INTRAOSSEOUS LIPOMA
Rare Benign Fat-Containing Bone Tumor | Classic Central Calcification | Calcaneus Most Common Site
MILGRAM CLASSIFICATION
Critical Must-Knows
- Calcaneus is the most common site - accounts for 60% of all intraosseous lipomas
- Central calcification on X-ray is pathognomonic - radiolucent lesion with dense central nidus
- MRI shows fat signal on all sequences - diagnostic feature distinguishing from other lucent lesions
- Completely benign - no malignant potential and excellent prognosis with simple curettage
- Milgram staging based on degree of fat necrosis and calcification, not biological behavior
Examiner's Pearls
- "Examiners love the central calcification pattern - it's pathognomonic for intraosseous lipoma
- "Fat signal on MRI (high T1, low T2 with fat suppression) clinches the diagnosis
- "Distinguish from bone infarct - infarcts have serpentine peripheral calcification, lipomas have central calcification
- "Simple curettage is curative - no wide margins needed as this is completely benign
Clinical Imaging
Imaging Gallery
Critical Intraosseous Lipoma Exam Points
Pathognomonic Imaging
Central calcification on X-ray - radiolucent lesion with dense central nidus of calcification. This is the classic radiographic appearance distinguishing lipoma from other lucent lesions.
MRI Fat Signal
High T1 signal that suppresses with fat saturation. This confirms fat content and distinguishes intraosseous lipoma from other radiolucent lesions like SBC or UBC.
Calcaneus Predilection
60% occur in calcaneus followed by proximal femur (20%). Rare in other sites. Think intraosseous lipoma for any lucent calcaneal lesion with central calcification.
Benign Biology
Completely benign with no malignant potential. Simple curettage is curative. Recurrence is rare (under 5%) and indicates incomplete excision.
Quick Decision Guide
| Presentation | Imaging Features | Management | Key Pearl |
|---|---|---|---|
| Asymptomatic, incidental finding | Radiolucent with central calcification, fat on MRI | Observation - no treatment needed | Benign, no growth potential |
| Mild pain, no fracture risk | Small lesion, intact cortex | Conservative - analgesia, activity modification | Most never become symptomatic |
| Persistent pain, large lesion | Cortical thinning, pathological fracture risk | Curettage with bone graft or substitute | Simple curettage is curative |
FAT CALCClassic Features of Intraosseous Lipoma
Memory Hook:FAT CALC - the FAT shows CALCification! This describes the classic central calcification in a fat-containing lesion.
STAGE 1-2-3Milgram Histological Staging
Memory Hook:Stages progress from Simple fat (Stage 1) to Transitional necrosis (Stage 2) to Advanced calcification (Stage 3). All are benign!
SAULICDifferential Diagnosis of Radiolucent Calcaneal Lesions
Memory Hook:SAULIC covers the differential for lucent calcaneal lesions - Lipoma has central calcification and fat signal!
Overview and Epidemiology
Clinical Significance
Intraosseous lipoma is a rare benign tumor composed of mature adipose tissue within the medullary cavity of bone. Despite being uncommon (under 0.1% of all bone tumors), it has a characteristic imaging appearance that makes it an important diagnosis to recognize. The pathognomonic central calcification on radiographs and fat signal on MRI allow confident diagnosis without biopsy in most cases.
Demographics
- Age: 40-60 years (middle-aged adults)
- Gender: Equal distribution (no gender predilection)
- Rare in children: Under 5% of cases
- Usually solitary: Multiple lipomas exceptionally rare
Anatomical Distribution
- Calcaneus: 60% (most common site by far)
- Proximal femur: 20% (intertrochanteric region)
- Tibia: 5% (proximal metaphysis)
- Fibula, ribs, skull: Rare (under 5% each)
- Never in spine: Unlike soft tissue lipomas
Pathophysiology and Mechanisms
Origin and Histogenesis
The exact origin of intraosseous lipoma is unknown. Several theories have been proposed:
Metaplasia Theory
Most accepted theory: Metaplastic transformation of bone marrow mesenchymal cells to adipocytes in response to:
- Trauma or microtrauma
- Ischemia or infarction
- Unknown stimulus
Developmental Theory
Alternative theory: Congenital nidus of ectopic fat cells that slowly expands over time.
Less favored as most cases present in adulthood, not childhood.
