Sinonasal Angiofibroma

Slide 1 · Sinonasal Angiofibroma

Clinicopathology • Morphology • Molecular basis • Diagnostic strategy

A benign fibrovascular neoplasm with potentially serious local effects

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Distinguish benign histology from locally aggressive behavior in sinonasal angiofibroma.

Link vascular–stromal architecture to epistaxis, imaging findings and biopsy risk.

Interpret CTNNB1/β-catenin and APC/FAP associations without overstating causation.

Plan a safe clinicopathologic diagnostic pathway and recognize important mimics.

Slide 3 · The entity: Vascular tissue and fibrous stroma

Angio-

Numerous vascular channels

And prominent blood supply

-fibroma

Collagen-rich stroma

With bland fibroblastic cells

Clinical behavior

Histologically benign

But often locally aggressive

Slide 4 · Why the modern name emphasizes “sinonasal”

Historically called juvenile nasopharyngeal angiofibroma (JNA).

Origin is not restricted to the nasopharyngeal mucosal compartment.

The posterolateral nasal cavity and nearby lateral nasopharyngeal region are implicated.

WHO 5th-edition terminology places sinonasal tract angiofibroma among sinonasal mesenchymal tumors.

Slide 5 · Posterolateral nasal cavity: Topologic relationships

Posterior nasal cavity

Pterygopalatine fossa

Nasopharynx

Orbit / orbit-adjacent space

Skull base / cranial cavity

Suspected origin zone

Topologic relationship schematic only — not a scaled anatomical section

Slide 6 · The sphenopalatine region as a disease hub

Anatomic neighborhood

Posterolateral nasal wall

Near sphenopalatine foramen

Vascular context

Arterial feeders can supply

A densely vascular mass

Extension context

Pterygopalatine compartment

Communicates with deeper spaces

Slide 7 · How a localized lesion becomes extensive

Origin

Posterolateral nasal cavity

Expansion

Nasopharyngeal / nasal lumen

Deep spread

Pterygopalatine fossa

Advanced disease

Orbit or skull base

Extent describes anatomical reach, not malignant histology.

Slide 8 · Anatomic planes help explain local extension

Medial / posterior

Nasal airway and choanal space

→ obstruction

Lateral

Pterygopalatine and adjacent

Infratemporal compartments

Superior

Skull-base and orbital proximity

→ serious complications

Slide 9 · Benign is a histologic classification—not a safety guarantee

The tumor is composed of bland vascular and stromal elements.

No malignant cytologic features are required for substantial morbidity.

Expansile growth and extension may compromise neighboring structures.

Hemorrhage can be a major procedural and clinical hazard.

Slide 10 · Clinical setting: The characteristic patient

The strongest epidemiologic clue is an adolescent male.

Occurrence outside this population is unusual, but not impossible.

Age and sex contribute to pre-test probability; They do not prove a diagnosis.

Consider the lesion particularly when a posterior nasal mass is also highly vascular.

Slide 11 · Why symptoms arise

Rich vascularity

Bleeding-prone channels

Intranasal growth

Reduced airway space

Local extension

Effects on adjacent structures

One lesion produces both hemorrhagic and obstructive symptom patterns.

Slide 12 · Epistaxis: The key presenting clue

Epistaxis is prominent in the Robbins description of sinonasal angiofibroma.

Fragile and numerous vascular channels provide a pathologic explanation.

Recurrent or marked bleeding should heighten concern before tissue sampling.

Blood-loss consequences must be evaluated clinically when episodes are significant.

Slide 13 · Nasal obstruction: Direct mechanical effect

Expansion within the nasal cavity or choana narrows the breathing passage.

Obstruction may be unilateral initially because of the mass location.

A vascular mass causing obstruction requires a different workup from an ordinary polyp.

Persistent obstruction plus epistaxis is more informative than either symptom alone.

Slide 14 · Features suggesting disease beyond the nasal lumen

Orbit-adjacent

Proptosis or orbital symptoms

May indicate extension

Cranial / neural

Neurologic findings can signal

Advanced skull-base involvement

Facial compartments

Facial contour or palatal changes

Can arise from mass effect

Slide 15 · Clinical problem: A posterior nasal mass

A 15-year-old boy presents with repeated brisk epistaxis and progressive unilateral nasal obstruction. Examination suggests a reddish posterior nasal lesion.

