Cancer Imaging (2010) 10, 62�72DOI: 10.1102/1470-7330.2010.0008

REVIEW

Cancer of the oral cavity and oropharynx

Dechen Wangmo Tshering Vogela, Peter Zbaerenb and Harriet C. Thoenya

aDepartment of Diagnostic, Interventional and Pediatric Radiology, bDepartment of Oto-Rhino-Laryngology,Head and Neck Surgery, Inselspital, University of Bern, Bern, Switzerland

Corresponding address: D.W. Tshering Vogel, Department of Diagnostic, Interventional and Pediatric Radiology,Inselspital, University of Bern, Freiburgstrasse, CH-3010 Bern, Switzerland.

Email: dechen.tshering@insel.ch

Date accepted for publication 8 January 2010

Abstract

Tumours in the oral cavity and oropharynx differ in presentation and prognosis and the detection of spread of tumourfrom one subsite to another is essential for the T-staging. This article reviews the anatomy and describes the patternof spread of different cancers arising in the oral cavity and oropharynx; the imaging findings on computerizedtomography and magnetic resonance imaging are also described. Brief mention is made on the role of newer imagingmodalities such as [18F]fluorodeoxyglucose-positron emission tomography/computed tomography, perfusion studiesand diffusion-weighted magnetic resonance imaging.

Keywords: Anatomy; oral cavity; oropharynx; carcinoma; magnetic resonance imaging; computerized tomography.

Introduction

The oral cavity and oropharynx are the uppermost part ofthe digestive tract and unique in the variety of tissuescontained within a small area. Knowledge of anatomyis essential in identifying the site of origin of thetumour, its pattern of spread and behaviour. Carcinomain this area is treated with surgery, chemotherapy andradiotherapy depending on the T-staging and it is there-fore very important to accurately stage the tumour toallow for optimum therapy and to avoid unnecessarymorbidity.

Epidemiology

The incidence of cancer of the oral cavity was reportedby Parkin et al.[1] as 2.6% of all cancers followed bypharyngeal (oro/hypo) cancers reported with 1.2%.It was more common in men than women; the M/Fratio for mouth cancer was 2.0 and for pharyngealcancers 4.4. In men, the incidence of oral cavity andpharyngeal cancers is high in western and southernEurope, whereas oral cavity cancers have a higher inci-dence in south-east Asia, southern Africa and Australia.In women, pharyngeal and oral cavity cancers have a

relatively high incidence in south-central Asia and oralcancers have a higher rate in south-east Asia andAustralia. These patterns reflect the prevalence of spe-cific risk factors, tobacco/alcohol in south Europe andAfrica and chewing of betel nuts in south-central andsouth-east Asia. In Australia, there is a high rate of lipcancer due to solar radiation. Oral cavity cancer is thesixth leading cause of cancer deaths in the world withcancer of the mouth and pharynx being the mostcommon head and neck tumours in the United States[2].

Anatomy

The oral cavity includes the lips, the hard palate, theupper and lower alveolar ridge, the anterior two-thirdsof the tongue, sublingual region, the buccal mucosa,the retromolar trigone and the floor of the mouth(mylohyoid, digastric, geniohyoid muscles)[3]. The retro-molar trigone is a small mucosal area on the mandibularramus behind the posterior molars. This is a junctionpoint between the oral cavity, oropharynx and nasophar-ynx allowing for complex spread of tumours[4].

The oral cavity is separated from the oropharynx by animaginary line drawn across the circumvallate papillae,anterior tonsillar pillars and junction of the hard and

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soft palate (Fig. 1). The oropharynx contains the poste-rior third (base) of the tongue, the tonsillar fossa andpillars, the soft palate and the posterior and lateral pha-ryngeal walls to the level of the hyoid bone inferiorly. Theanterior and posterior tonsillar pillars are mucosal foldsover the palatoglossus and palatopharyngeal muscles,respectively; the faucial or palatine tonsils are locatedbetween the tonsillar pillars bilaterally.

