Aneurysmal Bone Cyst

Slide 1 · Aneurysmal Bone Cyst

Mechanism • imaging • morphology • differential diagnosis

Pathology teaching lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Define aneurysmal bone cyst and explain why it is neoplastic yet benign.

Relate USP6 activation to osteolysis and characteristic cystic architecture.

Interpret imaging, gross appearance and septal microscopic features together.

Recognize recurrence and critical benign–malignant diagnostic differentials.

Slide 3 · Definition: A blood-filled bone neoplasm

Aneurysmal bone cyst (ABC) is a benign neoplasm of bone.

Its defining architecture is multiloculated, blood-filled cyst-like spaces.

Despite benign classification, tissue expansion and bone resorption can be locally destructive.

Blood-filled spaces

Fibrous septa

Schematic — not a specimen

Slide 4 · What the name does—and does not—mean

“Cyst” describes hemorrhagic, cavity-like spaces within bone.

“Aneurysmal” does not imply a true arterial aneurysm.

The spaces lack an endothelial lining: They are pseudocystic rather than vascular channels.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 5 · Biologic behavior: Benign, not innocuous

ABC is not classified as a malignant bone tumor.

Expansile growth can thin and remodel adjacent cortex.

Local aggressiveness explains symptoms, fracture-related problems and the need for treatment.

Local bone expansion

Pain / swelling

Fracture risk or neural compression

(dependent on site)

Schematic — not a specimen

Slide 6 · Age pattern

All age groups may be affected.

Most cases present during adolescence.

Age supports the clinical context, but cannot establish the diagnosis by itself.

Slide 7 · Predilection for major long bones

The femur and tibia are among the most frequent sites.

ABC can be considered when a young patient has an expansile lytic lesion in these bones.

Site is a clue that must be integrated with lesion position and internal architecture.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 8 · Vertebral involvement: Posterior elements

In the spine, ABC commonly involves the lamina and pedicles.

An enlarging lesion in this compartment can compress neural structures.

Neurologic manifestations depend on the lesion’s anatomy, not on malignant histology.

Vertebral body

Spinal canal

Posterior-element ABC

Schematic — not a specimen

Slide 9 · Clinical–pathologic framework

Bone resorption and expansion explain the radiographic appearance.

Hemorrhagic compartments account for internal fluid levels and gross cysts.

Fibroblastic septa, giant cells and woven bone form the diagnostic microscopic pattern.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 10 · How ABC came to be recognized as a neoplasm

The neoplastic element is a spindle-cell population within the septa.

Chromosomal rearrangements provide molecular evidence of clonal neoplasia.

This differs from interpreting a hemorrhagic cavity as a purely passive blood collection.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 11 · Cellular origin remains incompletely defined

The spindle-shaped neoplastic cells as being of uncertain origin.

The spindle cells coexist with osteoclast-like giant cells and osteoblastic bone repair.

Do not infer a proven specific cell of origin solely from morphology.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 12 · Chromosome 17p13 involvement

The defining molecular mechanism involves rearrangements at chromosome 17p13.

The locus contains USP6, the gene activated in many primary ABCs.

These are gene-regulatory rearrangements, not a general rule of chromosome loss.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 13 · USP6 activation: The essential molecular event

The USP6 coding region becomes juxtaposed to regulatory elements of partner genes.

The result is overexpression of USP6 protein.

Partner-gene diversity is compatible with a shared USP6-driven pathway.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 14 · CDH11 as a recurrent fusion partner

CDH11 as the most common USP6 regulatory partner.

The partner contributes gene-control elements; The USP6 coding sequence remains relevant.

A CDH11–USP6 example illustrates promoter swapping rather than a new chimeric enzyme domain.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 15 · Promoter swapping: Mechanism, not mere naming

A relatively active partner regulatory region becomes linked to USP6.

USP6 transcription is inappropriately enhanced in neoplastic septal cells.

The pathogenic point is deregulated expression, even when fusion partners differ.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 16 · USP6 is a deubiquitinating enzyme

USP6 encodes a deubiquitinating protein.

In ABC, its overexpression increases signaling activity downstream.

The clinically important result is a transcriptional program that promotes matrix breakdown.

USP6 overexpression

Increased NF-κB activity

MMP expression rises

Cystic bone resorption

Schematic — not a specimen

Slide 17 · NF-κB signaling downstream of USP6

The Robbins mechanism places increased NF-κB activity after USP6 overexpression.

NF-κB functions as a transcription factor that alters gene expression.

