R A D I O L O G I CC L I N I C S

O F N O R T H A M E R I C A

Radiol Clin N Am 45 (2007) 1–20

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Oral Cavity and Oropharynx TumorsHilda E. Stambuk, MDa,*, Sasan Karimi, MDa,Nancy Lee, MDb, Snehal G. Patel, MDc

- Oral cavityScreeningDiagnosisStagingDisease-specific follow-up

- Oropharynx

DiagnosisStagingDisease-specific follow-up

- Summary- References

Cancers of the oral cavity and pharynx are themost common head and neck cancers in the UnitedStates [1]. Most tumors are squamous cell carcino-mas (SCC), but other histologic types may includeminor salivary gland carcinomas and, rarely, lym-phomas and melanoma. For descriptive purposes,the mucosa of the oral cavity and oropharynx is di-vided into several anatomic sub sites (Fig. 1). Theanatomic division between the oral cavity andoropharynx is artificial, and in actual practice it isnot uncommon for a tumor to cross over into theoropharynx from the oral cavity and vice versa.The clinical behavior of tumors in these two loca-tions is distinct, however. As a general rule, regionallymph node and distant metastases are more fre-quently observed with involvement of the orophar-ynx by SCC. Clinical behavior is also dictated by thehistologic type of tumor; perineural spread of dis-ease and lung metastases are features associatedwith adenoid cystic carcinoma of minor salivarygland origin. Clinical examination and evaluationof local extent of disease are easier in the oral cavitybecause the mucosa of the oral cavity is more easilyaccessible to clinicians for clinical inspection and

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palpation. It is important for clinicians and radiol-ogists to understand these differences in clinical be-havior to direct patients to appropriate imaging inthe initial evaluation and subsequent follow-up oftheir disease. Radiologic issues pertaining to thesetwo anatomic sites are discussed under two separatesections in this article. The focus is on SCC, but raretumors such as adenoid cystic carcinoma are men-tioned briefly where appropriate.

Oral cavity

Screening

Clinical examination of the oral cavity is superior toradiologic imaging in assessing for mucosal lesions.There is no cost-effective role for imaging in screen-ing for index primary lesions of the oral cavity, evenin selected high-risk populations. Patients whohave SCC of the oral cavity are at a small butdefined risk for synchronous primary tumors[2,3]. Although most of these second primarytumors occur in the oral cavity and are easilydetected on clinical examination, a second primarycan be missed in patients who are difficult to

a Department of Radiology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY10021, USAb Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, NewYork, NY 10021, USAc Department of Surgery, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021,USA* Corresponding author.

ts reserved. doi:10.1016/j.rcl.2006.10.010

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Fig. 1. The anatomic sub sites of the oral cavity, (oral tongue, floor of mouth, lower alveolus, retromolar trigone,upper alveolus, hard palate, buccal mucosa), and oropharynx (base of tongue, soft palate, palatine tonsil).(Courtesy of Memorial Sloan-Kettering Cancer Center, New York, NY; with permission.)

examine because of pain or trismus. The radiologistautomatically should survey the upper aerodiges-tive tract for additional tumors when imaging stud-ies have been ordered for staging any oral cancer.Incidental discovery of a synchronous primary tu-mor may result in modification of the treatmentplan in a patient who is being evaluated for a knownoral cavity primary (Fig. 2).

Diagnosis

Most patients who have SCC come to imaging withthe diagnosis already made. The role of imaging asa diagnostic modality is limited. The radiologistshould not be satisfied with identifying the tumoralone but should provide the clinician with infor-mation about the local extent and regional spread

that can impact treatment. It is important to beaware of certain common imaging characteristicsthat might help in differentiating benign from ma-lignant lesions of the oral cavity (Table 1). SCC gen-erally only mildly enhances postcontrast on CTimaging and can be subtle (Fig. 3). On MR imagingscans, SCC is isointense to muscle on T1-weightedimages, tends to be of high T2 signal, and generallyexhibits mild to moderate homogeneous enhance-ment. CT is the more common imaging modalityin the evaluation of oral cavity cancers. CT imagingof the oral cavity and neck with contrast can be ac-quired within minutes with modern multidetectorscanners, and the raw data easily can be used forcoronal and sagittal reformation. CT is superior inevaluating the mandible for cortical bone invasion.

Fig. 2. (A) The patient presented with a clinically evident SCC of the left retromolar trigone (arrow) for whicha CT scan of the oral cavity was performed. (B) Incidental right base of tongue primary cancer (arrowhead)was discovered at imaging.

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Table 1: Imaging characteristics of benign versus malignant tumors of the oral cavity

Benign Malignant

Location Generally deep Generally superficialConfiguration Well defined Ill definedSurrounding tissue Normal or may be

displacedInvaded

Internal characteristics Fatty, cystic or vascular� flow voids but can beheterogeneous or solid

Solid and isodense tomuscle MR imaging;T1-weighted isointense,T2-weightedhyperintense to muscle,variable enhancement

Calcifications � No calcificationsBone Not affected or

regressively remodeledCortical invasion ordestruction

Nerves Not affected or focallesion if benign nervetumor

Perineural spread isgenerally diffuse orskips with associatedoral cavity mass

FDG-PET scan Generally no FDGuptake except ininfection

1 FDG uptake except intumors of minor salivarygland origin

MR imaging can be helpful in evaluating the fullextent of medullary cavity involvement once themandibular cortex has been violated. MR imagingis the imaging modality of choice in the evaluationof hard palate tumors, where replacement of bonemarrow by tumor is more easily appreciated on pre-contrast T1-weighted images (Fig. 4).

