Laryngeal squamous cell carcinoma (SCC) accounts for >95% of laryngeal malignancies and is the most common malignant tumor of the larynx. Smoking and alcohol are synergistic risk factors; the risk increases 10-15 fold in smokers. Anatomic subtypes show different clinical courses: glottic carcinoma (60-65%) is diagnosed early due to early hoarseness and has the best prognosis; supraglottic carcinoma (30-35%) metastasizes early due to rich lymphatic drainage and presents at advanced stages; subglottic carcinoma (2-5%) is rare but has poor prognosis due to late diagnosis. Key imaging roles include detection of cartilage invasion (T3-T4 staging), demonstration of paraglottic and pre-epiglottic space spread, evaluation of anterior commissure involvement, and cervical lymph node metastasis screening. MRI is superior for cartilage invasion and soft tissue spread, while CT excels for cartilage erosion and bony involvement.
Age Range
45-80
Peak Age
65
Gender
Equal
Prevalence
Common
The pathogenesis of laryngeal SCC follows the multi-step carcinogenesis model. Polycyclic aromatic hydrocarbons and nitrosamines in cigarette smoke cause DNA damage in basal cells of the laryngeal mucosa, initiating the dysplasia-carcinoma in situ-invasive carcinoma sequence. Alcohol disrupts the mucosal barrier, facilitating carcinogen penetration and showing synergistic effects with smoking. HPV (especially type 16) is an etiologic factor in a subset — particularly oropharyngeal SCC — but plays a more limited role in laryngeal SCC. In local tumor spread, the paraglottic space (internal fat tissue of the larynx) and pre-epiglottic space are natural pathways because perichondrial attachment points of the mucosal barrier are weak in these areas. Cartilage invasion occurs through the perichondrium; ossified cartilage areas are more resistant to tumor invasion because ossification alters the vascular architecture. On imaging, cartilage invasion manifests as sclerosis (reactive bone formation), erosion, or complete destruction; cortical irregularity on CT and signal increase in cartilage medulla on T2 fat-saturated MRI are early signs of invasion.
Sclerosis, cortical erosion, and/or complete destruction of laryngeal cartilages (thyroid, cricoid, arytenoid) due to tumor invasion — T3 (cartilage invasion) and T4 (extension beyond cartilage) staging criterion. Best on CT for ossified cartilage, more sensitive on MRI for non-ossified cartilage.
On contrast-enhanced CT, an irregularly marginated, heterogeneously enhancing soft tissue mass is seen in the larynx. In glottic tumors, it appears as vocal cord thickening and lumen narrowing; in supraglottic tumors, as an epiglottis or aryepiglottic fold mass. Necrotic areas appear as non-enhancing hypodense foci. The tumor tissue typically measures 40-70 HU and shows moderate enhancement compared to surrounding muscle.
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An irregularly marginated, heterogeneously enhancing soft tissue mass is seen in the left vocal cord, consistent with laryngeal SCC.
Cartilage invasion findings on non-contrast CT: 1) Sclerosis — increased density due to reactive bone formation; 2) Erosion — cortical contour irregularity or focal loss; 3) Complete destruction — replacement of cartilage structure by tumor tissue; 4) Extralaryngeal extension — spread through the cartilage wall into perilaryngeal fat. Thyroid and cricoid cartilages are most commonly invaded. Invasion is more easily detected in ossified cartilage areas.
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Cortical erosion and focal sclerosis are seen in the left posterior lamina of the thyroid cartilage, consistent with cartilage invasion (T3).
MRI shows obliteration of paraglottic fat by tumor soft tissue. The normal paraglottic space shows hyperintense fat signal on T1, which disappears with tumor invasion and is replaced by intermediate-intensity tumor tissue. On T2 fat-saturated sequences, the invaded paraglottic space becomes conspicuous with tumor signal (intermediate-high). This finding indicates deep tumor spread and affects suitability for partial laryngectomy. Pre-epiglottic space invasion is assessed similarly.
