Vertebral intraosseous lipoma

Introduction

Lipomatous tumours are ubiquitous and the commonest tumours to affect soft tissues. Despite the fat content of bone medulla, intra-osseous lipoma is the rarest primary tumour to afflict bones.¹ Here we present an unusual case of vertebral intraosseous lipoma in a young male with low backache. This article aims to discuss and highlight the radiological and pathological features of this rare entity which may often be missed or misinterpreted.

Case report

A 35-year-old male patient presented with chronic low backache of one year duration that was insidious in onset, moderate in intensity and aggravated by prolonged standing. The patient did not have radiculopathy or neurogenic claudication. There was no history of any comorbid condition, medication or spinal trauma. The patient's vital parameters were normal. Lower paraspinal muscle spasm was noted. There was no point tenderness, swelling, evidence of sacroiliitis or neurological deficit. All laboratory investigations were normal.

Lateral radiograph of the lumbosacral spine showed an ill-defined transradiant lesion in the superior part of L4 vertebral body (Fig. 1). Computerized Tomography (CT) revealed a sharply marginated ovoid intraosseous lesion of fat attenuation (−70 Hounsfield Units) at the same location. The lesion had a thin rim of sclerosis. A punctate calcific focus was noted within the lesion (Fig. 2). The overlying endplate cortex was thinned without any obvious disruption. Degenerative changes in the form of marginal osteophytes and semilunar-shaped areas of endplate sclerosis were present. Magnetic Resonance Imaging (MRI) confirmed the CT findings and revealed a lesion of fat intensity (hyperintense on both T1- and T2-weighted images). A thin rim hypointense on both T1- and T2-weighted images consistent with marginal sclerosis was present. Disc desiccation and Modic changes were also noted (Fig.3). There was no evidence of sacroiliitis. Based on these findings a diagnosis of lumbar spondylosis with intraosseous lipoma of L4 vertebral body was made.

Fig. 1.

Lateral radiograph of the lumbosacral spine reveals a subtle transradiant lesion (arrow) in the superior part of the body of L4 vertebra.

Fig. 2.

The panel of axial, coronal and sagittal CT images reveals a well-delineated lesion of fat attenuation with a central calcific focus in the body of L4 vertebra (arrow).

Fig. 3.

Sagittal T2 – (a) and T1-weighted images (b) reveal a lesion of fat intensity in the body of L4 vertebra adjacent the superior endplate (arrow). Also noted are disc desiccation and Modic type 2 endplate changes.

Discussion

Fatty tumours affecting bones may be classified as: (a) soft-tissue lipomata or liposarcomata with secondary bone involvement; (b) parosteal lipomata, which arise from the subperiosteal tissue; (c) intraosseous lipomata, which arise from the medullary cavity; (d) liposarcoma of bone and (e) liposclerosing myxofibrous tumour.^2,3

First reported in 1880,⁴ intraosseous lipoma is the rarest primary bone tumour with an incidence of 0.1%.^3,5,6 However, recent reports suggest a wider prevalence of up to 2.5%.^3,6 Intraosseous lipoma is underreported for many reasons: (a) non-specific radiographic appearances which may simulate other entities, (b) benign radiographic appearances which preclude further CT or MRI, (c) difficulty in histopathologic interpretation if not correlated with radiology as fat in these lesions may be indistinguishable from normal fat in yellow marrow, and osteonecrosis if ischaemic changes are present.³

Intraosseous lipoma has been reported most frequently in the 4th and 5th decades^3,7 and is slightly more common in males.⁷

Pain has been reported in up to 66% of cases.³ The aetiology of pain is speculated to be due to expansile remodelling of bone or co-existent intralesional ischaemic changes. Pathological fractures occur rarely.¹

Most of these tumours occur in the lower limb (71%). The commonest site is the calcaneum (32%) followed by the femoral sub-trochanteric region, proximal tibial and distal femoral shaft and the proximal and distal fibular shaft.⁷ Upper limb lesions usually involve the proximal and distal humeral and radial shafts. They are usually intramedullary, rarely intracortical and frequently eccentric in smaller long bones. They have also been reported in the spine,^8,9 skull and sinonasal cavities,^10,11 mandible, pelvis and ribs.⁵ Multiple intraosseous lipomata affecting multiple bones have also been reported.^3,4 Lesion size varies from 10 to 120 mm (mean 39 mm).^3,7

The aetiology and nature of intraosseous lipomas is controversial. While some regard them as benign tumours of the medullary adipose tissue, others consider them to be reactive changes secondary to infarcts, infections, or the result of healed bony infarcts secondary to trauma.¹² An association with hyperlipoproteinaemia¹ and chromosomal abnormalities has been reported.¹² The increased prevalence of intraosseous lipoma at sites with decreased trabecular bone, like the calcaneus, has led to the theory that they represent an ‘overshoot’ of haematopoietic to fatty marrow conversion, and may therefore be considered hamartomas.³

At gross examination, intraosseous lipomas are pale or bright yellow, may reveal lobulations with a thin capsule and septations.³ They are composed of mature adult fat and may contain a few atrophic trabeculae.