CT can be limiting in the evaluation of oral cavitytumors because of beam hardening artifact fromdental work. Susceptibility artifact from dentalwork is generally less obscuring of the underlying

Fig. 3. Contrast-enhanced CT scan of the oral cavity.Note that tumor in left floor of mouth (arrow) isonly mildly enhancing and relatively isodense to sur-rounding muscle.

anatomy on MR imaging than the artifact createdwith CT scanning. MR imaging shows superiortumor/muscle interface and better delineates peri-neural spread of disease; however, it is limited byits long acquisition time. An adequate MR imagingof the oral cavity takes approximately 30 minutes toacquire, with imaging of the neck requiring another30 minutes. Patients who have bulky tumors of theoral cavity have pooling of secretions and constantswallowing, which can render an MR imagingexamination nondiagnostic.

Fig. 4. Sagittal precontrast T1-weighted image showsbone marrow invasion by adjacent mucosal hard pal-ate adenoid cystic carcinoma. The normal higher sig-nal fatty marrow is replaced by grayish appearingtumor (arrow).

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The presence of nodal metastases is the most sig-nificant predictor of adverse outcome in head andneck SCC [4]. Extracapsular spread of diseasefrom a metastatic lymph node worsens the progno-sis further, and these patients may benefit frommore aggressive treatment [5,6]. CT shows focalnodal metastases/necrosis in ‘‘normal sized’’ lymphnodes and extracapsular spread of disease fromlymph nodes sooner than MR imaging and beforeit becomes apparent on clinical examination(Fig. 5).

Staging

SCC of the oral cavity tends to spread locally withinvasion of surrounding structures, and the riskand patterns of lymphatic spread to regional cervi-cal nodes vary with the anatomic location of theprimary tumor. Certain anatomic subsites, such asthe oral tongue and floor of the mouth, are richin lymphatics, and tumors of these areas havea higher risk of nodal metastases compared withother locations, such as the upper gum and hardpalate. Distant metastasis is not common inpatients with oral SCC, but tumors such as adenoidcystic carcinoma have a higher predilection forpulmonary metastases. Knowledge of the behaviorand patterns of spread of these tumors is essentialfor radiologists in accurate interpretation and stag-ing. The TNM staging system is used for epithelialtumors, including SCC and minor salivary glandcarcinoma only [7].

T stageThe anatomic imaging techniques of choice forlocal staging are contrast-enhanced CT and MR

Fig. 5. Focal low density within a normal sized lymphnode (arrow) on postcontrast CT scan indicates meta-static disease.

imaging, but CT is the workhorse. MR imaging of-ten complements CT and should be used to exam-ine specific questions, such as perineural spread ofdisease. If a patient is able to lie still without swal-lowing or moving, MR imaging provides betterdelineation of tumor from muscle. MR imaging isespecially useful in the evaluation of extent of in-volvement of the musculature of the tongue, whichcan be difficult to evaluate on clinical examinationin an awake patient. The precise delineation of localextent of tumor not only is important for assigningT stage (Table 2) but also is crucial in treatmentplanning.

CT must be performed with intravenous contrastto better identify the primary tumor and help differ-entiate nodal metastases from adjacent vasculature.These images should be provided in axial and coro-nal planes in standard and bone algorithms forcomplete evaluation of the soft tissues and bone.MR imaging scans always should be performedwith and without gadolinium intravenous contrast.The precontrast T1-weighted sequence is particu-larly useful in differentiating tumor from surround-ing fat, detecting neurovascular bundle encasement

Table 2: T staging of oral cavity tumors

TX Primary tumor cannot beassessed

T0 No evidence of primarytumor

Tis Carcinoma in situT1 Tumor 2 cm or less in

greatest dimensionT2 Tumor more than 2 cm

but not more than 4 cm ingreatest dimension

T3 Tumor more than 4 cm ingreatest dimension

T4aLip Tumor invades through

cortical bone, inferioralveolar nerve, floor ofmouth, or skin of face (ie,chin or nose)

Oral Cavity Tumor invades throughcortical bone, into deep(extrinsic) muscle oftongue (genioglossus,hyoglossus,palatoglossus, andstyloglossus), maxillarysinus, or skin of face

T4b Tumor involvesmasticator space,pterygoid plates, or skullbase and/or encasesinternal carotid artery

Oral Cavity and Oropharynx Tumors 5

(sublingual space), and detecting marrow involve-ment of the adjacent mandible and maxilla. SagittalT2-weighted images can be helpful in assessingdepth of invasion of the primary tumor of theoral tongue. The depth of invasion of the primarytumor has been shown to correlate with the riskfor nodal metastases and outcome [8]. Postcontrastfat saturation T1-weighted images also can be help-ful in differentiating tumor from adjacent muscle/fat and detecting perineural spread of disease.Tumors with an infiltrative border can be differenti-ated from those with a defined ‘‘pushing’’ border onimaging, and this information is helpful to clini-cians in predicting outcome [9].

Advanced lip cancers that occur along the muco-sal surface may abut the buccal cortex of the mandi-ble and may require CT imaging to assess theintegrity of the mandible. Imaging also may behelpful in evaluating for perineural spread oftumor, especially adenoid cystic carcinoma alongthe mental and inferior alveolar nerves. Otherwise,mucosal lip cancers do not require diagnostic imag-ing for assessment of local extension.

