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Glucocorticoid-Induced Osteoporosis – Causes & Treatment

Glucocorticoid-induced osteoporosis is a loss of bone density caused by long-term use of glucocorticoids. It significantly increases the risk of fractures, especially of the spine and hip.

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Things worth knowing about "Glucocorticoid-induced osteoporosis"

Glucocorticoid-induced osteoporosis is a loss of bone density caused by long-term use of glucocorticoids. It significantly increases the risk of fractures, especially of the spine and hip.

What is Glucocorticoid-Induced Osteoporosis?

Glucocorticoid-induced osteoporosis (GIOP) is a form of bone loss caused by long-term or high-dose use of glucocorticoids (also known as corticosteroids or steroids). Glucocorticoids are widely prescribed for inflammatory conditions such as rheumatoid arthritis, asthma, Crohn's disease, and lupus. While they are highly effective therapeutically, prolonged use significantly disrupts bone metabolism and leads to a reduction in bone density.

GIOP is the most common form of drug-induced osteoporosis and poses a serious health risk, as it greatly increases the likelihood of fractures – particularly of the vertebrae and the hip.

Causes and Mechanisms

Glucocorticoids affect bone metabolism through several pathways:

Inhibition of osteoblasts: Glucocorticoids reduce the activity and lifespan of bone-forming cells (osteoblasts), resulting in decreased new bone formation.
Promotion of osteoclast activity: At the same time, bone resorption by bone-degrading cells (osteoclasts) is indirectly increased.
Impaired calcium absorption: Glucocorticoids reduce intestinal calcium absorption and increase urinary calcium excretion, leading to a calcium deficiency.
Hormonal imbalance: They suppress sex hormones such as estrogen and testosterone, which normally have a protective effect on bone.
Muscle wasting: Glucocorticoids promote muscle breakdown, reducing the mechanical load on bones and increasing the risk of falls.

The extent of bone loss depends on the dose, duration, and route of administration of glucocorticoids. Even low doses can damage bone when taken over a long period.

Risk Factors

Certain factors increase the likelihood of developing GIOP:

Long-term glucocorticoid therapy (more than 3 months)
Daily dose exceeding 5 mg prednisolone equivalent
Older age
Female sex, especially after menopause
Pre-existing low bone density
Calcium and vitamin D deficiency
Physical inactivity and low body weight
Smoking and excessive alcohol consumption
Family history of osteoporosis

Symptoms

In its early stages, glucocorticoid-induced osteoporosis is often asymptomatic. Symptoms typically only become apparent once bone density has significantly decreased or a fracture has occurred:

Back pain, often caused by vertebral fractures
Loss of height and spinal curvature (kyphosis or dowager's hump)
Fractures occurring with minimal trauma (low-energy fractures)
Generalized skeletal pain

Diagnosis

The diagnosis of GIOP typically involves several assessments:

Bone density measurement (DXA): Dual-energy X-ray absorptiometry measures bone mineral density at the spine and hip.
Laboratory tests: Blood and urine tests to assess calcium, vitamin D, hormonal status, and bone turnover markers.
X-ray or MRI: Used when vertebral fractures are suspected.
Fracture risk assessment: The FRAX calculator estimates the individual 10-year probability of a major osteoporotic fracture.

Treatment and Prevention

General Measures

Once long-term glucocorticoid therapy is initiated, preventive strategies should be started promptly:

Calcium and vitamin D supplementation (recommended daily intake: 1000–1200 mg calcium and 800–1000 IU vitamin D)
Regular physical activity, especially strength and balance training
Calcium-rich diet (dairy products, leafy green vegetables)
Avoidance of smoking and excessive alcohol consumption
Fall prevention measures in daily life

Pharmacological Treatment

When fracture risk is elevated or osteoporosis is already present, specific medications are used:

Bisphosphonates (e.g., alendronate, zoledronic acid): First-line therapy to inhibit bone resorption.
Denosumab: A monoclonal antibody that inhibits bone breakdown, used when bisphosphonates are not tolerated.
Teriparatide: A bone-building agent (PTH analogue) for patients at very high fracture risk.
Hormone replacement therapy: In selected postmenopausal women.

Adjusting Glucocorticoid Therapy

Wherever possible, the glucocorticoid dose should be reduced to the lowest effective level or switched to an alternate-day regimen. Steroid-sparing agents (such as methotrexate or azathioprine) may also be used to reduce the need for glucocorticoids.

References

Buckley L et al.: 2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis. Arthritis & Rheumatology, 2017.
Compston J: Glucocorticoid-induced osteoporosis: an update. Current Rheumatology Reports, 2020.
Reid IR, Horne AM: Glucocorticoid-induced osteoporosis. In: Harrison's Principles of Internal Medicine, 21st edition, McGraw-Hill, 2022.

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