non oncologic imaging of the oral cavity and jaws

Otolaryngol Clin N Am

Non-Oncologic Imaging of the OralCavity and Jaws

Kristine M. Mosier, DMD, PhDSection of Neuroradiology, Department of Radiology, Indiana University School of Medicine,

950 West Walnut Street, RII E124, Indianapolis, IN 46202, USA

It is important to distinguish the oral cavity from surrounding spaces andthe oropharynx, as the presence of specialized hard and soft tissue structuresgives rise to different disease processes within the oral cavity than in the oro-pharynx. The oral cavity lies anterior to the oropharynx and is separatedfrom the oropharynx by the soft palate, tonsillar pillars, and at the tongue,the circumvallate papillae. Thus the oral tongue lies within the oral cavity,while the tongue base lies within the oropharynx. The oral cavity containsthe hard palate, alveolar processes of the maxilla and mandible, dentition,oral tongue, buccal vestibule, and lips. Within or bounding the oral cavityare three spaces formed by superficial layers of deep cervical fascia, mucosalsurfaces, or muscle boundaries. These are the sublingual and submandibularspaces inferiorly and the buccal spaces laterally.

The sublingual space (SLS) is formed by the genioglossus and geniohyoidmuscles medially and the mylohyoid muscle laterally and inferiorly(Fig. 1A,B). Anteriorly, the SLS is bounded by the lingual cortex of themandible. On its posterior boundary, the SLS is contiguous with the sub-mandibular space (SMS) and the parapharyngeal space. These anatomicalrelationships are critical to understanding the spread of infectious or neo-plastic processes, in particular, because the SLS is one of the spaces in thehead and neck not encapsulated by fascia. The SLS contains fat, the sublin-gual glands and ducts, the deep or uncinate portion of the submandibulargland and the submandibular duct (Wharton’s duct), the anterior marginof the hyoglossus muscle, the sublingual artery, the lingual nerve and artery,and distal branches of the glossopharyngeal and hypoglossal nerves. It isfurther important to recognize that the SLS is a continuous space anteriorly,ventral to the frenulum, permitting access across the midline.

41 (2008) 103–137

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The SMS (Fig. 1A–C) is a horseshoe-shaped space that lies laterally, in-feriorly, and posteriorly to the SLS, inferior to the mylohyoid and superiorto the hyoid bone. It is formed by superficial layers of deep cervical fasciathat split to envelope the space with the superficial layer of fascia extendingalong the medial margin of the platysma muscle and the deep layer extend-ing along the lateral margin of the mylohyoid. The SMS contains fat, thesuperficial portion of the submandibular gland and proximal portions ofWharton’s duct, submental and submandibular lymph nodes (level 1A

Fig. 1. (A) Axial CT view at the level of the oral cavity. Sublingual space (long black arrow), sub-

mandibular space (long white arrow), mylohyoid muscle (star), hyoglossus muscle (black arrow-

head). The root of the tongue is identified by the genioglossus (black circle) and the lingual

septum (white arrowhead). The lateral boundary of the submandibular space is formed by the fas-

cial layers on themedialmargin of the platysmamuscle (dashedwhite arrow). (B) CoronalCT view

at the level of the oral cavity. Sublingual space (long black arrow), submandibular space (longwhite

arrow), mylohyoid muscle (star), genioglossus (black circle), and the lingual septum (white arrow-

head), platysma muscle (dashed white arrow), buccinator muscle (curved arrow). (C) Inset: sche-

matic of coronal plane through the oral cavity. The shaded purple area illustrates the horseshoe

shaped configuration of the submandibular space and the bilateral continuity of the space ventral

to the mylohyoid and anterior belly of the digastric muscles. (Courtesy of Indiana University

School of Medicine Office of Visual Media, Indianapolis, IN; with permission.) Abbreviations:

ABD, anterior belly of the digastric muscle; SMG, submandibular gland.

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and B), the facial artery and vein, the inferior loop of the hypoglossal nerve,and the anterior belly of the digastric muscle. The SMS is continuouslyinferior to the mylohyoid muscle, thereby permitting midline transgression.The SMS is also contiguous on its posterior boundary with the SLS andwith the parapharyngeal space.

The oral tongue volumetrically constitutes the predominant organ of theoral cavity and is composed of the three orthogonally oriented intrinsictongue muscles (verticalis, longitudinalis, and transversus), and the extrinsicmuscles: genioglossus, hyoglossus, styloglossus, and palatoglossus. The rootof the tongue (see Fig. 1A, B) is formed by the genioglossus and geniohyoidmuscles and the lingual septum. Inferiorly, the root of the tongue extends tothe mylohyoid sling and anteriorly extends to the genial tubercles at the lin-gual mandibular symphysis.

Anatomical variants

The most common anatomical variants of clinical importance in the oralcavity arise from accessory or ectopic glandular tissue.

Accessory salivary tissue

Accessory salivary tissue arises from development of extra submandibulargland tissue. Accessory salivary tissue is composed of normal submandibularsalivary gland tissue (mixed mucinous and serous), and it is found in the SMSinferior to the mylohyoid muscle and anterior to the submandibular gland(Fig. 2). On imaging, this soft tissue mass in the SMS will have the same im-aging appearance and contrast enhancement as the submandibular glands.On CT imaging it will appear as a homogenous or mildly heterogenousmass with the same density as the submandibular gland. OnMRI it will followthe signal intensity of the submandibular glands on all sequences. Accessorysalivary tissue is a normally functioning salivary gland, and as such, it maydemonstrate ductal supply from branches off of the proximal or distal seg-ments of Wharton’s duct (Fig. 3). Accessory salivary gland tissue ranges insize from several millimeters up to 2 cm, and may, on occasion, attain thesize of a normal submandibular gland. In this scenario, it is important to de-termine whether the submandibular glands are present to distinguish this nor-mal variant from transposed submandibular glands used as a radiationtreatment procedure for beam sparing of the glands [1].

Lingual thyroid

Lingual thyroid is ectopic thyroid found in the tongue or tongue base.This arises because of failure of the thyroid anlage to descend during devel-opment from the foramen cecum along the thyroglossal duct tract to its finalposition in the visceral space of the anterior neck. On CT imaging, lingual

Fig. 2. Accessory salivary tissue. Axial (A) and coronal (B) CT views. Accessory salivary tissue

is seen as a soft tissue mass in the right submandibular space (white arrow) inferolateral to the

mylohyoid (star) and anterior to the submandibular gland. Note the characteristic extension of

the accessory salivary tissue through a dehiscence in the mylohyoid muscle (arrowhead).