Imaging: when and how

Evaluation of the oral cavity and oropharynx is primarilydone by clinical examination and with endoscopy.Diagnosis of cancer is made by biopsy. Cross-sectionalimaging is used for staging and allows visualization of thepathology beneath the mucosa, helps to determine thesize, thickness and depth of the tumour, detects invasionof neighbouring structures, bone or perineural spread,assesses lymph node metastases, excludes a secondtumour and assesses the teeth, and is used for treatmentplanning and follow-up during and after treatment.

Computerized tomography (CT) is usually the firstimaging modality used to assess and stage tumours ofthe oral cavity and oropharynx because it is widely avail-able, relatively cheap, quick and easy to perform. Thinsection (1 mm) scanning results in good quality coronaland sagittal reconstructions. CT can delineate the sizeand extent of the primary tumour, and assess bone invol-vement and metastatic lymph nodes. Disadvantagesinclude radiation exposure, the need to inject iodinatedcontrast medium, poor soft tissue contrast and artefactsdue to dental amalgam.

Magnetic resonance imaging (MRI) is complementaryto CT but offers distinct advantages such as better softtissue contrast, multiplanar capability and reduced

artefacts from dental fillings. It is superior in the detec-tion of early bone marrow involvement, pterygopalatinefossa infiltration, prevertebral muscle involvement andperineural tumour spread[5]. MRI entails no radiationand no iodinated contrast medium has to be adminis-tered. However, MR contrast medium has to be injectedin the evaluation of patients with tumours. Macrocyclicgadolinium chelates at low doses should be administeredto avoid the risk of nephrogenic systemic fibrosis inpatients with renal insufficiency.

The disadvantages of MRI include the long investiga-tion time with increased risk of motion artefacts andhigher cost. Contraindications to MRI include the pres-ence of pacemakers, metal foreign bodies andclaustrophobia.

CT and MR imaging appearance

Squamous cell carcinoma

On CT, tumours enhance after administration of contrastmaterial. Moderate enhancement may be difficult to iden-tify particularly when in the anterior part of the floor ofthe mouth, because of beam hardening artefacts due to adense mandible or dental amalgam. Large tumours tendto be heterogeneous because of necrosis[6].

On T1-weighted images, the tumour is hypointenseor isointense to muscle and on T2-weighted images, itis usually hyperintense. Solid tumours enhance withgadolinium (Fig. 2), whereas necrotic areas withinthe tumour remain hypointense[2]. The precontrastT1-weighted image is particularly useful in differentiatingtumour from surrounding fat, detecting neurovascularbundle encasement and bone marrow involvement[2].

MRI can overestimate the tumour due to haemorrhageand inflammatory changes.

H

M

GG

GH

S

HyE

Tr. Lg.

C

D

MH GG

SG

IM

H

BN

LHP

HS

Hy

A

OPOC

Figure 1 Sagittal T2-weighted MR image (A) in the median plane showing normal anatomy and the division of the oralcavity and oropharynx. Coronal T2-weighted image (B) and sagittal T2-weighted image (C) showing the variousstructures in the oral cavity. OC, oral cavity; OP, oropharynx; HP, hypopharynx; L, larynx; N, nasopharynx; H,hard palate; S, soft palate; Hy, hyoid bone; E, epiglottis. Muscles of the tongue: SG, styloglossus muscle; GG,genioglossus muscle; GH, geniohyoideus; IM, intrinsic muscles; Lg, superior longitudinal muscles; Tr, transverselingual muscles. Muscles of the floor of the mouth: MH, myelohyoid muscle; D, anterior belly of the digastric muscle.

Cancer of the oral cavity and opopharynx 63

The main drawback of both CT and MR imaging istheir lack of specificity; it is not possible to differentiatebetween tumour and inflammatory changes.

Bone involvement

Cortical bone invasion is depicted as an interruption oran erosion of the peripheral hyperattenuating rim at CTor hypointense rim at MR imaging in all sequences. CTdepicts cortical bone invasion best. Subtle cortical ero-sion is best detected by thin sectional CT with bone algo-rithm with coronal and sagittal reconstruction. The exactextent of the medullary bone invasion is better definedwith MR imaging. Low signal intensity on unenhancedT1-weighted images with high signal on T2-weightedimages and enhancement after intravenous (iv) contrastadministration may be considered to indicate marrowinvasion. These changes are unfortunately non-specificand also seen with peritumoural oedema, inflammation,coexisting periodontal disease, osteomyelitis, radiationfibrosis and osteoradionecrosis[3]. Sensitivity of bonemarrow involvement is high at 100%, specificity is how-ever relatively low at about 71�75% with MRI[4].Invasion of the maxilla is most often seen in retromolartrigone cancers and cancer of the hard palate[3].