This links a genetic alteration to a destructive tissue phenotype.

USP6 overexpression

Increased NF-κB activity

MMP expression rises

Cystic bone resorption

Schematic — not a specimen

Slide 18 · Matrix metalloproteinases and osteolysis

NF-κB–associated transcription increases proteins including matrix metalloproteinases.

These enzymes contribute to extracellular-matrix degradation.

Their increased activity helps explain cystic resorption of native bone.

USP6 overexpression

Increased NF-κB activity

MMP expression rises

Cystic bone resorption

Schematic — not a specimen

Slide 19 · Pathogenesis: Integrated sequence

Regulatory fusion → USP6 overexpression.

USP6 → enhanced NF-κB activity → matrix metalloproteinase expression.

Progressive matrix destruction produces characteristic cystic bone resorption.

USP6 overexpression

Increased NF-κB activity

MMP expression rises

Cystic bone resorption

Schematic — not a specimen

Slide 20 · Molecular mechanism explains the imaging

Resorption creates a lytic compartment in an otherwise mineralized organ.

Loculated hemorrhagic spaces produce internal structure rather than a single simple cavity.

Reactive bone at the periphery provides the characteristic thin shell.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 21 · Phenotype integrates neoplastic and reactive elements

Neoplastic spindle cells are embedded in a lesion with extensive secondary tissue responses.

Osteoclast-type giant cells and osteoblast-rimmed woven bone help shape the histology.

The presence of reactive structures does not negate the neoplastic USP6 driver.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 22 · Primary ABC versus secondary ABC-like change

A primary ABC is a distinct neoplastic lesion, commonly associated with USP6 rearrangement.

ABC-like cystic changes may occur within other bone tumors and require identification of that lesion.

The term “secondary ABC” must not obscure a different underlying diagnosis.

Primary aneurysmal bone cyst

USP6-driven neoplastic septal cells

ABC-like change within another lesion

Find and characterize underlying tumor

Schematic — not a specimen

Slide 23 · What USP6 testing can contribute

Detection of a USP6 rearrangement supports primary ABC in an appropriate context.

Molecular testing may clarify an equivocal hemorrhagic giant-cell-rich lesion.

A negative test does not automatically exclude ABC; Assay context and morphology remain necessary.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 24 · Molecular results cannot replace tissue assessment

USP6 activation can be shared across several other USP6-rearranged soft-tissue and bone processes.

Identify the anatomic site and characteristic architecture before assigning the diagnosis.

Conversely, hemorrhagic morphology alone does not establish USP6 status.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 25 · Localized pain: A principal symptom

ABC frequently presents with pain localized to the affected bone.

Expansile osteolysis and distortion of adjacent structures provide a clinicopathologic explanation.

Neither pain severity nor duration is specific for ABC.

Local bone expansion

Pain / swelling

Fracture risk or neural compression

(dependent on site)

Schematic — not a specimen

Slide 26 · Swelling as a sign of local expansion

Local enlargement may produce visible or palpable swelling.

A locally aggressive lesion can deform the bony outline despite benign classification.

Examination findings should be interpreted with bone site and imaging.

Local bone expansion

Pain / swelling

Fracture risk or neural compression

(dependent on site)

Schematic — not a specimen

Slide 27 · Spinal lesions and neurologic compromise

Lesions of vertebral posterior elements may compress nerves.

Clinical assessment should seek neurologic deficits when spine involvement is suspected.

Benign pathology does not imply an absence of urgent anatomic consequences.

Vertebral body

Spinal canal

Posterior-element ABC

Schematic — not a specimen

Slide 28 · Pathologic fracture and secondary changes

Cortical attenuation makes fracture a biologically plausible complication of expansion.

Fracture-related tissue damage can cause necrosis; Robbins otherwise describes necrosis as uncommon.

In a fractured lesion, do not overinterpret necrosis without the full clinical context.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 29 · Radiologic evaluation: The lesion as a whole

Describe location, centricity, margin, cortical shell and internal architecture.

ABC usually combines an eccentric expansile lytic component with a well-defined boundary.

Interpretation requires more than the presence or absence of fluid-fluid levels.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 30 · Eccentric lytic pattern

ABC is generally eccentric rather than uniformly centered within a long bone.

“Lytic” denotes loss of mineralized bone in the lesion.

Expansile behavior helps separate the lesion from a small static cortical defect.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 31 · Expansile growth and cortical remodeling

Growth can produce marked outward expansion of the bone.

An attenuated peripheral bony shell may remain as the lesion enlarges.