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thyroid will present as high-density or hyperdense soft tissue mass in themidline intrinsic muscles of the tongue or base of tongue, and which, follow-ing contrast, avidly and homogeneously enhances (Fig. 4). On MRI, a lin-gual thyroid will appear as a hyperintense mass on T1 and T2 weightedimages and will demonstrate considerable homogeneous enhancement. Animportant caveat to recognize is that these ectopic foci may consist of func-tioning thyroid and as such are susceptible to disease processes of the

Fig. 3. Accessory salivary tissue. Axial contrast enhanced CT (A) and anteroposterior view of

a right submandibular sialogram (B) show accessory salivary tissue (A, white arrow) extending

through a dehiscent mylohyoid and ductal supply from a branch off of the proximal segment of

Wharton’s duct (B, white arrow).

Fig. 4. Lingual thyroid. Axial contrast-enhanced CT at the level of the oral cavity (A) demon-

strates a homogenously enhancing mass at the midline tongue in the intrinsic muscles (black ar-

row). More inferiorly (B), there is absence of the left lobe of the thyroid (white arrow).


thyroid, including goiter or neoplasms. Moreover, because approximately25% to 75% of patients presenting with lingual thyroid will have eitheronly partial thyroid tissue in the cervical neck or a complete absence of thy-roid, it is imperative to ascertain the presence of functioning thyroid beforesurgical extirpation of the tongue mass. This is accomplished through visualsearch on contrast-enhanced CT or MRI studies and radionuclide iodine-123 to identify uptake in the lingual thyroid and any other cervical thyroidtissue [2].

Inflammation/infection

Oral cavity abscess/phlegmon

The presence of dentition, salivary tissue and mucosal barriers that maybe violated all predispose the oral cavity to infection or other inflammatoryprocesses. The most common inflammatory processes and infections arisefrom the dentition either from periapical infections or infections arisingfrom the supporting periodontium. Dental infection that transgress the lin-gual or buccal cortex may spread to the sublingual, submandibular, or buc-cal spaces within or surrounding the oral cavity. Spread of infection into theoral cavity from odontogenic sources depends on the relationship of thealveolar source to the attachment of the mylohyoid muscle at the mylohyoidline on the lingual aspect of the mandible (Fig. 5). The root apices of premo-lar and often first molar teeth lie superior to the attachment of the mylo-hyoid, and infections from these teeth will spread into the sublingualspace. The root apices of the second and third molars lie inferior to the my-lohyoid attachment; thus, infections from these teeth tend to extend into thesubmandibular space. Infection from odontogenic sources will appear as

Fig. 5. Schematic diagram of the relationship of the tooth roots to the sublingual, submandib-

ular, and buccal spaces. Infection extending through the lingual cortex from premolar and

molar teeth will involve the sublingual space, whereas infection from molar teeth will involve

the submandibular space. (Courtesy of Indiana University School of Medicine Office of Visual

Media, Indianapolis, IN; with permission.)

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a fluid collection in the sublingual or submandibular space, with a periapicallesion and typically with a focal area of erosion or dehiscence of the mandib-ular cortex. Suspicion or clinical impression of infection from odontogenicsources is evaluated best with contrast-enhanced CT imaging windowedwith both bone and soft tissue algorithms. On CT, the fluid collection willappear as a low-density area in the sublingual, submandibular, or buccalspace with enhancement at the rim (Fig. 6). The presence of anaerobicorganisms may produce gas, which appears as very hypodense collectionsor bubbles having the same density as air. Inflammation of the surroundingfascial planes and muscles will appear as increased linear density (stranding)

Fig. 6. Submandibular space abscess or phlegmon. Axial contrast-enhanced CT (A) shows

a large fluid collection within the right submandibular space (arrow), with thickening of the buc-

cinator muscle on the lateral aspect of the mandible and stranding in the subcutaneous tissues

representing myositis and cellulits respectively. (B) Axial bone CT shows an endodontically

treated (root canal) second molar root with apical periodontitis (C).


in the subcutaneous tissues and along fascial planes, or increased densityand enhancement of involved muscles.

Necrotizing fasciitis is a rapidly progressive and often fatal infection ofsubcutaneous tissues and deep facial planes caused either by group Abeta-hemolytic streptococci or mixed aerobic and anaerobic organismsincluding Staphylococcus aureus, Bacteroides, Clostridium, or Escherichiacoli.Necrotizing fasciitis may be seen in immunocompromised or debilitatedpatients and even in healthy patients accompanying minor trauma or sur-gery. Although the imaging findings are relatively nonspecific, it is neverthe-less critical to recognize this presentation to ensure prompt surgicaldebridement. Necrotizing fasciitis generally is characterized by extensive col-lections of subcutaneous and subfascial gas and fluid and marked cellulitisor myositis involving the deep fascial planes and sublingual, submandibular,and or buccal spaces (Fig. 7A, B) [3].

The midline continuity between the sublingual or submandibular spacesand the contiguity between the sublingual and submandibular spaces pro-vides a conduit for egress of abscess or phlegmon resulting in Ludwig’s an-gina. Ludwig’s angina will present as large fluid collections or edemainvolving the sublingual and submandibular spaces bilaterally (Fig. 8), oftenwith an identifiable source of odontogenic infection, trauma, or sialolithia-sis/sialoadenitis.

Sialolithiasis and sialoadenitis

Sialolithiasis or salivary stone formation is the most common disease ofthe salivary glands, with an estimated incidence of approximately 12/1000,and it occurs most commonly in the submandibular glands. Submandibularsialolithiasis is believed to result from a stagnation of calcium rich saliva.Formation of sialoliths is thought to arise from deposition of calcium salts

Fig. 7. Necrotizing fasciitis. Axial contrast-enhanced CT at the level of the oral cavity (A) and

base of tongue (B) shows extensive subcutaneous and subfascial gas in the submandibular space

(long arrows) with significant edema, multiple fluid collections (short arrows), myositis, and

cellulitis.

Fig. 8. Ludwigs angina. 80-year-old woman presents in acute respiratory distress. Axial (A) and

coronal (B) contrast-enhanced CTs demonstrate extensive edema and soft tissue thickening of

the tongue, sublingual, and submandibular space seen clinically as angioedema, cellulitis, and

hematoma. A calcification lies within the genioglossus muscle (arrow), representing either a for-

eign body or displaced sialolith and is the likely initiating factor.

