Recent evidence demonstrates that tobacco smoking causes an imbalance in bone turnover, leading to lower bone mass and making bone vulnerable to osteoporosis and fracture. Tobacco smoke influences bone mass indirectly through alteration of body weight, parathyroid hormone-vitamin D axis, adrenal hormones, sex hormones, and increased oxidative stress on bony tissues. Also, tobacco smoke influences bone mass through a direct effect on osteogenesis and angiogenesis of bone. A RANKL-RANK-OPG pathway is an essential regulatory pathway for bone metabolism and its importance lies in its interaction with most of the pathophysiologic mechanisms by which smoking influences bone mass. Both first- and secondhand smoke adversely affect bone mass; smoking cessation seems to reverse the effect of smoking and improve bone health. Recent advances in research on bone turnover markers could advance scientific knowledge regarding the mechanisms by which smoking may influence bone mass.