An expanding benign process can resemble aggressive disease on a single imaging feature.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 32 · Well-defined margin and reactive eggshell

Most ABCs are circumscribed and radiographically well defined.

A thin sclerotic peripheral eggshell reflects reactive bone deposition.

This rim is a pattern clue; It is not proof of an exclusive diagnosis.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 33 · Internal septa on cross-sectional imaging

Computed tomography and magnetic resonance imaging can show internal septation.

Multiloculation on imaging corresponds to the fibrous partitions visible grossly.

The septa are relevant targets for histologic examination and differential diagnosis.

Blood-filled spaces

Fibrous septa

Schematic — not a specimen

Slide 34 · Fluid–fluid levels: Characteristic imaging clue

CT and MRI can reveal fluid–fluid levels within cystic spaces.

Levels provide a useful clue to compartmentalized hemorrhagic contents.

They should be interpreted with lesion margins, septa and other imaging features.

Horizontal interfaces between

Layered hemorrhagic contents

Schematic — not a specimen

Slide 35 · Why fluid–fluid interfaces develop

Different-density hemorrhagic components can settle into layers within a cavity.

Cross-sectional imaging depicts the resulting interfaces between fluid components.

This physical interpretation does not prove that the underlying lesion is benign.

Horizontal interfaces between

Layered hemorrhagic contents

Schematic — not a specimen

Slide 36 · Fluid levels are not pathognomonic

Other hemorrhagic bone tumors may also contain fluid–fluid levels.

Telangiectatic osteosarcoma is an important malignant mimic.

An indeterminate aggressive lesion requires attention to solid septa and tissue diagnosis.

Horizontal interfaces between

Layered hemorrhagic contents

Schematic — not a specimen

Slide 37 · Structured imaging report for suspected ABC

Specify bone, anatomic compartment and distance to adjacent critical structures.

Describe lesion margins, cortical integrity, expansion and internal septation.

Report fluid levels and identify solid components requiring scrutiny.

Slide 38 · Gross appearance: Multiple blood-filled cavities

A sectioned ABC has a hemorrhagic, sponge-like appearance.

Numerous cystic spaces are separated by pale tan-white septa.

The macroscopic anatomy matches the multiloculated appearance seen on imaging.

Blood-filled spaces

Fibrous septa

Schematic — not a specimen

Slide 39 · Gross septa are diagnostically important

Blood may dominate a sectioned lesion visually, but the septa contain the tissue architecture.

Septal tissue is therefore essential for identifying neoplastic and reactive components.

An isolated blood sample cannot adequately characterize the whole lesion.

Blood-filled spaces

Fibrous septa

Schematic — not a specimen

Slide 40 · Microscopic architecture: Pseudocysts

Spaces contain blood yet lack endothelial lining.

Fibrous, cellular septa partition adjacent cavities.

The lesion is therefore not a conventional vascular malformation or true endothelial-lined aneurysm.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 41 · Septal plump spindle cells

The septa contain plump spindle-shaped lesional cells.

These form part of the neoplastic tissue compartment.

Interpret spindle cells in relation to giant cells, woven bone and overall morphology.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 42 · Osteoclast-type multinucleated giant cells

Multinucleated osteoclast-like cells occur in the septa.

Giant cells are a morphological feature, not a uniquely diagnostic marker.

The differential includes other giant-cell-rich bone lesions.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 43 · Reactive woven bone in the septa

Irregular woven bone is present within the fibrous septa.

Bony deposition often follows the contours of septal structures.

This pattern helps explain osseous material within a largely hemorrhagic lesion.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 44 · Osteoblastic rimming of reactive bone

Reactive woven bone lined by osteoblasts.

This is a recognizable component of the septa, not evidence of malignant osteoid production.

Evaluate lining cells and matrix together in the context of the full section.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 45 · Blue bone: A distinctive metaplastic matrix

Approximately one-third of ABCs contain densely calcified basophilic metaplastic matrix.

This material is termed “blue bone”.

Its presence supports a morphologic pattern but is not a universal requirement.

Pseudocyst

Cellular septum

Basophilic metaplastic matrix

Schematic — not a specimen

Slide 46 · Necrosis: An important contextual observation

Necrosis is uncommon in ABC without associated pathologic fracture.

Fracture can produce secondary necrosis within an otherwise benign process.

Extensive atypia or concerning solid tissue should not be dismissed as a fracture effect.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 47 · Integrated microscopic diagnostic pattern

Blood-filled non–endothelial-lined spaces are separated by cellular septa.