Perineural spread

CT can show enlargement of the nerve foramina andreplacement of fat in the presence of perineural spread(Fig. 3). MRI can show the enlargement of the nerve andenhancement and replacement of the fat in the pterygo-palatine fossa (Fig. 4)[7]. Perineural spread can be ante-grade or retrograde and skip lesions may occur.Therefore meticulous evaluation of the skull base is ofutmost importance in order to detect perineural spread.However, inflammatory or oedematous enlargement ofthe nerves can simulate perineural spread so thesechanges are not specific for perineural spread[8].Secondary signs of denervation such as atrophy of themuscles innervated by the involved nerve or abnormal

enhancement of the denervated muscle can be helpfulin making the correct diagnosis.

Lymph node staging

The status of the lymph nodes is the most significantpredictor of outcome in patients who have squamouscell carcinoma (SCC) of the oral cavity[2]. The oraltongue and floor of the mouth are rich in lymphaticsand tumours in these areas have a higher risk of nodalmetastases compared with the hard palate and alveolarridge. Level I�III nodes are at highest risk from oralcancers. In previously untreated neck cancers, metastasesin nodes at level IV and V are rare in the absence oflymph node involvement at levels I�III.

Most metastatic nodes are abnormally enlarged. Forlevel II nodes, the size criterion used is more than1.5 cm transversal short axis; for all other nodes, morethan 1 cm is pathological. Normal-sized nodes can havefocal metastases or necrosis that is more easily seen onCT than on MRI[2]. Necrosis should be differentiatedfrom the fat hilus of lymph nodes by measuring theHounsfield units and looking at the shape of the lymphnode. Other features include heterogeneous enhancementand stranding or involvement of the adjacent soft tissue ifextracapsular nodal spread is present. This is morecommon in larger nodes. The current staging systemfor the neck does not take into account the presence ofextracapsular spread but is based on the site, number andlaterality of the lymph nodes relative to the primarytumour[2].

N staging of lymph nodes

Nx regional lymph nodes cannot be assessedN0 no nodesN1 ipsilateral lymph node 3 cm or less in greatest

dimensionN2a ipsilateral lymph node between 3 and 6 cmN2b multiple ipsilateral lymph nodes less than 6 cm

A B C

Figure 2 Axial MR images in a patient with proven cancer of the left tonsil. The tumour (arrow) is well delineated,hypointense on T1-weighted (A), hyperintense on T2-weighted (B) with enhancement after contrast injection (C).

64 D.W. Tshering Vogel et al.

N2c bilateral or contralateral lymph nodes less than6 cm

N3 lymph nodes larger than 6cm

Cancers of the oral cavity

SCC accounts for 90�95% of tumours. Other tumoursinclude minor salivary gland tumours, lymphomas andrare tumours such as melanomas, liposarcomas, rhabdo-myosarcomas[2,6]. SCC of the oral cavity tends to spreadlocally with invasion of surrounding structures; the riskand pattern of spread varies with the anatomic locationof the tumour[6]. Adenoid cystic carcinoma is well knownfor its propensity to perineural spread but this is not

specific and is also observed in squamous cell cancerwhich is more common[8].

T-staging of oral cavity cancer (TNM 2009)

T-staging of the tumour depends on size criteria andextension of the tumour in neighbouring structures. Txindicates that the primary tumour cannot be assessed, T0no evidence of tumour, T1 tumours are less than 2 cm inthe greatest dimension, T2 between 2 and 4 cm, T3 morethan 4 cm. T4a tumours show invasion of the corticalbone, deep or extrinsic muscles of the tongue, maxillarysinus and skin of the face. T4b tumours show infiltrationof the masticator space, pterygoid plates, skull base orencasement of the internal carotid artery.

