SCC of maxillary CARCINOMA. Classification, investigation for staging and diagnosis, management and clinical features in detail from standard ENT textbook in simplified manner for long question answer

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Squamous Cell Carcinoma (SCC) of the Maxillary Sinus

Sources: Scott-Brown's Otorhinolaryngology Head & Neck Surgery, KJ Lee's Essential Otolaryngology, Cummings Otolaryngology

1. INTRODUCTION & EPIDEMIOLOGY

Sinonasal malignancies are uncommon, accounting for less than 1% of all neoplasms and around 3% of upper aerodigestive tract tumours. The incidence is 0.5-1 per 100,000 per year. They mostly develop in the fifth and sixth decades, with men affected twice as often as women.
The maxillary sinus is the most common site (55%) followed by the nasal cavity (35%), ethmoid sinuses (9%), and rarely the frontal and sphenoid sinuses (1%). SCC is the most common histological type.
Diagnosis is frequently delayed - the average time from first symptom to diagnosis is approximately 6 months. Only 25% of maxillary sinus carcinomas are still confined within the antrum at the time of presentation.
  • Scott-Brown's Otorhinolaryngology, Ch. 7

2. AETIOLOGY / RISK FACTORS

CarcinogenAssociation
Hardwood dust (furniture workers)70x increased risk for adenocarcinoma; African mahogany most carcinogenic
Softwood dustAssociated with SCC
Nickel compounds250x increased risk of sinonasal SCC; latent period 18-36 years
Chromium, polycyclic hydrocarbonsSinonasal malignancy
Aflatoxin, mustard gas, thorotrastSinonasal malignancy
Cigarette smokingSynergistic with wood dust
Inverted (Schneiderian) papilloma14.6% risk of transformation to SCC
Radiation, viral (HPV)Proposed role
  • Occupational exposure accounts for ~40% of reported sinonasal malignancies.
  • Chronic sinusitis does NOT predispose to cancer.
  • Scott-Brown's, p.117

3. SURGICAL ANATOMY (Relevant to Spread)

The maxillary sinus (antrum of Highmore) has 6 walls:
  • Anterior wall - thin; tumours erode through to the cheek/skin
  • Posterior wall - overlies the pterygopalatine and infratemporal fossa
  • Medial wall - separates from the nasal cavity; contains the ostium; close to the nasolacrimal duct
  • Superior wall (roof) - floor of the orbit; contains the infraorbital nerve in the infraorbital canal
  • Inferior wall (floor) - close to the roots of upper molar/premolar teeth
  • Superolateral wall - forms the orbital floor laterally
Lymphatic drainage is scant. Two pathways:
  • Anterior pathway: to facial, parotid, and submandibular nodes → upper deep cervical chain
  • Posterior pathway: retropharyngeal nodes → upper deep cervical chain

4. CLASSIFICATION OF MAXILLARY SINUS TUMOURS

4a. Histological Classification

CategoryTypes
Epithelial (most common)SCC (most common), Adenocarcinoma, Adenoid cystic carcinoma, Mucoepidermoid carcinoma, Undifferentiated carcinoma (SNUC)
Non-epithelialLymphoma, Melanoma, Sarcoma, Olfactory neuroblastoma (OAN/Esthesioneuroblastoma)
Benign with malignant potentialInverted papilloma
SCC specifically:
  • Approximately 85% are well-differentiated
  • Papillary, exophytic, fungating, friable, and keratinizing patterns are recognized
  • Macroscopically may be polypoid or fungating
  • Transformation from Schneiderian papilloma is a recognized pathway

4b. Ohngren's Classification (Prognostic)

Ohngren's line = a theoretical plane joining the medial canthus of the eye to the angle of the mandible.
This divides the maxilla into:
DivisionLocationPrognosis
Anteroinferior (Infrastructure)Below and in front of Ohngren's lineBetter prognosis - surgical access easier, less critical structures
Posterosuperior (Superstructure)Above and behind Ohngren's lineWorse prognosis - proximity to skull base, orbit, cavernous sinus, pterygoid region
Tumours antero-inferior to this line have better treatment outcomes. - KJ Lee, p.597

4c. Anatomical Infrastructure vs Superstructure Division

Based on an imaginary horizontal plane through the floor of the antrum at the level of the hard palate:
  • Infrastructure lesions - involve the floor of the antrum, alveolus, hard palate
  • Superstructure lesions - involve the roof of the antrum (orbital floor) and above

5. PATTERNS OF TUMOUR SPREAD

Local Spread - Maxillary Sinus

DirectionStructures Involved
MediallyLateral wall of nasal cavity; nasal obstruction, epistaxis
Anteriorly/LaterallyAnterior wall of maxilla → cheek swelling; skin involvement
PosteriorlyPosterior wall → pterygopalatine fossa → infratemporal fossa → trismus, cranial nerve involvement
SuperiorlyOrbital floor → proptosis, diplopia
InferiorlyPalate → oral mass, dental loosening
Along infraorbital nerveFacial pain and sensory change over cheek

Regional (Lymph Node) Spread

  • Lymphatic spread becomes apparent in 25-35% at some point during disease
  • Only ~10% present with nodal disease (marker of locally advanced disease)
  • Most commonly: submandibular and jugulodigastric nodes
  • Bilateral involvement possible when tumour involves midline structures

Distant Metastases

  • Uncommon at presentation; develop in ~10% of SCC (vs 20% of adenocarcinomas)
  • Sites: bone, brain, liver, lung, skin
  • Almost always associated with local recurrence
  • Scott-Brown's, pp.118-119

6. CLINICAL FEATURES

Symptoms arise late - typically once the sinus is filled and tumour erodes its walls.