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around an initial organic nidus consisting of altered salivary mucins, bacte-ria, and desquamated epithelial cells. The inorganic composition of the sia-lolith consists of calcium phosphate, hydroxylapatite, magnesiumphosphate, and sodium hydroxide. Intermittent stasis produces a changein the mucoid element of saliva forming a gel that provides a frameworkfor the deposition of salts. Sialolithiasis is found more commonly in the sub-mandibular glands than in the parotid or sublingual glands because of threeprimary factors: more alkaline saliva in the submandibular glands, increasedconcentration of calcium and phosphate in the submandibular saliva, andhigher mucous content than saliva of the parotid or sublingual glands [4].Sialolithiasis involving the submandibular gland is appreciated best on CTimaging with bone algorithms and appears as a hyperdense mass or nodulewith the same or similar density as bone located within the submandibularparenchyma or along the course of Wharton’s duct in the submandibular orsublingual space (Fig. 9A). Chronic obstruction can result in an inflamma-tory infiltrate of the ductal walls of Wharton’s duct, which on CT imagingappears as a thickened, enhancing wall of a dilated duct (Fig. 9B). On MRI,susceptibility effects of the calcified stone make the sialolith appear largerthan its actual size (Fig. 9C, D). Ductal obstruction of Wharton’s duct orthe sublingual ducts with accompanying weakening of the ductal walls bychronic inflammation can result in rupture of the duct with formation ofa sublingual or submandibular space abscess or sialocele.

Sialadenditis involving the submandibular gland occurs largely as a resultof ductal obstruction or stenosis, or secondary to autoimmune disorders orinvolvement by malignancies of the floor of the mouth. Clinical presentation

Fig. 9. Sialolithiasis. (A) Axial contrast-enhanced CT. Calcified sialolith in Wharton’s duct at

the junction of the superficial lobe with the deep lobe of the submandibular gland. (B) Axial

contrast-enhanced CT from the same patient in A. The black arrow points to a thickened

and enhancing wall of the dilated submandibular duct. (C) Contrast-enhanced axial T1-

weighted MRI of a different patient demonstrating a calcified sialolith in left Wharton’s duct

(arrow). (D) Axial T2 weighted MRI of the same patient in C showing the sialolith with sur-

rounding fluid (arrow). The actual size of this stone was approximately 20% smaller than mea-

sured on the MRIs. Size inaccuracies for sialoliths generally would only affect sialoendoscopic

or interventional retrieval or lithotripsy.


suggestive of sialoadenditis is evaluated best with contrast-enhanced CT im-aging, which demonstrates, in the acute phase, an enlarged enhancing sub-mandibular gland often with a dilated submandibular duct, most often atthe hilum, although secondary ducts may be dilated also (Fig. 10). Chronicsialadenditis, caused by repeated cycles of inflammation, often presents assmall atrophic gland. Chronic sclerosing sialadenditis, also known as Kutt-ner’s tumor, may present a diagnostic dilemma. This is a unilateral chronicsialadenditis secondary to sialolithiasis characterized histologically by anintense lymphoplasmacytic periductal infiltrate and fibrotic encasement ofthe ducts [5]. On CT and MRI, this often presents as an enhancing masswithin the gland parenchyma, making it indistinguishable from benign neo-plasms such as pleomorphic adenoma or occasionally malignant neoplasms(Fig. 11). Although clinical history may point to an inflammatory etiology,in many cases, the chronic course is sufficiently indolent to warrant suspi-cion of neoplasm, and in this setting the diagnosis most often is confirmedfollowing sialodenectomy.

Fig. 10. Acute sialoadenditis. Axial contrast-enhanced CT. The affected gland is larger,

enhances more, and has dilatation of the hilum (short arrow) and the proximal segment of

Wharton’s duct (long arrow).

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Sialocele

Sialoceles can be divided into true sialoceles and false sialoceles. Truesialoceles are caused by distention or expansive spherical dilatation ofWharton’s duct in the SLS with the distinction that the ductal walls remainintact. These commonly present on CT as ovoid- or lenticular-shaped fluidmasses within the SLS, often in association with a sialolith. In contrast, theducts of the sublingual glands or the submandibular duct may becomeobstructed and rupture leading to a false sialocele. False sialoceles represent

Fig. 11. Chronic sclerosing sialoadenditis (Kuttner’s tumor). Axial T2 weighted (A) and con-

trast-enhanced T1-weighted (B) images demonstrate a well-demarcated mildly T2 hyperintense,

enhancing mass in the superficial lobe of the submandibular gland. On the basis of imaging

appearance alone, this lesion would be impossible to differentiate from a benign neoplasm.


local extravasation of salivary fluid with a pseudocapsule and as such pres-ent on CT imaging as a thin-walled fluid mass within the sublingual spaceseparate from the submandibular duct (Fig. 12). Clinically, patients willpresent with a fluctuant or soft and painless mass in the floor of the mouthor oral cavity following obstructive episodes or following trauma. Contrast-enhanced CT with soft tissue and bone algorithm is the modality of choicefor evaluating suspected siaoceles to determine the presence of associatedobstructing sialoliths. It is always prudent to recall that obstruction of sub-lingual glands or the submandibular duct may occur secondary to neoplasticinvolvement, most commonly by squamous cell carcinoma of the floor ofthe mouth. If a neoplastic or infiltrative mass is identified on CT imagingor on clinical examination, contrast-enhanced MRI would the modality ofchoice to determine the extent of glandular, tongue, oral cavity, or mandib-ular marrow involvement.

Ranula and plunging ranula

Ranulas are mucous retention cysts or mucoceles arising within the sub-lingual or minor salivary glands, and they may arise as the sequelae ofinflammation or trauma. Composed of mucin and salivary fluids with anepithelial lining, the simple ranula on CT imaging will appear as a circum-scribed homogenous hypodense unilocular cystic-appearing mass witha well-defined thin wall contained within the sublingual space (Fig. 13).On MRI, ranulas are homogenously hypointense on T1 weighted imagesand hyperintense on T2 weighted images, with enhancement only of thewall. Although an inflammatory process may underlie the genesis of a simpleranula, ranulas may be distinguished from abscesses by the absence of septicsymptomology, attendant cellulitis, and additional multiple fluid or gas col-lections. Ranulas, however, may be difficult to differentiate from other

Fig. 12. Sialocele. Axial (A) and coronal (B) contrast-enhanced CT. The fluid collection in the

left sublingual space (arrow) is well-defined with a thin wall, but not within the duct, making this

a false sialocele.

