Table 1.
Pharmacologic treatment options for bone health optimization.
Class | Agent | Brand Name | Mechanism of Action |
---|---|---|---|
Vitamin and mineral supplements | Calcium | N/A | The main mineral component of bone. Forms calcium salts (mostly calcium phosphate) by osteoblasts which harden cartilaginous bone matrices and thus bone building |
Vitamin D | N/A | Activates intestinal absorption of calcium and maintaining calcium homeostasis | |
Antiresorptive agents | Bisphosphonates | Reclast, Boniva, Fosamax, Zoneta, Actonel Aclasta | Inhibits osteoclast function, thus allowing osteoblasts to more efficiently build bone mass |
Anabolic agents | Denosumab | Prolia | Monoclonal antibody that inhibits receptor activator of nuclear factor kappa-B ligand (RANKL), resulting in decreased osteoclast development |
Romosozumab | Evenity | Monoclonal antibody that binds and inhibits sclerostin, a protein secreted by osteocytes that inhibits osteoblast function increases RANKL which activates osteoclasts (PMID: 30775535). Thus, romosozumab is unique in that it increases bone formation and decreases bone resorption | |
Parathyroid hormone (PTH) analogs | Teriparatide | Forteo | Regulates calcium and phosphate metabolism in bone and the kidneys. Counterintuitively increases bone resorption, thus resulting in increased serum calcium levels. However, low-dose and intermittent exposure (i.e., once daily) disproportionately activate osteoblasts with increased serum calcium more than osteoclast function, thus having a net effect of increased bone mineral density |
Abaloparatide | Tymlos | Similar to teriparatide, but with different pharmacokinetics that may confer some advantages in bone mineral density improvements |