Most cases of oral tongue SCC are located alongits lateral border or ventral surface. The prognosisof these tumors depends on their depth of invasion.Although superficial tumors are difficult to assesson radiologic imaging, involvement of the extrinsicmuscles of the tongue (genioglossus, hyoglossus,palatoglossus, and styloglossus) is relatively easyto detect (Fig. 6). Another feature of interest iswhether the tumor approaches or crosses themidline fibrofatty septum of the tongue. Posteriorextension of an oral tongue tumor into the baseof tongue should be noted because this findinghas the potential to change treatment. Oral tongueSCC commonly extends into the floor of mouth.The neurovascular bundle (particularly the lingualartery and hypoglossal nerve and their branches)traverses the sublingual space and can be in closeproximity to tumor (Fig. 7). Surgical excision of a le-sion such as this requires sacrifice of the ipsilateralneurovascular bundle but leaves viable remnanttongue based on the intact contralateral neurovas-cular bundle. In contrast, if an oral tongue tumoris extensive enough to require surgical sacrifice ofboth neurovascular bundles (Fig. 8), the patientwould require total glossectomy, which can befunctionally crippling. Nonsurgical management(radiation with or without chemotherapy) shouldbe considered in these situations. Tumors of theanterior floor of mouth can obstruct the openingsof the Wharton’s ducts (submandibular salivarygland ducts). Radiologically evident dilatation ofWharton’s ducts should prompt a thorough searchfor a mucosal primary tumor in the absence ofobvious calculous disease (Fig. 9).

Evaluation of the mandible for invasion bytumor is an important consideration in stagingand treatment planning. Tumors at certain loca-tions, such as the floor of mouth, retromolar trig-one, and the lower alveolus, can invade themandible directly. Although gross invasion is rela-tively easy to identify, early cortical bone loss di-rectly adjacent to obvious tumor should beconsidered indicative of bone invasion (Fig. 10).If bone invasion is present, it is important for theradiologist to define its extent so that the surgeonis able to determine the extent of mandibular resec-tion. In most situations CT is adequate for this de-termination, but the bone marrow may be furthercharacterized by MR imaging if appropriate.

Fig. 6. CT imaging shows obvious SCC involvement ofthe extrinsic muscles of the tongue, including thepaired genioglossus muscles (arrows).

Fig. 7. CT of the oral cavity shows tumor of the rightlateral tongue (arrow) in close proximity to butnot involving the right neurovascular bundle(arrowhead).

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Fig. 8. Extensive tumor involving the right neurovas-cular bundle that would have required sacrifice ofthe uninvolved left neurovascular bundle and totalglossectomy to achieve adequate surgical margins.

Fig. 9. Left anterior floor of mouth cancer (arrow) ob-structing left Wharton’s duct with subsequent ductaldilatation (arrowhead).

Resection of the involved segment of the mandiblebecomes necessary if there is direct invasion of thebone. On the other hand, if the primary tumor isin close proximity to but does not directly invadethe mandible, marginal mandibulectomy providesan adequate surgical resection while maintainingintegrity of the bone (Fig. 11). On rare occasions,segmental mandibulectomy may become necessaryin the absence of direct bone invasion. Marginalresection of the mandible is technically not possibleif the tumor is in close proximity to a substantialdepth along its lingual (inner) cortex. Clinicalexamination is generally unreliable in differentiat-ing direct tumor extension through the musculardiaphragm of the oral cavity from metastaticlymphadenopathy or an obstructed submandibularsalivary gland (Fig. 12). This information hasimportant implications in the staging and thesurgical approach and should be reported clearly.

The mandible also should be evaluated in certainother situations in which mandibulotomy is re-quired for surgical access to the primary tumorthat may not necessarily be in proximity to thebone. Tumors of the posterior oral cavity and oro-pharynx are difficult to resect through the openmouth. The mandibular ‘‘swing’’ approach (mandi-bulotomy) can provide excellent exposure of thesetumors and allow adequate resection and appropri-ate reconstruction of the surgical defect. A parame-dian osteotomy is usually placed between thelateral incisor and canine teeth, after which thefloor of mouth is incised so that the mandibularsegment can be retracted laterally. Unrelated butunexpected lesions at the proposed mandibuloto-my site should be recognized and reported to avoidsurprises during the surgical procedure (Fig. 13).

The retromolar trigone is the part of the buccalmucosa located posterior to the last lower molartooth along the ascending ramus of the mandible.Because the periosteum of the mandible is in close

Fig. 10. (A) CT scan of the oral cavity showing early invasion of the mandibular cortex from a lower alveolar ridgeSCC. (B) CT scan of the oral cavity with gross invasion of the mandible from gingival SCC.

Oral Cavity and Oropharynx Tumors 7

Fig. 11. The relationship of the primary tumor to the mandible determines the extent of surgical resection of thebone. (A) If the bone is directly invaded by tumor (arrow), a segmental mandibulectomy is necessary and theresultant defect may need reconstruction. (B) Marginal mandibulectomy involves resection of a rim of mandibleto provide a surgical margin for tumors that are in close proximity but not invading bone (arrow). The procedureis technically feasible only if there is sufficient vertical height of bone stock and the mandibular canal with itsneurovascular bundle does not get exposed or resected. The patient is at risk for stress fracture if the remnantmandible has insufficient vertical height/stock or its vascular supply is compromised.

proximity, tumors of the retromolar trigone havea higher propensity to invade bone. The pterygo-mandibular raphe is a fibrous band that runsfrom the hamulus of the medial pterygoid plate tothe posterior end of the mylohyoid line of the man-dible. The fibers of the buccinator and superior con-strictor muscles interdigitate along this raphe. Oncea retromolar trigone tumor infiltrates the pterygo-mandibular raphe, it has access to the buccinatormuscle and buccal space, pterygoid musculatureand pterygoid plates, posterior maxillary alveolarridge, or skull base (Fig. 14). The inferior alveolarnerve is also located in close proximity to the retro-molar trigone and is at risk for direct invasion andperineural spread. Perineural spread of tumor alongthe inferior alveolar nerve is identified by enlarge-ment and enhancement of the nerve more easilyseen on MR imaging and widening of the bonycanal on CT scan (Fig. 15).

