Sarah was 38 when her GP connected the dots. She had been diagnosed with premature ovarian insufficiency two years earlier - her periods had stopped in her mid-30s - and had been told it was something to monitor. Nobody had mentioned her bones. A DEXA scan, ordered as part of a routine health review, came back showing osteopenia in her lumbar spine. The finding wasn't a disaster, but it was unexpected. More to the point, it was preventable - or at least, it could have been caught and managed earlier.
This kind of story is more common than most people realise. Osteoporosis is not simply a disease of old age. A significant proportion of people who develop it - across all age groups - have an identifiable underlying cause: a condition that disrupts how bone is built, maintained, or broken down. These are called secondary causes, and finding them changes what can be done.
Note: The case examples in this article are illustrative composites. They do not represent any individual patient.
What does 'secondary' osteoporosis mean?
Osteoporosis is described as primary when it occurs as part of the natural ageing process - driven by the gradual decline in oestrogen after menopause, or by the slow loss of bone density that comes with advancing age in men. It is described as secondary when there is a specific underlying driver: a medical condition, a treatment, or a medication that accelerates bone loss beyond what age alone would explain.
The distinction matters clinically because secondary osteoporosis often requires a different approach. Treating only the bone loss - without addressing what is causing it - rarely achieves the best outcome. In some cases, treating the underlying condition substantially improves bone health in its own right. In others, knowing the cause changes how aggressively the bone loss needs to be managed and what protective measures are appropriate.
Secondary causes are far more prevalent than most patients expect. Research shows they are present in over half of premenopausal women with low bone density, and in approximately two-thirds of older men. Even among postmenopausal women, a secondary contributing factor is found in roughly one in three cases.
Hormonal causes: when oestrogen or testosterone drops early
Oestrogen plays a central role in maintaining bone density throughout a woman's life. It slows the natural process by which old bone is broken down, keeping bone resorption in balance with new bone formation. When oestrogen levels fall - whether gradually through menopause or abruptly through another cause - that balance tips, and bone loss accelerates.
In natural menopause, this process begins in a woman's late 40s to early 50s. In premature ovarian insufficiency (loss of ovarian function before age 40) and early menopause (before age 45), it begins much earlier - sometimes by a decade or more - and the cumulative impact on bone is significant.
Studies in women with POI and early menopause consistently show that at the time of diagnosis, more than 40% already have osteopenia, and around one in ten have osteoporosis. Women who experience menopause before age 45 face a 1.5 to 3 times higher fracture risk compared with those who reach menopause at the typical age. Australian longitudinal data tracking nearly 9,000 women over 23 years found that almost 50% of women with POI or early menopause had developed osteoporosis or experienced a fracture by their late 60s, compared with around 37% of women with usual-age menopause.
One of the most clinically important findings in this area is the relationship between diagnostic delay and bone outcomes. The longer the gap between when ovarian function is lost and when it is diagnosed and managed, the worse the bone health tends to be - particularly in lean women and those with very low oestrogen levels.
Sarah, 38. Diagnosed with premature ovarian insufficiency at 36. Periods had been irregular from her early 30s. By the time a DEXA scan was arranged, she had already lost measurable bone density in her lumbar spine. With appropriate management - including hormone therapy discussed with her GP - her bone health is now monitored and on a protective trajectory. Looking back, earlier investigation would have been possible, and beneficial.
For men, the equivalent of oestrogen deficiency is low testosterone - a condition called hypogonadism. Like POI in women, male hypogonadism at any age significantly increases bone loss. It can arise from primary testicular failure, pituitary conditions, or as a consequence of certain medical treatments. Men with confirmed low testosterone on blood testing are eligible for a Medicare-rebated bone density scan under MBS item 12312.
In younger women, a further hormonal cause worth mentioning is significant energy deficiency - whether from an eating disorder, extreme dietary restriction, or very high athletic training loads without adequate fuel. In all these situations, oestrogen production falls even in the absence of any ovarian disease, and bone loss follows.
The most common secondary cause: glucocorticoids
Glucocorticoid-induced osteoporosis is the most frequent and well-documented form of secondary osteoporosis. Glucocorticoids - steroid tablets prescribed for conditions including asthma, rheumatoid arthritis, Crohn's disease, lupus, polymyalgia rheumatica, and many others - affect bone through several mechanisms. They suppress bone formation directly, increase calcium loss through the kidneys, and in higher doses can suppress sex hormone production as well.
Bone loss from glucocorticoids can occur relatively quickly. Significant reductions in density are measurable within the first few months of treatment, and the risk of vertebral fracture is elevated even at relatively low doses. Current Australian guidelines recommend that anyone starting oral glucocorticoid treatment expected to last four months or more should have formal fracture risk assessment and bone density monitoring.
James, 54. Managing Crohn's disease for 15 years, with periodic courses of oral corticosteroids - sometimes for months at a stretch during flares. Bone health had never been discussed as part of his gastroenterology or GP care. When a new GP reviewed his full medication history, a DEXA scan was arranged. His lumbar spine T-score was more than expected for his age. With the underlying diagnosis acknowledged, he is now on a bone-protective plan alongside his Crohn's management.
