Three-phase Model for Crack Behavior in Functionalized Carbon Nanotube Reinforced Bone Tissue
نویسندگان
چکیده
INTRODUCTION Due to the extraordinary mechanical properties of CNTs, hydroxyapatite (HAp) precipitation on functionalized carbon nanotubes (f-CNTs) suggests using CNTs as reinforcing scaffolds, in order to obtain a mechanically enhanced bone tissue. Moreover, deposition and regeneration of bone mineral phase is enhanced by the help of f-groups on CNT surface/head, even in the absence of the organic component (i.e. collagen fibers) [1]. As discussed in [2], the carboxyl (COOH) f-group contributes to the attachment of calcium and phosphate ions to the CNT through ionic interactions, forming the HAp nanoparticles on the CNT scaffold. The f-site also takes part in the reinforcing mechanism and load transfer from the HAp matrix to the CNT, giving rise to a mechanically improved artificial bone tissue. In addition, the presence of CNTs also enhances the fracture properties in the bone matrix, by decreasing the tendency of microcracks to grow/propagate when exposed to the CNT stiff inclusion(s) [3]. By its nature, bone is in direct relation with the applied mechanical loads, and its living functions depend on the external mechanical stimuli. The improvement of the mechanical response of the proposed synthetic bone may be promising from the view point of engineering a stronger, stiffer bone tissue for implantation or as a cure to diseases such as osteoporosis. However, alterations in the mechanical behavior of this new bone tissue can have a definite impact on its mechanical and living functions (e.g., the rate of the bone remodeling process, which ultimately dictates the mechanical properties of the bone tissue) [4]. In this study, a 2D model is developed to look at the interactions between a crack and an fCNT inclusion in the HAp matrix. The objective is to observe the effect of elastic property mismatch on crack behavior and its influence on the microcracking mechanism which is hypothesized to be a toughening mechanism in living bone that is responsible for stimulating bone remodeling [5].
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