6a. Early (Non-specific) Symptoms

  • Unilateral nasal obstruction
  • Unilateral blood-stained nasal discharge (epistaxis)
  • Facial pain/pressure
These mimic sinusitis, which is why diagnosis is often delayed.

6b. Symptoms by Direction of Spread

Symptom/SignMechanism
Facial pain + cheek numbnessInfiltration of the infraorbital nerve (CN V2) through the roof of the sinus
Epistaxis + epiphoraMedial wall erosion + nasolacrimal duct obstruction
TrismusSpread posteriorly into pterygoid muscles / pterygopalatine fossa
Facial numbnessMaxillary (V2) and mandibular (V3) trigeminal nerve deficits
Oral mass / loose teethInferior spread to hard palate/alveolus
Proptosis + diplopiaSuperior spread into the orbit (orbital floor erosion)
Cheek swellingAnterolateral wall breach
TrismusPosterior spread into infratemporal fossa
Diplopia / CN palsyCavernous sinus involvement (very advanced)

6c. Key Clinical Sign

A palpable mass in the cheek, palate, or gingiva; orbital displacement; unilateral facial numbness are red flags requiring urgent workup.
  • Scott-Brown's, pp.124-125

7. INVESTIGATIONS

7a. Endoscopy

  • Rigid nasal endoscopy is mandatory in any suspected sinonasal malignancy
  • May show ulcerative growth, polypoid reaction, or friable mass
  • Some tumours produce a polypoid reaction in overlying mucosa - casual outpatient biopsy may be non-diagnostic

7b. Imaging

CT scan (preferred for bone)
  • Required for ALL patients
  • Both axial and coronal views are necessary
  • Demonstrates bone erosion, extent of antral destruction
  • Better for skull base involvement and bone integrity
  • May be compromised by dental amalgam artefact
MRI (preferred for soft tissue)
  • Gadolinium-enhanced MRI is superior for:
    • Distinguishing tumour from retained secretions (T2 and diffusion-weighted sequences)
    • Perineural spread (most malignant tumours enhance diffusely vs rim enhancement of secretions)
    • Intracranial and dural infiltration
    • Orbital invasion
    • Extent in pterygopalatine fossa and infratemporal fossa
  • CT + MRI together are complementary and both are commonly required
Chest X-ray / CT Chest
  • To exclude pulmonary metastases
  • Mandatory before planning curative treatment
FDG-PET/CT
  • Not usually needed for staging the primary
  • Useful for excluding distant disease (e.g., melanoma)
  • Helpful if concern exists that sinus disease is metastatic
Arteriography - Rarely needed; used if pre-operative embolization is planned for highly vascular tumours

7c. Biopsy

  • Tissue diagnosis is mandatory before any treatment
  • Sinus tumours can be excessively vascular - outpatient biopsy must have facilities to arrest haemorrhage
  • Biopsy under general anaesthesia preferred - reduces non-diagnostic rate, allows sampling from within the sinus
  • Caldwell-Luc approach should be avoided if it might seed tumour or compromise resection

7d. Examination Under Anaesthesia (EUA)

  • Thorough examination including palpation of the palate, alveolus, and posterior pharynx

7e. MDT Discussion

  • All cases to be discussed in a multidisciplinary team (MDT) forum before treatment planning, including surgical oncology, radiation oncology, reconstructive surgery, prosthetics.
  • Scott-Brown's, pp.124-126

8. TNM STAGING (AJCC)

Maxillary Sinus T Staging

StageDefinition
TisCarcinoma in situ
T1Tumour limited to maxillary sinus mucosa, no bone erosion
T2Tumour causing erosion/destruction of bone, including hard palate and/or middle meatus (but NOT the posterior antral wall or pterygoid plates)
T3Tumour invades: posterior wall of maxillary sinus, orbital floor/medial wall, subcutaneous tissues of cheek, pterygoid fossa, or ethmoid sinuses
T4aModerately advanced: invades anterior orbital contents, skin of cheek, pterygoid plates, infratemporal fossa, cribriform plate, sphenoid or frontal sinuses
T4bVery advanced: invades orbital apex, dura, brain, middle cranial fossa, cranial nerves other than V2, nasopharynx, or clivus

N (Nodal) and M (Distant) Staging

  • Same as routine head and neck SCC staging
  • N0: no regional node metastasis
  • N1: single ipsilateral node ≤3cm
  • N2: larger/multiple nodes
  • M1: distant metastases present

Staging Matrix (Overall Stage)