Milgram Histological Classification
The Milgram staging system classifies intraosseous lipomas based on histological features reflecting the natural evolution from viable fat to necrosis and calcification.
| Stage | Histology | Radiographic Appearance | Clinical Significance |
|---|---|---|---|
| Stage 1 | Viable adipose tissue only | Radiolucent, no calcification | Early lesion, purely fatty |
| Stage 2 | Fat necrosis with focal calcification | Radiolucent with central calcification | Classic appearance - most common |
| Stage 3 | Extensive calcification and cyst formation | Heavily calcified, may mimic bone infarct | Advanced involution, difficult to diagnose |
Staging Does Not Indicate Malignancy
Important concept: The Milgram staging system reflects the natural involution of the lipoma from viable fat to necrotic calcified tissue. It does NOT indicate biological behavior or malignant potential. All stages are equally benign.
Why Central Calcification?
The characteristic central calcification occurs due to:
- Fat necrosis in the center of the lesion (ischemia or outgrowth of blood supply)
- Dystrophic calcification of necrotic fat cells
- Progressive calcification from center outward as lesion involutes
This contrasts with bone infarct, which shows peripheral serpentine calcification delineating the infarct margin.
Classification and Staging
Milgram Histological Classification (1988)
Gold standard for intraosseous lipoma classification based on histological appearance.
Stages and Natural History
Histology: Mature adipose tissue with intact cell membranes, normal nuclei, and viable fat cells.
Radiology: Purely radiolucent lesion, no calcification visible.
Prevalence: Uncommon (10-15% of cases) - most lesions progress to Stage 2 before clinical detection.
Histology: Viable fat at periphery, central fat necrosis with dystrophic calcification.
Radiology: Radiolucent lesion with central calcification - pathognomonic appearance.
Prevalence: Most common (60-70% of cases) - this is the classic imaging appearance.
Histology: Extensive calcification, minimal residual fat, cyst formation, reactive bone.
Radiology: Heavily calcified lesion, may mimic bone infarct or enchondroma.
Prevalence: Less common (20-25%) - advanced involution, difficult diagnosis.
Stage 2 is Classic
Stage 2 lesions represent the classic intraosseous lipoma with pathognomonic central calcification on X-ray. This is the most commonly encountered stage and the easiest to diagnose radiographically. Stage 1 (no calcification) and Stage 3 (extensive calcification) can be more challenging to recognize.
Clinical Presentation
Symptoms
- Asymptomatic: 50-70% (incidental finding on imaging)
- Pain: 30-50% - dull, aching, activity-related
- No systemic symptoms: Never presents with fever, weight loss, malaise
- Pathological fracture: Rare (under 5%) but possible if large lesion with cortical thinning
Duration
- Chronic pain: Months to years if symptomatic
- Stable size: No progressive enlargement (unlike malignant lesions)
- Incidental discovery: Often found during imaging for other reasons
- Slow involution: May calcify and become more apparent over years
Physical Examination
Inspection and Palpation
- No visible swelling: Intramedullary location prevents external mass
- No skin changes: No erythema, warmth, or overlying soft tissue abnormality
- Tenderness: May have mild focal tenderness over lesion site
- Normal neurovascular exam: No nerve or vessel involvement
Functional Assessment
- Full range of motion: Adjacent joints unaffected
- Normal gait: If calcaneal, may have antalgic gait if painful
- No deformity: Unless pathological fracture occurred
- Weight-bearing: Tolerated unless fracture or severe pain
Red Flags Against Intraosseous Lipoma
These features suggest alternative diagnosis:
- Rapid growth or increasing size (consider malignancy)
- Soft tissue mass extending beyond bone (not characteristic of intraosseous lipoma)
- Systemic symptoms (fever, weight loss - consider infection or malignancy)
- Pathological fracture through aggressive-appearing lesion (reassess diagnosis)
Clinical Scenarios
Common Presentations
| Scenario | Typical Patient | Imaging Indication | Management |
|---|---|---|---|
| Incidental finding | 50-year-old, ankle X-ray for sprain | X-ray shows lucent calcaneal lesion with central calcification | Reassure patient, no treatment needed |
| Chronic heel pain | 45-year-old with 6 months heel pain, no trauma | MRI confirms fat signal lesion in calcaneus | Trial conservative management, consider curettage if persistent |
| Proximal femur lesion | 60-year-old with hip pain, large lesion with cortical thinning | MRI shows fat signal, concern for fracture risk | Consider prophylactic curettage with bone graft |
Imaging and Diagnosis
Plain Radiographs
Radiographic Features
Well-defined radiolucent lesion with narrow zone of transition. Geographic Type IA or IB (Lodwick classification).
Located in metaphysis or diaphysis of long bones, or within calcaneus body.
Dense central nidus of calcification within the lucent lesion. This is the PATHOGNOMONIC feature.
Calcification is typically round or oval, centrally located, distinct from peripheral rim calcification of bone infarct.