Fig. 13. Ranula. Axial CT shows a cystic mass in the right sublingual space with a thin wall

(long arrow). Note that as it expands in the sublingual space, it has pushed the mylohyoid mus-

cle laterally (short arrow).

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benign masses in the floor of the mouth such as epidermoid or dermoid onCT imaging. These, however, generally can be differentiated on the basis oftheir MRI appearance [6].

Plunging ranulas are enlarged simple ranulas that rupture from the sub-lingual space over the free edge of the mylohyoid into the submandibularspace (Fig. 14A–C). Because of rupture out of the epithelial wall, plungingranulas are by definition extravasation pseudocysts lacking an epithelial lin-ing. Plunging ranulas will appear on CT imaging as homogenous hypodenseunilocular or multiolobar cystic-appearing mass in the submandibular spacecharacteristically with a tail extending into the SLS (see Fig. 14B, C). Occa-sionally plunging ranulas can attain large size, and because of the commu-nication between the submandibular space and parapharyngeal space, canextend into the parapharyngeal space [7], necessitating differentiationfrom other cystic masses of the neck, particularly lymphangioma (cystichygromas).

Developmental lesions

Lymphovascular malformation (lymphangioma/cystic hygroma)

Lymphovacular malformations arise most commonly during the mostactive period of lymphatic system development: during infancy and earlychildhood. These are benign hamartomas that are believed to developfrom sequestra of primitive lymphatic sacs derived from the venous system[8–10], most commonly from the jugular lymph sac [10,11]. In older childrenand the occasional adult, lymphovascular malformations are seen morecommonly involving the sublingual and submandibular spaces; these arepostulated to arise from trauma rather than as a developmental hamartoma[11–13]. Within the oral cavity, lymphangiomas most typically appear asmutliloculated or unilocular trans-spatial nonenhancing cystic-appearing

Fig. 14. Plunging ranula. (A) Schematic diagram in the axial plane showing the plunging ranula

as a cystic mass extending from the sublingual space to the submandibular space. (Courtesy of

Indiana University School of Medicine Office of Visual Media, Indianapolis, IN; with permis-

sion.) (B) Axial contrast-enhanced CT shows the characteristic tail extending between the sub-

mandibular and sublingual space. The dimple of the tail (arrow) is caused by the ranular contents

spilling over the free edge of the mylohyoid. This is appreciated better on the reformatted sagittal

view. (C) Mylohyoid (black arrow), submandibular gland (white arrow).


masses that insinuate through the sublingual, submandibular, and/or theroot of tongue or buccal space. On contrast-enhanced CT imaging, lym-phangiomas are hypodense nonenhancing cystic-appearing masses thatmay demonstrate internal septations or fluid–fluid levels (Fig. 15). Becauseof their lymphovascular content, these lesions are delineated best with

Fig. 15. Lymphangioma. Axial contrast-enhanced CT shows a hypodense nonenhancing cystic

mass in the submandibular space (arrow) with a somewhat serpiginous medial margin along the

mylohyoid characteristic of these lesions (A). When larger, these lesions may form internal sep-

tations (B).

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contrast-enhanced MRI. On T1 weighted MRI, lymhangiomas typically ap-pear hypointense, although intralesional hemorrhage or a higher proteina-ceous content will appear T1 hyperintense. On T2 weighted images, theselesion will appear homogenously hyperintense (Fig. 16). The pattern of mag-netic resonance contrast enhancement may reveal the nature of the lymphaticor vascular contents. Most commonly, these lesions show only subtle rim en-hancement suggestive of the cystic hygroma type composed predominately ofendothelial lined lymphatic spaces. Internal enhancement may suggest thecavernous or capillary lymphangioma subtypes, while enhancement withflow voids may suggest the end spectrum lymphovascular malformation con-sisting of mixed lymphatic and venous vascular malformation [14].

Dermoid and epidermoid

Epidermoids and dermoids arise from the inclusion of surface ectodermalelements from the first and second branchial arches during development.Epidermoids are inclusion cysts containing only epithelium, whereasdermoids are inclusion cysts containing epithelium and dermal structuresincluding dermal appendages. Although only about 7% of epidermoidsand dermoids occur in the head and neck, of these, less than 25% occurin the oral cavity, typically in the SLS or SMS or the root of the tongue[15,16], and typically they present in adolescents or in the second to third

Fig. 16. Lymphangioma. The fluid contents and internal architecture are appreciated better on

this axial T2 weighted MRI. This is a classic appearance of a lymphangioma.


decade. On CT, epidermoids appear as a well-circumscribed fluid mass withonly subtle or no evidence of a wall, thus rendering them difficult to differ-entiate from a simple ranula when they occur in the SLS (Fig. 13). Der-moids, because of the presence of fat or other structures, maydemonstrate some inhomogenous increased fluid density. MRI is the pre-ferred modality to distinguish between epidermoids and dermoids. Epider-moids will demonstrate diffuse homogenous hyperintensity on both T1and T2 weighted images because of increased protein content. Dermoidswill demonstrate focal areas of hyperintensity on T1 weighted images andheterogenous T2 signal; the use of fat suppression sequences will distinguishintralesional fat from calcification more rarely present in dermoids.

Benign neoplasms of the oral cavity

Lipoma

The sublingual and submandibular spaces and root of the tongue all con-tain fat and as such have the potential to give rise to lipomas. Most lipomasin the oral cavity arise within the buccal mucosa, submandibular or sublin-gual space, and rarely, the tongue. Classically, lipomas present as a homog-enous generally ovoid mass having fat density on CT and following fatsignal intensity on MRI (Fig. 17).

Hemangioma

Hemangiomas are benign vasoformative tumors that develop from endo-thelial cell proliferation. The endothelial cell proliferation distinguishes

Fig. 17. Lipoma. (A) Axial and (B) coronal contrast-enhanced CT. The lipoma caused by its fat

content appears as an expansion of the submandibular space (A, arrow). This expansion nicely

demonstrates the continuity between the bilateral submandibular spaces (B, white arrow) infe-

rior to the mlyohyoid muscle (B, black arrow). (C) Axial contrast-enhanced CT. The rare li-

poma within the tongue.

