In this work, a bone damage resorption finite element model based on the disruption of the inhibitory signal transmitted between osteocytes cells in bone due to damage accumulation is developed and discussed. A strain-based stimulus function coupled to a damage-dependent spatial function is proposed to represent the connection between two osteocytes embedded in the bone tissue. The signal is transmitted to the bone surface to activate bone resorption. The proposed model is based on the idea that the osteocyte signal reduction is not related to the reduction of the stimulus sensed locally by osteocytes due to damage, but to the difficulties for the signal in travelling along a disrupted area due to microcracks that can destroy connections of the intercellular network between osteocytes and bone-lining cells. To check the potential of the proposed model to predict the damage resorption process, two bone resorption mechano-regulation rules corresponding to two mechanotransduction approaches have been implemented and tested: (1) Bone resorption based on a coupled strain-damage stimulus function without ruptured osteocyte connections (NROC); and (2) Bone resorption based on a strain stimulus function with ruptured osteocyte connections (ROC). The comparison between the results obtained by both models, shows that the proposed model based on ruptured osteocytes connections predicts realistic results in conformity with previously published findings concerning the fatigue damage repair in bone.
Keywords: Bone; Cracks; Fatigue; Finite element model; Remodelling; Ruptured osteocytes.
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