Tumors like lesions of bone

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Tumor-Like Lesions of Bone

These are non-neoplastic bone lesions that mimic true bone tumors clinically and radiographically. They are classified under "Lesions Simulating Primary Neoplasms" in pathology. The major categories are covered below, along with key primary bone tumors for context.

Source: Robbins & Kumar Basic Pathology (Robbins Pathology)

Classification of Primary Bone Tumors (Overview)

Category	Behavior	Tumor Type	Common Location	Age (yr)
Bone forming	Benign	Osteoid osteoma	Metaphysis of long bones	10-20
Bone forming	Benign	Osteoblastoma	Vertebral column	10-20
Bone forming	Malignant	Osteosarcoma	Distal femur, proximal tibia	10-20
Cartilage forming	Benign	Osteochondroma	Metaphysis of long bones	10-30
Cartilage forming	Benign	Chondroma	Small bones of hands/feet	30-50
Cartilage forming	Malignant	Chondrosarcoma	Pelvis, shoulder	40-60
Unknown origin	Benign	Giant cell tumor	Epiphysis of long bones	20-40
Unknown origin	Benign	Aneurysmal bone cyst	Proximal tibia, distal femur, vertebra	10-20
Unknown origin	Malignant	Ewing sarcoma	Diaphysis of long bones	10-20

True Tumor-Like Lesions (Lesions Simulating Primary Neoplasms)

These are the three classic tumor-like (non-neoplastic) lesions:

1. Fibrous Cortical Defect and Nonossifying Fibroma

Nature: Common developmental abnormality - fibrous connective tissue replaces bone
Incidence: Present in up to 50% of children older than 2 years
Location: Eccentrically in the metaphysis of the distal femur and proximal tibia; almost half are bilateral or multiple
Size distinction: <0.5 cm = fibrous cortical defect; those that grow to 5-6 cm = nonossifying fibroma
Radiology: Sharply demarcated radiolucent masses surrounded by a thin rim of sclerosis - appearance is specific enough that biopsy is rarely necessary

Morphology: Gray to yellow-brown cellular lesions with cytologically bland fibroblasts arranged in a storiform (pinwheel) pattern, with macrophages that may be foamy or form multinucleate giant cells. Hemosiderin is commonly present.

Clinical: Most small lesions resolve spontaneously. Progressive enlargement may cause pathologic fracture. Treatment is curettage with possible bone grafting.

2. Fibrous Dysplasia

Nature: Benign lesion resulting from a localized developmental arrest - all bone components are present but fail to differentiate into mature structures
Genetics: Somatic gain-of-function mutations in GNAS1 (same gene mutated in pituitary adenomas) → constitutively active Gs-protein → increased cAMP → promotes cellular proliferation and disrupts osteoblast differentiation
Phenotype depends on when during embryogenesis the mutation was acquired and what proportion of mesenchymal cells are affected

Forms:

Monostotic - single bone involvement (most common)
Polyostotic - multiple bones; may cause deformities and fractures into adulthood
Mazabraud syndrome - fibrous dysplasia + soft tissue myxoma
McCune-Albright syndrome - polyostotic fibrous dysplasia + café-au-lait skin pigmentations + endocrine abnormalities (especially precocious puberty)

Morphology: Intramedullary lytic lesions that may expand and cause bowing/cortical thinning. Periosteal reaction is usually absent. Composed of curvilinear trabeculae of woven bone without an osteoblast rim, surrounded by a moderately cellular fibroblastic proliferation. Cystic degeneration, hemorrhage, and foamy macrophages are common.

Fibrous Dysplasia histology - curvilinear trabeculae of woven bone lacking osteoblastic rimming in a fibrous background

Fibrous dysplasia: curvilinear trabeculae of woven bone that lack conspicuous osteoblastic rimming, arising in a background of fibrous tissue.

Key distinguishing feature: Absence of osteoblastic rimming of trabeculae (the "Chinese letters" pattern of woven bone in a fibrous stroma - likened to "alphabet soup")

Clinical:

Monostotic disease often stops enlarging at growth plate closure
Symptomatic lesions treated by curettage (recurrence common)
Bisphosphonates reduce bone pain in polyostotic disease
Rare complication: malignant transformation into sarcoma (usually polyostotic)

3. Aneurysmal Bone Cyst (ABC)

Nature: Characterized by multiloculated blood-filled cystic spaces - not a true cyst and not truly aneurysmal
Age: All age groups affected; most cases present in adolescence
Location: Most frequently the femur, tibia, and vertebral body posterior elements
Genetics: Spindle-shaped cells frequently demonstrate rearrangements of chromosome 17p13 → fusion of USP6 gene (encodes a deubiquitinating enzyme) regulatory elements to COL1A1 → USP6 overexpression → upregulates NF-κB → increases matrix metalloproteases → cystic bone resorption

Morphology:

Radiography: Eccentric, expansile, lytic, metaphyseal lesion with well-defined margins
CT/MRI: Internal septa and characteristic fluid-fluid levels (pathognomonic)
Gross: Multiple blood-filled cystic spaces separated by thin tan-white septa
Micro: Septa lack endothelial lining and are composed of plump uniform fibroblasts, multinucleate osteoclast-like giant cells, and reactive woven bone

Aneurysmal bone cyst - axial MRI showing fluid-fluid levels (arrow), and gross specimen showing hemorrhagic spongelike appearance

ABC: (A) MRI showing characteristic fluid-fluid levels (arrow). (B) Gross specimen - hemorrhagic, spongelike bisected proximal fibula.

Clinical: Presents with localized pain and swelling. Although benign, it is locally aggressive. Treatment: curettage or excision. Recurrence in 10-50% of cases.

Related: Giant Cell Tumor (True Tumor Often Grouped Here)

Although a true neoplasm, Giant Cell Tumor (GCT) is often discussed alongside tumor-like lesions:

Age: 20-40 years (adults after skeletal maturity)
Location: Epiphysis of long bones (distal femur, proximal tibia - around the knee)
Behavior: Locally aggressive, can rarely metastasize
Genetics: H3F3A mutations (histone H3.3) in stromal cells; RANKL-dependent osteoclast recruitment
Radiology: Lytic, expansile, destroys medullary canal and cortex; extends to subchondral bone
Morphology: Sheets of uniformly distributed multinucleate osteoclast-like giant cells (up to 50+ nuclei) with background mononuclear stromal cells

Giant cell tumor histology showing abundant multinucleate giant cells with background mononuclear stromal cells

Giant cell tumor: abundance of multinucleate giant cells with background mononuclear stromal cells.

Treatment: Curettage with bone cement/grafting; denosumab (anti-RANKL) for unresectable cases. Recurrence ~50% after curettage alone.

Quick Comparison Summary

Lesion	Age	Location	Key Feature	Radiology	Genetics
Fibrous cortical defect / NOF	Children/teens	Metaphysis of distal femur/tibia	Storiform fibroblasts, hemosiderin	Radiolucent with sclerotic rim	-
Fibrous dysplasia	Any (presents young)	Variable	Woven bone without osteoblast rimming	Lytic, bowing, "ground glass"	GNAS1 mutation
Aneurysmal bone cyst	Adolescents	Femur, tibia, vertebra	Blood-filled cysts, no endothelial lining	Eccentric lytic + fluid-fluid levels	USP6-COL1A1 fusion
Giant cell tumor	20-40	Epiphysis	Sheets of giant cells	Lytic, epiphyseal	H3F3A mutation

Robbins & Kumar Basic Pathology, pp. 780-789

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