A B

Figure 3 CT images, coronal reconstruction (A) and axial images (B) showing a histologically proven case ofadenoid cystic carcinoma of the hard palate (star) with extension along the greater palatine nerve and replacementof fat (arrow) in the greater palatine foramen. Compare the normal foramen on the right side.

A B C

Figure 4 Axial T1-weighted MR images before contrast injection (A,B) showing the hypointense tumour of the hardpalate on the left (star) with loss of normal fat signal in the pterygopalatine fossa on the left (arrow) in a patient withproven lymphoma and perineural extension of the tumour. The coronal image after gadolinium injection with fatsuppression (C) shows enhancement of the greater palatine nerve on the left (arrows).

Cancer of the oral cavity and opopharynx 65

Lips

SCC of the lip is the most common malignant neoplasmof the oral cavity with an incidence of 40%. Cancer of thelip usually arises from the vermillion border and canspread to involve adjacent skin or underlying musclessuch as the orbicularis oris muscle. Early lesions areeasier to detect clinically. Imaging plays a role withmore advanced lesions with indeterminate margins. Therole of imaging is to determine the full extent of thelesion including possible perineural spread, lymph nodemetastases and the integrity of the adjacent bone. If thereis invasion of bone, the carcinoma is upstaged to a T4[4].

On CT and MRI the primary tumour may appear as amass with or without areas of ulceration. Subtle boneerosion usually occurs along the buccal surface of the

mandibular or maxillary alveolar ridge and is bestdetected with CT. Large tumours may extend directlyinto the mandible or involve the mental nerve withoutcortical bone destruction[3].

Floor of the mouth

Most SCCs originate within 2 cm of the anterior midlinefloor of the mouth[6]. They spread beneath the mucosainto the sublingual gland and can obstruct the Whartonduct resulting in submandibular gland sialadenitis. This isoften the first clinical manifestation and therefore carefulexamination of the floor of the mouth is mandatory incases of an enlarged submandibular gland (Fig. 5).Invasion of the mylohyoid muscle signifies submandibu-lar spread. Superiorly and posteriorly the tumours tend toinvolve the ventral surface of the tongue, the adjacentlingual neurovascular bundle and the base of thetongue. Anteriorly and laterally, the neoplasm mayadvance into the adjacent gingival mucosa and thendestroy the lingual cortex and involve the marrow ofthe mandible[3].

The less common tumours arising from the lateral floorof the mouth show similar dissemination patterns.Advanced lesions may extend beyond the oral cavityand infiltrate the contiguous spaces of the suprahyoidneck particularly the parapharyngeal space and the mas-ticator space. The medial pterygoid muscle inserts intothe inner cortex of the angle of the mandible, and can beinvaded by tumours of the lateral floor of the mouth. Theprevalence of lymph node metastases is between 30% and70%[3]. Lymph nodes that should be assessed includelevel I to III nodes[4].

Retromolar trigone

Retromolar trigone tumours (Fig. 6) account for 7% oftumours affecting the oral cavity. Cancers originating inthe retromolar trigone can spread to any of the adjacentstructures, including the tonsils, the base of the tongue,

Figure 5 Axial T2-weighted MR image of a patient withhistologically proven squamous cell cancer of the floor ofthe mouth showing the tumour with involvement of themandible and extension into the adjacent soft tissues ante-riorly (star). Note obstruction with dilatation of theWharton duct on both sides (arrows).

A B

Figure 6 Axial T1-weighted MR images before (A) and after contrast administration with fat saturation (B) in apatient with proven cancer of the retromolar trigone on the right (star). Note infiltration of the buccinator muscle andextension along the alveolar ridge (arrow).

66 D.W. Tshering Vogel et al.

along the pterygomandibular raphe superiorly to the tem-poralis muscle, medial to the pterygomandibular spacewhere the lingual and inferior alveolar nerves run, infer-iorly into the floor of the mouth or anteriorly from themedial pterygoid plate into the pterygopalatine fossa[7].

