Sinonasal squamous cell carcinoma (SCC) is the most common malignant neoplasm of the paranasal sinuses and nasal cavity, accounting for approximately 50-80% of all sinonasal malignancies. It most commonly originates from the maxillary sinus (60-70%), followed by the nasal cavity (20-30%) and ethmoid sinuses (10-15%). Histopathologically, keratinizing and non-keratinizing squamous cell carcinoma subtypes exist, with the HPV-associated non-keratinizing variant showing better prognosis. Clinically, it presents with unilateral nasal obstruction, epistaxis, facial pain, and cranial nerve palsies. Aggressive bone destruction on CT and marked diffusion restriction with solid enhancement on MRI are typical findings. Perineural spread (especially V2 — infraorbital nerve) and orbital invasion are common. TNM staging and multidisciplinary treatment approach (surgery + radiotherapy ± chemotherapy) are required. Overall 5-year survival is between 40-60%, varying by stage and location.
Age Range
50-80
Peak Age
65
Gender
Male predominant
Prevalence
Uncommon
Sinonasal SCC develops through malignant transformation of the respiratory epithelium (Schneiderian membrane) or metaplastic squamous epithelium; chronic inflammation, tobacco/nickel/wood dust exposure, and HPV infection (types 16/18) are the main risk factors. Tumor growth produces osteolytic destruction of surrounding bony structures — matrix metalloproteinases (MMP-2, MMP-9), cathepsins produced by malignant cells and RANKL-mediated osteoclast activation trigger bone resorption, which translates to irregular bone destruction on CT. High cellularity and high nucleus-to-cytoplasm ratio restrict the extracellular space, impeding water molecule movement — this is seen as marked diffusion restriction (low ADC) on DWI. Tumor neoangiogenesis produces solid enhancement on contrast-enhanced imaging through vascular endothelial growth factor (VEGF) production. Perineural spread (PNS) results from the ability of tumor cells to migrate along nerve sheaths and particularly shows spread along the V2 branch (infraorbital nerve → foramen rotundum → cavernous sinus → Meckel's cave) — this is seen as nerve thickening and enhancement on MRI.
The triad of a unilateral sinus/nasal cavity mass with aggressive irregular bone destruction (moth-eaten/permeative pattern), solid enhancement on MRI, and marked diffusion restriction (ADC <1.0 × 10⁻³ mm²/s) is the strongest diagnostic combination for sinonasal SCC. This triad has high diagnostic value in differentiating from benign lesions (polyposis, inverted papilloma) and other malignant lesions (lymphoma — homogeneous enhancement + very low ADC, melanoma — T1 hyperintensity).
On CT, sinonasal SCC is characterized by aggressive irregular bone destruction. The destruction pattern is 'moth-eaten' (multiple small osteolytic foci) or permeative (cortical integrity loss across a wide area). In maxillary sinus SCC, the anterior, posterior, and medial walls along with the orbital floor are the most commonly affected locations. Posterior wall destruction leads to pterygopalatine and infratemporal fossa invasion, orbital floor destruction to orbital invasion, and superior wall destruction to intracranial extension. Unlike the smooth pressure remodeling in benign lesions (polyposis, inverted papilloma), destruction in SCC is irregular, fragmented, and surrounded by soft tissue mass. The extent of bone destruction is critically important in determining T stage and surgical planning.
Report Sentence
A soft tissue density mass is noted in the left/right maxillary sinus with aggressive irregular bone destruction of the sinus anterior/posterior/medial walls and orbital floor.
On DWI, sinonasal SCC shows marked diffusion restriction. At high b-values (b=1000 s/mm²), the tumor shows hyperintense signal while low signal is seen on the ADC map (ADC typically 0.6-0.9 × 10⁻³ mm²/s). These low ADC values reflect the tumor's high cellularity, high nucleus-to-cytoplasm ratio, and restricted extracellular space. DWI plays a critical role in differentiating tumor from retention secretions: obstructed sinus secretions may show variable DWI signal depending on T2 pattern, but tumoral tissue consistently shows low ADC. In treatment response assessment, ADC increase indicates treatment success, while ADC decrease or stability indicates residual/recurrent tumor. DWI also helps differentiate tumor from peritumoral edema and post-therapeutic changes.
