Interstitial fluid velocity is decreased around cortical bone vascular pores and depends on osteocyte position in a rat model of disuse osteoporosis.

Muscle paralysis induced with botulinum toxin (Botox) injection increases vascular porosity and reduces osteocyte lacunar density in the tibial cortical bone of skeletally mature rats. These morphological changes potentially affect interstitial fluid flow in the lacunar-canalicular porosity, which is thought to play a role in osteocyte mechanotransduction. The aim of this study was to investigate the effects of disuse-induced morphological changes on interstitial fluid velocity around osteocytes in the bone cortex.

Botox-induced muscle paralysis alters intracortical porosity and osteocyte lacunar density in skeletally mature rats.

Reduced mechanical loading can lead to disuse osteoporosis, resulting in bone fragility. Disuse models report macroscopic bone loss due to muscle inactivity and immobilization, yet only recently has there been quantification of the effects of disuse on the vascular pores and osteocyte network, which are believed to play an important role in mechanotransduction via interstitial fluid flow. The goal of this study was to perform a high-resolution analysis of the effects of muscle inactivity on intracortical porosity and osteocyte lacunar density in skeletally mature rats.

The effects of estrogen deficiency on cortical bone microporosity and mineralization.

Recent studies have demonstrated matrix-mineral alterations in bone tissue surrounding osteocytes in estrogen-deficient animals. While cortical bone porosity has been shown to be a contributor to the mechanical properties of bone tissue, little analysis has been done to investigate the effects of estrogen deficiency on bone's microporosities, including the vascular and osteocyte lacunar porosities. In this study we examined alterations in cortical bone microporosity, mineralization, and cancellous bone architecture due to estrogen deficiency in the ovariectomized rat model of postmenopausal osteoporosis.

Microstructural changes associated with osteoporosis negatively affect loading-induced fluid flow around osteocytes in cortical bone.

Loading-induced interstitial fluid flow in the microporosities of bone is critical for osteocyte mechanotransduction and for the maintenance of tissue health, enhancing convective transport in the lacunar-canalicular system. In recent studies, our group has reported alterations of bone's vascular porosity and lacunar-canalicular system microarchitecture in a rat model of postmenopausal osteoporosis. In this work, poroelastic finite element analysis was used to investigate whether these microstructural changes can affect interstitial fluid flow around osteocytes.

Lactation-Induced Changes in the Volume of Osteocyte Lacunar-Canalicular Space Alter Mechanical Properties in Cortical Bone Tissue.

Osteocytes can remove and remodel small amounts of their surrounding bone matrix through osteocytic osteolysis, which results in increased volume occupied by lacunar and canalicular space (LCS). It is well established that cortical bone stiffness and strength are strongly and inversely correlated with vascular porosity, but whether changes in LCS volume caused by osteocytic osteolysis are large enough to affect bone mechanical properties is not known. In the current studies we tested the hypotheses that (1) lactation and postlactation recovery in mice alter the elastic modulus of bone tissue, and (2) such local changes in mechanical properties are related predominantly to alterations in lacunar and canalicular volume rather than bone matrix composition.