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Over the years, numerous mechanisms have been identified through which homocysteine affects osteoblast functioning. These include alterations in collagen structure, epigenetic modifications and changes in RANKL-OPG production by osteoblasts. These mechanisms are reviewed in this chapter. We have also herein discussed how homocysteine affects osteocyte behavior. With onset of hyperhomocysteinemia induction of osteocyte 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.

How Homocysteine Modulates the Function of Osteoblasts and Osteocytes