Hemangioma of Bone

Haemangioma is the most common benign vascular tumour of bone. It is usually an incidental finding in an adult, and it does not undergo malignant transformation.

How common. Autopsy studies find haemangiomas in 10-12% of all spines. The true prevalence is unknown, because many are never detected, and fewer than 1% become symptomatic over a lifetime.

Who. Detection peaks at 40-60 years (mean 50). The lesion can occur at any age after skeletal maturity but is rare in children, under 5% of cases; it is likely congenital and only becomes clinically apparent in adulthood. Women are affected twice as often as men overall and three times as often in the spine, whereas skull haemangiomas show no significant gender predilection.

Where. By site:

• Vertebral bodies - 28-30%, thoracic more than lumbar more than cervical
• Skull and calvarium - 20%, mainly the frontal and parietal bones
• Facial bones - 10%: maxilla, mandible, zygoma
• Long bones - 5%: femur, humerus, tibia
• Other - ribs, pelvis and scapula, rarely

Within the spine. The thoracic spine carries 55-60% of vertebral lesions, most often T4-T9. The lumbar spine carries 30-35% (L1-L3), the cervical spine 5-10% and the sacrum less than 5%. Multiple levels are involved in 30-40% of vertebral cases.

What it is. Likely a hamartoma: a developmental malformation, present from birth and growing slowly over decades, rather than a true neoplasm. The WHO classification nonetheless lists it as a benign vascular neoplasm (see the Evidence Base). The female predominance suggests a hormonal role (see pregnancy, under Clinical Presentation).

Histological types. Three are described:

• Cavernous - large, thin-walled, blood-filled channels lined by endothelium, separated by fibrous stroma with fatty marrow between the vessels. The more common type, and the more symptomatic
• Capillary - small, thin-walled, densely packed capillary-sized vessels with less fatty stroma. Less aggressive
• Mixed - capillary and cavernous elements together

How symptoms arise. Four mechanisms, plus pregnancy (see Clinical Presentation):

1. Expansion - slow growth expands the vertebral body and causes pain
2. Fracture - pathological fracture of the weakened vertebral body
3. Compression - epidural extension compresses the spinal cord or nerve roots
4. Haemorrhage - acute bleeding into the lesion, very rare

Typical and aggressive lesions. A typical lesion is quiescent and found by chance; a lesion becomes symptomatic when it behaves aggressively, with rapid growth or cortical destruction, and symptomatic haemangiomas usually have posterior-element involvement or epidural extension.

The typical case. A 50-year-old woman has a lumbar spine MRI while being evaluated for mechanical back pain. The L3 vertebral body shows bright T1 and T2 signal, a lateral radiograph shows the corduroy appearance, and the lesion itself is asymptomatic.

The incidental lesion. At least 95% of haemangiomas are asymptomatic, found on spine MRI or CT done for an unrelated complaint. There are no local symptoms or neurological findings, the lesion is confined to the vertebral body with no posterior-element involvement or soft-tissue component, and it needs no intervention.

Pain. The symptomatic minority present with pain of one of four kinds:

• Localised back pain - mechanical, worse with activity
• Night pain - may be present with active expansion
• Radicular pain - nerve-root compression from epidural extension
• Acute pain of sudden onset - pathological fracture

Neurological presentations. These are rare:

• Radiculopathy - dermatomal pain, sensory change, weakness
• Myelopathy - spastic gait, hyperreflexia, bowel and bladder dysfunction
• Cauda equina syndrome - rare, from lumbar lesions with massive epidural extension
• Acute paraplegia - extremely rare, from acute haemorrhage or fracture

Pregnancy. A lesion may enlarge rapidly during pregnancy, an oestrogen effect; this is rare, and it can bring new back pain or neurological symptoms; the lesion usually regresses postpartum, but cord compression may require urgent intervention. Counsel women of childbearing age accordingly.

Skull lesions. A skull haemangioma without symptoms presents as a palpable mass and a cosmetic concern. It can erode through the inner or outer table, dural involvement can bring headache or seizures (rare), and it bleeds profusely if traumatised or at surgery.

Long-bone lesions. Localised pain and swelling, a palpable mass where the bone is superficial, and, rarely, a pathological fracture.

Examination. Inspection may show a visible deformity over a skull lesion or a kyphotic deformity after a vertebral fracture; the overlying skin is normal. Palpation may find tenderness to percussion over a vertebral lesion, a bony prominence over a skull lesion, and a soft-tissue mass with an aggressive lesion.

The neurological examination is usually normal in asymptomatic cases. When it is not, look for radicular findings (dermatomal sensory loss, weakness), upper motor neuron signs of myelopathy, and bowel or bladder dysfunction from cauda equina compression.

