Discussion
Intraosseous lipomas are very rare benign tumors of bones with an
incidence of less than 0.1% of all primary bone tumors mostly affecting
the bones of lower extremities with calcaneum being a common location
like in our case.2 Other long bones femur, tibia, and
fibula are also affected in metaphyseal and diaphyseal regions. They are
mostly solitary and unifocal. Lipomas are derived from mature
adipocytes, but the exact etiology is poorly understood. Many believe in
a primary origin from bone marrow fat, while others support trauma and
fat degeneration, infective pathologies, and fat metaplasia. Age and sex
predilection are also not fully agreed upon. Several cases are
asymptomatic and detected as incidental findings while working on some
other conditions. Symptomatic cases may present with pain, swelling, and
tenderness.3 Intraosseous lipomas can undergo changes
like fat necrosis, cystic degeneration, dystrophic calcification,
fibrosis, bone infarction, etc. Malignant transformation has been
documented in very few cases of intraosseous lipomas.4
Diagnosis with simple plain x-ray alone is difficult for an intraosseous
lipoma; the presence of benign-appearing osteolytic bone lesion with
well-defined margins with intralesional calcification commonly referred
to as Cockade sign may be a useful clue.5 With the
advent of CT and MRI, we can detect the nature of the lesion without the
need for biopsy or surgical excision.6 However, it is
important to understand histopathology to better recognize the imaging
features of intraosseous lipomas. Based on the histopathological
features, intraosseous lipomas are divided into three types: stage 1
includes solid tumors of viable lipocytes, stage 2 includes transitional
cases with partial fat necrosis and focal calcification but with areas
of viable lipocytes, and stage 3 includes advanced cases where fat cells
have died with varying degree of changes like calcification, cyst
formation, and reactive new bone formation.7 The
radiological features including CT scan findings correspond to the
histologic stages of the lesion. Stage 1 lesions are lucent representing
viable, non-necrotic fat with resorption of bony trabeculae; stage 2
lesions have lucent areas of viable fat along with radiodense areas of
fat necrosis and dystrophic calcification and may be expansile too.
Stage 3 lesions are heterogenous, more radiodense due to calcification
and extensive fat necrosis along with the thick sclerotic border, and
may show cystic changes within. 8
MRI is also an excellent method for the identification of intraosseous
lipomas by visualizing fat within the lesions.2 Stage
1 lipomas show viable fat isointense to subcutaneous fat on T1-weighted
sequences and show low signal intensity with fat suppression on
T2-weighted images. A thin surrounding circumferential rim consistent
with reactive sclerosis with low signal intensity on T1- and T2-
weighted sequences demarcating the margin of the fatty lesion may be
present. Stage 2 lesions also show fat and the circumferential rim of
decreased signal on T1- and T2-weighted images along with the
low-signal-intensity areas in the central portion of the lesion
consistent with calcifications. Stage 3 lesions have a thin peripheral
rim of fat, central calcification, and a thick rim of surrounding
sclerosis with low signal intensity on T1- and T2-weighted sequences. A
variable signal is seen on T1-weighted and an increased signal is seen
on T2- weighted images in areas of fat necrosis.9
The differential diagnoses for this condition include bone infarct,
unicameral bone cyst, aneurysmal bone cyst, chondromyxoid fibroma,
fibrous dysplasia, osteoblastoma, giant cell tumor and liposclerosing
myxofibrous tumors (LSMFT).9 Clinicoradiological
correlation is essential to determine the diagnosis of intraosseous
lipoma. Most cases can be managed conservatively. The prognosis is very
good and the chance of recurrence is negligible. The possible surgical
indications for management can be the presence of a painful lesion,
pathological fracture, necessity for histological diagnosis or to
decrease the risk of malignant transformation.10,11Common surgical options are curettage with or without bone grafting, or
with a bone graft substitute.