SOURCE: Corrado A, et al. Osteoblast as a target of anti-osteoporotic treatment. Postgrad Med 2017;129:858-865.
In healthy bones, osteoclast activity is balanced with osteoblast activity to produce a continuing stream of freshly created bone by degradation of aging bone and replacement with new bone. After attainment of the peak level of mature bone in early adulthood, osteoclast activity modestly exceeds osteoblast activity, leading to a gradual decline in bone mineral density that we call age-related bone loss to distinguish it from the more rapid bone loss seen at menopause (regardless of age) due to estrogen loss that characteristically outpaces simple age-related bone loss.
Most pharmacologic interventions currently in use for treatment or prevention of osteoporosis rely on osteoclast inhibition to enhance (or at least maintain) bone mineral density. In contrast, teriparatide primarily works by stimulation of osteoblasts. Estrogen also produces some positive activity on osteoblasts, such as inhibition of osteoblast apoptosis. Finally, even though the primary mechanism of bisphosphonates is inhibition of osteoclastic activity, even this pharmacologic class produces some favorable effects on osteoblasts.
One additional class of pharmacologic agent has shown promising effects: The anti-sclerostin antibody agent romosozumab provides both stimulation to osteoblasts and diminution of osteoclast activity. This agent is pending FDA approval.