bone and possible biomechanical pathways for osteoporosis.

Background: The rapid loss of trabeculae as observed during osteoporosis is attributed to pathological changes in the bone remodelling process. In this study, it is proposed that osteoporosis is due to altered signals resulting from either (i) a decrease in the mechanosensitivity of the sensor cells or (ii) an increase in the bone tissue elastic modulus.

Methods: To test these hypotheses, a mechanobiological algorithm was developed and applied to simulate the remodelling cycle in a realistic trabecular strut.

An algorithm for bone mechanoresponsiveness: implementation to study the effect of patient-specific cell mechanosensitivity on trabecular bone loss.

The rate of bone loss is subject to considerable variation between individuals. With the 'mechanostat' model of Frost, genetic variations in bone mechanoresponsiveness are modelled by different mechanostat 'setpoints'--which may also change with age or disease. In this paper, the following setpoints are used: epsilonmin (strain below which resorption is triggered); epsilonmax (strain above which deposition occurs); omegacrit (microdamage-level above which damage-stimulated resorption occurs).

Loss of trabeculae by mechano-biological means may explain rapid bone loss in osteoporosis.

Osteoporosis is characterized by rapid and irreversible loss of trabecular bone tissue leading to increased bone fragility. In this study, we hypothesize two causes for rapid loss of bone trabeculae; firstly, the perforation of trabeculae is caused by osteoclasts resorbing a cavity so deep that it cannot be refilled and, secondly, the increases in bone tissue elastic modulus lead to increased propensity for trabecular perforation. These hypotheses were tested using an algorithm that was based on two premises: (i) bone remodelling is a turnover process that repairs damaged bone tissue by resorbing and returning it to a homeostatic strain level and (ii) osteoblast attachment is under biochemical control.