Perineural spread of tumor is a particular featureof adenoid cystic carcinomas, which are generallysubmucosal in location and tend to occur on thehard palate. Tumors of the hard palate can spreadalong the greater and lesser palatine nerves intothe pterygopalatine fossa and along V2 and thevidian nerve (Fig. 16). Radiologic evaluation ofhard palate tumors should include a careful surveyof these routes of spread, including the entirecourse of the trigeminal nerve. The submucosalextent of the lesion, involvement of the underlyingbone of the hard palate, and extension into thenasal cavity or maxillary sinus also should be noted(Fig. 17).

N stageThe status of the cervical lymph nodes is the mostsignificant predictor of outcome in patients whohave SCC of the oral cavity. The risk of nodal

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Fig. 12. Coronal imaging is helpful in delineating the relationship of the primary tumor to the lingual cortex ofthe mandible. It is also important to differentiate direct tumor extension through the mylohyoid muscle into thesubmandibular space (A) from a metastatic lymph node (B) or an enlarged submandibular gland from tumorobstructing Wharton’s duct (C).

metastases depends on the anatomic site of the pri-mary tumor within the oral cavity. Tumors of theoral tongue, floor of mouth, and buccal mucosahave a higher propensity to metastasize to cervicallymph nodes compared with hard palate and alve-olar tumors. SCCs generally metastasize to thedraining cervical lymph nodes in a predictable pat-tern [10]. For ease of description and consistency,the cervical lymph nodes are arbitrarily groupedinto levels I-V (Fig. 18) (Table 3). Levels I-III areat highest risk for nodal metastases from oral cavitySCC. In the previously untreated neck, metastasesto levels IV or V are rare in the absence of obviouslymphadenopathy at levels I-III.

Most metastatic lymph nodes from SCC areabnormally enlarged, but the size criteria for desig-nating cervical lymph nodes as metastatic are notuniversally accepted. As a general rule, lymph nodesR1.5 cm at levels I and highest level II (jugulodi-gastric) and R1 cm at all other levels are considered

abnormal. Normal sized lymph nodes can havefocal metastasis or necrosis that is more easilyseen on CT than MR imaging (Fig. 19). Other radio-logic features of metastatic lymphadenopathy fromSCC include heterogeneous enhancement andstranding or involvement of the adjacent soft tissueif extracapsular nodal spread is present (Fig. 20).Extracapsular nodal spread is generally seen inlarger lymph nodes but can be seen in small lymphnodes. The current staging system for the neck doesnot take into account the presence of extracapsularspread but is based on the size, number, and later-ality of the metastatic lymph nodes relative to theprimary tumor (Table 4).

The radiologist also should look for and reportcertain other features of metastatic lymphadenopa-thy that may be valuable in therapeutic decisionmaking. The relationship of metastatic lymphade-nopathy to the great vessels of the neck, particularlythe carotid artery, is an important consideration in

Oral Cavity and Oropharynx Tumors 9

Fig. 13. (A) The mandibular osteotomy is placed ina paramedian location on the anterior mandible,and division of the soft tissue structures of the floorof mouth allows lateral retraction for access to theposterior oral cavity and oropharynx. (Courtesy ofMemorial Sloan Kettering Cancer Center, New York,NY; with permission.) (B) Panorex shows incidentallytic lesion of the anterior mandible. Failure to recog-nize this lesion preoperatively places the patient atrisk for poor healing and nonunion of themandibulotomy.

determining surgical resectability. If more than 270�

of the circumference of the carotid artery are sur-rounded by tumor, it is considered ‘‘encased’’ andthe tumor is generally surgically unresectable.Similarly, extension of nodal disease into the pre-vertebral musculature is an adverse indicator ofprognosis and should be reported.

M stageDistant metastases from oral cavity SCC are rare atpresentation. There is no cost-effective role for rou-tine positron emission tomography (PET) scan inmost patients who have oral SCC. Patients whopresent with locoregionally advanced tumor maybe at higher risk for distant metastasis, especiallyto the lungs. Noncontrast chest CT may be indi-cated to assess for distant metastases in this selectedgroup and in patients who have adenoid cysticcarcinoma.

Disease-specific follow-up

The pattern of recurrence in oral cavity SCC isdifferent from oropharyngeal SCC because nodaland distant metastases are more frequently seen inpatients who have oropharyngeal SCC. Mostrecurrences occur at the local site or in the neck,which should be the primary focus of posttreat-ment surveillance. The risk for distant failure aftersuccessful treatment of oral cavity SCC is low.Patients who have multiply recurrent tumors andbulky nodal metastases may be at higher risk.

Clinical evaluation of the oral cavity for localrecurrence is relatively easier than examination oforopharyngeal sites, such as the base of tongue.Conversely, submucosal and deep-seated

Fig. 14. (A) The buccinator and superior constrictor muscles interdigitate along the pterygomandibular raphe,which is attached to the medial aspect of the mandible in the vicinity of the retromolar trigone. (Courtesy ofMemorial Sloan-Kettering Cancer Center, New York, NY; with permission.) (B) CT scan of the oral cavity showsspread of a right retromolar trigone tumor into the right buccal space involving the posterior aspect of the buc-cinator muscle.

