The pathophysiology of CN is not yet completely understood, although it is associated with an activation of inflammation processes and bone remodeling markers [11], the disruption of the osteoblast and osteoclast system [12], the activation of the receptor activator of nuclear factor-kappa B ligand (RANKL) system and its antagonist osteoprotegerin (OPG) [13,14], and often stress fractures due to physical activity [15]. This evidence concerns the gene TNFSF11 and cyclic hematopoiesis.