Myeloma is a cancer of plasma cells, a type of white blood cell that normally lives in the bone marrow and makes antibodies. Because the disease is inside bone from the outset, its effect on the skeleton is not a late complication: it is the defining feature of the illness.
This page is about that skeletal side, and particularly about the point at which an orthopaedic operation becomes part of the treatment. The myeloma itself is managed by a haematologist, and that treatment is summarised briefly at the end.
The essentials
- Myeloma weakens bone, and the weak spots do not reliably heal, even when the myeloma itself is responding well to treatment. That is why surgery sometimes has a role in a disease treated mainly with drugs.
- Pain when you put weight through a limb is the symptom to report. It is different from general aching, and it is the most useful warning that a bone is in mechanical trouble. Tell your haematologist specifically.
- Fixing a bone before it breaks is better than repairing it afterwards: better survival, fewer complications, and a much better chance of walking normally again.
- The operations are about strength, not about removing the cancer. A rod down the bone, cement to fill a cavity, or a joint replacement, each designed to let you bear weight immediately.
- Surgery does not treat the myeloma. Your haematology treatment continues, and radiotherapy is often given to the operated area afterwards.
What myeloma does to bone
Healthy bone is constantly renewed. Cells called osteoclasts dissolve old bone; cells called osteoblasts lay down new bone. The two are normally coupled, and the skeleton stays in balance.
Myeloma uncouples them. It drives osteoclasts to work harder and suppresses osteoblast activity, so bone is removed and not replaced. On imaging this shows as lytic lesions: punched-out areas where bone has been dissolved away. Bone involvement of this kind occurs in up to 80 to 90% of people with myeloma, at diagnosis or later.
One consequence deserves emphasis, because it explains most of what follows:
A myeloma lesion does not reliably fill back in, even when the myeloma is responding well. Research on myeloma bone disease notes that lesions persist under current standard treatment even in patients in complete remission, and that available bone-protecting drugs act almost entirely on the bone-dissolving side of the equation rather than stimulating new bone formation.
So a patient whose blood results and marrow have improved dramatically may still have a hole in the femur that is no stronger than it was. That is a mechanical problem requiring a mechanical solution, and it is why surgery has a role in a disease treated principally with drugs.
When the bone is at risk of breaking
A fracture through diseased bone is called a pathological fracture. When a bone is weakened enough that it is likely to break but has not yet done so, that is an impending fracture.
Myeloma is a common cause. In an analysis of over 400,000 patients with cancer affecting bone, myeloma was the second commonest cause of pathological fracture of a long bone, behind kidney cancer. In one surgical series of pathological lesions and fractures of the upper femur, myeloma was the single commonest underlying diagnosis, accounting for 22% of cases.
How the risk is judged
Several things are weighed together:
- How much of the bone’s width the lesion occupies. A lesion crossing more than about two-thirds of the diameter is much more concerning than a small one.
- Whether the outer shell (the cortex) is breached. In humeral lesions specifically, cortical breach has been found to be the single strongest predictor of fracture, with an odds ratio of 21.
- Which bone, and where in it. Weight-bearing bones matter more than others, and the region just below the hip is the highest-risk site of all.
- Pain on loading. Pain that comes on when you put weight through the limb, rather than pain at rest, is the most informative symptom, and often the earliest sign that the bone is failing mechanically.
A scoring system published by Mirels in 1989 combines four of these factors into a single number and is still the most widely used tool for the purpose. It is genuinely useful for structuring the conversation, and it has real limitations that are worth knowing about:
- When eight experienced surgeons and radiologists scored the same radiographs, agreement between them was poor, worse than for the older, simpler system it replaced.
- In the upper limb it performs badly. Across dedicated studies of humeral lesions, the standard threshold detected only around 14% of the bones that went on to break, no better than chance.
- It was originally derived in patients with metastases from solid cancers who were treated with radiotherapy. It was not developed in myeloma.
That last point matters in practice, because myeloma responds to radiotherapy and to drug treatment more readily than most cancers that spread to bone. A lesion that looks alarming on a scan may become less pressing once systemic treatment takes effect. There is a published case of exactly that: a patient with a high-scoring impending hip fracture in whom chemotherapy made prophylactic nailing unnecessary. That is a single case rather than a rule, but it is the reason these decisions are made jointly with the haematology team rather than from a score alone.
Why fixing a bone before it breaks is preferable
The argument for operating on an impending fracture rather than waiting is reasonably well supported.
In the 400,000-patient analysis, patients treated for an impending fracture had better survival at both 90 and 360 days than those treated after the bone had broken, with significantly fewer blood clots in the legs, fewer pulmonary emboli, fewer urinary infections and fewer blood transfusions.
A smaller study comparing nailing of impending against completed femoral fractures found the pre-emptive operations had shorter operating times, less blood loss, shorter hospital stays and, most importantly for daily life, significantly more patients regained the ability to walk. That study excluded blood cancers, so it does not speak directly to myeloma, but the mechanical logic carries across: a bone that is still in one piece is easier to stabilise well than one that has shattered, and the patient has not spent the intervening period immobile and in pain.
One common claim about prophylactic surgery does not hold up, and it is worth being straight about. It is often said to be cheaper. The best-adjusted study (265 patients, propensity matched) found no difference in hospital costs between operating before and after fracture. What it did find was that patients who broke the bone first were far more likely to need discharge to a rehabilitation facility: 57% against 30%. The real cost of waiting is not measured in hospital bills. It is measured in independence.
What the operations involve
The aim of surgery in myeloma is different from the aim of sarcoma surgery. Here the objective is not to remove the tumour with a margin: the myeloma is treated with drugs throughout the body. The objective is to make the bone able to bear load reliably, immediately, and for as long as the patient needs it.
