on June 23, 2026
Osteoporosis is often thought of as an inevitable consequence of aging or menopause. In fact, a significant proportion of cases are not caused solely by age or physiology, but represent a condition known as secondary osteoporosis, that is, a reduction in bone strength due to medical conditions or medication use.
Recognizing secondary osteoporosis is essential because the most effective treatment does not always involve adding an anti-osteoporosis therapy, but rather identifying and addressing the underlying cause whenever possible.
The most common causes include certain long-term treatments, particularly corticosteroids, endocrine therapies for cancer, and other medications that can interfere with the delicate balance of bone remodeling.
Understanding these mechanisms helps patients take a more informed part in treatment decisions and improves long-term adherence.
What is secondary osteoporosis?
Secondary osteoporosis is a condition in which reduced bone strength can be attributed to an identifiable cause.
The conditions most commonly associated with it include:
- chronic medication use;
- endocrine disorders;
- chronic inflammatory diseases;
- gastrointestinal disorders causing malabsorption;
- kidney disease;
- cancer;
- prolonged immobilization;
- nutritional deficiencies.
International guidelines recommend a full diagnostic evaluation to rule out secondary causes before starting specific osteoporosis treatment.
Bone is a dynamic organ: why some medications affect it
Bone tissue is continuously remodeled through the coordinated activity of:
- osteoblasts (bone formation);
- osteoclasts (bone resorption).
Many medications disrupt this balance by:
- reducing the formation of new bone tissue;
- increasing bone resorption;
- altering muscle function;
- changing calcium metabolism;
- interfering with the endocrine system.
Over the long term, this can increase the risk of skeletal fragility.
Corticosteroids: the most common medication-related cause of secondary osteoporosis
Glucocorticoids are among the best-documented causes of drug-induced osteoporosis.
Commonly used examples include:
- Prednisone
- Prednisolone
- Methylprednisolone
These medications are prescribed for many conditions:
- autoimmune diseases;
- respiratory diseases;
- chronic inflammatory diseases;
- immunosuppressive therapy.
How they affect bone
Corticosteroids can:
- reduce osteoblast activity;
- increase bone resorption;
- decrease intestinal calcium absorption;
- increase urinary calcium loss;
- promote muscle loss and reduced physical activity.
Fracture risk increases early and can become clinically significant within the first few weeks of treatment.
International guidelines recommend assessing bone health risk in advance for patients being considered for long-term treatment.
Cancer endocrine therapies and bone health
Some cancer treatments can cause an accelerated loss of bone mass.
Breast cancer and aromatase inhibitors
Frequently used drugs:
- Anastrozole
- Letrozole
- Exemestane
These therapies reduce estrogen production.
Since estrogens play a central role in maintaining bone remodeling, their decline accelerates the loss of mineral density.
Prostate cancer and androgen deprivation
Drugs used:
- Leuprorelin
- Goserelin
- Bicalutamide
The reduction of androgens affects:
- muscle mass;
- body composition;
- bone metabolism.
For this reason, the assessment of skeletal health is now an integral part of oncological management.
Other drugs associated with bone loss
The literature has identified further pharmacological classes associated with alterations in bone metabolism:
- some anticonvulsants;
- excess thyroid replacement hormones;
- some immunosuppressants;
- some proton pump inhibitors used chronically;
- some antidepressants;
- antiandrogen treatments.
This association does not necessarily imply the development of osteoporosis but requires individual assessment.
Antiresorptive therapies: benefits and possible side effects
Antiresorptive therapies are one of the cornerstones of fracture prevention in high-risk patients.
Among the most commonly used:
- Alendronate
- Risedronate
- Zoledronic acid
- Denosumab
Evidence shows a significant reduction in fracture risk in selected patients.
Atypical femoral fractures
They are rare events.
The risk is especially high with very prolonged treatments and is assessed individually by the doctor.
For some patients, a periodic reassessment of therapeutic necessity may be considered.
Osteonecrosis of the jaw
It is a rare complication.
The risk is much higher in cancer patients treated with high doses compared to patients treated for osteoporosis.
Preventive dental management is a useful measure.
Pain in osteoporosis: it does not always depend on the bone
An often underestimated aspect is that chronic pain does not always correlate with bone density.
Factors that may contribute:
- osteoarthritis;
- muscular alterations;
- microtrauma;
- joint stiffness;
- reduced physical activity.
Therefore, therapeutic success does not necessarily coincide with a rapid reduction in symptoms.
Is there a role for complementary approaches?
Complementary interventions can be considered as integrated and non-substitutive support.
Therapeutic physical activity
The strongest evidence concerns:
- resistance exercise;
- strength training;
- balance exercises.
Acupuncture
It can help control musculoskeletal pain in some patients, but it does not replace osteoporosis treatment.
Nutrition and phytotherapy
Some plants have been studied for their content of:
- silicon;
- polyphenols;
- minerals.
However, clinical evidence remains limited and does not allow for specific therapeutic indications for the treatment of osteoporosis.
Communication and adherence: an essential part of care
One of the main problems in the management of osteoporosis is early discontinuation of therapy.
The most frequent reasons are:
- fear of side effects;
- absence of immediate symptoms;
- unrealistic expectations.
The patient should know that:
- treatment is generally long-term;
- the main benefit is the reduction of fracture risk;
- regular monitoring helps personalize the treatment plan.
Secondary osteoporosis reminds us that bone health does not depend on age alone.
Many drugs can affect bone metabolism, but this does not mean they should be avoided when clinically necessary.
Individual risk assessment, monitoring, and clear communication help build more effective and sustainable treatment plans over time.
Bibliography
SIOMMMS. Guidelines for the diagnosis, prevention, and treatment of osteoporosis.
Compston J et al. Glucocorticoid-induced osteoporosis. Lancet.
Buckley L et al. American College of Rheumatology Guideline for Prevention and Treatment of Glucocorticoid-Induced Osteoporosis.
JAMA. 2016;316(7):722–733.
N Engl J Med. 2016;375:1532–1543.
PNAS. 2015;112(39):12157–12162.
Eastell R et al. Management of osteoporosis in postmenopausal women.
Black DM et al. Bisphosphonates and fracture prevention.
Khosla S et al. Pathophysiology of osteoporosis.
Endocrine Society Clinical Practice Guidelines.