Questions to answer

Which diagnosis should immediately enter the differential?

Which commonly used office procedure could cause severe hemorrhage?

Slide 16 · The key safety rule: Avoid an unplanned biopsy

Sinonasal angiofibroma is highly vascular and can bleed profusely.

Suspected cases are generally characterized using cross-sectional imaging first.

Biopsy is not routine when clinical and imaging findings are characteristic.

If diagnostic tissue is necessary, the approach requires specialist planning and bleeding control.

Slide 17 · Safe initial diagnostic sequence

Clinical suspicion

Young male + epistaxis / obstruction

Imaging

Contrast CT and MRI for extent

Multidisciplinary plan

Vascular mapping; Resection strategy

Avoid an unplanned office biopsy of a highly vascular suspected angiofibroma.

Slide 18 · Nasal endoscopy: Evaluate without traumatizing

An endoscopic examination may reveal a vascular-appearing posterior nasal or nasopharyngeal mass.

Inspection can establish laterality, accessible surface appearance and obstruction.

Surface appearance alone cannot determine the full extent or histology.

Avoid forceful instrumentation or routine tissue sampling of a suspected vascular lesion.

Slide 19 · Imaging answers distinct clinical questions

CT

Bone remodeling / erosion

And compartment anatomy

MRI

Soft-tissue extent

And intracranial relations

Angiography

Arterial supply

And embolization planning

Slide 20 · Contrast-enhanced CT: Establishing lesion geography

Avid contrast enhancement supports the presence of a hypervascular mass.

CT maps nasal, nasopharyngeal and paranasal sinus involvement.

It can show altered bony contours and widened deep facial spaces.

Interpret a characteristic location and enhancement pattern together—not in isolation.

Slide 21 · Bone on CT: Remodeling versus destructive reach

Displacement

Progressive mass effect can

Bow neighboring bony walls

Remodeling

Expansion changes the shape

Of adjacent structures

Advanced extent

Skull-base erosion may occur

Even though tumor is benign

Slide 22 · Holman–Miller sign: A cause–effect sequence

Tumor reaches

Pterygopalatine fossa

Space expands

Posterior maxillary wall displaced

CT appearance

Anterior wall bowing

Supportive imaging sign, not a standalone histologic diagnosis.

Slide 23 · MRI clarifies soft-tissue extension

MRI is helpful for defining the interface with orbit and skull base.

It identifies disease extending toward the cranial cavity or soft-tissue compartments.

Contrast enhancement and vascular flow phenomena provide clues to tumor vascularity.

MRI is valuable in assessing residual or recurrent tissue after treatment.

Slide 24 · Flow voids: The imaging correlate of moving blood

Histologic premise

Abundant vascular channels

Carry flowing blood

MR observation

High-flow channels may appear

As internal signal voids

Interpretation

A vascular clue that complements

Location and enhancement

Slide 25 · CT versus MRI: Complementary roles

Feature

CT emphasizes

MRI emphasizes

Anatomic overview

Bone and sinonasal boundaries

Soft-tissue compartments

Tumor vascularity

Contrast enhancement

Flow voids and enhancement

Deep extension

Pterygopalatine bony changes

Orbit / intracranial relationships

After treatment

Remodeling and anatomy

Residual or recurrent enhancing tissue

Slide 26 · Angiography: Not simply another diagnostic picture

Catheter angiography delineates feeding arterial branches and vascular anastomoses.

The arterial map informs hemorrhage-reduction strategies.

Embolization can be performed when appropriate to the vascular anatomy.

Potential hazardous anastomoses make specialist technique and patient selection essential.

Slide 27 · Before surgery, imaging should answer four questions

What is the full extent of the mass and its deep-space involvement?

Does it abut or extend through the skull base or toward the orbit?

Where are major arterial feeders and potentially dangerous connections?

What boundaries will influence the feasibility and completeness of excision?

Slide 28 · Macroscopic appearance: Integrate, do not overdiagnose

Angiofibroma is often described as a vascular, firm or lobulated soft-tissue mass.

Visible vessel-rich areas correspond to the “angio-” component.

Fibrous texture corresponds to the collagenized stromal component.

Gross appearance is nonspecific: Definitive tissue interpretation uses microscopy and context.

