PTH may directly affect the
response of bone cells to mechanical stimulation, but it may also affect the
perception of mechanical stimuli in vivo. Continuously elevated levels of PTH cause osteocytic osteolysis [
71], thereby affecting the architecture of the lacunacanalicular system that forms the niche for the osteocytes embedded within the bone matrix. Altered lacunar shape alters the quantity of local strains occurring around the osteocytes during daily activities and exercise, as outlined elsewhere in this issue, thereby effectively altering the height of the mechanical stimulus experienced by osteocytes [
72]. Thus, dietary components that alter osteocyte lacunar shape will most likely interact with mechanotransduction by osteocytes. Regarding matrix strains transduced to osteocytes, dietary components that significantly alter the mineralization of the bone matrix, thereby rendering it more stiff or compliant, will theoretically affect the amount of strain elicited on osteocytes. Dietary components that significantly alter the mineralization of the bone matrix could also affect the ability of osteocytes to maintain an unmineralized layer of matrix surrounding their cell fingers. It is generally assumed that this layer is essential for the transmission of mechanical signals, since loading-induced shifts in interstitial fluid through the canaliculi wherein the osteocyte cell extensions reside is considered an important amplification mechanism for mechanical signals exerted on bone [
17]. Factors produced by osteoblasts and osteocytes that affect mineralization include osteocalcin (OC) and matrix GLA protein (MGP). MGP has been found in bone, dentine, cartilage, and soft tissue, including blood vessels, and is associated with the organic matrix and mobilization of calcium. Animal studies show that MGP prevents the calcification of soft tissue and cartilage while facilitating normal bone growth and development. The synthesis of OC and MGP is regulated by calcitriol, retinoic acid, vitamin K, and vitamin D [
73]. In addition, it was shown that feeding rats olive extract at 250 mg per day for 12 months increases serum osteocalcin [
74]. Whether this also affects matrix mineralization and transmission of mechanical loads towards the osteocytes is unknown. Matrix mineralization is definitely affected by retinol intake in mice, at least under extreme conditions of disturbed matrix mineralization [
75]. X-linked hypophosphatemic rickets is caused by inactivation of the PHEX gene. Phex is expressed by very late differentiated osteoblasts and early osteocytes in mice and humans, while it is exclusively expressed by osteocytes in chickens [
16]. Feeding mice with a mutant PHEX gene, a retinol-free diet results in a partial rescue of growth plate and bone mineralization defects, while the amount of non-mineralized bone matrix is reduced more than 70%, showing the impact of retinol on the cell-autonomous mineralization defect of Phex-deficient osteoblasts [
75]. Whether retinol in the diet will have a similar effect on matrix mineralization in otherwise healthy humans remains to be seen. Taken together, vitamin D may affect the transmission of mechanical signals to osteocytes if it affects lacuna shape, but whether any other dietary component will affect transmission of mechanical signals is uncertain.