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these lesions from other vascular malformations or lympovascular malfor-mations in which there is abnormal development of vascular or lymphovas-cular plexuses and a normal endothelial cell cycle. Although generallyuncommon, hemangiomas are the most common tumors to affect the oralcavity in infants and young children. In addition, hemangiomas occurin association with several syndromes including Rendu-Osler-Weber,Sturge-Weber-Dimitri, von Hippel-Lindau, Posterior fossa malformations,Hemangioma, Arterial anomalies, Cardiac defects and coarctation of theaorta, Eye abnormalities, and Sternal abnormalities/ventral developmentaldefect syndrome. Klippel-Trenaunay-Weber, Kasabach-Merritt, and Maf-fucci. Characteristically, hemangiomas present in the first few months oflife as submucosal or intramuscular bluish-colored lesions that are soft,compressible, and fill upon digital pressure release. In contrast to othervascular malformations, hemangiomas involute over time. Hemangiomasare classified into three subtypes: capillary, cavernous, and mixed, with


the cavernous subtype the most common in the oral cavity [17,18]. The CTappearance of these lesions is somewhat nonspecific, frequently presentingas a moderately hyperdense mass, having a similar density to muscle withor without enhancement. When present, venous calculi (phleboliths) will dif-ferentiate hemiangioma from other lesions. Because of their vascular com-position, these lesions are evaluated best with MRI and will demonstratean insinuating T1 hypointense, T2 heterogenous hyperintense, and heteroge-neously enhancing mass (Fig. 18).

Benign mixed tumor (pleomorphic adenoma) of the submandibulargland

Benign mixed tumors of the submandibular gland often present clinicallyas a slowly enlarging painless mass of the SMS, thus making clinical differ-entiation from nodal disease or other masses of the floor of the mouthdifficult. Benign mixed tumors develop from neoplastic proliferation ofa mixture of epithelial, myoepithelial, and stromal elements. On contrast-enhanced CT, pleomorphic adenomas, when small, typically appear asa well-defined, well-circumscribed homogenous mild-to-moderately enhanc-ing mass in the parenchyma of the superficial lobe of the submandibulargland. Pleomorphic adenomas are encapsulated thinly, and in the subman-dibular gland, often are encased in a fibrous capsule. On MRI, these lesionswill appear hypointense on T1 weighted images, heterogenous or hyperin-tense on T2 and STIR (short Tau inversion recovery) sequences, and char-acteristically with increasing enhancement on contrast images acquired withlonger delay times (Fig. 19A–E). Larger lesions tend to develop areas ofmixed density on CT or signal intensity on MRI because of focal areas ofnecrosis, hemorrhage, or calcification [19–21].

Fig. 18. Hemangioma. Axial T1 weighted (A), T2 weighted (B), and contrast-enhanced (C)

MRIs show a hetergenous T2 hyperintense, enhancing mass with punctuate flow voids in the

right tongue. Note that the lesion is difficult to visualize on the T1 weighted images.

Fig. 19. Pleomorphhic adenoma. Axial T1 weighted (A), T2 weighted (B), short Tau inversion

recovery (C), and contrast- enhanced axial (D) and coronal (E) MRIs. The pleomorphic

adenoma is characteristically well -defined, hetergenously T2 hyperintense and mildly to avidly

enhancing. The coronal images (E) were acquired with a delay and show increased enhancement

(compared with D). Note that this lesion would be difficult to differentiate from chronic scleros-

ing sialoadenitis (compare with Fig. 11).

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Other rare benign lesions of the oral cavity

Neurogenic neoplasms
Neurogenic neoplasms involving the oral cavity are predominately neuro-
fibromas seen in association with von Recklinghausen’s syndrome, orschwannomas. Neurofibromas are rare within the oral cavity but typicallyinvolve the tongue or the buccal mucosa and present as circumscribed nod-ules or masses or macroglossia [22]. Schwannomas of the oral cavity accountfor only 1% of the schwannomas in the head and neck and typically presentas encapsulated masses involving the tongue or floor of mouth isodense orisointense to muscle that when larger may be cystic and show little enhance-ment [23]. In contrast to schwannomas in other sites in the head and neck,the nerve of origin for schwannomas of the oral cavity (lingual, hypoglossal,glossopharyngeal) is difficult if not impossible to identify in most cases [24].Although they contain skeletal muscle and histiocytes, granular cell tumors


nevertheless are considered neurogenic because of their neurogenous com-ponents. The epulis form occurs as a congenital infanile lesion, whereasthe adult form is termed granular cell myoblastoma. Granular cell myoblas-toma of the oral cavity typically occurs in the tongue of young adults andpresents nonspecifically on CT as an infiltrative soft tissue mass. TheMRI appearance is more distinctive, demonstrating low signal on both T1and T2 weighted images, reflecting the myogenous and fibrotic components,but robustly enhancing with contrast.

Maxilla and mandible

Inflammation/infection

Infection within the jaws arises predominately from inflammation orinfection affecting the dental pulp or the supporting periodontal ligament.Other much less common sources of infection include the sequelae of traumaor hemotogenous spread. The presence of dental infection is appreciatedbest on CT with bone algorithm. Infection of the dental pulp follows trans-gression of the enamel and dentin by dental caries or microleakage throughdental restorations. Infection spreads through the pulp tissues into the peri-apical tissues and causes widening of the periodontal ligament space fromedema and inflammatory exudate (Fig. 20). Apical periodontitis, or moreaccurately, apical rarefying osteitis, is the term used to describe apicalinflammatory lesions, and it includes all histological variants of inflamma-tion from edema to granuloma formation to cysts and abscess. Radiolo-graphically apical rarefying osteitis is characterized by widening of theperiodontal ligament space at the root apex, with or without the loss ofthe lamina dura (bone lining the tooth socket), and with or without lytic ero-sion of the surrounding periapical trabeculation. In more advanced disease,

Fig. 20. Apical periodontitis. Axial bone CT. There is widening of the periodontal ligament

space and thickening of the lamina dura (arrow) around the root apex of this mandibular molar.

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there may be resorption of the root apex. Inflammatory lesions involving theroot apex also may arise because of horizontal alveolar bone loss as a sequelaof chronic periodontal inflammation and infection.