The septa contain spindle cells, osteoclast-type giant cells and reactive osteoblast-rimmed woven bone.

A broad specimen and radiologic correlation increase confidence.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 48 · Radiologic–gross–histologic correspondence

Radiology

Gross specimen

Histology

Expansile lysis

Loculated hemorrhagic cavity

Bone resorption and fibrous septa

Fluid–fluid levels

Blood-filled compartments

Hemorrhage within pseudocysts

Thin reactive shell

Peripheral bone remodeling

Reactive bone formation

Internal septa

Tan-white fibrous partitions

Spindle cells, giant cells, woven bone

Slide 49 · Why sampling may mislead

A cavity may yield blood rather than diagnostic septal tissue.

Cystic change may mask a pre-existing tumor within the same lesion.

Review discordance between imaging and limited histology before committing to ABC.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 50 · ABC versus giant cell tumor of bone

Feature

Aneurysmal bone cyst

Giant cell tumor

Typical context

Adolescence; long bones and posterior spine

Usually adults, often epiphysis of long bones

Dominant pattern

Blood-filled pseudocysts with septa

Solid mononuclear stroma with abundant giant cells

Molecular clue

USP6 regulatory rearrangement

H3-3A mutation in neoplastic cells

Clinical note

Expansile and locally aggressive

Locally destructive, may recur

Slide 51 · ABC versus nonossifying fibroma

Feature

Aneurysmal bone cyst

Nonossifying fibroma

Typical imaging

Expansile lytic cavity; fluid levels possible

Eccentric metaphyseal lucency with sclerotic rim

Histologic architecture

Blood-filled spaces and cellular septa

Storiform bland fibroblasts and foamy macrophages

Characteristic cells

Spindle cells; osteoclast-type giant cells

Fibroblasts, macrophages, giant cells

Molecular context

USP6 regulatory fusion

RAS-pathway alterations described

Slide 52 · ABC versus fibrous dysplasia

Feature

Aneurysmal bone cyst

Fibrous dysplasia

Architecture

Multiloculated hemorrhagic pseudocysts

Fibroblastic stroma with curvilinear woven bone

Woven bone

Reactive; often osteoblast-rimmed

Typically without prominent osteoblastic rimming

Molecular context

USP6 regulatory rearrangement

Somatic activating GNAS alterations

Important caution

May be a distinct primary lesion

May show superimposed ABC-like change

Slide 53 · ABC-like change within another bone lesion

Other benign and malignant tumors may develop secondary hemorrhagic cystic architecture.

Reported examples include giant cell tumor, fibrous dysplasia and osteosarcoma.

The final diagnosis should name the underlying process when it is identified.

Primary aneurysmal bone cyst

USP6-driven neoplastic septal cells

ABC-like change within another lesion

Find and characterize underlying tumor

Schematic — not a specimen

Slide 54 · Telangiectatic osteosarcoma: Do not miss

Both lesions can be expansile, hemorrhagic and show fluid–fluid levels.

Malignant atypical stromal cells within septa favor telangiectatic osteosarcoma.

Suspicious enhancing solid components or malignant osteoid demand complete evaluation.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 55 · Evaluate the septa, not only the blood

The central diagnostic distinction often lies in tissue within septa or solid portions.

Look for bland ABC spindle cells versus cytologically malignant stroma.

A targeted, representative sample is essential when imaging and histology disagree.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 56 · Diagnostic integration: Practical pathway

Begin with clinical age and precise skeletal site.

Review lesion boundaries, cortical expansion, septa and solid nodules on imaging.

Examine representative septal tissue; Investigate underlying tumors and use USP6 testing if unresolved.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 57 · Local aggressiveness without metastasis as a defining feature

ABC can be locally destructive despite benign histologic categorization.

Pain, mass effect and compromised adjacent structures are consequences of location and expansion.

The principal management issue is local control rather than systemic oncologic staging.

Local bone expansion

Pain / swelling

Fracture risk or neural compression

(dependent on site)

Schematic — not a specimen

Slide 58 · Treatment: Curettage or excision

Curettage or excision as treatment approaches.

Choice of intervention depends on anatomy and clinical management considerations.

These treatment names do not imply that every lesion has an identical surgical plan.

Locally aggressive growth

Curettage or excision

Local recurrence remains possible

Reassess new pain / swelling

Schematic — not a specimen

Slide 59 · Recurrence is a clinically important outcome

Local recurrence in 10%–50% of cases.

The range is broad and should not be presented as an individual-patient probability.