Oral tongue

The tongue is composed of intrinsic and extrinsic musclefibres and a midline fibrous septum extending from thehyoglossus membrane and the midportion of the hyoidbone. The main bulk of the tongue is made up of the fourinterdigitating intrinsic muscles: the superior and inferiorlongitudinal, transverse and oblique muscles. The extrin-sic muscles originate from bony attachments external tothe tongue and include the genioglossus, styloglossus,hyoglossus and palatoglossus muscles. These interdigitatewith the intrinsic muscles (Fig. 1).

Nearly all SCCs of the oral tongue occur on the lateraland undersurface of the tongue. Most of the lateralborder lesions occur on the middle and posterior thirdsof the oral tongue[6]. SCCs tend to remain in the tongueuntil they are quite large. The prognosis is generallybetter than that of carcinoma of the tongue base. Largetumours tend to grow into the glossotonsillar sulcus, baseof the tongue, tonsillar fossa and floor of the mouth. Inaddition to routine axial images, coronal MR images mayprovide additional information about the exact extent oftongue neoplasms and their relationship to the neurovas-cular bundle. Infiltrating lesions extend medially in thetongue itself. They first invade the muscles located later-ally (the hyoglossus, styloglossus and palatoglossus mus-cles). Then they reach successively the lingual pedicle,the genioglossus muscle, the lingual septum and the con-tralateral half of the tongue. Tumour extension across themidline with involvement of the contralateral lingualartery or nerve makes surgical resection for cure difficultbecause of the morbidity associated with total

glossectomy (Fig. 7). Tumours may also extend in theanteroposterior direction, from the tip to the base of thetongue.

Because of the anatomic disposition of the genioglos-sus muscle, it constitutes a natural route for advancedlesions to extend towards the anterior floor of the mouth.Middle-third lesions invade the lateral floor of the mouthand mandible. Lesions of the posterior third grow intothe floor of the mouth, the glossotonsillar sulcus, theoropharyngeal tonsil and underlying deep spaces.Lesions may extend superiorly to the soft palate via thepalatoglossus muscle and from the soft palate to the naso-pharynx via the veli palatini muscles. Detection of poste-rior extension into the base of the tongue is importantsince it can change treatment. The oral tongue is mobileand therefore evaluation is easier in the sagittal and cor-onal planes than on axial images.

T-staging and tumour thickness is important for thecorrect choice of therapy. Tumour thickness or depthof tumour can predict the presence of cervical lymphnode metastases[9�11]. Cancer of the tongue is knownto have a high incidence of nodal metastases even inthe early T1 and T2 stages. The pathophysiology ofnodal metastases is not known but could be relatedto the abundant submucosal lymphatic vessels. Theincidence of nodal metastases increases rapidly whenthe muscles of the tongue are infiltrated and postulatedexplanations include the more invasive behaviour ofdeeply infiltrating cancer or the contraction of thetongue muscles which could promote lymphaticspread[9].

Tumour thickness is also reported to influence thelocal recurrence rate. The most important risk factorfor local recurrence is the histological resection margin,the deep margin is frequently the site of inadequate resec-tion because it is more difficult to assess accurately withpalpation. Therefore, the deeper the infiltration, thehigher the chances of an inadequate resection margin[9].

A B

Figure 7 Axial T1-weighted MR images before (A) and after contrast injection with fat saturation (B) in a patient withcancer of the tongue on the left side (star). The tumour does not cross the midline which is represented by the fatty signalintensity of the lingual septum (arrow).

Cancer of the oral cavity and opopharynx 67

Incidence of subclinical nodal metastases with tumourthickness of 3 mm has been reported to be 8% with nolocal recurrence. For tumour thickness between 3 and9 mm, the incidence of subclinical nodal metastasesreported was 44% with 7% local recurrence. Tumourthickness more than 9 mm was associated with subclini-cal nodal metastases in 53% and local recurrence in24%[11].

Hard palate

Here it is important to assess the degree of bone invasionand to exclude perineural spread for these tumours.Adenoid cystic cancers in this area have a propensityfor perineural spread along the greater and lesser palatinenerves into the pterygopalatine fossa (Fig. 3). Perineuralspread can also occur with lymphoma (Fig. 4). From thepterygopalatine fossa, tumour can travel along the max-illary nerve into the foramen rotundum or anteriorly intothe infraorbital foramen or along the vidian nerve in thevidian canal.