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recurrences are more easily detected on radiologicimaging (Fig. 21). Some radiographic features thatmay indicate locally recurrent disease includemass-like lesion with or without enhancement, ab-normality along the margins of previous resectionor reconstruction, bone invasion, and perineuralspread. As on clinical examination, recurrence canbe difficult to appreciate on diagnostic imaging

Fig. 15. Precontrast T1-weighted MR imaging showsdiffuse enlargement of the right inferior alveolarnerve compatible with perineural spread of SCC. Be-cause the inferior alveolar nerve is surrounded byfatty marrow, the enlarged nerve is easily seen onthe precontrast T1-weighted sequence. The abnormalinferior alveolar nerve enhances postcontrast admin-istration, which makes it blend in with the surround-ing fatty marrow. Postcontrast T1-weighted sequenceneeds fat suppression for reliable identification ofperineural spread.

because of treatment-related changes, such asedema, fibrosis, and distortion of local anatomy af-ter surgical manipulation. Unless otherwise indi-cated, it is advisable to wait approximately 12weeks after completion of treatment before imagingto reduce false-positive results. In the appropriatecircumstances, FDG PET scans can provide addi-tional information and help direct the need for tis-sue diagnosis. Patients who have received radiationtherapy as part of their treatment program may beat risk for developing osteoradionecrosis if the radi-ation portals include the mandible. Although theincidence of osteoradionecrosis is low in modernpractice, its consequences, such as orocutaneous fis-tulas and pathologic fracture, can be devastating tothe patient and treatment can be complicated. Thedifferential diagnosis from recurrent tumor maybe difficult, and unfortunately, PET scan is not spe-cific in differentiating between these two entities.

The clinically node-negative neck in selected oralcancers can be managed safely by close surveillance.Clinical examination has been shown to be unreli-able in detecting early nodal metastases comparedwith CT or MR imaging [11,12]. Although ultraso-nography is not commonly used in the UnitedStates, it has become widely accepted in Europe[13]. Lymphatic metastases after treatment of theneck can be unpredictable because of distortion ofnormal lymphatic pathways. It is important toscrutinize the neck and upper mediastinum for un-usual metastases, such as lateral retropharyngealand paratracheal lymph nodes.

The lungs are the most common site for distantmetastases from head and neck SCC. Routinescreening for pulmonary metastases is generallylimited to an annual chest radiograph, but CT ofthe chest may be appropriate for selected high-risk

Fig. 16. The maxillary branch of thetrigeminal nerve innervates the mu-cosa of the hard palate and upper al-veolus. Perineural spread can occuralong branches of these nerves ina retrograde fashion into the ptery-gopalatine fossa, where it can gainaccess to V2, or antegrade alongany of the peripheral branches.(Courtesy of Memorial Sloan Ketter-ing Cancer Center, New York, NY;with permission.)

Oral Cavity and Oropharynx Tumors 11

patients. No conclusive evidence supports thehypothesis that routine screening is cost-effectivein improving overall outcome [14–16].

The risk for metachronous (subsequent) primarycancers increases progressively with time after suc-cessful treatment of the index primary oral cavitycancer [17]. Most of these tumors occur in locationsthat are easily accessible to the clinician, and there isno cost-effective role for imaging in screening forsubsequent mucosal primary lesions of the headand neck. Patients who have oral cancers are alsoat risk for developing primary lung cancer, but therole for routine radiologic screening in this popula-tion remains undefined [17]. Annual chest radio-graphs have been recommended for earlydetection of subsequent primary lung cancer, butCT of the chest is a more sensitive examinationthat may be useful in selected high-risk patients [18].

The role of functional imaging (FDG-PET scan)has been investigated in screening after treatmentof other head and neck cancers, such as laryngealand hypopharyngeal [19]. The relatively lower riskfor subsequent primary tumors and distant metas-tases in patients who have oral cancer makes itunlikely that this investigation will prove cost-effective.

Oropharynx

The oropharynx is the part of the upper aerodiges-tive tract that is immediately posterior to the oralcavity. It includes the base of tongue, tonsils, tonsil-lar pillars, posterior and lateral pharyngeal walls,and the inferior (anterior) surface of the soft palate.The oropharynx is separated from the oral cavity by

Fig. 17. Axial postcontrast T1-weighted MR imagingshows perineural spread involving V2 from the fora-men rotundum, cavernous sinus, Meckel’s cave, cister-nal segment of the trigeminal nerve, and root entryzone in the pons.

the plane formed by the circumvalate papilla, ante-rior tonsillar pillars, and junction of the hard andsoft palate. Superiorly, it extends to the level ofthe Passavant’s ridge of the superior constrictormuscle, which is approximately at the plane of thehard palate. Inferiorly, the oropharynx ends at thelevel of pharyngoepiglottic folds.

This article focuses on SCC of the base of thetongue, tonsils/tonsillar pillars, and the soft palatesubsites of the oropharynx. One should keep inmind that different subsites within the oropharynxcontain a variable amount of lymphoid tissue. Lym-phoma should be included in the differential diag-nosis. Although less common, non–squamous cellmalignancies, such as tumors that originate fromthe minor salivary glands, also can arise in theoropharynx.

Diagnosis

Base of the tongue carcinomaThe base of the tongue is the posterior third of thetongue or the part posterior to the circumvalatepapilla. It extends inferiorly to end at the level ofvallecula and houses the lingual tonsil [20]. SCCof the base of the tongue is often occult andasymptomatic; the lesions are often large by thetime they cause symptoms, such as dysphagia or re-ferred ear pain. Some patients present with nodalmetastases without signs of a primary tumor [21].These mucosal lesions can be invasive with deep

Fig. 18. Division of the neck into levels of lymphaticdrainage. (From Shah JP, Patel SG. Head and neck sur-gery and oncology. 3rd edition. New York: ElsevierScience; 2003. p. 355; with permission.)

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Table 3: Levels of lymphatic drainage

Level Definition

I Submental and submandibularnodes. They lie above the hyoidbone, below the mylohyoid muscle,and anterior to the back of thesubmandibular gland.

IA Submental nodes. They lie betweenthe medial margins of the anteriorbellies of the digastric muscles.

IB Submandibular nodes. On each side,they lie lateral to the level IA nodesand anterior to the back of eachsubmandibular gland.

II Upper internal jugular nodes. Theyextend from the skull base to thelevel of the bottom of the body ofthe hyoid bone. They are posteriorto the back of the submandibulargland and anterior to the back of thesternocleidomastoid muscle.