That goal shapes every technical decision.
Prophylactic intramedullary nailing
A metal rod is passed down the hollow centre of the bone. Because it supports the bone along its full length rather than at a single point, it protects the lesion that prompted the operation and any other lesions in the same bone, which matters in a disease that is rarely confined to one spot.
Nails can usually be inserted through small incisions without opening the lesion itself, so blood loss is modest and recovery is quick. Weight-bearing is generally permitted straight away, which is the whole point of doing it.
A theoretical concern about nailing through a tumour is that instrumenting the marrow cavity might spread disease along the tract. This has been studied: in 122 patients, local progression around the nail occurred in 6%, and only 2% ever needed a further operation because of it. Worth knowing about; not a reason to avoid the operation.
Fixation with cement augmentation
Where a lesion has hollowed out a segment of bone, a nail or plate alone may have insufficient bone to grip. Bone cement (polymethylmethacrylate) is placed into the cavity, filling the defect and providing immediate structural support. It sets within minutes and does not depend on biology.
In myeloma this is more than a convenience. Since the lesion cannot be relied upon to reossify, cement substitutes permanently for the bone that will not come back. A construct that is stable on the day of surgery is one that does not need the patient to wait, and does not fail while waiting for healing that may never arrive.
Cement is also used to fill defects around implants and to augment screw fixation in soft, disease-affected bone. In biomechanical modelling of segmental replacements, cemented fixation reduced stress in the surrounding bone, although that is a computational study rather than a clinical trial, so it supports the reasoning rather than proving the outcome.
Joint replacement and segmental reconstruction
When the disease has destroyed bone next to a joint, or the joint surface has already collapsed, there may be too little sound bone for fixation to hold. In that situation the affected segment and the adjacent joint are removed and replaced with an implant. Around the hip, knee or shoulder this may mean a standard replacement using a long-stemmed, cemented implant, or a larger segmental reconstruction.
Replacement is a bigger undertaking. In a comparison of the two approaches at the proximal humerus, patients having a prosthesis had considerably more blood loss and longer operations than those treated with a plate and cement. That series was small, retrospective and its authors were explicit that the groups were not comparable, so it should not be read as showing one operation is better. What it does illustrate is the trade-off: replacement solves problems fixation cannot, at a greater physiological cost.
What happens afterwards
Radiotherapy is commonly given to the operated site once the wound has healed, to treat the disease that the surgery did not address. Systemic treatment continues under the haematology team. Surgery is a component of the plan, never the whole of it.
Why durability increasingly matters
For many years surgery for bone disease in cancer was framed as palliative: get the patient comfortable and mobile for the time they have. Myeloma has been moving away from that framing.
Population data from 1975 to 2023 show myeloma mortality rising until the mid-1990s, then falling in successive steps, with the steepest decline of the whole period occurring between 2021 and 2023. Those inflection points line up with the arrival of stem cell transplantation, then proteasome inhibitors, then the newer agents.
The practical implication for surgery is straightforward: a reconstruction may now need to last many years rather than many months. That argues for constructs chosen for durability rather than expedience, and it is a reason to plan these operations properly rather than treat them as holding measures.
Treatment of the myeloma itself
Briefly, because this is led by your haematologist rather than by a surgeon.
Initial treatment usually combines several classes of drug: proteasome inhibitors, immunomodulatory drugs, antibodies targeting markers on the surface of myeloma cells, and corticosteroids. For patients well enough, this is often followed by a stem cell transplant using the patient’s own cells, and then by ongoing maintenance treatment.
Bone-protecting drugs are given alongside. Zoledronic acid and pamidronate are long-established and reduce skeletal complications; kidney toxicity can limit their use. Denosumab, an antibody that blocks the signal driving osteoclasts, can be given where kidney function is impaired. In myeloma specifically the evidence shows denosumab is non-inferior to zoledronic acid rather than superior: its advantage is renal safety, not fewer fractures. Notably, a large meta-analysis found that denosumab’s edge in delaying skeletal events, which is real in solid tumours, was not seen in myeloma.
CAR T-cell therapy has become an established option for myeloma that has relapsed. The patient’s own T-cells are collected, genetically modified to recognise myeloma cells and returned as a single infusion. Two randomised trials define its current place:
- In patients who had already had two to four lines of treatment, idecabtagene vicleucel extended median progression-free survival to 13.8 months against 4.4 with standard regimens, with complete response in 44% against 5%.
- In patients who were refractory to lenalidomide after one to three prior lines, ciltacabtagene autoleucel had not reached median progression-free survival at 33.6 months, against 11.8 months for standard care, and improved overall survival, with a hazard ratio of 0.55. Deaths occurred in 24% against 39%.
Both are demanding treatments. Severe reductions in blood counts are very common and infection is the main cause of treatment-related death. They are delivered only at specialist centres.
The reason this matters on a surgical page is that it changes the horizon. Patients receiving these treatments may do well for years, and the skeleton has to keep working for that whole time.
If you have myeloma and something hurts
The most useful thing to report, and the thing most often left unmentioned, is pain when you put weight through a limb. Bone pain affects around half of patients with myeloma, and lesions judged to be at risk of fracture are among the strongest predictors of it. Pain that appears or worsens on loading (standing, walking, pushing up from a chair, lifting) is different from generalised aching, and it is the pattern that most often signals a bone in mechanical trouble.
Mention it specifically to your haematologist. Imaging is straightforward, and the difference between dealing with a bone before and after it breaks is substantial.
Assessment of a lesion like this is arranged through your treating haematologist, and the plan is agreed between the haematology and orthopaedic teams. The broader steps involved in investigating a bone lesion are set out in tests and diagnosis.
Myeloma affecting the spine is common and is assessed and managed differently from disease in the limbs; it is not covered here.