Cortex is intact or mildly thinned but not destroyed. No periosteal reaction unless pathological fracture.
Sclerotic rim may be present at margin between lesion and normal bone.
No extension beyond bone cortex. Intraosseous lipomas are purely intramedullary.
Central vs Peripheral Calcification
Distinguish intraosseous lipoma from bone infarct:
- Intraosseous lipoma: Central round/oval calcification (fat necrosis)
- Bone infarct: Peripheral serpentine calcification (geographic map pattern outlining infarct)
This is a classic exam distinction!
MRI - Gold Standard for Diagnosis
Fat Signal Characteristics
Diagnostic feature: Signal identical to subcutaneous fat on all sequences.
- T1-weighted: High signal (bright)
- T2-weighted: Intermediate to high signal
- STIR/Fat saturation: Signal SUPPRESSES completely
- No enhancement: Fat does not enhance with gadolinium
Additional MRI Features
- Central calcification: Low signal nidus on all sequences
- Well-defined margins: Smooth interface with normal marrow
- No soft tissue extension: Confined within bone cortex
- No edema: Surrounding bone marrow normal (unless fracture)
Fat Suppression Confirms Diagnosis
The key to MRI diagnosis is demonstrating that the high T1 signal SUPPRESSES with fat saturation sequences (STIR or fat-sat T2). This proves the lesion contains fat, distinguishing it from other T1 hyperintense lesions like hemorrhage or proteinaceous cyst fluid.
CT Scan
CT is rarely needed but may show:
- Fat density (-40 to -120 Hounsfield units)
- Central calcification well-delineated
- Cortical integrity assessment
CT is useful for surgical planning if curettage planned, to assess cortical thinning and structural integrity.
Differential Diagnosis
| Condition | Key Distinguishing Feature | Imaging Clue |
|---|---|---|
| Bone infarct | Peripheral serpentine calcification | Geographic map pattern at periphery, NOT central |
| Simple bone cyst | No central calcification, younger age | Fallen fragment sign, fluid signal on MRI |
| Aneurysmal bone cyst | Expansile, fluid-fluid levels | Blow-out appearance, hemorrhagic fluid on MRI |
| Enchondroma | Chondroid matrix calcification | Rings and arcs calcification, no fat signal |
| Fibrous dysplasia | Ground-glass matrix, no fat signal | Expansile, no central calcification pattern |
When to Biopsy
Biopsy is RARELY needed if imaging is classic (central calcification on X-ray, fat signal on MRI).
Observation Without Biopsy
Classic imaging features allow confident diagnosis:
- Radiolucent lesion with central calcification
- Fat signal on MRI (high T1, suppresses with fat-sat)
- Typical location (calcaneus, proximal femur)
- Middle-aged patient
Consider Biopsy If
Atypical features raise diagnostic doubt:
- No fat signal on MRI (not a lipoma)
- Aggressive features (cortical destruction, soft tissue mass)
- Rapid growth or change in appearance
- Patient symptoms out of proportion to imaging
Pathology
Gross Pathology
Macroscopic appearance: Yellow, greasy, soft tissue indistinguishable from normal adipose tissue. May have areas of white chalky calcification (fat necrosis).
Size: Typically 2-5 cm diameter, rarely larger.
Histology
Microscopic Features
- Mature adipocytes: Large cells with single lipid vacuole displacing nucleus to periphery
- Minimal atypia: Cells look like normal fat
- Fat necrosis (Stage 2-3): Ghost cells, loss of cell membranes
- Dystrophic calcification: Calcium deposits in necrotic fat
- Reactive bone: Woven bone at periphery in some cases
Differential Histology
Distinguish from:
- Normal marrow fat: Lipoma is expansile mass, not just fatty marrow
- Liposarcoma: Lipoblasts (cells with scalloped hyperchromatic nuclei), not present in benign lipoma
- Bone infarct: Geographic necrosis of bone and marrow, calcification at periphery
Histology Pearl
Histologically, intraosseous lipoma is indistinguishable from soft tissue lipoma - both show mature adipose tissue. The key is the intramedullary location within bone and the central calcification pattern that is unique to intraosseous lipoma.
Management and Treatment
Observation Protocol
Indications for observation:
- Asymptomatic lesion discovered incidentally
- Classic imaging appearance (no diagnostic uncertainty)
- Small size with no risk of pathological fracture
- Patient preference to avoid surgery
Surveillance Schedule
Repeat X-ray at 6 months to confirm stability. Intraosseous lipomas do not grow.
If stable at 6 months, repeat X-ray at 1 year. If still stable, discharge from follow-up.
Educate patient that this is benign. Advise to return if new pain or symptoms develop.
