Indeed, both oxidative stress and inflammation can be involved in the development of osteoporosis by preventing the differentiation of osteoblasts, inducing the differentiation and activity of osteoclasts, enhancing apoptotic osteocytes, and increasing the expression of RANKL and the RANKL/OPG-ratio [24,25,26,27,28]. This evidence concerns the gene TNFSF11 and osteoporosis.