Abstract
The present study aimed to investigate the role of magnitude in adaptive response of osteoblasts exposed to compressive stress. Murine primary osteoblasts and MC3T3-E1 cells were exposed to compressive stress (0, 1, 2, 3, 4, and 5 g/cm2) in 3D culture. Cell viability was evaluated, and expression levels of Runx2, Alp, Ocn, Rankl, and Opg were examined. ALP activity in osteoblasts and TRAP activity in RAW264.7 cells co-cultured with MC3T3-E1 cells were assayed. Results showed that compressive stress within 5.0 g/cm2 did not influence cell viability. Both osteoblastic and osteoblast-regulated osteoclastic differentiation were enhanced at 2 g/cm2. An increase in stress above 2 g/cm2 did not enhance osteoblastic differentiation further but significantly inhibited osteoblast-regualted osteoclastic differentiation. This study suggested that compressive stress regulates osteoblastic and osteoclastic differentiation through osteoblasts in a magnitude-dependent manner.
Highlights
The present study aimed to investigate the role of magnitude in adaptive response of osteoblasts exposed to compressive stress
A previous study reported that a compressive stress of 1.0 g/cm[2] is optimal for osteoblastic differentiation[13], but another study observed enhanced osteoblastic differentiation when compression was raised from 2.0 g/cm[2] to 4.0 g/cm[2 11]
After application of compressive stress, the collagen gels containing cells were submerged into α-minimal essential medium (αMEM) containing 10% fetal bovine serum (FBS)
Summary
The present study aimed to investigate the role of magnitude in adaptive response of osteoblasts exposed to compressive stress. Results showed that compressive stress within 5.0 g/cm[2] did not influence cell viability Both osteoblastic and osteoblastregulated osteoclastic differentiation were enhanced at 2 g/cm[2]. By inducing bone resorption around the roots, vertical compressive stress can intrude teeth into sockets, and horizontal compressive stress leads to teeth movement. Deguchi et al found that compressive stress enhances the osteogenesis of cortical bone around miniscrews and the miniscrew-bone contact rate[7] These findings suggested that compressive stress may regulate activities of both osteoblast and osteoclast. In vitro studies showed contradictory results on the responses under compressive stress: inhibited/enhanced osteoblastic differentiation and inhibited/enhanced osteoblast-regulated osteoclastic differentiation have both been reported[9,10,11,12]. Magnitude may be one of the parameters that determine the role of mechanical stress in bone remodeling
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