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Marked diffusion restriction is noted in the mass on DWI with low signal on the ADC map (ADC: approximately ... × 10⁻³ mm²/s); this finding is consistent with high cellularity and favors malignancy.
On contrast-enhanced T1-weighted sequences, sinonasal SCC shows heterogeneous solid enhancement. Enhancement is generally moderate to marked, with necrotic areas within the tumor appearing as non-enhancing hypointense foci. Central necrosis is more prominent in large tumors and may be surrounded by a peripherally enhancing rim. The most important contribution of contrast-enhanced MRI is distinguishing tumor from obstructed sinus secretions: tumor enhances while retention secretions do not — this distinction cannot be reliably made on CT. Peritumoral dural enhancement indicates intracranial extension, nerve thickening and enhancement indicates perineural spread, and loss of orbital fat plane with extraocular muscle enhancement indicates orbital invasion. Fat-suppressed contrast-enhanced sequences provide superiority particularly in orbital and intracranial extension evaluation.
Report Sentence
On fat-suppressed contrast-enhanced T1 sequences, the mass shows heterogeneous solid enhancement with non-enhancing necrotic areas within; tumor-secretion differentiation has been made.
On fat-suppressed contrast-enhanced T1 sequences, perineural spread (PNS) findings may include nerve thickening and pathological enhancement along the infraorbital nerve (V2). PNS shows retrograde spread along the V2 branch from the infraorbital canal → foramen rotundum → Meckel's cave → cavernous sinus. Widening of the infraorbital canal and destruction of surrounding bone walls are accompanying findings on CT. Loss of normal fat signal in the pterygopalatine fossa (replacement by enhancement on fat-suppressed sequences) is an early PNS finding. Widening of the foramen rotundum and filling of Meckel's cave with enhancing tissue indicates intracranial PNS. Detection of PNS is clinically critical because it expands the radiotherapy field and has a negative impact on prognosis.
Report Sentence
On fat-suppressed contrast-enhanced T1 sequences, pathological thickening and enhancement along the left/right infraorbital nerve (V2) is noted, consistent with perineural tumor spread; loss of normal fat signal in the pterygopalatine fossa is present.
On T2-weighted sequences, sinonasal SCC shows intermediate signal — generally slightly hyperintense or isointense to muscle. Intratumoral necrotic areas may be hyperintense on T2 while fibrotic/desmoplastic areas may be hypointense. T2's most important contribution is tumor-secretion differentiation: retention secretions show very hyperintense (serous type) or hypointense (desiccated type) signal on T2 while tumor shows intermediate signal. In orbital invasion evaluation, T2 enables detection of tumor tissue (intermediate) within the orbital fat plane (hyperintense). T2 is also useful in dural invasion evaluation — the contrast between CSF (very hyperintense) and tumor (intermediate) allows assessment of subarachnoid space invasion.
Report Sentence
On T2-weighted sequences, the mass demonstrates intermediate signal intensity, clearly differentiated from high-signal retention secretions in surrounding sinuses.
On FDG PET-CT, sinonasal SCC shows intense FDG uptake (SUVmax typically >8-10). FDG uptake reflects the high metabolic activity of the tumor and is used in primary tumor evaluation, cervical/distant metastasis screening, and treatment response assessment. The primary tumor shows marked heterogeneous FDG uptake with necrotic areas showing no uptake. PET-CT provides high sensitivity in screening for cervical lymph nodes and distant metastases (lung, bone, liver). In post-therapeutic evaluation, differentiation is made between residual/recurrent tumor (high FDG uptake) and post-radiotherapy changes (low/isometabolic). PET-CT also enables targeting of the most metabolically active area for biopsy planning.
