INTRODUCTION
Osteoporosis is a systemic skeletal disease characterized by decreased bone formation by osteoblasts with increased osteo-clastic bone resorption.1 Unlike postmenopausal osteoporosis, which occurs due to a sudden withdrawal of circulating estrogens leading to markedly increased osteoclast bone resorption, aging affects both osteoclast and osteoblast lineages. Aging-related bone loss was associated with increased osteoclastogenesis2 and altered the conditions that may facilitate the differentiation of mesenchymal stem cells into adipocytes and possibly reduce osteoblast differentiation.3–4 Therefore, novel and improved therapies are critically needed to target osteoclast activity more efficiently without affecting osteoblasts' function.