Slide 29 · The biphasic histologic pattern

Original morphology schematic — not a histology specimen

What to recognize

Numerous endothelial-lined vascular spaces

Fibrous, collagen-rich supporting tissue

Scattered bland stromal fibroblasts

Slide 30 · Vascular channels: Varying size and shape

Original morphology schematic — not a histology specimen

What to recognize

Vascular profiles vary in caliber and contour

Thin or incomplete muscular vessel walls

Fragile channels help explain brisk epistaxis

Slide 31 · Endothelial lining is deceptively simple

Vessel lumina are lined by a single layer of endothelial cells.

Vascular spaces may be irregular, angulated or variably dilated.

The lesion’s diagnostic pattern depends on the vessel–stroma relationship.

Endothelial cellular atypia is not the defining abnormality in this benign neoplasm.

Slide 32 · Vessel walls and bleeding propensity

Original morphology schematic — not a histology specimen

What to recognize

Vascular profiles vary in caliber and contour

Thin or incomplete muscular vessel walls

Fragile channels help explain brisk epistaxis

Slide 33 · Collagen-rich stroma and bland fibroblasts

Original morphology schematic — not a histology specimen

What to recognize

Pink field depicts collagen (conceptually)

Small dark ovals represent bland stromal nuclei

Diagnosis requires real specimen evaluation

Slide 34 · What the microscope should separate

Vascular element

Endothelial-lined lumina

With diverse caliber

Stromal element

Collagenous matrix with

Small bland fibroblasts

Overall pattern

Mixed fibrovascular architecture

Without a malignant phenotype

Slide 35 · Interpretation pitfall: Architecture outranks one shape

A staghorn-like or branching vessel contour is not unique to angiofibroma.

Collagenization can vary between cases and microscopic fields.

Limited sampling may fail to show the overall vascular–stromal architecture.

Age, site, imaging and histology must be integrated when morphology overlaps mimics.

Slide 36 · Prior embolization can modify histologic vessels

Original morphology schematic — not a histology specimen

What to recognize

Gray intraluminal material is schematic embolus

Actual treated tissue may show vascular changes

Interpret treatment effects with procedure history

Slide 37 · Handling a vascular excision specimen

Confirm procedure history, especially whether preoperative embolization occurred.

Assess the fibrovascular lesion on multiple representative sections.

Correlate cautery, hemorrhage and treatment-related material with operative context.

Communicate uncertainty rather than forcing a diagnosis from a fragmented small sample.

Slide 38 · β-catenin is part of the tumor’s molecular story

Most sporadic sinonasal angiofibromas harbor CTNNB1 mutations.

CTNNB1 encodes β-catenin, a protein involved in cellular signaling regulation.

Abnormal nuclear β-catenin localization provides a tissue-level correlate.

Association with a molecular alteration does not equate to an independently sufficient diagnostic test.

Slide 39 · From CTNNB1 to nuclear β-catenin

CTNNB1 alteration

Somatic mutation in many

Sporadic lesions

β-catenin signaling

Abnormal nuclear

Localization / activity

Stromal phenotype

Nuclear staining can be

Identified in tumor cells

Genotype → pathway implication → tissue-level immunophenotype

Slide 40 · Nuclear β-catenin staining: What it can support

WHO review describes nuclear β-catenin localization in nearly all cases.

The relevant positive cells are the neoplastic stromal component.

The pattern supports altered β-catenin regulation when paired with morphology.

It is not pathognomonic: Other sinonasal tumors can share nuclear staining.

Slide 41 · Sporadic CTNNB1 versus syndromic APC context

Sporadic sinonasal angiofibroma

Commonly associated with somatic

CTNNB1 mutations

β-catenin pathway activation

Syndromic context (FAP)

Germline APC predisposition

Can converge on altered

β-catenin regulation

Different upstream genetic events can affect the same regulatory pathway.

Slide 42 · Familial adenomatous polyposis: The association

An angiofibroma can occur in the context of familial adenomatous polyposis (FAP).

In the hereditary setting, germline APC mutation is the stated driver context.

APC perturbation also converges on β-catenin regulation.

The association should prompt appropriate consideration of personal or family history.

Slide 43 · Androgen receptor: Relevant but not an explanation by itself

WHO review notes androgen receptor immunoreactivity in stromal cells is common.

Clinical predilection for adolescent males is consistent with biological interest in hormonal pathways.