Report Sentence
On FDG PET-CT, intense heterogeneous FDG uptake is noted in the mass in the left/right maxillary sinus (SUVmax: ...); pathological uptake in cervical lymphadenopathies/distant metastasis is present/not identified.
Criteria
Most common subtype. Keratin pearls and intercellular bridges are typical on histology. Usually HPV-negative, associated with smoking/environmental exposure. More aggressive course.
Distinct Features
Prominent bone destruction and heterogeneous density on CT (keratinized areas may show slightly higher density). More prominent tendency for necrosis. 5-year survival 35-50%.
Criteria
HPV type 16/18 positive. Basaloid/transitional morphology on histology, absence of keratinization. p16 immunohistochemistry positive. Usually in younger age group.
Distinct Features
Better prognosis (5-year survival 60-80%). May show more homogeneous density and enhancement on CT. Better response to chemoradiotherapy. Cervical lymph node metastasis rate is higher.
Criteria
SCC developing in the setting of existing inverted papilloma. Synchronous (5-10%) or metachronous (5-10%). Associated with p53 mutation and cyclin D1 overexpression.
Distinct Features
Focal loss of cerebriform pattern and replacement with homogeneous solid enhancement on MRI. Decrease in ADC values. Increase in bone destruction aggressiveness. Two different tissue components (papilloma + carcinoma) may be visible within the lesion.
Distinguishing Feature
Inverted papilloma shows cerebriform enhancement pattern (absent in SCC), demonstrates remodeling rather than bone destruction, and shows mild diffusion restriction on DWI (ADC 1.0-1.4 — higher than SCC's <0.8). Attachment point hyperostosis is specific to inverted papilloma.
Distinguishing Feature
Lymphoma shows homogeneous enhancement (different from SCC's heterogeneous enhancement), demonstrates very low ADC values (<0.6 × 10⁻³), and exhibits a 'bone replacement' pattern — bone marrow infiltration without prominent bone destruction. SCC shows irregular osteolytic bone destruction.
Distinguishing Feature
Adenoid cystic carcinoma shows prominent perineural spread (more frequent and extensive than SCC), demonstrates less bone destruction with slow growth, may show hyperintense tubular/cribriform pattern on T2, and distant metastasis appears late (lung). SCC shows more aggressive bone destruction and early local spread.
Distinguishing Feature
Melanoma shows hyperintense signal on T1 and hypointense signal on T2 due to melanin content (paramagnetic melanin effect) — this signal characteristic is not seen in SCC. Amelanotic melanoma may not show this signal characteristic. Melanoma more commonly originates from the nasal cavity/septum while SCC more commonly originates from the maxillary sinus.
Urgency
urgentManagement
surgicalBiopsy
NeededFollow-up
Tedavi sonrası ilk 2 yıl her 3 ayda bir, 3-5 yıl arası 6 ayda bir klinik muayene + MRG; PET-BT tedavi sonrası 3-6 ay arası baseline değerlendirme ve rekürrens şüphesinde.Sinonasal SCC requires a multidisciplinary approach. In early-stage disease (T1-T2), endoscopic or open surgical resection is the primary treatment; in advanced-stage disease (T3-T4), surgery + adjuvant radiotherapy ± chemotherapy is applied. The goal of surgical resection is to achieve negative surgical margins; postoperative radiotherapy is mandatory in positive surgical margin status. In the presence of perineural spread, the radiotherapy field is expanded to include up to the cavernous sinus. In orbital invasion, orbital exenteration may be required — orbital preservation may be considered in periosteal-limited invasion. TNM staging uses AJCC 8th edition. Prognosis is better in HPV-associated non-keratinizing SCC and de-escalation strategies are being investigated.
Treatment of sinonasal SCC is surgical resection ± adjuvant radiotherapy/chemotherapy. Staging is performed with CT + MRI (CT for bone, MRI for soft tissue/perineural spread). Prognosis depends on stage and surgical margins. 5-year survival is 40-60%. Cervical lymph node metastasis worsens prognosis.