A cellular automata model of bone formation

•In this paper we present the first towards the larger goal to construct biomimetic multi-sale mathematial models to understand the underlying mehanisms, pathways and multicellular interactions that regulate bone remodeling.–The team will work to isolate each cell involved in the bone remodeling process in in vitro characterizations and experiments to analyze the mechanisms underlying this complex process by using mathematical modeling and statistical tools.–As a first step, this manuscript presents the isolation of osteoblasts in an in vitro characterization and the accompanying cellular automata model that mimics the behaviour of osteoblastics cells.•This paper is truly multi disciplinary approach to understanding the bone formation process. The team includes two biomedical engineers, two statisticians and two mathematical modelers. By taking a multidisciplinary approach, we are able to utilize the strengths of three different areas to better understand the dynamics of bone formation.–One feature that makes this paper unique is the use of statistical methods to validate the cellular autodata model.–The use of statistical tools assess how effectively the mathematical model represents the biological phenomenon provides an innovative way to improve mathematical modeling of highly stochastic biological processes.–We are hoping that making mathematical models more realisticbecomes a trend in mathematics. Bone remodeling is an elegantly orchestrated process by which osteocytes, osteoblasts and osteoclasts function as a syncytium to maintain or modify bone. On the microscopic level, bone consists of cells that create, destroy and monitor the bone matrix. These cells interact in a coordinated manner to maintain a tightly regulated homeostasis. It is this regulation that is responsible for the observed increase in bone gain in the dominant arm of a tennis player and the observed increase in bone loss associated with spaceflight and osteoporosis. The manner in which these cells interact to bring about a change in bone quality and quantity has yet to be fully elucidated. But efforts to understand the multicellular complexity can ultimately lead to eradication of metabolic bone diseases such as osteoporosis and improved implant longevity. Experimentally validated mathematical models that simulate functional activity and offer eventual predictive capabilities offer tremendous potential in understanding multicellular bone remodeling. Here we undertake the initial chal