One of the most intriguing aspects of bone is its ability to grow, repair damage, adapt to mechanical loads, and maintain mineral homeostasis [1]. It is generally accepted that bone adaptation occurs in response to the mechanical demands of our daily activities; moreover, strain and microdamage have been implicated as potential stimuli that regulate bone remodeling [2]. Computational models have been used to simulate remodeling in an attempt to better understand the metabolic activities which possess the key information of how this process is carried out [3]. At present, the connection between the cellular activity of remodeling and the applied mechanical stimuli is not fully understood. Only a few mathematical models have been formulated to characterize the remolding process in terms of the cellular mechanisms that occur [4,5].

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