Bone is much more dynamic than it may appear, constantly undergoing a remodeling process of resorption and new bone formation. Whether or not bone mass is lost through resorption or gained is determined by the balance between osteoclast cells, which carry out bone resorption, and osteoblast cells, which form new bone tissue. The ability of bone to undergo dynamic remodeling is important for regulating calcium and phosphate levels in the body, as well as healing bone fractures and adapting to different mechanical stimuli.^[8]

osteoporosis, which literally means “porous bone”, is caused by an imbalance between osteoblasts and osteoclasts, favoring the bone- resorbing activity of the latter. The risk of such an imbalance greatly increases after about age 50, particularly so in women at the time of menopause. Osteoporosis is a common cause of bone fractures in older adults.^[9]

Since weight-bearing exercise increases mechanical loading on bones, such exercises act as a positive stimulus for increased bone mass. It would follow that obesity might have a similar effect, promoting increased bone mass in response to the higher forces on the skeleton imposed by moving around at a higher body weight. Although some human studies have indicated that bone mass does increase with obesity,^[10] results have been mixed, with other studies finding the opposite effect: a paradoxical decrease in bone mineral density (BMD) and an increase in fracture risk.^[11]

The reason for variation in associations between obesity and BMD across different studies and populations is an ongoing area of research. Animal studies have shed further light on the complex effects of obesity on bones, with one mouse study revealing an increase in bone mass during the early stages of obesity, but impaired bone formation with chronic obesity.^[12] In populations where it occurs, obesity-associated loss of BMD may be partially explained by the effects of obesity on mesenchymal stem cells (MSCs), a stem cell population in bone marrow capable of differentiating into a number of different tissues including muscle, bone (osteoblasts), fat (adipocytes), and cartilage.^[13] Since adipocytes and bone-building osteoblast cells arise from the same MSC progenitor cells, a shift in the differentiation of MSCs to adipocytes causes a reciprocal decrease in the number of osteoblasts.^[14] A change in the balance of osteoblasts to osteoclasts would reduce bone mineral density over time and increase risk of osteoporosis.