Radiographs of the spine. The lateral view shows the corduroy or jail-bar appearance: vertical striations made by thickened vertical trabeculae, with loss of the horizontal trabeculae and a coarse trabecular pattern. The striations are less apparent on the AP view. The cortex is usually intact, although aggressive lesions may destroy it, and the vertebral body rarely expands with increased height.

Radiographs of the skull. Skull lesions are typically well defined, with sclerotic margins, in one of three patterns:

• Sunburst - trabeculae radiating from the centre, the classic appearance
• Honeycomb - multiple small lucencies
• Soap-bubble - an expansile lytic lesion with septa

Radiographs of long bones. A lytic lesion with a trabeculated, soap-bubble or honeycomb pattern, and cortical thinning or expansion.

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CT. On axial slices the thickened vertical trabeculae are cut in cross-section and appear as dots in low-attenuation marrow, the polka-dot (or corduroy) sign; sagittal and coronal reconstructions show the vertical striations. CT also assesses cortical integrity and any epidural soft tissue extending into the spinal canal. In the skull it shows radiating trabeculations and expansion of the diploe between the inner and outer tables, with a soft-tissue mass if the dura is involved.

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MRI of the typical lesion. The typical haemangioma is bright on T1 and bright on T2. The T1 signal comes from fat between the vascular spaces and matches subcutaneous fat; the T2 signal is a heterogeneous hyperintensity from slow-flowing blood and oedema. On STIR or fat-suppressed images the signal drops out, which confirms the fat.

Why the T1 signal matters. Most other vertebral lesions contain no fat. Metastases and myeloma are both dark on T1 and bright on T2, so bright T1 with bright T2 is virtually diagnostic of a typical haemangioma. Such a lesion is a haemangioma until proven otherwise, and biopsy is usually not needed.

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MRI of the aggressive lesion. These are the features that mark it:

• Extension into the posterior elements (pedicles, lamina)
• An epidural soft-tissue mass
• Spinal cord compression or displacement
• Vertebral body expansion (greater than 50% canal compromise)
• Heterogeneous signal, with less fat and more vascular tissue

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Contrast. Usually not needed for the diagnosis. The lesion enhances if contrast is given, because it is vascular, and contrast helps delineate the epidural extent for surgical planning.

Angiography. Used for preoperative planning, for embolisation of a symptomatic lesion, and to confirm the vascular nature of a lesion when imaging is ambiguous. It shows a hypervascular lesion with an intense blush, arterial feeders from the vertebral, intercostal or lumbar arteries, and arteriovenous shunting in some cases.

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When to biopsy. A classic lesion is diagnosed on imaging. Biopsy is for:

• Atypical radiographic features - cortical destruction, a soft-tissue mass
• Concern for malignancy (angiosarcoma)
• A neurological deficit without a clear diagnosis
• A young patient, since haemangiomas are rare in children

Pathology. The specimen is soft, red-purple, spongy tissue with blood-filled spaces. The endothelial cells are bland, with no atypia and no mitoses: a benign proliferation.

Immunohistochemistry. The expected panel:

• CD31 positive (endothelial marker)
• CD34 positive (vascular marker)
• ERG positive (endothelial transcription factor)
• Ki-67 proliferation index low, less than 2%
• Cytokeratin negative, excluding carcinoma

Histological differential. Angiosarcoma shows cellular atypia, mitoses and infiltrative growth. Haemangioblastoma is a CNS lesion, not a bone primary. A vascular malformation looks similar but is a developmental anomaly, not a tumour.

In the vertebral body. The table sets the haemangioma against metastasis, myeloma and Paget disease.

Beyond the table. A metastasis usually occurs in a patient older than 50, comes with a known primary malignancy and often destroys the pedicle, which a haemangioma usually spares. Myeloma shows diffuse marrow infiltration on MRI and a monoclonal protein, hypercalcaemia and anaemia on blood tests. Paget disease is mixed lytic and sclerotic on radiographs, raises the alkaline phosphatase and is common in the pelvis.

Other spinal and skull lesions. The remaining differentials, grouped by the site where they mimic a haemangioma:

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• The danger is a shared radiculomedullary feeder. The segmental (intercostal/lumbar) arteries that supply a vertebral hemangioma can also give off a radiculomedullary branch to the anterior spinal artery - in the lower thoracic/upper lumbar spine this is the artery of Adamkiewicz (arteria radicularis magna, usually left, T9-L2). Embolic material that passes into that branch causes anterior spinal artery infarction and paraplegia - the catastrophic complication of spinal tumour embolization.
• How the risk is minimised. Embolization is done by superselective microcatheterisation of the tumour's feeding pedicles, with careful pre-embolization angiography (and provocative testing where indicated) to confirm that the vessel about to be embolized does not supply the cord; the particle size is chosen large enough not to pass through arteriovenous shunts into the cord or lungs; and the operator stops if a radiculomedullary/cord feeder is identified. Liquid agents and ethanol (alcohol) are powerful but higher-risk (reflux, cord infarction, skin necrosis, cardiovascular effects), so they are used cautiously.
• Timing and purpose. Particulate transarterial embolization is performed 24-48 hours before surgery (not the same day) so the tumour bed thromboses and intraoperative blood loss falls; it is also used as a stand-alone or vertebroplasty-adjunct treatment for painful non-compressive lesions.