Osteomyelitis by definition involves inflammation and infection of thebone and bone marrow and occurs most commonly in association with api-cal or periodontal dental disease. The early acute stage of osteomyelitis maypresent with no identifiable radiographic changes; however, acute suppura-tive osteomyelitis will demonstrate an osteolytic nonexpansile lesion of thecancellous and cortical bone with cortical erosion and in the subacute orchronic state, with bony sequestra (Fig. 21). A chronic low-grade infectioninstead may result in deposition of bone within the trabeculae or along thecortex in either a focal or diffuse pattern, resulting in sclerosing osteomye-litis. Chronic infection often is accompanied by periosteal reaction on eitherthe buccal or lingual cortex, with the periosteal deposition notably parallelto the surface of the bone. This appearance stands in contrast to the perios-teal reaction occasionally seen with malignant lesions in which the perios-teum is lifted off perpendicular to the cortical surface, giving rise to thesunburst appearance (Fig. 22). Garre’s sclerosing osteomyelitis (proliferativeperiostitis) is a low-grade chronic osteomyelitis most frequently seen in chil-dren and young adults, and it is associated with infection involving develop-ing tooth follicles (folliculitis), unerupted teeth, or erupted teeth with cariouslesions. Garre’s sclerosing osteomyelitis is characterized by significant peri-osteal reaction, often out of proportion to the level of dental disease, andfrequently with accompanying cellulitis and myositis (Fig. 23A–D). The

Fig. 21. Osteomyelitis. Axial bone CT (A) and axial contrast-enhanced CT (B) shows an

irregular lytic area in the mandibular body with cortical erosion and sequestra (A) and cellulitis

of the overlying buccinators muscle (B).

Fig. 22. Osteosarcoma: periosteal reaction. Axial bone CT. The malignant periosteal prolifer-

ation is lifted off perpendicular to the surface of the mass (arrow), creating the classic ‘‘sun-

burst’’ appearance in this patient who has a mandibular osteosarcoma. The patient has

fibrous dyplasia in the maxilla.


appearance of Garre’s sclerosing osteomyelitis can be very aggressive, lead-ing to potential misinterpretation as osteosarcoma. The presence of odonto-genic etiology, periosteal bone layering parallel to the cortex, and clinicalhistory or symptoms supportive of infection primarily should suggest thisvariant of osteomyelitis.

Another variant of inflammatory disease to be critically aware of isbisphosphonate-induced osteonecrosis (BRON) of the jaws. This entity firstwas described in 2003 [25–27] and occurs in patients treated with bisphos-phates (Pamidronate, Tiludronate, Alendronate sodium, Etidronate,Risedronate, Zoledronic acid, Ibandronate) for treatment of osteolyticlesions in multiple myeloma, metatstatic osteolytic bone lesions, hyper-calcemia of malignancy, Paget’s disease, and osteoporosis. Although theincidence of BRON is highest in patients receiving intravenous bisphospho-nate therapy for oncologic purposes, it also has been reported in patients re-ceiving oral bisphosphonates for postmenopausal or glucocorticoid-inducedosteoporosis. BRON occurs most commonly following dentoalveolartrauma or surgery, although it also occurs spontaneously. Patients presentwith pain, tooth mobility, or ulceration and occasionally altered sensationin the affected quadrants [27]. Suspicion of BRON should be evaluated ra-diographically with CT [28], which demonstrates irregular osteolytic loss oftrabeculation, cortical erosion, sequestrum, and in some cases, periosteal re-action (Fig. 24). Although these findings are identical for osteomyelitis, an-ecdotally, the extent of necrosis at the time of imaging tends to be moresignificant than would be expected for osteomyelitis of odontogenic origin

Fig. 23. Garre’s sclerosing osteomyelitis. Axial (A) and coronal (B) bone CT. There are multi-

ple irregular lytic areas and involvement of the follicle in this patient. Note the significantly

thickened periosteum laid down parallel to the surface of the bone (arrows, A and B). Axial

(C) and coronal (D) MRIs from the same patient showing the accompanying T2 hyperintense

myositis of the masseter and pytergoid muscles.

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in the absence of bisphosphonates. Depending on the stage of necrosis,BRON is treated with oral antimicrobial therapy, conservative surgical re-moval of sequestra, marginal or segmental surgical resection in refractorycases, and hyperbarric oxygen therapy, although the latter has shown lim-ited success [27,28].

Fibro-osseous lesions

Fibro-osseous lesions represent a broad spectrum of lesions characterizedhistologically by the replacement of normal bone with a benign proliferationof fibrous connective tissue and varying amounts of new bone deposition[29,30]. Fibro-osseous lesions range from common to rare in the jaws andbecause of their proliferative nature, they may be confused with other neo-plasms. Because of the common histological picture of these lesions, diagno-sis often is made radiographically based on the location, presence or absence

Fig. 24. Bisphonsphonate-induced osteonecrosis. Axial (A) and coronal (B) bone CT shows ex-

tensive osteomyelitis of the right maxilla with sequestration of the entire right maxillary

alveolus.


of mulitcentricity, lesion contents, and pattern of effect on the involvedbone. Periapical cement dysplasia (periapical cementoosseous dysplasia) isthe most common and localized fibro-osseous lesion to affect the jaws. Itis found in approximately 0.3% to 0.5% of the adult population. It occurstypically in middle-aged women, and it appears to have a predilection forthe African-American population. Characteristically, these lesions presentinitially as a solitary focal radiolucent area at the apex of the central man-dibular incisors, with the important distinction that the teeth are vital. Overtime, the radiolucent area fills in with a fluffy-appearing conglomerate ofbone (Fig. 25A–C). The lesions typically are encapsulated by a rim ofbone and may cause buccal or lingual expansion of the cortex. Becausethe teeth are vital, these lesions are not treated except for secondary infec-tion or for purposes of cosmesis when there is bone expansion. Florid osse-ous dysplasia (florid cementoosseous dysplasia) represents the exuberantmore geographically diffuse form of periapical cemental dysplasia. Floridosseous dysplasia usually involves the entire mandible, and in about 60%of cases, the maxilla also. Lesions present as circumscribed radiolucent orlytic areas inferior to the root apices that characteristically scallop betweenthe tooth roots and contain varying amounts of ossification (Fig. 26A–D)that when mature may resemble pagetoid bone. Florid osseous dysplasiamay cause significant bone expansion and in some cases, ulceration of theoverlying gingiva. Like periapical cemental dysplasia, florid osseous dyspla-sia is not treated except as relief for pain, secondary infection or cosmesis.Ossifying fibroma is a benign neoplasm whose histological composition isidentical to that of the cemento-ossifying dysplasias. Ossifying fibromaspresent as a solitary expansile mass typically located in the premolar ormolar region of the mandible inferior or separate from the root apiceswith varying amounts of central ossification and a lucent rim caused bya fibrous capsule (Fig. 27). Most lesions are small (up to 2 cm); however,

Fig. 25. Periapical cemental dysplasia. Intraoral periapical radiographs (A) demonstrate the

evolution of these lesions starting out on the left image as a lucent area at the apices of the man-

dibular incisors with a small central opacification that over time enlarges and fills the lucent

space (middle and right images). Axial (B) and coronal (C) bone CT images in a different patient

show a somewhat expansile lytic area with several islands of opacification at the apices of the

mandibular central incisors.