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The left paraglottic fat plane is obliterated by tumor soft tissue, suggesting deep paraglottic space invasion.
Laryngeal SCC shows marked diffusion restriction on DWI — the tumor is hyperintense at high b-values (b=1000) and hypointense on the ADC map. ADC values typically range 0.8-1.2 × 10⁻³ mm²/s (normal muscle ~1.5-2.0). The degree of diffusion restriction is directly proportional to tumor cellularity and correlates with histopathologic grade. DWI also plays a critical role in treatment response assessment and recurrence detection.
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Marked diffusion restriction (ADC: 0.9 × 10⁻³ mm²/s) is seen in the left glottic-supraglottic mass, consistent with a highly cellular malignant process.
Cartilage invasion on MRI is best assessed on T2 fat-saturated sequences. Normal cartilage medulla appears hypointense with fat suppression, while invaded cartilage shows tumoral signal increase (hyperintensity) in the medulla. MRI offers higher sensitivity (89-95% vs 66-80%) but lower specificity (74-84% vs 87-94%) compared to CT. Reactive inflammation and edema can be sources of false positives. Disruption of cartilage perichondrium integrity and extralaryngeal fat invasion determine T4a staging.
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Abnormal signal increase in the medulla of the left lamina of the thyroid cartilage is seen on T2 fat-saturated sequence, consistent with cartilage invasion.
Cervical lymphadenopathy is common in laryngeal SCC; especially in supraglottic tumors, early and bilateral metastasis is likely due to rich lymphatic drainage. Levels II-IV are most commonly involved. Metastatic lymph node is recognized on CT as ≥10 mm short axis, central necrosis (hypodense center, rim enhancement), round shape (long/short axis ratio <2), and conglomerate structure. Extranodal extension is seen as perinodal fat infiltration and determines N3b stage.
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Conglomerate lymphadenopathies with central necrosis measuring up to 15 mm in short axis are seen at left levels II and III, consistent with metastatic lymphadenopathy.
Criteria
Originates from vocal cords (60-65%)
Distinct Features
Early diagnosis due to early hoarseness, late metastasis due to poor lymphatic drainage, best prognosis. T1 single cord, T2 both cords, T3 cartilage invasion/vocal cord fixation
Criteria
Originates from epiglottis, aryepiglottic fold, false vocal cords (30-35%)
Distinct Features
Late symptoms (dysphagia, throat pain), early bilateral lymphatic metastasis, pre-epiglottic space invasion common
Criteria
Originates from subglottic region down to inferior border of cricoid cartilage (2-5%)
Distinct Features
Rare, late diagnosis (asymptomatic growth), cricoid cartilage invasion common, paratracheal/paraesophageal lymph node metastasis
Distinguishing Feature
SCC shows deep invasion + cartilage invasion; papillomatosis superficial mucosal involvement, no deep invasion
Distinguishing Feature
SCC mucosal origin, no calcification; chondrosarcoma cartilage origin, ring-and-arc calcification pathognomonic
Distinguishing Feature
SCC solid enhancing mass; laryngocele cystic/air-filled structure, no enhancement
Distinguishing Feature
SCC mass + enhancement; paralysis no mass, vocal cord atrophy, piriform sinus dilatation
Urgency
urgentManagement
surgicalBiopsy
NeededFollow-up
specialist-referralHistopathologic diagnosis via direct laryngoscopy + biopsy is required when laryngeal SCC is suspected. Staging is performed with CT+MRI. In early glottic (T1-T2) tumors, voice preservation is possible with radiotherapy or laser surgery (90%+ control). Advanced stages require total laryngectomy + neck dissection ± adjuvant RT/CRT. Multidisciplinary tumor board decision is required.
Treatment of laryngeal SCC depends on tumor stage and location. In early glottic tumors (T1-T2), voice preservation is possible with radiotherapy or laser surgery. Advanced tumors may require total laryngectomy and neck dissection. Cartilage invasion and extralaryngeal spread are critical factors in surgical planning. 5-year survival is >90% for early glottic carcinoma and 30-50% for advanced stages.