Why "drug holiday" is not one thing
The phrase gets used as though all osteoporosis medicines behave alike when you stop them. They do not. What happens after your last dose depends entirely on which class you were on, and the difference is large enough to change how the decision should be made.
Bisphosphonates: a real reservoir
Alendronate, risedronate, ibandronate and zoledronic acid bind to the mineral surface of bone and stay there. When you stop, the drug already in the skeleton keeps exerting an effect that fades over months to years rather than switching off. This is why a planned pause — commonly discussed after roughly five years of oral treatment or three years of annual infusions in women who are no longer at high risk — is a reasonable conversation.
A pause is not automatic, and it is not for everyone. Women who have already had a fracture, who have very low density, or who are on long-term glucocorticoids are usually kept on treatment rather than paused.
Denosumab: the opposite behaviour
Denosumab does not bind to bone mineral. It clears, and when it does, bone resorption rebounds above baseline. Density gained is lost within roughly 6 to 12 months, and spontaneous vertebral fractures — frequently multiple — have been reported in women who stopped without follow-on treatment.
So there is no such thing as a denosumab drug holiday. Coming off it requires a planned handover to another agent, usually a bisphosphonate, and evidence shows that bridging reduces but does not entirely eliminate the loss. See our full page on denosumab for the detail.
Anabolic drugs: a fixed course that must be followed
Teriparatide and abaloparatide build bone rather than only slowing its breakdown, and they are given for a limited course. Gains from these drugs are lost if nothing follows. Standard practice is to move to an antiresorptive afterwards to lock in what was built. Finishing the course and stopping is not a neutral option.
Raloxifene and hormone therapy
Both work while you take them and stop working when you do not, without a rebound overshoot of the denosumab kind. Density drifts back toward where it would otherwise have been. For hormone therapy, this is one reason the bone benefit is not a reason to stay on it indefinitely by itself — the protection lasts as long as the treatment does.
What a well-run pause looks like
- A documented reason: how long you were treated, what your density did, whether you fractured.
- A monitoring plan: repeat bone density testing at a stated interval rather than "we will see."
- Defined restart triggers: a new fracture, a meaningful fall in density, or a new risk factor such as starting steroids.
- Calcium, vitamin D, resistance and weight-bearing exercise continuing throughout — the pause applies to the drug, not to everything else.
Questions worth asking
- "Which class am I on, and does it have a reservoir effect?"
- "If we pause, when do we retest and what result would make us restart?"
- "If I am on denosumab, what exactly is the handover plan and its timing?"
The classes side by side
| Class | Examples | What happens when you stop |
|---|---|---|
| Bisphosphonates | Alendronate, risedronate, ibandronate, zoledronic acid | Effect fades over months to years; a planned pause can be reasonable |
| RANKL inhibitor | Denosumab | Rebound above baseline; requires handover, never a pause |
| Anabolic | Teriparatide, abaloparatide | Gains lost unless an antiresorptive follows |
| SERM | Raloxifene | Protection stops with the drug; no rebound overshoot |
| Hormone therapy | Estradiol, combined MHT | Protection stops with the drug; bone loss resumes |
What monitoring during a pause should look like
A pause without monitoring is not a pause, it is simply stopping. A reasonable structure:
- Bone density repeated at a stated interval — commonly around two years, sooner if risk is higher
- Height measured at each review; loss of height can be the first sign of a vertebral fracture that caused no pain
- A note of any fall, whether or not it caused injury
- A review of anything new that changes risk: glucocorticoids, an aromatase inhibitor, a new diagnosis, significant weight loss
Triggers to restart
- Any new fragility fracture — a break from a fall at standing height or less
- A meaningful fall in bone density on repeat testing
- Starting a medicine that accelerates bone loss
- Height loss or new back pain suggesting a vertebral fracture
Why anyone pauses at all
The rationale is the small long-term risks that accumulate with continuous antiresorptive use — atypical femoral fracture and osteonecrosis of the jaw — both rare, both more associated with longer duration. In a woman at high fracture risk, those risks remain much smaller than the risk of the fracture being prevented, which is why high-risk women generally continue rather than pause. The pause is a tool for the lower-risk end, not a default endpoint for everyone.