Return of local symptoms after treatment warrants reassessment for recurrent or residual lesion.

Locally aggressive growth

Curettage or excision

Local recurrence remains possible

Reassess new pain / swelling

Schematic — not a specimen

Slide 60 · Follow-up relates to local behavior

Clinical surveillance focuses on recurrent pain, swelling and site-specific deficits.

Imaging is used as indicated to evaluate residual or recurrent expansion.

A follow-up plan is individualized; Robbins does not provide a universal surveillance interval.

Locally aggressive growth

Curettage or excision

Local recurrence remains possible

Reassess new pain / swelling

Schematic — not a specimen

Slide 61 · Case 1: Adolescent with distal femoral pain

A 15-year-old has several months of focal pain and swelling near the knee.

Imaging shows a circumscribed eccentric expansile lytic lesion with a thin shell.

MRI demonstrates septated cavities with multiple fluid–fluid levels.

Eccentric lytic cavity

Thin reactive shell

Long bone (section)

Schematic — not a specimen

Slide 62 · Case 1: What would establish ABC?

The imaging pattern supports ABC but is insufficient on its own.

Histology should show hemorrhagic pseudocysts and bland fibroblastic septa with giant cells and woven bone.

A malignant solid component or marked septal atypia would require reconsideration.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 63 · Case 2: Vertebral posterior-element lesion

An adolescent develops focal spinal pain with progressive nerve-related symptoms.

Cross-sectional imaging reveals an expansile lesion centered in the posterior elements.

The diagnostic problem includes both lesion identification and anatomic compression.

Vertebral body

Spinal canal

Posterior-element ABC

Schematic — not a specimen

Slide 64 · Case 2: Clinicopathologic priority

Robbins supports ABC in posterior vertebral elements as a recognized site.

Neural compression can explain neurologic deficits without requiring malignant pathology.

Urgency follows the neurologic findings and degree of compression.

Vertebral body

Spinal canal

Posterior-element ABC

Schematic — not a specimen

Slide 65 · Case 3: A fluid-level diagnostic trap

A rapidly enlarging bone lesion has fluid–fluid levels and thick enhancing internal tissue.

A limited sample contains mostly blood and a small amount of reactive bone.

The available material does not safely exclude a malignant hemorrhagic bone tumor.

Horizontal interfaces between

Layered hemorrhagic contents

Schematic — not a specimen

Slide 66 · Case 3: Resolving the discrepancy

Correlate sampling with the suspicious solid or thick septal areas.

Evaluate for atypical malignant stromal cells and neoplastic osteoid.

Do not label the entire lesion “ABC” solely because fluid levels and blood are present.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 67 · Knowledge check: USP6 mechanism

Which molecular change is central to primary ABC?

USP6 coding sequence becomes controlled by partner-gene regulatory elements.

The resulting overexpression promotes NF-κB activity and matrix-degrading proteins.

Normal gene regulation

CDH11 regulatory region

USP6 coding region

Promoter swapping / fusion

USP6 overexpression

Schematic — not a specimen

Slide 68 · Knowledge check: Microscopic triad

What should a representative ABC septum contain?

Bland plump spindle cells, osteoclast-like giant cells and reactive woven bone.

The adjacent blood-filled spaces are not lined by endothelium.

Pseudocyst

Cellular septum

Schematic — not a specimen

Slide 69 · Diagnostic synthesis

The lesion is benign but can be locally aggressive.

USP6-driven signaling and matrix degradation underpin the neoplastic mechanism.

Morphologic diagnosis depends on septa and blood-filled pseudocysts, not fluid levels alone.

A malignant mimic or underlying tumor must be excluded when findings are discordant.

Expansile hemorrhagic bone lesion

Review imaging + septal histology

Exclude underlying tumor and

Malignant septal cells

Consider USP6 testing in equivocal cases

Schematic — not a specimen

Slide 70 · References and source boundaries

Primary textbook

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. Chapter 26: Bones, Joints, and Soft Tissue Tumors. pp. 1084–1086.

Supplementary diagnostic context

Nasri E, Reith JD. Aneurysmal bone cyst: a review. J Pathol Transl Med. 2023;57:81–87. doi:10.4132/jptm.2023.02.23.

Restrepo R, Zahrah D, Pelaez L, et al. Update on aneurysmal bone cyst: pathophysiology, histology, imaging and treatment. Pediatr Radiol. 2022;52:1601–1614. doi:10.1007/s00247-022-05396-6.

All diagrams are original editable schematics; no diagnostic specimen images are reproduced.