Overall StageT/N/M
Stage IT1 N0 M0
Stage IIT2 N0 M0
Stage IIIT3 N0 M0, or T1-3 N1 M0
Stage IVAT4a any N M0, or any T N2 M0
Stage IVBT4b any N M0, or any T N3 M0
Stage IVCAny T any N M1
  • KJ Lee's Essential Otolaryngology, pp.596-597; Scott-Brown's, p.119

9. MANAGEMENT

9a. General Principles

  • Patients with T1 tumours may be cured with surgery alone
  • The majority require combination (multimodality) therapy
  • Surgery + radiotherapy ± chemotherapy is the standard curative approach
  • IMRT (Intensity Modulated Radiotherapy) is the preferred radiotherapy technique
  • Cases should be discussed at MDT before treatment

9b. Surgery

Types of Maxillectomy:
ProcedureIndication
Partial maxillectomy (infrastructure)Infrastructure tumours - involves medial wall/floor resection; alveolus and palate resection
Total maxillectomyTotal removal of the upper jaw as a "bony box" containing the tumour
Extended maxillectomyTumour extends beyond the upper jaw; includes orbital exenteration, skull base, pterygoid plates
Craniofacial resectionSkull base involved (anterior cranial fossa)
Endoscopic resectionSelected cases without significant orbital/intracranial involvement or lateral disease
Surgical Approaches:
  1. Lateral rhinotomy (Michaux/Moure) - excellent exposure of nasal cavity and medial maxilla; cosmetically acceptable incision in the lateral nasal crease
  2. Weber-Fergusson incision - for total maxillectomy; combines lateral rhinotomy with a lip-splitting incision for wider exposure
  3. Midfacial degloving - avoids facial scars; useful for bilateral access
Neck dissection:
  • Elective levels I-III neck dissection considered for T2 or greater lesions
  • Cervical metastasis demonstrated in 35% of hard palate/maxillary alveolar carcinomas
  • Facial lymph nodes should be considered during neck dissection for maxillary tumours

9c. Radiotherapy

  • Post-operative radiotherapy (PORT) should start within 6 weeks of surgery
  • Dose: 60-65 Gy over 30 fractions (IMRT technique)
  • PORT indications: T3 or greater disease, positive margins, perineural or perivascular invasion, multiple cervical nodes (especially with extracapsular spread)
  • Elective neck irradiation considered for locally advanced (T3-T4) disease due to 23% risk of locoregional recurrence

9d. Chemotherapy

  • Used in multimodality regimens for advanced or metastatic disease, or SCC/SNUC
  • Cisplatin-based protocols most commonly used
  • Concurrent chemoradiotherapy for non-resectable cases
  • Palliative chemotherapy for unresectable/metastatic disease

9e. Combined Modality Therapy

  • For SCC and SNUC: surgery + post-operative radiotherapy ± chemotherapy has the best outcomes
  • If operable: surgery first, then post-operative radiotherapy with concurrent chemotherapy where indicated
  • IMRT with advanced planning and concurrent chemotherapy provides significant value

9f. Reconstruction

  • Small defects: buccal fat pad, temporalis flap, facial artery musculomucosal flap
  • Large defects: free tissue transfer (soft tissue or composite flaps)
  • Palatal resection: obturator prosthesis (fitted with teeth to restore speech and deglutition) OR composite free flap
  • Orbital resections: titanium implants for facial prostheses
  • Multidisciplinary prosthetic rehabilitation is an essential component
  • Scott-Brown's, pp.126-130

10. PROGNOSIS

FactorSignificance
T stageMost direct survival impact
Resection margin statusIndependent predictor of survival
Intracranial/orbital involvementIndependent predictor
Nodal diseasePoor prognosis marker
Distant metastasisPoor prognosis
Previous radiation / incomplete resectionWorse outcome
Histological subtypeMelanoma worst; minor salivary gland/low-grade sarcoma best
  • 5-year absolute survival for hard palate carcinoma: 57%; alveolar carcinoma: 49%
  • Locoregional control of maxillary tumours after initial therapy: ~40-45%
  • Over 90% of recurrences occur within the first 2 years
  • Distant metastases in ~10% of SCC (vs 20% adenocarcinoma)
  • Scott-Brown's, p.131; KJ Lee, p.597

SUMMARY TABLE

AspectKey Points
Most common typeSCC (~85% well-differentiated)
Most common siteMaxillary sinus (55% of sinonasal malignancies)
Age/sex5th-6th decade; men > women (2:1)
Key risk factorsNickel (SCC), hardwood dust (adenocarcinoma), smoking
Ohngren's lineMedial canthus to angle of mandible; anteroinferior = better prognosis
Diagnosis delayedAverage 6 months; only 25% confined within antrum at presentation
InvestigationsNasal endoscopy + biopsy, CT (bone), MRI (soft tissue), CXR
StagingTNM (AJCC) - T1 to T4b based on extent of invasion
TreatmentSurgery (maxillectomy) + PORT (60-65Gy IMRT); chemo for advanced cases
Node managementElective levels I-III ND for T2+ disease
Prognosis~40-45% locoregional control; 5-yr survival ~50-60% for early disease; poor for advanced
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