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they can reach several centimeters in dimension with significant expansionof the cortices (Fig. 28). Juvenile ossifying fibroma is a rare variant of themore common ossifying fibroma that has a predilection for children, adoles-cents, or young adults and has a more aggressive clinical course with bonedestruction and extension into adjacent soft tissues (Fig. 29). Fibrous dys-plasia represents the end spectrum of dysplastic fibro-osseous lesions toinvolve the jaws and occurs as either the monostotic form, as part of thepolyostotic type, or as part of the McCune-Albright syndrome. It more of-ten presents in the monostotic form and involves the maxilla, presenting aseither as irregular lytic areas interspersed with sclerotic areas (Fig. 30) or asthe typical ground glass appearance in which the trabeculae become blurred

Fig. 26. Florrid osseous dysplasia. Axial bone CT images show the classic pattern of a multicen-

tric (A–C), expansile lytic areas (A, arrow) intermixed with areas of opacification with the lucent

areas scalloping up between the roots of the teeth (B, arrow). This is appreciated on the lateral

oblique radiograph of a different patient (D).

Fig. 27. Ossifying fibroma. Axial bone CT demonstrates a mixed lucent–opaque mass in the

premolar–molar region of the mandible with a characteristic lucent rim (arrow) representing

the fibrous capsule.


Fig. 28. Ossifying fibroma. Ossifying fibromas may become large and cause significant expan-

sion of the buccal or lingual cortices and tend to have wispy to coarse internal septations as seen

in this axial bone CT.

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and hazy-appearing because of fibrous replacement. In the mandible, fi-brous dysplasia may appear as a fusiform enlargement of the ramus oralveolus with hazy loss of trabeculation (Fig. 31). CT is the modality ofchoice to depict the bony changes; however, the emergence of positron emis-sion tomography (PET)/PET-CT as a routine tool for differentiating benignand malignant neoplasia bears mention. In the active stage, areas of fibrousdysplasia undergo fibroblastic, osteoclastic, and osteoblastic turnover result-ing in avid FDG (fluorodeoxyglucose) uptake such that the standardizedmeasure of activity for 18FDG may be in the range considered neoplasticand even exceed that of some malignant neoplasms (Fig. 32).

Fig. 29. Juvenile ossifying fibroma. The juvenile variant tends to grow rapidly and cause signif-

icant expansion as seen in this axial noncontrast CT showing considerable expansion of the

mandibular ramus. The ossifying fibromas undergo ossification first centrally and progress to

the periphery.

Fig. 30. Fibrous dysplasia. Axial bone CT shows the characteristic expansile mixed lucent and

sclerotic appearance of the left maxilla and mandibular ramus. Note that in the sclerotic or os-

sified areas, the individual trabeculae are hazy and indistinct. This is typical of the ground glass

appearance.

Fig. 31. Fibrous dysplasia. Axial bone CTs (A, B) show fusiform enlargement of the mandib-

ular ramus with preservation of the cortical boundaries. Axial noncontrast CT (C) shows an

absence of cellulits or myositis that would point to an inflammatory process.


Fig. 32. Fused axial CT and positron emission tomography (PET). The bright (hypermetabolic)

areas in the left maxilla and mandible in the same patient as Fig. 30 represent the degree of Flu-

orodeoxyglucose uptake by fibrous dysplasia. The standard uptake value in the areas of fibrous

dysplasia was 13, which is well within the expected range for malignancy.

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Odontogenic cysts

By far the most common odontogenic cyst is the periapical or radicularcyst, which arises in response to periapical infection or inflammation andradiographically is generally indistinguishable from periapical granulomaor abscess. The dentigerous cyst is the most common developmental cyst,although the incidence is far lower than radicular cysts, on the order of0.001%. Dentigerous cysts develop from the reduced enamel epithelial ofthe dental follicle after development of the crown but before the root de-velops. Thus the resultant lesion appears characteristically as a unilocularradiolucent lesion surrounding the crown of an unerupted or impactedtooth, typically in the mandibular third molar region (Fig. 33). On MRI,these lesions are nonenhancing with T1 hypointensity and T2 hyperinten-sity. Large lesions frequently are expansile, with a thin rim of intact cortex,

Fig. 33. Dentigerous cyst. Axial (A) and coronal (B) bone CTs demonstrate a unilocular cyst

surrounding the crown of an unerupted tooth. This is the classic appearance of a dentigerous

cyst.


and those in the maxilla often extend into the maxillary antrum. Odonto-genic keratocyts (OKC) are also developmental cysts, although less commonthan dentigerous cysts. OKCs arise from rests of dental lamina normallypresent in the developing tooth germ. Although cysts, OKCs demonstrateaggressive clinical behavior and have a high recurrence rate. MultipleOKCs are described classically as a component of Gorlin’s syndrome (basalcell nevus syndrome). OKCs appear as a unilocular or multilocular radiolu-cency within tooth-bearing areas of the alveolus, most often in the posteriormandible, frequently with bone expansion and focal erosion of the cortex(Fig. 34). Because of their viscous parakeratin and protein content, theselesions occasionally will appear slighty hyperdense on CT (compared withother cysts) and with low to intermediate T1 signal on MRI [31]. Large max-illary lesions may involve the orbit or pytergoid plexus, complicating surgi-cal enucleation.

Odontogenic tumors

The most common odontogenic tumor, the odontoma, is a benign tumorcomposed of a hamartomatous malformation of the odontogenic apparatusin varying stages of development: enamel, dentin, cementum, and pulptissues. These lesions account for approximately 67% of all odontogentictumors and are classified according to the degree of tooth development.Compound odontomas are composed of identifiable tooth forms, whereascomplex odontomas consist of an amorphous mass of dental tissue. Theselesions typically present from the first to third decade as a well-circumscribed calcified mass with a radiolucent rim typically in the premolaror molar regions of the mandible, or less often, in the anterior maxilla(Fig. 35). The ameloblastoma is among the most common benign odonto-genic tumors, characterized by its local aggressiveness and high recurrencerate. Ameloblastomas arise from retained ameloblasts of the odontogenic

Fig. 34. Odontogenic keratocyst. Axial (A) and coronal (B) bone CTs demonstrate a large

expansile unilocular cyst extending through the mandibular alveolus and into the ramus. The

lingual cortex is thinned and eroded (arrows), permitting egress of cystic contents into the

adjacent submandibular space.