When to Observe
Most intraosseous lipomas can be observed without treatment. Surgery is only indicated for symptomatic lesions or those with fracture risk. Asymptomatic incidental lesions require only reassurance and brief radiographic follow-up to confirm stability.
Postoperative Care
Post-Curettage Rehabilitation Protocol
Wound care and dressing changes. Weight-bearing status depends on site: calcaneus - partial weight-bearing in boot; proximal femur - protected weight-bearing with crutches.
Suture removal at 2 weeks. Progressive weight-bearing as tolerated. X-ray at 6 weeks to assess graft incorporation.
Full weight-bearing for most patients. Transition to normal footwear (calcaneus). Resume light activities.
Return to full activity including sports. Final X-ray to confirm healing and no recurrence. Discharge if stable.
Follow-up Protocol
- X-ray at 6 weeks and 3 months post-curettage
- Annual follow-up not required for confirmed benign lipoma
- Recurrence is rare (under 5%) - patient can be reassured
Outcomes and Prognosis
Surgical Outcomes
Curettage with or without bone graft is curative in over 95% of cases.
Expected Outcomes
- Pain resolution: 95% of patients have complete pain relief
- No recurrence: Under 5% recurrence rate with complete curettage
- Bone healing: Grafted defects heal within 6-12 weeks
- Return to activity: Full activity by 3-6 months post-op
Potential Complications
- Recurrence: Under 5% (incomplete curettage)
- Wound infection: Standard surgical site infection rates (2-3%)
- Pathological fracture: Rare if prophylactic measures taken
- Nerve injury: Site-specific (sural nerve in calcaneus)
Long-term Prognosis
Excellent. Intraosseous lipoma is completely benign with no malignant potential.
- No malignant transformation: Never reported
- No metastases: Does not metastasize
- No growth: Stable size, does not enlarge
- Natural involution: May calcify and involute (Stage 2 to Stage 3)
Prognosis Pearl
The prognosis is 100% excellent. This is a completely benign lesion with no malignant potential. Simple curettage is curative, and recurrence is rare. Patients can be confidently reassured that this is not cancer and will not become cancer.
Complications
Surgical Complications
| Complication | Incidence | Prevention | Management |
|---|---|---|---|
| Recurrence | Under 5% | Complete curettage of all walls | Re-curettage if symptomatic recurrence |
| Pathological fracture | Rare (under 3%) | Prophylactic fixation if large lesion with cortical thinning | ORIF with bone graft |
| Wound infection | 2-3% | Standard sterile technique, prophylactic antibiotics | Antibiotics, irrigation and debridement if deep infection |
| Nerve injury | Under 2% | Careful approach avoiding neurovascular structures | Observation for neuropraxia, exploration if transection suspected |
Disease-Related Complications
Natural History Complications
- Pathological fracture: Rare (under 5%), occurs with large lesions and cortical thinning
- Chronic pain: Mechanism unclear, may be due to microfractures or pressure
- No systemic complications: Does not affect other organs
No Long-term Risks
- No malignant transformation: Never reported in literature
- No recurrence after observation: Lesions do not grow
- No metastases: Does not spread
- No death: Never causes mortality
Evidence Base and Key Studies
Milgram Classification of Intraosseous Lipoma
- Landmark classification system based on 55 cases of intraosseous lipoma
- Three stages based on histological appearance: viable fat (Stage 1), fat necrosis with calcification (Stage 2), extensive calcification (Stage 3)
- Stage 2 most common (60-70%), representing the classic central calcification pattern
- All stages are benign - staging reflects involution, not biological behavior
Radiological Features of Intraosseous Lipoma
- Review of imaging features in 21 cases of intraosseous lipoma
- Central calcification present in 81% of cases on radiographs (pathognomonic when present)
- MRI shows fat signal (high T1, suppresses with fat saturation) in 100% of cases
- Calcaneus was most common site (62%), followed by proximal femur (24%)
Surgical Management and Outcomes of Intraosseous Lipoma
- Case series of 16 intraosseous lipomas treated surgically
- Simple curettage curative in all cases (100% success rate)
- No recurrences with mean follow-up of 4.2 years
- Bone grafting recommended for large defects to prevent pathological fracture
Intraosseous Lipoma: Report of 35 Cases and Review
- Largest radiologic series analyzing 35 cases of intraosseous lipoma
- Calcaneus most common location (60%), followed by proximal femur and tibia
- Central calcification present in 81% of cases - pathognomonic when present
- MRI diagnostic in all cases - fat signal (high T1, suppresses with fat saturation)
Exam Viva Scenarios
Practice these scenarios to excel in your viva examination
Scenario 1: Incidental Calcaneal Lesion
"A 52-year-old woman presents after ankle sprain. X-ray shows a well-defined radiolucent lesion in the calcaneus with a central dense calcification. She has no heel pain. What is your diagnosis and management?"