One aspect of glucocorticoid-induced osteoporosis that I see regularly in practice is that younger patients are often not considered for monitoring at all. The evidence shows that even premenopausal women on high doses of glucocorticoids face a meaningful risk of vertebral fracture - yet they are the group least likely to receive preventive care. If you take steroid tablets regularly for any reason, bone health should be part of the ongoing conversation with whoever manages your care.
High-dose inhaled corticosteroids - used for conditions like severe asthma or COPD - are also associated with increased bone loss and fracture risk, specifically at doses equivalent to 800 micrograms or more of standard inhaler medication per day. This is the dosing threshold recognised by Medicare for eligibility under MBS item 12312. Low and moderate doses of inhaled corticosteroids do not appear to carry the same risk. If you use a high-dose preventer inhaler long-term, it is worth raising bone health at your next GP review.
Gut conditions, joints, and glands
Several common medical conditions affect bone health through pathways that have nothing to do with age or hormone levels. Some of the better-documented ones include the following - though this is not a complete list, and there may be other conditions relevant to your individual situation.
Coeliac disease and malabsorption
Coeliac disease disrupts the small bowel's ability to absorb calcium and vitamin D - the two nutrients most critical to maintaining bone density. This can produce significant bone loss even before coeliac disease is diagnosed, and in some cases bone fragility is among the first clinical clues that something is wrong. Systematic reviews consistently show high rates of osteopenia and osteoporosis in people with coeliac disease, including in premenopausal women and men. Strict adherence to a gluten-free diet substantially reduces - and in many cases partially reverses - the bone loss.
Inflammatory bowel disease (Crohn's disease and ulcerative colitis) affects bone through a combination of mechanisms: direct inflammatory bone loss driven by cytokines, malabsorption of calcium and vitamin D in Crohn's disease, and the frequent use of glucocorticoids to manage flares. Other conditions causing malabsorption - including some bariatric surgeries, particularly procedures that reduce nutrient absorption - carry similar bone risks.
Overactive thyroid and parathyroid
An overactive thyroid (hyperthyroidism) accelerates bone turnover: the rate at which old bone is broken down exceeds the rate at which new bone is laid down, and the net result over time is bone loss. This applies to overt hyperthyroidism - including the hyperthyroidism caused by Graves' disease - as well as, to a lesser extent, subclinical hyperthyroidism.
A less intuitive cause in this category is over-treatment of an underactive thyroid. If a person taking thyroid hormone replacement has their dose set slightly too high, the resulting suppressed TSH can quietly accelerate bone resorption over months and years. This is worth checking at regular thyroid reviews, particularly in postmenopausal women.
Primary hyperparathyroidism - in which overactive parathyroid glands drive calcium out of bone into the bloodstream - is another well-documented cause. It is often discovered incidentally when a routine blood test shows a raised calcium level. Bone loss from primary hyperparathyroidism can be significant and is eligible for monitoring under MBS item 12315.
Inflammatory and autoimmune conditions
Chronic inflammatory conditions including rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and lupus (systemic lupus erythematosus) affect bone through inflammatory cytokines that promote osteoclast activity - the cells that break down bone. The frequent use of glucocorticoids to manage these conditions adds a second, independent source of bone loss. Reduced mobility from joint disease is a further contributing factor in some patients.
Chronic kidney disease also significantly affects bone through a distinct mechanism (CKD-mineral bone disease), in which the kidney's role in vitamin D activation and calcium-phosphate balance is progressively impaired. Other conditions that may contribute to secondary bone loss include chronic liver disease, type 1 diabetes, certain blood disorders, and - rarely - conditions like mastocytosis. If you have a complex medical history, it is worth discussing bone health with your GP even if you do not fit the more familiar profile.
Medications that can silently affect bone health
Many people are surprised to learn that some of the most commonly prescribed medications in Australia are associated with reduced bone density when taken long-term. The following are among the drug classes your GP may ask about - though other medications can also be relevant, and this list is not exhaustive.
The key message here is not to alarm you or prompt you to change anything on your own. These medications are often prescribed for very good reasons, and the benefits frequently outweigh the bone-related risk. What matters is whether bone health has been factored into your ongoing monitoring and management.
Diane, 48. Diagnosed with coeliac disease in her early 30s - mostly adherent to a gluten-free diet, but not perfectly. Also takes a daily acid reflux tablet for reflux, prescribed years earlier and never reviewed. At a comprehensive health check, her GP notes both factors and arranges blood tests and a DEXA. Vitamin D is low, BMD is in the osteopenic range. Better dietary adherence, vitamin D and calcium correction, and a medication review with her GP shift her trajectory. The PPI is not stopped - her reflux history is significant - but it is reviewed and dose-optimised, and her bone health is now actively monitored.
