Secondary osteoporosis is bone loss caused by an underlying medical condition, medication, or disease, rather than by aging or menopause alone. While most people associate thinning bones with getting older, roughly two-thirds of men with osteoporosis and about one in five women with osteoporosis have a secondary cause driving their bone loss. This distinction matters because identifying and treating the root cause can slow or even reverse the damage in ways that standard osteoporosis treatment alone cannot.
How It Differs From Primary Osteoporosis
Primary osteoporosis is the type most people know about. It develops gradually as part of aging: women lose bone rapidly after menopause when estrogen drops, and men experience a slower decline in bone density over decades. No specific disease is triggering the loss.
Secondary osteoporosis, by contrast, has a clear culprit. Something in the body, whether a hormone disorder, a chronic illness, or a medication, is actively accelerating bone breakdown or blocking the body’s ability to build new bone. It can strike at any age, including in younger adults who wouldn’t normally be at risk. A 30-year-old with celiac disease or a man on long-term steroids can develop fragile bones well before aging would typically play a role.
Endocrine Conditions That Weaken Bone
Hormones regulate the constant cycle of bone being broken down and rebuilt, so disorders of the endocrine system are among the most common secondary causes.
Overactive parathyroid glands pull calcium out of bones and into the bloodstream. This condition is relatively common, affecting about 233 per 100,000 women and 85 per 100,000 men, and it typically shows up after age 50. Cushing syndrome, where the body produces too much cortisol, speeds up bone breakdown while simultaneously reducing new bone formation, a double hit. Hyperthyroidism has long been recognized as destructive to bone; unchecked, it can make bones appear porous and fragile. Early menopause, meaning loss of ovarian function before age 40, removes the protective effect of estrogen years ahead of schedule, leaving bones vulnerable during what should be peak bone-health years.
Diabetes also plays a role, though differently depending on type. People with type 1 diabetes face a 3-fold increased risk of fractures overall and a 7-fold increased risk of hip fracture compared with the general population. Type 2 diabetes raises fracture risk as well, though more modestly, likely through changes in bone quality rather than bone density alone.
Chronic Inflammatory and Lung Diseases
Chronic inflammation is corrosive to bone. In rheumatoid arthritis, nearly one-third of patients develop osteoporosis, and their rate of fragility fractures is almost double that of people the same age without the condition. The inflammatory molecules that drive joint pain also stimulate the cells that break down bone.
Lung diseases carry a surprisingly high bone cost. About one-third of people with COPD worldwide have osteoporosis, driven by inflammation, reduced physical activity, low body weight, and the frequent use of steroid inhalers or oral steroids. Cystic fibrosis causes both softening and thinning of bone, leading to high rates of spinal and other fractures.
Gut Diseases and Malabsorption
Your bones depend on a steady supply of calcium and vitamin D absorbed through the gut. When digestive diseases interfere with that absorption, bones pay the price.
Celiac disease is a prime example. Damage to the intestinal lining reduces calcium absorption, which triggers the parathyroid glands to compensate by pulling calcium from bone. At the same time, celiac disease raises levels of inflammatory molecules that accelerate bone breakdown. Inflammatory bowel disease, whether Crohn’s or ulcerative colitis, creates a similar combination of malabsorption and chronic inflammation that significantly raises osteoporosis and fracture risk.
Chronic liver disease, including hepatitis B and C, is another overlooked cause. Patients awaiting liver transplants have notably high rates of osteoporosis and fractures. Gastric bypass surgery deserves mention here too: surgical techniques that bypass portions of the intestine lead to calcium and vitamin D deficiency, triggering the same chain reaction of parathyroid overactivity and accelerated bone loss.
Medications That Cause Bone Loss
Several widely prescribed drug classes can thin bones, sometimes at surprisingly low doses.
Glucocorticoids (Steroids)
Steroid medications like prednisone are the single most common drug-related cause of secondary osteoporosis. Between 30% and 50% of people on long-term steroids develop fractures. The risk begins at very low doses: even 2.5 mg of prednisone daily is associated with increased spinal fracture risk. At 10 mg daily for more than 90 days, the risk of spinal fractures jumps 17-fold and hip fractures increase 7-fold.
Steroids damage bone through three mechanisms at once. They extend the lifespan of the cells that break bone down, they kill the cells embedded within bone that sense damage and signal for repairs, and they reduce the production of new bone-building cells. This is why fractures from steroid use often happen before a bone density scan shows significant decline. The bone’s internal quality deteriorates before its overall density drops.
Acid-Reducing Medications (PPIs)
Proton pump inhibitors, commonly taken for acid reflux, carry a modest but real risk when used long-term. Short-term use shows no increased fracture risk, but after more than a year of continuous use, the odds of hip fracture rise by 20% to 62%, and vertebral fracture risk increases by 40% to 60%. After seven or more years of use, fracture risk climbs substantially higher. The likely mechanism involves reduced calcium absorption in a less acidic stomach environment.
Anti-Seizure Medications
All classes of anti-seizure drugs are associated with bone loss, roughly doubling the overall fracture risk. Older medications like phenytoin, phenobarbital, and carbamazepine are particularly harmful because they speed up the breakdown of vitamin D in the liver, reducing calcium uptake and setting off the same parathyroid-driven bone loss seen in gut diseases. Even newer anti-seizure drugs that don’t affect vitamin D still contribute to bone loss through other pathways.
Who Gets Screened and How
Secondary osteoporosis should be suspected whenever bone loss is more severe than expected for someone’s age, when fractures occur without significant trauma, or when osteoporosis appears in a younger person. Men with osteoporosis and premenopausal women with low bone density are particularly likely to have a secondary cause.
The initial screening typically involves blood tests for calcium, phosphate, vitamin D levels, parathyroid hormone, thyroid function, and liver and kidney function, along with a complete blood count. If calcium or parathyroid hormone levels come back abnormal, a 24-hour urine calcium collection helps pinpoint the problem.
For people with severe osteoporosis, meaning multiple fractures or a bone density T-score below -3.0, without an obvious explanation, additional testing looks for less common causes. This can include screening for blood cancers, celiac disease, abnormal sex hormone levels, and excess cortisol production.
How Secondary Osteoporosis Is Managed
The most important step is addressing whatever is causing the bone loss. For someone with undiagnosed celiac disease, adopting a strict gluten-free diet restores intestinal absorption and allows bone to recover. For hyperparathyroidism, correcting the overactive gland stops the calcium drain. For someone on long-term steroids, reducing the dose or switching medications when possible removes the primary driver of bone damage.
In many cases, treating the underlying cause alone isn’t enough. Bone that has already been lost needs active rebuilding. Calcium and vitamin D supplementation form the baseline, particularly for people with malabsorption or documented deficiencies. Bone-specific medications that slow breakdown or stimulate new bone growth are often added, especially when fracture risk is high or bone density is severely reduced.
The outlook for secondary osteoporosis is generally more favorable than for primary osteoporosis, precisely because there’s a treatable cause. When the underlying condition is identified early and managed well, bone density often stabilizes and can partially recover. The challenge is that secondary causes frequently go unrecognized, particularly in men and younger adults, where osteoporosis isn’t always on the radar. Anyone diagnosed with osteoporosis before age 50, or who fractures a bone from a minor fall, benefits from a thorough workup to rule out a secondary cause.