Osteoporosis and bone loss

Osteoporosis associated with age-related bone loss is an enormous and growing public health problem, and current approaches to treat osteoporosis with skeletal-specific agents clearly have limitations. As such, there is considerable interest in targeting fundamental aging mechanisms, including cellular senescence, to prevent or treat osteoporosis. There is now considerable evidence that senescent cells accumulate in the bone microenvironment with aging in mice and in humans. Moreover, at least in mice, reducing the burden of senescent cells or inhibiting their proinflammatory senescence-associated secretory phenotype can prevent age-related bone loss. Cellular senescence also appears to play a role in mediating the skeletal fragility associated with diabetes and following radiation or chemotherapy. Thus, targeting senescent cells holds the promise of preventing or treating bone loss associated with a number of conditions while at the same time also ameliorating other age-related comorbidities, including frailty.