Ascribing involutional changes to the histopathologic features of intraosseous lipomata, Milgram subdivided them into 3 stages: Stage 1 lesions consist of viable adipocytes without abnormal cytologic features (normal fat); Stage 2 lesions are composed of viable adipocytes, fat necrosis and dystrophic calcification; Stage 3 lesions exhibit extensive fat necrosis, calcification, cyst formation, reactive peripheral or intralesional ossification, with occasional viable adipocytes.^3,12 There is no preponderance of stage 2 and 3 lesions with advancing age.⁷ It is speculated that the enlargement of these lesions in the confined space of the intramedullary canal raises the intramedullary pressure causing ischaemic fat necrosis and calcification. An alternate theory propounds that the calcification seen in these tumours might be a product of the mesenchymal cells in the lesion.³ Stages 2 and 3 lesions are thus most frequently confused with bone infarct histologically.

The radiologic appearance of an intraosseous lipoma parallels its Milgram stage.^3,6 On plain radiography, Milgram stage 1 lesions are well-circumscribed, transradiant lesions occasionally associated with mild focal expansile remodelling. Bone expansion is more prominent in thin long bones such as the fibula. Stage 1 lesion may simulate unicameral bone cyst, aneurysmal bone cyst, fibrous dysplasia, and plasmacytoma.^3,6 Overall marginal sclerosis and calcification are seen in 45% and 42% of lesions, respectively, however these findings are more common in lesions located in the calcaneum (61%).⁸ Bone expansion is noted in 33% of sites overall, but infrequently in the calcaneum (13%).⁷ CT demonstrates the intralesional fat (−600 HU to −100 HU), a thin rim of sclerosis and, if present, expansile remodelling of the intramedullary canal. On MRI, the intralesional fat appears similar to subcutaneous fat. Normal yellow marrow shows signal intensity lower than that of the intraosseous lipoma on T1-weighted images, related to cellular elements. Fat can also be demonstrated on MRI by fat suppression sequences.

Milgram stage 2 or 3 lesions appear as transradiant lesions with central or ring-like calcification or ossification. The ossification may be extensive, leading to the term ossifying lipoma.³ A predominantly calcified or ossified lesion may mimic an enostosis. Partially mineralized lesions may be mistaken for chondroid lesions or osteonecrosis on radiographs. On CT and MRI, intralesional fat (unless it is completely calcified or ossified) distinguishes the intraosseous lipoma from tumours of chondroid, osteoid, or fibrous origin. On MRI, calcification is seen as foci of low signal intensity on both T1- and T2-weighted images. Intraosseous lipoma may be difficult to differentiate from osteonecrosis at MR imaging and CT because both lesions contain intrinsic fat with a rim of tissue separating the lesion from surrounding marrow. Expansile remodelling of bone, osteolysis, and a rounded rather than irregular serpentine margin suggest an intraosseous lipoma.

With progressive ischaemia and involution, fibrous proliferation and cystic degeneration occurs in an intraosseous lipoma (Milgram stage 3 lesions). This and a skeletal distribution similar to unicameral bone cysts in adults has led to the postulation that unicameral bone cysts may represent completely involuted intraosseous lipomas. On radiographs, severely involuted lesions demonstrate a thick peripheral rind of ossification with variable amounts of central ossification-calcification producing a distinctive ‘bull’s-eye’ appearance. Despite the heterogeneous appearance of a severely involuted intraosseous lipoma on both CT and MR images, the identification of intralesional fat permits a definitive diagnosis.

Bone scintigraphy of intraosseous lipomas demonstrates radionuclide uptake ranging from absent to moderate.³

Intraosseous lipoma in the vertebra may occasionally mimic haemangioma and osteoporotic bone with increased fatty marrow.⁸ Abnormal biomechanical stress due to endplate cortical thinning as in our case may be a contributor to backache and it may be worthwhile to carefully look for these lesions.

Conclusion

Intraosseous lipoma is the rarest primary bone tumour that often poses a diagnostic dilemma on plain radiography because it may be confused with a bone infarct, chondroid neoplasm, fibrous dysplasia, or other benign conditions. CT and MRI are helpful in diagnosis by elucidating intralesional fat.

Conflicts of interest

All authors have none to declare.