Although SCC of the hard palate is often confined toits site of origin at the time of diagnosis, advancedtumours may invade the maxilla, nasal cavity, buccalmucosa, tongue or retromolar trigone. Therefore, coronalsections are extremely useful for evaluating thesetumours. Lymphatic spread occurs along the facial andretropharyngeal lymph nodes and along the upper jugularchain.

Buccal region including gingival andalveolar ridges

Although less than 10% of oral cavity tumours arise inthis region, proximity of these tumours to bony corticalmargins is worrying due to potential bony invasion andperineural spread (Fig. 8). Buccal carcinomas usuallyarise along the lateral margins and common routes ofspread include lateral submucosal extension along thebuccinator muscle towards the ptyeromandibular raphe

and subsequent bony involvement. SCC of the buccalmucosa tends to invade the masticator space, the bucci-nator muscle with subsequent involvement of the skin,the anterior tonsillar pillars and the soft palate.Infiltration of the medial pterygoid muscle causes tris-mus. Pathways of lymphatic spread are variable andinclude the submandibular, facial, intraparotid andpreauricular nodes. SCC of the gingiva frequentlyoccurs in the molar and premolar regions along the gin-gival margin of a tooth and bone destruction is a frequentfinding. Nearly 50% of patients have level II lymph nodeinvolvement at presentation.

Cancer of the oropharynx

Oropharyngeal SCCs are usually poorly differentiatedand locally advanced at the time of clinical presentation.The overall incidence of cervical lymph node metastasesis 50�70%[3]. Submucosal tumour extension within theoropharynx is common. Extension across the midlineusually precludes surgical cure in tongue base tumours.The commonest sites of cancers in the oropharynx arethe tonsils and the tongue base[7]. Tonsils are a prime sitefor lymphoma.

T-staging of oropharyngeal cancer(TNM 2009)

T-staging of oropharyngeal cancer depends on tumoursize and local infiltration. Tx when the primary tumourcannot be assessed, T1 tumours are less than 2 cm in thegreatest dimension, T2 between 2 and 4 cm, T3 morethan 4 cm. T4a tumours show invasion of the larynx,deep/extrinsic muscles of the tongue, medial pterygoidmuscle, hard palate and mandible. T4b tumours showinvasion of the lateral pterygoid muscles, pterygoidplates, lateral nasopharynx, skull base or encasement ofthe internal carotid artery.

BA

Figure 8 Axial CT images in soft tissue (A) and bone window (B) showing the histologically confirmed alveolar SCC(star) and the bony erosion (arrow).

68 D.W. Tshering Vogel et al.

The lymph nodes in the upper jugular and spinalaccesssory chain and the retropharyngeal nodes aremost commonly involved by oropharyngeal cancers.Oropharyngeal metastases most commonly are to levelI�IV with level II being the most common site. Nodalmetastases to both sides of the neck are common becauseof rich lymphatics.

Tonsils

Tumours arising from the tonsillar pillars and the tonsilsare grouped together. SCC of the tonsils is the mostcommon tumour in this region followed by lymphoma(Fig. 2). Nodal drainage of tonsils is primarily unilateralto levels II and III. Tonsillar carcinoma can present asunilateral metastatic lymph nodes[2]. It is prone to spreadposterolateraly to the lateral pharyngeal wall, paraphar-yngeal space and pterygoid muscles, inferiorly to theglossotonsillar sulcus, base of the tongue, floor of themouth and superiorly to the soft palate and nasopharynx.

Base of the tongue

The base of the tongue is the posterior third of the tongueand it extends inferiorly to end at the level of the valle-cula and houses the lingual tonsil. Tumours here areoften occult and asymptomatic, the lesions are oftenlarge by the time they cause symptoms such as dysphagiaor otalgia. Some patients present with lymph node metas-tases without signs of a primary tumour. Invasion can bedeep or the lesions can be exophytic and protrude intothe airway. Small lesions are difficult to detect due to thesurrounding lymphoid tissue which also enhances[2].