IIA A level II node that lies eitheranterior, medial, lateral, or posteriorto the internal jugular vein. Ifposterior to the vein, the node isinseparable from the vein.

IIB A level II node that lies posterior tothe internal jugular vein and hasa fat plane separating it and thevein.

III Middle jugular nodes. They extendfrom the level of the bottom of thebody of the hyoid bone to the levelof the bottom of the cricoid arch.They lie anterior to the back of thesternocleidomastoid muscle.

IV Low jugular nodes. They extendfrom the level of the bottomof the cricoid arch to the levelof the clavicle. They lie anterior toa line connecting the back of thesternocleidomastoid muscle and theposterolateral margin of theanterior scalene muscle. They arealso lateral to the carotid arteries.

V Nodes in the posterior triangle. Theylie posterior to the back of thesternocleidomastoid muscle fromthe skull base to the level of thebottom of the cricoid arch andposterior to a line connecting theback of the sternocleidomastoidmuscle and the posterolateralmargin of the anterior scalenemuscle from the level of the bottomof the cricoid arch to the level of theclavicle. They also lie anterior to theanterior edge of the trapeziusmuscle.

extension or can be exophytic and protrude into theairway (Fig. 22). Small lesions are difficult to detecton imaging because of lymphoid tissue at the baseof the tongue, which normally enhances. The onlyfinding on cross-sectional imaging when lesionsare small may be subtle asymmetry at the base ofthe tongue. Unlike superficial spread of disease,deep plane infiltration is easily detected on imaging(Fig. 23). The extent of superficial spread is betterappreciated clinically during endoscopic examina-tion. On CT and MR imaging the tumors demon-strate mild to moderate enhancement. They areoften isointense to muscle on T1-weighted imagesbut are generally slightly hyperintense relative tomuscle on T2-weighted images. The extent of thetumors is more easily appreciated on postcontrastimages with fat saturation (Fig. 24).

In general, MR imaging is the preferred modalityfor evaluation of oropharyngeal tumors because of

Table 3: (continued)

Level Definition

VA Upper level V nodes extend from theskull base to the level of the bottomof the cricoid arch.

VB Lower level V nodes extend from thelevel of the bottom of the cricoidarch to the level of the clavicle, asseen on each axial scan.

From Som PM, Curtin HD, Mancuso AA. An imaging-based classification for the cervical nodes designed asan adjunct to recent clinically based nodal classifications.Arch Otolaryngol Head Neck Surg 1999;125:388–96; withpermission.

Fig. 19. A normal sized lymph node at left level II thathas an eccentric focal metastatic deposit (arrow). Thisfeature should be differentiated from a normal fattyhilum, which also would be eccentric but would belower density and is seen in a reniform-shaped ratherthan round lymph node.

Oral Cavity and Oropharynx Tumors 13

superior soft tissue contrast and less amalgam arti-fact. Motion artifact can degrade image quality inpatients who have bulky tumors, however. PET im-aging, particularly when co-registered with CT, maylocalize the primary tumor in patients with un-known primaries.

Conservation therapy with chemotherapy andradiation has become the mainstay treatment of oro-pharyngeal cancers. Treatment is governed by tumorsize, but tumor volume seems more important fortherapy than T staging. Small-volume tumors canbe treated with equivalent cure rates using surgeryor radiation therapy, but definitive radiation therapyis the preferred treatment approach because surgicalaccess via mandibulotomy is more invasive and hasthe potential for producing postoperative dysfunc-tion [22]. Larger T-staged lesions are generallytreated with concurrent chemotherapy and radia-tion therapy in an attempt to preserve functionand the quality of life [23].

Tonsillar carcinomaThe anterior and posterior tonsillar pillars aremucosal folds over the palatoglossus and palato-pharyngeal muscles, respectively. The faucial or pal-atine tonsils are located between the tonsillar pillarsbilaterally. In this section, neoplasms that arisefrom the tonsillar fossa and the anterior and poste-rior pillars are grouped together. Carcinomas thatarise at the tonsillar fossa are most common fol-lowed by lesions that arise from the anterior andthe posterior pillars.

Small or early lesions are typically superficial andmay be located within a tonsillar crypt so that theymay be undetectable on CT/MR imaging. As the

Fig. 20. Stranding of the soft tissue adjacent to a met-astatic node indicates extracapsular nodal spread ofdisease. This feature is seen earlier on CT than MR im-aging and portends a poorer prognosis for thepatient.

tumor grows it tends to create asymmetry of thetonsils, which can be indistinguishable from subtletonsillar asymmetry that sometimes can be presentin normal individuals (Fig. 25). The incidence of anasymmetric tonsil harboring cancer in a patientwith an otherwise normal examination (ie, normalmucosa and no cervical adenopathy) is approxi-mately 5% [24]. Tonsillar asymmetry should raisesuspicion for tumor, particularly in a symptomaticpatient. The larger or more advanced lesions maybe exophytic or locally infiltrate the adjacent softtissues of the neck (Fig. 26).