Receptor expression is not proof that androgen signaling solely causes the neoplasm.

Do not replace an integrated diagnosis with a single immunostain.

Slide 44 · What molecular findings actually mean

Feature

Observation

Interpretive limit

CTNNB1

Mutated in majority of sporadic cases

Not a universal standalone diagnostic criterion

β-catenin IHC

Nuclear localization is common

Pattern overlaps other mesenchymal tumors

Germline APC

FAP-associated pathogenesis

Association ≠ all cases hereditary

Androgen receptor

Stromal immunoreactivity reported

Expression ≠ established sole cause

Slide 45 · Differential diagnosis begins before pathology

Posterior nasal symptoms occur in both benign and malignant diseases.

Epistaxis, enhancement, demographics and epicenter change the differential.

Do not biopsy a presumed benign inflammatory polyp before recognizing suspicious vascularity.

Context determines the safest route to definitive characterization.

Slide 46 · Angiofibroma versus inflammatory nasal polyp

Clue

Angiofibroma

Inflammatory polyp

Typical context

Adolescent male / recurrent bleeding

Inflammatory nasal symptoms

Tissue structure

Vascular channels + fibrous stroma

Edematous inflamed mucosal stroma

Vascularity

Marked; Biopsy hazard

Usually far less conspicuous

Imaging priority

Map deep extension and feeders

Assess extent and sinus disease

Slide 47 · Angiofibroma versus sinonasal papilloma

Dimension

Angiofibroma

Papilloma

Cell of origin

Fibrovascular mesenchymal lesion

Schneiderian epithelial neoplasm

Age/setting

Predominantly adolescent males

Commonly adults

Microscopic hallmark

Thin-walled vessels in collagen

Epithelial proliferation / inversion

Molecular context

CTNNB1 / β-catenin

EGFR mutation in many inverted cases

Slide 48 · Angiofibroma versus glomangiopericytoma

Diagnostic element

Angiofibroma

Glomangiopericytoma

Dominant pattern

Numerous vessels + fibrous stroma

Perivascular myoid spindle-cell tumor

Stromal character

Bland fibroblasts; Collagenized

Cellular perivascular myoid growth

β-catenin IHC

Nuclear expression common

Nuclear expression may also occur

Clinical integration

Young male; Classic site

Often older patients; Other sinonasal sites

Slide 49 · Other vascular-appearing lesions to consider

Vascular malformation

Vessel-rich lesion without

The classic neoplastic stroma

Hemangioma and analogues

Distinct vessel architecture

And clinical setting

Other mesenchymal tumors

Perivascular or stromal lesions

May mimic selected fields

Slide 50 · When to broaden the differential to malignancy

Assessment

Angiofibroma pattern

Concern for alternative

Presentation

Classic demographic and vascular pattern

Atypical age/site or aggressive symptoms

Imaging

Characteristic hyperenhancing epicenter

Infiltrative noncharacteristic pattern

Microscopy

Bland endothelial and stromal cells

Atypia, mitoses, necrosis or epithelial cancer

Decision

Integrated clinicoradiologic diagnosis

Targeted investigation by specialist team

Slide 51 · Diagnostic reasoning is multimodal

Clinical context

Sex / age / epistaxis

Imaging

Epicenter / enhancement / extent

Pathology

Vessels + collagen + bland cells

Optional ancillary

Selected IHC or genetics

Each domain supports interpretation; None replaces the others.

Slide 52 · Locally aggressive growth is the chief paradox

The underlying cytology is benign rather than frankly malignant.

Growth can extend into complex facial spaces and the cranial cavity.

Risk therefore depends strongly on anatomical extent and proximity to critical structures.

“Benign” must never be interpreted as negligible surgical or clinical risk.

Slide 53 · Major complications follow location, not atypia

Blood supply

Severe bleeding during symptoms

Or instrumentation

Orbital relationship

Extension may threaten

Orbital structures

Intracranial reach

Skull-base extension

Raises treatment complexity

Slide 54 · Surgical excision is the principal treatment

Surgery as the treatment of choice.

The operative route depends on size, site, vascular supply and deep extension.

Complete removal may be difficult when disease involves complex skull-base anatomy.

High-quality preoperative anatomical mapping is therefore part of treatment planning.

