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Hormone treatments, chemotherapy that stops the ovaries and long courses of steroids all thin the bones, fast enough to measure within a year. Some of it comes back when the treatment stops, and the drugs that prevent fracture while it is going on are well proven.
Four cancer treatments take bone, and each has been measured.
Androgen deprivation for prostate cancer: in the trial that first quantified it, men on leuprolide alone lost 3.3 per cent of lumbar spine bone mineral density, 2.1 per cent at the trochanter and 1.8 per cent at the total hip over 48 weeks, with trabecular spine density falling 8.5 per cent (Smith, NEJM 2001).
Aromatase inhibitors: in the bone substudy of the ATAC trial, median bone mineral density over five years of anastrozole fell 6.08 per cent at the lumbar spine and 7.24 per cent at the total hip, while the tamoxifen group gained 2.77 and 0.74 per cent. The same substudy recorded the reassurance that is usually left out: "No patients with normal BMD at baseline became osteoporotic at 5 years."
Chemotherapy that stops the ovaries: among 35 premenopausal women whose ovaries failed during adjuvant chemotherapy, median spine density fell 4.0 per cent in the first six months and a further 3.7 per cent in the next six, while the 14 who kept ovarian function had no significant loss (Shapiro, JCO 2001). The loss tracks the oestrogen, not the drug.
Steroids: weeks to months of dexamethasone or prednisolone, standard in myeloma and lymphoma, cause glucocorticoid bone loss on top of any of the above.
What to do about it. ASCO's 2019 guideline advises assessing fracture risk with an established tool first, obtaining a bone density scan for those at substantial risk, optimising nutrition, exercise and lifestyle for everyone, and, where a drug is indicated, using "bisphosphonates or denosumab at osteoporosis-indicated dosages". The randomised evidence behind that is strong: in ABCSG-18, denosumab 60 mg twice a year in 3,420 postmenopausal women on an aromatase inhibitor halved the risk of a first clinical fracture (hazard ratio 0.50, 92 fractures against 176), with no adjudicated osteonecrosis of the jaw. In men on androgen deprivation, the same dose raised lumbar spine density by 5.6 per cent at 24 months against a 1.0 per cent loss on placebo and cut new vertebral fractures at 36 months from 3.9 to 1.5 per cent.
Vitamin D and calcium are where the honest answer disappoints. Correcting a genuine deficiency is worth doing and guidelines advise adequate intake alongside any bone drug, but supplements are not a substitute for one: in VITAL, 2,000 international units of vitamin D3 daily in 25,871 generally healthy adults made no difference to total, non-vertebral or hip fractures over a median 5.3 years. Those people were not selected for low bone density or on bone-losing cancer treatment, so the trial does not say vitamin D is useless in this setting; it says it is not the treatment.
What comes back, and when: partial, and slowly. After five years of anastrozole stops, lumbar spine density rose again by a median 2.35 per cent in the sixth year and 4.02 per cent in the seventh, so the aromatase-inhibitor loss is not permanent. Bone lost on androgen deprivation recovers if testosterone returns, and bone lost to chemotherapy-induced ovarian failure recovers if ovarian function returns, which is itself age-dependent. A fracture that has already happened does not reverse, which is the argument for measuring and treating early rather than waiting.
Oestrogen and testosterone restrain osteoclasts. Removing either, by an aromatase inhibitor, androgen deprivation or chemotherapy-induced ovarian failure, raises bone resorption above formation and density falls fastest in trabecular bone, which is why the spine goes first. Bisphosphonates and the anti-RANKL antibody denosumab suppress the osteoclast side of the balance.
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