SCC in this location is an aggressive, deeply infiltrativetumour with a 75% incidence of lymph node metastasesat presentation. It may extend laterally to involve themandible and medial pterygoid muscles, superiorlyto involve the tonsillar fossa and soft palate, anteriorly

to involve the mobile tongue and floor of the mouth andinferiorly to involve the vallecula, preepiglottic space, andepiglottis or portions of the hypopharynx. Neoplasmsand normal lymphoid tissue at the base of the tonguecan be confused at both CT and MRI because of theirT2 signal characteristics and enhancement patterns, anddeep endoscopic biopsies are the only way to differentiatebetween the two. In addition to routine axial images,sagittal and coronal MR images may provide an excellentappreciation of the volume of the tumour in the tonguebase[3]. Cancer of the base of the tongue can invade thepreepiglottic fat space and this may require a supraglotticlaryngectomy if not a total laryngectomy (Fig. 9). Sincethe combined resection of the base of the tongue andlarynx diminishes the quality of life with compromisedswallowing and speaking, the correct diagnosis is veryimportant[3]. The preepiglottic fat is best assessed withsagittal T1-weighted scans and axial T1-weighted scans inwhich soft tissue signal intensity within the fat suggestscancerous involvement. Occasionally, adjacent inflamma-tion or peritumoural oedema or partial volume effectsmight simulate preepiglottic fat invasion[7].

Lymph nodes commonly involved are level II to IVnodes. Involvement can be bilateral due to rich lympha-tics and can be seen in up to 30% of patients[2].

Posterior pharyngeal wall

Carcinomas of the posterior oropharyngeal wall have theworst prognosis of all squamous cell oral cavity and oro-pharyngeal carcinomas[3]. These tumours spread both ina caudal direction into the hypopharynx and a cranialdirection into the nasopharynx. They commonly presentas a flat, thick tumour spreading at the mucosal surfaceusually involving both the oropharynx and hypopharynxand are readily diagnosed on endoscopy. On axial CTor MR images, they appear as thickening of the posteriorwall of the pharynx (Fig. 10). They commonly

A B

Figure 9 Axial CT image (A) in a patient with proven SCC of the base of the tongue showing the tumour (arrows) withcentral necrosis and a necrotic lymph node on the right side (star). The tumour extends into the valleculae on both sidesand displaces the epiglottis posteriorly. Sagittal reconstruction (B) showing the tumour (star) with infiltration of thepreepiglottic space (arrow).

Cancer of the oral cavity and opopharynx 69

spread submucosally, invading the retropharyngeal fat.The prevertebral fascia acts as a barrier to tumourspread and invasion of the prevertebral muscles isuncommon at initial presentation. Invasion of the prever-tebral muscles, the longus colli and longus capiti musclesprecludes surgical resection. This can, however, be diffi-cult to assess since abnormal signal intensity, attenuationvalues and enhancement of the muscles which couldindicate involvement can be misleading, and the surgicalevaluation at the time of panendoscopy or open explora-tion remains the gold standard[7]. Demonstration of aretropharyngeal fat plane has a high negative predictivevalue for tumour involvement[5].

Soft palate

Soft palate tumours present as soft tissue swelling andcan be difficult to assess radiologically unless they arelarge (Fig. 11). They can spread laterally, anteriorlyor superiorly. Minor salivary gland tumours are oftenassociated with perineural spread and may extend alongthe lesser palatine nerve to involve the pterygopalatine

fossa or along the trigeminal nerve branches to the cav-ernous sinus and Meckel cave. Neural involvement maybe discontinuous[5].

Bone erosion is an unusual finding and is presentonly in advanced soft palate carcinoma invading thehard palate. Extensive invasion of the parapharyngealand masticator spaces may be associated with carotidartery encasement or extension superiorly along the fas-cial and muscle planes into the skull base. If the tumourencompasses more than 270 degrees of the circumfer-ence of the carotid artery on axial images it becomesunlikely that it can be removed without resectingthe vessel. Lymph node metastases occur primarily inthe upper jugular or retropharyngeal nodes. It is presentin 60% of tumours at presentation[2].

