Osteocyte mechanotransduction: changes with age - a parametric finite element study

Abstract

The nature of bone is to adapt its structure in response to mechanical loading. When the bone is loaded, it is remodeled to be able to support the increased loads. Bone resorption can occur resulting in bone loss from lack of mechanical loading. Bone adaptation is controlled by: (1) osteoclasts, which resorb bone, (2) osteoblasts, which lay down new bone, and (3) osteocytes, which send signals of bone remodeling. Studies have shown that in the absence of mechanical loading, osteocytes send signals of bone resorption. Understanding the microarchitecture of bone is essential to understanding the mechanotransduction within the osteocyte network. The purpose of this study was to analyze the effect of age on the microarchitecture of murine bone and use the data to conduct a finite element analysis of strains imposed on the lacuna. Ten murine femur bone samples were studied; 5 old (2-years-old), and 5 young (5-months-old). Each sample was resin-embedded, acid etched according to protocol, and imaged. ImageJ was utilized to quantitatively assess changes in the number of canaliculi, the diameter of the canaliculi, lacunar size, and lacunar density. The total number of canaliculi per osteocyte decreased with age, specifically in the periosteal region. A greater number of canaliculi were found in the periosteal region than the endosteal region of the young samples. The canalicular diameter increased with age, specifically in the periosteal region from young to old. In the old samples the canalicular diameter decreased from the periosteal region to the endosteal region. The lacunar size decreased in the periosteal region from young to old. It also decreased across the young sample with larger lacuna in the periosteal region. The lacunar density increased with age. The finite element analysis revealed strain amplification factors of 2.19 for the young, young endosteal, and young periosteal models. The finite element analysis revealed strain amplification factors of 2.15, 1.89, and 2.10 for the old model, the old endosteal, and the old periosteal models, respectively. The lower strains predicted in the old bone compared to the young bone may be responsible for the well-known resistance to loading that occurs with aging.