• The lesion is plumbed into the epidural veins. A hemangioma's dilated intraosseous vascular channels communicate directly with the basivertebral vein and the valveless epidural and paravertebral venous plexus (Batson's plexus). Injecting PMMA cement into this high-flow vascular space therefore risks the cement tracking into the epidural space (cord/root compression) or embolizing through the veins to the lungs (pulmonary cement embolism) - a greater risk than in an ordinary osteoporotic fracture.
• Reduce the flow before you inject. This is the rationale for pre-procedural sclerosis/embolization (transarterial particles or intralesional alcohol) before cement in an aggressive or epidural-extending hemangioma - occluding the vascular channels first lowers the leak risk and improves the durability shown in the alcohol-embolization-plus-vertebroplasty series.
• Inject safely. Use higher-viscosity cement injected slowly under continuous ("live") biplane/lateral fluoroscopy, and stop at the first sign of posterior or venous filling; a kyphoplasty balloon cavity can allow a more controlled, lower-pressure fill. The goal is pain relief and stabilisation, not complete filling.

The principle. Only symptomatic haemangiomas need treatment, and the invasiveness of the treatment is matched to the disease, from observation for the incidental lesion to embolisation, decompression and stabilisation for cord compression.

The asymptomatic lesion. An incidental lesion without symptoms or aggressive features is observed. No follow-up imaging is required and there are no activity restrictions; the lesion stays stable for life and intervention is rarely needed. Explain that it is a benign vascular tumour, not cancer, with no risk of malignant transformation, that it will not cause symptoms in the vast majority, and that new back pain or neurological symptoms are a reason to return. For the asymptomatic patient it is safe to ignore, and the patient can be discharged.

Pain without a neurological deficit. Radiotherapy is first-line, vertebroplasty or kyphoplasty the alternative, and embolisation is used if both are contraindicated.

Radiotherapy. The conventional dose is 20-40 Gy fractionated over 10-20 fractions; within that range, the largest multicentre series found that a total of 34 Gy or more gave significantly better symptom relief than a lower dose (Heyd, in the Evidence Base). Radiotherapy scleroses the vascular channels and reduces tumour volume, and gives pain relief in 80-90%, gradually over weeks to months. The contraindications are a neurological deficit, where surgery is preferred, and young age.

Vertebroplasty and kyphoplasty. For a painful vertebral haemangioma with partial collapse, cement is injected percutaneously into the vertebral body. It gives immediate pain relief in 80-90%, is minimally invasive, and recovery is quick; its complications are set out below.

Embolisation alone. Transarterial embolisation of the feeding vessels, with PVA particles, coils or Onyx liquid embolic, reduces tumour vascularity and palliates pain. Pain relief is variable (50-70%) and recurrence is common as the blood supply reconstitutes. Its best use is as a preoperative adjunct to surgery.

Pathological fracture. Kyphoplasty if the fracture is stable and there is no neurology; surgical stabilisation if it is unstable or there is a neurological deficit. Operative treatment of the fracture is surgical fixation with curettage and bone grafting.

Neurological deficit or cord compression. Obtain an urgent MRI to confirm the compression, embolise preoperatively (see Surgical Technique), then decompress and fuse, and consider adjuvant radiotherapy postoperatively. The indications for decompression and stabilisation are:

1. Neurological deficit (myelopathy, radiculopathy)
2. Spinal instability or pathological fracture
3. Epidural extension with cord compression
4. Failed radiation or vertebroplasty
5. Rapidly progressive symptoms

Aggressive features (cortical destruction, a soft-tissue component). Biopsy to exclude angiosarcoma, then en bloc resection if feasible; radiotherapy with embolisation if the lesion is unresectable.

Surgical Technique

Preparing for the bleeding. Surgery on a haemangioma carries a risk of profuse bleeding. Preoperative embolisation, performed 24-48 hours before the operation, is essential for these vascular lesions and decreases intraoperative blood loss by 40-60%. Type and cross-match 4-6 units of packed red cells for potentially massive bleeding, have a cell saver available for autotransfusion, and plan the approach on an updated MRI.

Posterior decompression. A laminectomy decompresses the spinal cord and removes the epidural component of the haemangioma. Instrumented fusion is added for instability and is usually required. Avoid aggressive curettage of the vertebral body, because of the bleeding risk.