Scenario 2: Proximal Femur Lesion with Fracture Risk
"A 58-year-old man presents with 6 months of hip pain. Imaging shows a 5cm radiolucent lesion in the intertrochanteric region of the proximal femur with central calcification and significant cortical thinning. MRI confirms fat signal. How do you manage this?"
Scenario 3: Differential Diagnosis Challenge
"A 45-year-old presents with a radiolucent lesion in the calcaneus. Your colleague suggests this is a simple bone cyst. The X-ray shows some central density. How do you differentiate between intraosseous lipoma and simple bone cyst? What additional imaging would you order?"
MCQ Practice Points
Most Common Site
Q: What is the most common site for intraosseous lipoma? A: Calcaneus accounts for 60% of all intraosseous lipomas, followed by proximal femur (20%). This is a high-yield fact.
Pathognomonic Imaging
Q: What is the pathognomonic radiographic finding of intraosseous lipoma? A: Central calcification within a radiolucent lesion. This dense central nidus of calcification distinguishes intraosseous lipoma from simple bone cyst and other lucent lesions.
MRI Diagnosis
Q: What MRI finding confirms the diagnosis of intraosseous lipoma? A: High T1 signal that suppresses with fat saturation sequences. This proves fat content and allows confident diagnosis without biopsy.
Milgram Classification
Q: What does the Milgram classification of intraosseous lipoma indicate? A: The Milgram classification (Stages 1-3) reflects the histological evolution from viable fat to necrosis and calcification. It does NOT indicate biological behavior or prognosis - all stages are equally benign.
Treatment Indications
Q: What are the indications for surgical treatment of intraosseous lipoma? A: Surgery indicated for: persistent pain unresponsive to conservative treatment, pathological fracture or imminent fracture risk (large lesion with cortical thinning), or diagnostic uncertainty. Asymptomatic lesions can be observed.
Malignant Potential
Q: What is the malignant potential of intraosseous lipoma? A: Zero. Intraosseous lipoma is completely benign with no reported cases of malignant transformation. Prognosis is excellent.
Australian Context
Referral Pathway
- Most cases managed in general orthopaedic practice
- Musculoskeletal radiologists can confirm diagnosis on MRI
- Oncology referral NOT required (benign lesion)
Imaging Access
- MRI widely available for confirming fat signal
- Medicare rebates available for MRI of bone lesions
- CT rarely needed unless planning complex reconstruction
Fellowship Examination Relevance
For Orthopaedic fellowship examination, be prepared to describe the pathognomonic imaging features (central calcification on X-ray, fat signal on MRI), the Milgram classification (Stages 1-3 based on fat necrosis and calcification), and explain why this lesion is completely benign with no malignant potential.
INTRAOSSEOUS LIPOMA
High-Yield Exam Summary
Key Facts
- •Rare benign tumor - under 0.1% of all bone tumors
- •Calcaneus most common site (60%), proximal femur (20%)
- •Age 40-60 years, equal gender distribution
- •Completely benign - no malignant potential
Pathognomonic Imaging
- •Central calcification on X-ray - dense nidus within radiolucent lesion
- •Fat signal on MRI - high T1, suppresses with fat saturation
- •Distinguish from bone infarct - infarct has peripheral serpentine calcification
- •MRI diagnostic - biopsy rarely needed if imaging classic
Milgram Classification
- •Stage 1: Viable fat only - no calcification visible
- •Stage 2: Fat necrosis with central calcification - most common (60-70%)
- •Stage 3: Extensive calcification with cyst formation
- •Staging reflects involution, NOT biological behavior - all benign
Clinical Presentation
- •Asymptomatic (50-70%) - incidental finding
- •Pain (30-50%) - dull, aching, activity-related
- •Pathological fracture rare (under 5%) with large lesions
- •No systemic symptoms
Management
- •Asymptomatic: Observation with 6-month X-ray to confirm stability
- •Symptomatic or fracture risk: Curettage with bone graft
- •Prophylactic fixation if large lesion with cortical thinning
- •Recurrence rare (under 5%) with complete curettage
Exam Pearls
- •Central calcification = pathognomonic (vs peripheral in bone infarct)
- •Fat on MRI confirms diagnosis - high T1, suppresses with fat-sat
- •Calcaneus is #1 site - always think lipoma for lucent calcaneal lesion with central calcification
- •Simple curettage curative - no wide margins needed (benign)