Similar to mucosal tumors at other sites, tonsillarcarcinoma can present as a nonhealing, painless ul-cer at first. As the tumor grows, however, the patientmay develop painful swallowing, ipsilateral referredotalgia, and neck adenopathy. Advanced tonsillarfossa carcinomas can transgress the superior con-strictor muscle to invade the parapharyngeal space.The tumors also can involve the anterior and poste-rior tonsillar pillars and grow along the palatoglos-sus and palatopharyngeal muscles, respectively.Lesions of the anterior tonsillar pillars can extendsuperiorly to the soft and hard palate and inferiorlyto the tongue base [20]. Anteriorly, they can extendalong the pharyngeal constrictor to the pterygo-mandibular raphe. When lesions involve the

Table 4: N staging for oral cavity andoropharyngeal tumors

Nx Regional lymph nodes cannot beassessed

N0 No regional lymph node metastasisN1 Metastasis in a single ipsilateral

lymph node, 3 cm or less in greatestdimension

N2 Metastasis in a single ipsilaterallymph node, more than 3 cm but notmore than 6 cm in greatestdimension; or in multiple ipsilaterallymph nodes, none more than 6 cmin greatest dimension; or in bilateralor contralateral lymph nodes, nonemore than 6 cm in greatestdimension

N2a Metastasis in a single ipsilaterallymph node more than 3 cm but notmore than 6 cm in greatestdimension

N2b Metastasis in multiple ipsilaterallymph nodes, none more than 6 cmin greatest dimension

N2c Metastasis in bilateral orcontralateral lymph nodes, nonemore than 6 cm in greatestdimension

N3 Metastasis in a lymph more than6 cm in greatest dimension

Stambuk et al14

Fig. 21. CT scan of a patient with multiply recurrent SCC of the oral cavity. (A) Baseline posttreatment scan showsa right maxillectomy defect. (B) Recurrent tumor was easily seen on clinical examination (arrow). Note the ad-ditional submucosal recurrence (arrowhead) that could not be appreciated on clinical examination. (C) Recur-rent disease was FDG avid on PET scan, which was obtained for distant metastatic evaluation.

posterior tonsillar pillars they tend to grow alongthe palatopharyngeus muscle. They can extend su-periorly to soft palate and inferiorly to involve thepharyngoepiglottic fold, middle constrictor, andeven the upper thyroid cartilage [25]. The posteriororopharyngeal wall may get involved with posteriorextension.

On CT the tumors can enhance similar to the ton-sils. Invasion of the masticator and parapharyngealspace in advanced tumors is often readily detectedon imaging (Fig. 27). On MR imaging the lesionsare isointense to muscle on T1-weighted imagesbut are slightly hyperintense relative to muscle onT2-weighted images. Fat-saturated postcontrast

Fig. 22. Axial postgadolinium (A) and coronal T2-weighted fat saturated (B) images demonstrate an exophyticmass arising from the base of the tongue on the left side.

Oral Cavity and Oropharynx Tumors 15

Fig. 23. Recurrent SCC of the tongue base involving the root of the tongue with extensive anterior extension isevident on the axial postcontrast (A) and sagittal T2-weighted image (B).

imaging helps in improving tumor delineation. PETCT can be helpful in localizing the primary tumorand guiding biopsy in patients who have ‘‘occultprimaries’’ [26].

For early T1-T2 tonsillar lesions, definitive radia-tion therapy is the primary treatment of choice.Excellent locoregional control can be obtained.On the other hand, more advanced T3-T4 disease

Fig. 24. Pre- (A) and postgadolinium with fat saturation (B) T1-weighted images. Advanced SCC of the tonguebase extending to retromolar trigone abutting the mandible without mandibular invasion (A, B) (arrows). Cor-onal postcontrast image (C) demonstrates involvement of the posterior mylohyoid muscle with tumor extendinginto the submandibular space (arrow).

Stambuk et al16

is treated with concurrent chemotherapy and radia-tion therapy. Surgery is reserved for salvage [27].

Soft palateThe soft palate is a much less frequent subsite forSCC than the faucial tonsils or the base of thetongue. Carcinomas of the soft palate most com-monly involve the oral aspect of the palate. As ex-pected, SCC is the most common tumor of thesoft palate, but minor salivary gland cancers arenot infrequent [21].

When small, soft palate lesions may be undetect-able on imaging and are best visualized duringclinical evaluation. Early cancers appear as ulcera-tive mucosal lesions on direct visualization.Patients may have velopharyngeal insufficiency,hypernasal speech, difficulty swallowing, and

Fig. 25. Axial CT image demonstrates subtle asymmet-ric fullness of the left tonsil in a patient without priortonsillectomy.

referred otalgia on presentation. Patients whohave advanced lesions may have symptoms relatedto the sites of involvement by tumor, such as tris-mus and malocclusion—signs of pterygoid muscleinvasion. These tumors commonly extend anteri-orly to the hard palate or inferiorly to the tonsillarpillars (Fig. 28). They also can extend along theveli palatini muscles to involve even the skullbase. The pterygopalatine fossa can become in-volved by tumor once the palatine nerves are dis-eased [21]. The tumors are best evaluated by MRimaging, particularly in the coronal plane.

Radiation therapy is the primary treatment mo-dality for small tumors in many centers to preservequality of life. More advanced T3 and T4 cancers aretreated with radiation concurrent with chemother-apy. Surgery is reserved for salvage.

Fig. 27. Axial CT. Large left tonsillar mass extends intomasticator space. The tumor abuts the medial ptery-goid muscle without infiltrating the muscle (arrows).

Fig. 26. Mildly enhancing left tonsillar mass on axial CT image (A). Coronal T2 fat-saturated image (B) of a differ-ent patient demonstrates superior extension of tonsillar SCC to left side of the soft palate (arrow).

Oral Cavity and Oropharynx Tumors 17

Fig. 28. Axial (A) and sagittal (B) T2-weighed images reveal a soft palate mass extending to the uvula. Postga-dolinium image in the coronal plane (C) shows extension of tumor to the tonsillar fossae.

Staging

The TNM staging system is applicable to SCC andminor salivary gland carcinoma and not to nonepi-thelial tumors, such as those of mesenchymal ori-gin. Although the surface extent of oropharyngealcancer is best determined on clinical examination,cross-sectional imaging is invaluable in assessmentof certain other features, such as deep tumor inva-sion and nodal staging.