- Oral corticosteroids taken for 3 months or more (at any point in your history)
- High-dose inhaled corticosteroids (800 mcg/day or above of the equivalent standard inhaler)
- Breast cancer treatments that lower oestrogen levels (aromatase inhibitors)
- Prostate cancer treatments that lower testosterone (androgen deprivation therapy)
- Long-term proton pump inhibitors (daily acid reflux tablets, taken for more than a year)
- Certain long-term epilepsy medications - particularly older enzyme-inducing types
- Thyroxine replacement at a dose that results in a suppressed TSH
- Depot contraceptive injections (bone loss from this is largely reversible after stopping)
A note on proton pump inhibitors: multiple large meta-analyses, including an umbrella review of 27 systematic reviews and meta-analyses published in 2024, have found a statistically significant association between long-term PPI use and fractures at the hip, spine, and other sites. The evidence is observational and does not prove causation - many factors may contribute. It is sufficient to warrant a discussion with your GP if you have been taking a PPI daily for more than a year, particularly if other bone risk factors are present.
Important
Any change to a PPI is something to plan together with your GP rather than stop on your own. Stopping acid reflux medication without a plan can cause rebound acid, where the stomach's acid surges back and reflux symptoms worsen, and it can affect conditions like Barrett's oesophagus and peptic ulcer disease. So the right step is to raise bone health as part of your ongoing review, and to work out any medication change with your doctor.
For long-term epilepsy medication: not all anti-seizure medications carry the same bone risk. The concern is primarily with older enzyme-inducing types, which affect how the body metabolises vitamin D. Newer medications including some commonly prescribed today do not appear to carry the same risk. If you take medication for epilepsy and are unsure whether your specific type is associated with bone loss, it is worth asking your prescribing doctor or pharmacist.
Does this apply to me?
Tick any boxes that apply to you. This is a conversation starter, not a medical test - it does not diagnose osteoporosis or replace an assessment by your GP. Individual eligibility for bone density scans and further investigation depends on clinical factors your GP will assess.
This tool is for general information only and does not constitute a medical assessment. The presence of one or more factors does not mean you have osteoporosis. Eligibility for bone density scans depends on specific clinical criteria assessed by your GP. Always discuss your individual circumstances with a qualified health practitioner.
Want the whole series on one page? I've put every bone-health habit, graded by the evidence, into a free one-page shortlist that comes with the newsletter.
What does a workup for secondary causes look like?
If your GP suspects a secondary cause - or is screening for one as part of a bone health assessment - the workup is typically straightforward and low-burden. It usually involves a clinical history review, some targeted blood tests, and a DXA bone density scan.
Depending on your individual circumstances, some of the blood tests your GP may request include:
- Calcium, phosphate, and alkaline phosphatase
- Parathyroid hormone (PTH)
- Thyroid function (TSH)
- Coeliac antibodies (tissue transglutaminase IgA)
- 25-OH vitamin D
- Kidney function (eGFR, creatinine)
- Liver function
- Full blood count and inflammatory markers
- Sex hormones (as relevant to age and clinical picture)
- Serum protein electrophoresis if a blood disorder is suspected
Not every test is appropriate for every person. Your GP will tailor the investigation to what is most relevant given your history, rather than ordering everything for everyone. An elevated PTH result, for example, needs to be interpreted alongside the calcium and vitamin D - a high PTH in the setting of low vitamin D is usually a normal physiological response, not a sign of disease.
A note on FRAX - the tool used to estimate 10-year fracture risk: it is most useful in people aged 40 to 90. In younger patients, including women with POI or other conditions causing bone loss before age 40, it has limited applicability, and your GP will rely on clinical judgment and history rather than a calculated score.
Medicare rebates for bone density scans (DXA)
This is a summary of the main bone densitometry items. Each item has specific clinical eligibility criteria that your GP will assess. Medicare criteria may be updated - confirm current eligibility at the time of referral. Item descriptions are simplified for patient understanding; full clinical descriptors apply.
My scan came back borderline - does that change things?
A result in the osteopenic range (T-score between -1.0 and -2.5) is common and does not automatically indicate something is wrong beyond what ageing would predict. In a person in their 70s without other risk factors, mild osteopenia may reflect normal age-related bone change.
The question worth asking is: does this result make sense given your age and history? If you are younger than the result would suggest - or if you have any of the conditions or medication exposures described in this article - it is worth discussing whether a secondary causes screen is appropriate. In some cases, what appears to be mild or unexplained bone loss has a specific, treatable underlying cause. Identifying it can meaningfully change the trajectory of your bone health.
A result that surprises your GP is itself a reason to investigate further. If you were told your scan result was borderline and you weren't sure what it meant, that is a conversation worth returning to at your next appointment - particularly if your history includes anything covered in this article.
Something in this article
apply to you?
A bone health assessment - including secondary causes screening - is something I can help with at a GP appointment.
Common questions about secondary osteoporosis
Clinical references: RACGP/Healthy Bones Australia Osteoporosis Guidelines 2024 (3rd ed, Wong et al.); Hosein-Woodley et al., Biomedicines 2024 (secondary osteoporosis review); Monash University/Australian Women's Midlife Health Study (POI/EM longitudinal cohort); PMID 38701099 (POI bone health 23-year longitudinal); Tazzyman et al. (ICS meta-analysis, 2024); Umbrella review: Bone Reports 2024 (PPI and bone). MBS item details verified against MBS Online, December 2024.