How Homocysteine Modulates the Function of Osteoblasts and Osteocytes

Abstract

Over the years, numerous mechanisms have been identified through which homocys - teine affects osteoblast functioning. These include alterations in collagen structure, epi genetic modifications and changes in RANKL-OPG production by osteoblasts. These mechanisms are reviewed in this chapter. We have also herein discussed how homocys teine affects osteocyte behavior. With onset of hyperhomocysteinemia induction of osteo - cyte specific genes particularly the mineralization genes like Dmp1 and Sost is facilitated producing untoward mineralization, osteocyte apoptosis, deviations from regular bone remodeling process and onset of targeted remodeling in bone. These modifications have immense effect on the overall mechanical stability of bone. Homocysteine thus represents an independent risk factor for bone fragility. parathyroid hormone, growth hormone, thyroid hormones, glucocorti -coids, bone morphogenetic proteins, prostaglandins, sex hormones, various cytokines and the molecular triad comprising of OPG (osteoprotegerin), receptor activator of nuclear factor-κB ligand (RANKL) and receptor activator of nuclear factor-κB (RANK). The cells involved in the process are osteoblasts, osteoclasts, osteocytes, immune cells, megakaryocytes and osteomacs. suggested a 3 levels) homocysteine levels. conclusions that cbs is a primary 1,25(OH) 2 D 3 target gene which renders homocysteine metabolism responsive to 1,25(OH) 2