Table 5: Tumor (T) staging for squamous cellcarcinoma of the oropharynx

T1 Tumor %2 cm in maximal diameterT2 Tumor 2–4 cm in maximal diameterT3 Tumor >4 cm in maximal diameterT4 4a Tumor invades the larynx,

deep/extrinsic muscles of tongue,medial pterygoid, hard palate, ormandible4b Tumor invades lateralpterygoid muscle, pterygoid plates,lateral nasopharynx, or skull base orencases carotid artery

T stageThe primary tumor (T) staging depends mainly ontumor size (Table 5), and the treatment is deter-mined by CT/MR features in addition to clinicalfindings [7]. The root of the tongue and the floorof the mouth should be inspected for possible ante-rior spread of a base of the tongue carcinoma. Baseof the tongue carcinoma can spread posterolaterallyto anterior tonsillar pillars and the faucial tonsils orinferiorly to pre-epiglottic fat or supraglottic larynx(Fig. 29) [25]. The third division of the trigeminalnerve should be inspected for signs of perineuralspread.

Accurate staging of SCC arising from the palatinetonsils also depends on physical/endoscopic exam-inations and imaging. In advanced cases, numbnessin the distribution of V3 and trismus indicate mas-ticator space extension with involvement of V3.Numbness of the chin indicates mandibular exten-sion and involvement of the inferior alveolar nerve.Fasciculation and atrophy of the hemitongue aresigns of tumor in posterior sublingual space involv-ing the twelfth nerve.

Stambuk et al18

Fig. 29. Axial postgadolinium (A) and sagittal T1-weighted image (B) in a patient with base of the tongue SCCwith involvement of the pre-epiglottic space and supraglottis. (C) Companion sagittal image of a different pa-tient with base of the tongue SCC without involvement of the pre-epiglottic space. The pre-epiglottic fat and itsreplacement with tumor are marked with arrows (B, C).

N stageNodal staging of oropharyngeal carcinoma isthe same as for cancers of the oral cavity (seeTable 4). The oropharynx has the second highestincidence of nodal disease at presentation amongother SCCs of the head and neck [28]. The lymphnodes in the upper jugular and spinal accessorychains and the retropharyngeal nodes are mostcommonly involved by oropharyngeal SCC. Nodalassessment is best performed on imaging at thetime of primary tumor assessment. The oropharyn-geal lymphatic metastases are mainly to level I-IVnodes, with level II being the most common site.The base of the tongue lymphatic drainage is mostlyto level II-IV nodes. Nodal metastasis to both sidesof the neck is common because of rich lymphaticsand can be seen in up to 30% of patients whohave tongue base carcinoma. Soft palatal carcino-mas have a high incidence of nodal metastasis.

Approximately 60% of patients have nodal diseaseat the time of diagnosis [21].

Predominantly cystic SCC metastasis in theneck is most commonly seen with primary tumorsof the palatine and lingual tonsils. Such cystic me-tastases should be differentiated from liquefactionnecrosis that can occur in solid adenopathy [29].These primary tumors arise in the tonsillar cryptepithelium and are of the transitional type insteadof the usual SCC [30]. Cystic nodal metastases arenot uncommonly confused for a branchiogeniccyst, and it is important to understand that the di-agnosis of metastatic carcinoma must be ruledout, especially in adults. It is crucial to alert theclinician when cystic metastases are encounteredin the neck on imaging because such primarieshave a different behavior than the usual SCC.Such primary tumors can have different diagnos-tic/surgical implications when the primary site is

Oral Cavity and Oropharynx Tumors 19

Fig. 30. Axial T2- (A) and T1-weighted (B) images of a patient with left tongue base SCC. Note lack of a significantmass at the tongue base and predominantly cystic metastasis on the left side containing hemorrhagic fluid.

not evident. The primary tumors of the orophar-ynx responsible for cystic metastases are oftensmall and indolent and may be clinically occult.Patients are often younger and may not havehistory of risk factors, such as tobacco or alcoholuse. Despite the typical small size of tumors of thetonsillar crypt epithelium, they metastasize earlyand lead to moderately large nodes (Fig. 30) [29].In a patient who has cystic upper internal jugularchain nodal metastasis without a known primary,the ipsilateral faucial or lingual tonsil should behighly considered as a potential site for the occult tu-mor. The adenoidal pad of the Waldeyer’s ring isa less frequent site responsible for cystic metastases.It should be noted that cystic metastases can bepresent in the setting of other tumors, such aspapillary carcinoma of the thyroid [29,30].

M stageThe lungs are the most common site of distantmetastases. Bony and hepatic metastases are lesscommon in oropharyngeal SCC. Mediastinal nodemetastases are considered distant metastasis [7].

Disease-specific follow-up

Patients who have oropharyngeal cancer should beclinically followed with physical examinationsevery 6 to 8 weeks initially after treatment thenevery 2 months for the first 2 years, every 4 to 6months the third and fourth years, and yearly inthe fifth year. Posttreatment MR imaging shouldbe obtained at least 3 months after completion ofradiation therapy to minimize the confoundingeffect of posttreatment inflammatory changes.Close follow-up of high-risk patients or patientswho are at high risk for tumor recurrence is encour-aged, particularly during the 2 years after treatment[31]. Follow-up is important because most

recurrences occur during this time period. Imagingplays a crucial role during this period because it isnot unusual for posttreatment changes to limitphysical evaluation of the neck. FDG-PET hasbeen shown to be a highly sensitive tool in detect-ing recurrent SCC of the head and neck [32,33].

In general, patients who have head and neck SCChave a 10% risk of developing a second aerodiges-tive tract primary malignancy. This number iseven higher—approximately 15%—for tonsillarand base of the tongue cancers. It is important tobe cognizant of this fact when following up patientswho have a history of SCC.

Summary

In addition to familiarity with the locoregionalanatomy, radiologists must have a solid under-standing of the clinical behavior and spreadpatterns of oral cavity and oropharyngeal SCC tomake a meaningful contribution to the treatmentof patients.

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