Disease specific follow-up

The current goal of treatment is to achieve locoregionalcontrol with chemotherapy, radiotherapy and surgeryto enable organ preservation with maintenance of

A B

Figure 11 Axial T2-weighted MR image (A) and axial T1-weighted image (B) after contrast injection with fat sup-pression showing the large soft palate tumour (star) with enlargement of the retropharyngeal lymph nodes on both sides(arrows) in a patient with cancer of the uvula.

BA

Figure 10 Axial (A) and sagittal (B) T1-weighted MR images after contrast injection with fat saturation showing theenhancing tumour of the posterior pharangeal wall presenting as a submucosal mass crossing the midline.

70 D.W. Tshering Vogel et al.

function[5]. Cancers of the oral cavity and oropharynxcan recur locally, present with recurrent lymph nodemetastases or less commonly distant metastases.Follow-up imaging should be performed at regular inter-vals for the first 2 years. It is advisable to wait 3 monthsafter completion of therapy before performing morpho-logical imaging studies.

Radiological features indicating recurrence include amass-like lesion with or without enhancement, abnormal-ity along the margins of previous resection or reconstruc-tion, bone invasion and perineural spread. Clinical andradiological assessment is difficult due to treatmentchanges such as oedema, fibrosis and distortion of anat-omy due to surgery. Newer imaging techniques havealready shown promising results in the detection oftumour recurrence where conventional imaging failed.These techniques are described briefly in the next section.

Newer imaging modalities

[18F]Fluorodeoxyglucose-positronemission tomography/CT

[18F]Fluorodeoxyglucose (FDG)-positron emissiontomography (PET)/CT is a well-established tool for theassessment of both lymph node involvement and recur-rences. It has been found superior to conventional ima-ging workup in the evaluation of patients with head andneck malignancies. It can be used in pretreatment stag-ing, treatment monitoring and evaluation of the treatmentresponse. Current clinical practice, however, doesnot favour the use of PET in staging of all newlydiagnosed SCCs, it can, however, detect metastasesand other primary tumours more than 1 cm in size[12].Inflammation cannot be differentiated from tumour andspecificity can further be reduced due to physiologicaluptake in lymphoid tissue, nasal mucosa, salivaryglands and muscle activity.

Diffusion-weighted MR imaging

This relies on the relative movement of water in differentbiological tissues. In normal tissues or tissues with vaso-genic oedema, there is no limitation of water diffusion. Intissue with cytotoxic oedema or hypercellular areas, thereis diffusion restriction which can be assessed both quali-tatively and quantitatively. While conventional MR ima-ging is usually adequate for demonstrating the primarytumour before treatment, diffusion-weighted imaging canaid in the post-treatment evaluation since post-treatmentchanges can be difficult to delineate from small foci oftumour recurrence as they can both enhance similarlywhen using conventional MR or CT. Post-treatmenttissue is oedematous and relatively hypocellular andthus does not demonstrate restricted diffusion, whereastumour recurrence contains areas of increased cellularityand should demonstrate restriction of diffusion[12�14].The reported sensitivity, specificity and accuracy for

detecting malignancy were 94.6%, 95.9% and 95.5%,respectively[13].

Perfusion imaging

This can be performed with CT or MRI and evaluatesdynamic microscopic blood flow changes through aregion of interest. Changes in signal intensity (MRI) orattenuation (CT) are measured during a dynamic con-trast infusion[12]. Oropharyngeal tumour tissues report-edly demonstrate increased blood volume and blood flowwith decreased times in comparison with normal tis-sues[15]. Blood flow and blood volume within recurrenttumour tissue are also reported to be elevated in compar-ison with therapy-altered tissue with correspondingdecreases in transit time[16].

Conclusion

Treatment of patients with cancer of the oral cavity andoropharynx is a challenge for the head and neck surgeonand oncologist. Therefore, accurate diagnosis and stagingof these cancers are prerequisites for choice of optimaltreatment. CT and MRI are excellent imaging techniquesfor tumour detection and for providing information onthe exact extension.

The evaluation of the neck after treatment, however,poses a special problem using CT and MRI. In this par-ticular setting newer modalities such as PET-CT, diffu-sion-weighted MRI and perfusion imaging either with CTor MR are promising tools for detection of residualtumour or recurrence. However, larger scale studies arerequired to confirm these initial promising results.

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