Osteoporosis is characterized by low bone mineral density and the structural deterioration of bone tissue, making bones porous and fragile. This fragility significantly increases the risk of fractures, often from minor trauma or simply from a fall. While aging and hormonal changes are common factors, many people develop secondary osteoporosis due to necessary medical treatments. Certain medications, while treating one serious condition, can inadvertently interfere with the body’s natural process of bone maintenance. Understanding which drugs disrupt bone health is the first step toward prevention.
The Highest Risk: Glucocorticoids and Steroids
Glucocorticoid medications, such as prednisone, cortisone, and dexamethasone, are the single most frequent cause of drug-induced bone loss. These powerful anti-inflammatory drugs manage conditions including rheumatoid arthritis, asthma, inflammatory bowel disease, and various autoimmune disorders. The resulting bone disease is formally known as Glucocorticoid-Induced Osteoporosis (GIOP).
The risk of bone loss relates directly to the dose and duration of the steroid treatment. Significant loss can begin within the first three to six months of therapy, making early monitoring crucial. Fracture risk is present even at low doses, such as 2.5 milligrams of prednisolone per day, and increases substantially with daily doses of 5 milligrams or more taken for three months or longer. This rapid initial bone loss predominantly affects the trabecular bone found in the spine, leading to vertebral compression fractures.
Other Medications That Affect Bone Density
Several other widely prescribed drug classes carry a risk of secondary osteoporosis. Hormonal therapies used to suppress sex hormones significantly impact bone density. Gonadotropin-releasing hormone (GnRH) agonists, used for prostate cancer, breast cancer, or endometriosis, induce a state of sex hormone deficiency. Since estrogen and testosterone regulate bone health, their suppression accelerates bone turnover and increases fracture risk.
Proton Pump Inhibitors (PPIs), common medications for acid reflux and ulcers like omeprazole and lansoprazole, are associated with increased fracture risk with long-term use. One proposed mechanism is that reducing stomach acid impairs the body’s ability to absorb dietary calcium. This triggers a hormonal response that pulls calcium from the bones to maintain blood levels.
Anticonvulsant medications, particularly older agents like phenytoin and carbamazepine, interfere with the body’s vitamin D metabolism. These drugs induce liver enzymes that accelerate the breakdown of active vitamin D into inactive metabolites. Because vitamin D is necessary for intestinal calcium absorption, this deficiency compromises bone mineralization and strength.
Selective Serotonin Reuptake Inhibitors (SSRIs), a frequent treatment for depression and anxiety, have been linked to lower bone mineral density and increased fracture risk. The mechanism is complex, but bone cells have serotonin receptors. Research suggests the drug’s effect on serotonin signaling may reduce bone formation.
Other immunosuppressants used after organ transplantation, such as cyclosporine and tacrolimus, also contribute to accelerated bone loss. This often occurs in combination with steroid therapy.
Understanding Drug-Induced Bone Loss
The skeleton is a dynamic structure constantly undergoing remodeling, a balance between building new bone and breaking down old bone. This process involves two cell types: osteoblasts, responsible for formation, and osteoclasts, responsible for resorption. In a healthy individual, the activity of these cells is tightly coupled to maintain skeletal integrity.
Certain medications disrupt this balance, leading to a net loss of bone mass. Drugs like glucocorticoids create a double negative effect by decreasing the function of bone-building osteoblasts while increasing the activity of bone-resorbing osteoclasts. This rapid shift favoring breakdown causes severe bone loss.
Other medications interfere with the body’s ability to utilize raw materials for bone building. For example, anti-seizure medications increase the metabolism of vitamin D, removing the active form from circulation. Without sufficient active vitamin D, the intestines cannot properly absorb calcium from the diet, creating a mineral deficit that the body corrects by dissolving existing bone.
Monitoring and Protecting Bone Health
Individuals taking medications known to affect bone density should work closely with their healthcare team to mitigate fracture risk. The first step involves regular bone mineral density (BMD) testing, typically using a Dual-Energy X-ray Absorptiometry (DXA) scan. This test establishes a baseline and monitors the rate of bone loss, allowing for timely intervention.
Lifestyle adjustments are a key protective strategy. Ensuring adequate intake of calcium and vitamin D, through diet or supplementation, provides the necessary materials for bone maintenance. Weight-bearing and muscle-strengthening exercises, such as walking or lifting weights, mechanically stimulate bone formation and help preserve mass.
In high-risk cases, such as with long-term glucocorticoid use, a bone-preserving medication may be prescribed alongside the high-risk drug. These medications, such as bisphosphonates or anabolic agents, counteract the bone-depleting effects of the primary treatment. The goal is to maximize the benefit of the primary medication while protecting the skeleton from known side effects.