Vertebrectomy and reconstruction. Indicated for extensive vertebral body involvement, instability or failed decompression. The vertebrectomy is en bloc or piecemeal, through an anterior or posterior approach or both, with cage reconstruction (titanium mesh, PEEK or allograft strut) and posterior instrumented fusion. It is definitive treatment with low recurrence, but the morbidity is significant and it often requires an anterior approach.

Long-bone lesions. Thorough intralesional curettage with local adjuvants (phenol, cryotherapy), bone grafting with autograft or allograft, and prophylactic fixation if a structural defect remains.

The percentage ranges in this section are conventional teaching estimates, not single-study measurements. The measured figures are in the Evidence Base cards: Fox (11 of 11 with full neurological recovery, and recurrence split by radiotherapy dose), Heyd (90.5% response at 34 Gy or more) and Premat (VAS 7.2 to 3.1, with 88% sensory regression).

Spontaneous complications. All are rare. Pathological fracture, a vertebral compression fracture, occurs in less than 5%; spinal cord compression from epidural extension in less than 1%; and acute haemorrhage, presenting with an acute neurological deficit, is extremely rare.

Treatment complications. Each treatment has its own profile:

Prognosis. Excellent: most patients remain asymptomatic for life. Symptomatic lesions respond well to treatment: 85-95% of patients with a preoperative deficit improve neurologically after surgery, quality of life is excellent after successful treatment, and the majority return fully to their activities.

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Global Epidemiology

• Most common benign vascular tumour of bone; found in 10-12% of spines at autopsy worldwide
• Vertebral body (28-30%) and calvarium (about 20%) are the dominant sites; thoracic spine predominates
• Peak detection 4th-5th decades, female-to-male ratio about 2:1 (up to 3:1 for vertebral lesions)
• Under 1% of all hemangiomas ever become symptomatic, and progression of an incidental lesion is rare (2 of 59 over a mean 7.4 years in the Mayo series)

Side-by-Side Guidance

Bone hemangioma has no single dedicated society guideline; recommendations are derived from tumour-classification bodies and spine-oncology consensus. Where they converge and where emphasis differs:

WHO Classification of Tumours (5th ed, 2020) anchors the benign biology. Imaging-society guidance (ACR Appropriateness Criteria, ESR/European radiology consensus) drives the no-biopsy, no-surveillance approach for classic lesions. Spine-oncology consensus (e.g. AO Spine, Acosta/UCSF framework) governs the graded intervention ladder.

Registry and Resource Considerations

• No arthroplasty-style registry tracks hemangioma; evidence rests on institutional series (Mayo, UCSF, Pitie-Salpetriere) and the German multicenter radiotherapy cohort
• High-resource settings: Interventional radiology enables preoperative or stand-alone transarterial/alcohol embolization and vertebroplasty, shifting many aggressive epidural cases away from open surgery
• Limited-resource settings: Where embolization and cell-salvage are unavailable, open surgery for vascular lesions carries higher haemorrhage risk; radiotherapy (widely available, dose at least 34 Gy) becomes a key first-line option for painful lesions, and conservative observation is emphasised for incidental findings
• MDT coordination between spine surgeon and interventional radiologist is the practice standard wherever embolization is offered

• Surveillance of "atypical" but asymptomatic lesions: Low-T1 (fat-poor) lesions can look worrying yet behave indolently. There is no consensus on whether to image-monitor a fat-poor lesion without Laredo aggressive features; most authors observe, but interval MRI is sometimes used.
• Vertebroplasty alone for aggressive epidural lesions: Cementoplasty (with or without alcohol embolization) controls pain and sensory symptoms durably, but is unreliable for motor deficit. The threshold for choosing percutaneous treatment over open decompression in patients with mild myelopathy is debated.
• Embolization technique and timing: Particulate transarterial embolization 24-48 hours preoperatively is standard, but direct intralesional alcohol/Onyx and the optimal interval are not standardised, and radicular feeders raise spinal-cord-infarction concerns.
• Adjuvant radiotherapy after subtotal resection: Historical data show recurrence with under-dosed radiotherapy; the role of routine postoperative radiotherapy after modern gross-total or near-total resection is unsettled, and long-term radiation risk must be weighed in young patients.
• Pregnancy-associated enlargement: The reported rapid growth and regression of vertebral hemangiomas in pregnancy is based on case reports; the true magnitude of estrogen sensitivity and how aggressively to intervene during pregnancy remain uncertain.
• Biopsy safety: Bright-T1/T2 classic lesions need no biopsy, but when imaging is atypical the bleeding risk of percutaneous biopsy of a vascular lesion versus the need to exclude angiosarcoma is a genuine trade-off.