Slide 55 · Why embolization precedes selected operations

Angiography

Identify arterial feeders

Embolization

Reduce tumor perfusion

Resection

Lower anticipated blood loss

Preoperative embolization is often useful, but the vascular map determines feasibility and risk.

Slide 56 · Embolization is an intervention with its own risks

Dangerous extracranial–intracranial arterial connections require recognition.

Nontarget embolization may injure ophthalmic or cerebral circulation.

Preoperative endovascular treatment must be performed by an experienced team.

Embolization modifies surgical risk; It does not substitute for definitive assessment of extent.

Slide 57 · What increases the chance of persistence or recurrence?

Anatomically inaccessible or deeply extended tumor may be difficult to clear.

Residual tumor after excision can later be detected as persistent or recurrent disease.

Imaging surveillance is particularly relevant in patients with complex or advanced lesions.

Recurrence estimates should be interpreted in relation to tumor stage and treatment series.

Slide 58 · How to read published outcome percentages

Recurrence rates can approach 20% in some settings.

The same brief textbook section cites a 9% fatal-case figure without a defined contemporary denominator here.

Do not communicate either number as a universal individual prognosis or modern treatment benchmark.

Current counseling requires disease extent, treatment details and population-specific outcome data.

Slide 59 · Post-treatment assessment: Persistent disease is not invisible

Contrast-enhanced MRI can help detect and characterize residual or recurrent tumor.

Interpret enhancing tissue in relation to operative anatomy and previous imaging.

Follow-up strategy is individualized rather than based on a single universal interval.

New epistaxis or progressive obstruction after therapy warrants reassessment.

Slide 60 · Case exercise: Protect the patient first

An adolescent male has repeated spontaneous epistaxis. CT shows an enhancing posterior nasal mass and enlargement of the pterygopalatine region. A clinic considers endoscopic biopsy.

Questions to answer

What features suggest sinonasal angiofibroma?

What immediate change to the diagnostic plan is appropriate?

Slide 61 · Case answer: Imaging before tissue

Demographics + recurrent epistaxis + hypervascular posterior mass point toward angiofibroma.

Pterygopalatine involvement further supports the characteristic anatomic pattern.

Avoid an unplanned biopsy because of hemorrhage risk.

Arrange specialist cross-sectional mapping and appropriate vascular/surgical assessment.

Slide 62 · Case exercise: Interpret a vascular–stromal lesion

Resection tissue shows bland spindle fibroblasts in dense collagen. Numerous irregular, thin-walled channels have a single endothelial lining. Nuclear β-catenin is seen in stromal nuclei.

Questions to answer

Which components establish the morphologic pattern?

What is the correct interpretation—and limitation—of β-catenin staining?

Slide 63 · Case answer: Architecture plus contextual molecular support

The key morphologic feature is a mixture of vascular channels and collagenized bland stroma.

Nuclear β-catenin is compatible with the CTNNB1/APC-associated biological context.

β-catenin expression alone is not uniquely diagnostic of angiofibroma.

Site, demographic context, imaging and overall morphology complete the diagnosis.

Slide 64 · Synthesis: Clinicopathologic correlations

Finding

Underlying explanation

Recurrent epistaxis

Abundant, vulnerable vascular channels

Obstructive symptoms

Space-occupying posterior sinonasal mass

Avid enhancement / flow voids

Rich blood supply / flowing vascular channels

Firm fibrous lesion

Dense collagenous stroma

Local aggressiveness

Expansion into deep adjacent compartments

Postoperative recurrence

Residual tissue in anatomically complex sites

Slide 65 · Final diagnostic take-home points

An adolescent male with recurrent epistaxis and a posterior hypervascular nasal mass warrants consideration of angiofibroma.

Do not undertake an unplanned biopsy; Map vascularity and extent first.

Histology is fibrovascular and cytologically benign, yet local extension can be serious.

CTNNB1 / β-catenin abnormalities and occasional APC/FAP association inform biological interpretation.

Slide 66 · Selected references for further reading

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. 2026; Ch. 16, p. 673.

WHO Classification of Head and Neck Tumours (5th ed.): sinonasal tract angiofibroma; update review, 2022 (PMC9018924).

Imaging in the Diagnosis of Juvenile Nasopharyngeal Angiofibroma. J Clin Imaging Sci. 2013 (PMC3716018).

Kothari et al. Preoperative Embolization Techniques. Otolaryngol Head Neck Surg. 2023;169:454–466.