Fig. 35. Odontoma (complex). Axial (A) and coronal (B) bone CTs show a corticated largely

cystic or lucent mass with a central hyperdensity similar to bone or cementum. The differential

for this lesion would include the fibro-osseous lesions such as periapical cemental dysplasia or

ossifying fibroma.

132 MOSIER

epithelium and predominately occur in the third to fourth decade in the pos-terior mandible. The unicystic ameloblastoma appears as a unilocular cysticmass near the apices, or around the crown of an impacted tooth, makingdistinction from other odontogenic cysts difficult. More typically, amelo-blastomas will show a large expansile multilocular cystic-appearing masswith coarse septations and/or a soap bubble appearance (Fig. 36). Corticalerosion and extension into adjacent soft tissues is common, and lesionsinvolving the maxilla may involve the orbits or ptyergopalatine fissure.The ameloblastic fibroma and ameloblastic fibro-odontoma, although nottrue variants of ameloblastoma, contain varying amounts of primitive ame-loblastic epithelium, connective tissue, and/or odontomatous components.These rare lesions occur in younger patients, being very uncommon beyond

Fig. 36. Ameloblastoma. Axial bone CT (A) and noncontrast CT (B) in two different patients

show expansile multilocular masses within the mandibular alveolus. Note the coarse, thick

internal septations that give these lesions a bubbly appearance. The central hyperdensities

seen in B are the residual islands of destroyed bone.

Fig. 37. Central giant cell granuloma. Axial (A), coronal (B), and sagittal (C) images from a 9-

year-old girl show an expansile unilocular cystic appearing mass centered within the anterior

mandible (A, B). These lesions often are loculated with thin, wispy septations that give them

a honeycomb or soap bubble appearance (C). Note, however, that the sepatations tend to be

thinner and finer than the septations seen with ameloblastomas. They are considerably less ag-

gressive than ameloblastomas and will attain larger dimensions before bone is eroded.


the second decade. Additionally, they occur most often in the premolar andmolar regions of the mandible. Radiographically, they may be indistinguish-able from ameloblastomas or odontomas. The Odontogenic myxoma isa mesodermal-derived tumor likewise often indistinguishable from amelo-blastomas, demonstrating an expansile multiloculated lesion in the posterior

Fig. 38. Eosinophilic Granuloma. Axial bone CT of a 9-year-old boy who presented with jaw

pain. Note that although there is buccal cortex erosion (arrow), the lesion is small and the

remaining margins sharp, giving it a punched-out appearance.

Fig. 39. Aggressive fibromatosis. Axial bone (A) and contrast-enhanced (B) CT images demon-

strate irregular lytic destruction of the left mandibular ramus (A) and a nonenhancing hypo-

dense mass involving the surrounding masticator space (masseter and pyterogoid muscles,

arrows). The differential for this lesion would include rhabdomyosarcoma, although rhabdo-

myosarcomas tend to be more dense and usually demonstrate more enhancement.

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mandible or maxilla, A subtle distinguishing feature, however, is that occa-sionally the septations are more coarse than those of the ameloblatoma. Thepresence of internal calcifications within a generally radioloucent mass dis-tinguishes the uncommon calcifying epithelial odontogenic tumor (CEOT;Pindborg tumor) found in the posterior mandible and often associatedwith the crowns of impacted teeth [29,32].

Miscellaneous nonodontogenic lesions involving the jaws

The central giant cell granuloma is found uniquely in the jaws, and con-troversy remains over whether it is a reactive lesion or a neoplasm. Theselesions are found characteristically in the anterior mandible during the firstand second decades, predominately in females. They present as an expansilemultilocular radiolucency with a classically described honeycomb appear-ance (Fig. 37) [29]. Note that these lesions, although sharing some histolog-ical features with giant cell tumors of the bone, are considered a separateentity.

Table 1

Differential diagnosis chart. Major pathologic entities of the oral cavity are categorized by their

imaging findings

SLS SMS ROT

Fluid A, S, R, L A, S, R, L A, L

Fat D, T D, T D, T

Calcification C C D

Mixed soft tissue E/D, T E/D, T E/D, L

Abbreviations: A, abscess / infection; C, calcified sialolith; E/D (D), epidermoid /dermoid;

L, lymphangioma; S, sialocele; R, ranula; ROT, root of tongue; T, tumor.

Table 2

Differential diagnosis chart. Major pathologic entities of the jaws are categorized by their

imaging findings

Radiolucent Radiopaque Mixed

Unilocular Multilocular Solitary Multicentric Solitary Multicentric

Tooth- bearing

alveolus

I, C, Ta, O T, O F, T F I, F, C, T I, F

Extra alveolar

maxilla and

manidble

O F, O F, T F I, F, T I, F

Abbreviations: I, infection/inflammation; C, cyst; F, fibro-osseous; O, other (central giant

cell granuloma, eosinophilic granuloma, fibromatosis); T, tumor.a unicystic ameloblastoma.


Eosinophilic granuloma is the mildest form of histocytosis X, and whenit affects the jaws, it typically appears at a later age than lesions elsewhere.Eosinophilic granulomas appear as a punched-out radiolucent defect com-monly in tooth-bearing areas of the alveolus (Fig. 38). This punched-out ap-pearance is distinct from the lytic areas seen with odontogenic inflammatorydisease, cyst, or tumors.

Fibromatosis (aggressive fibromatosis) is an extra-abdominal desmoidtumor that although benign is locally aggressive. These tumors more com-monly involve the neck or supraclavicular region and arise within skeletalmuscle, periosteum, or fascia. These typically infiltrate the jaws secondarilyfrom the buccal mucosa, tongue, or submandibular space, although rarelythey may arise primarily within the jaws. On imaging, they present as a sol-itary, homogenous, minimally enhancing mass that infiltrates through thecortex (Fig. 39) [33].

Algorithms for differential diagnosis of lesions in the oral cavity and jaws

Within the oral cavity, the key to arriving at the differential diagnosis liesin the concept of spaces. Recognition of whether the lesion lies within theSLS, SMS, or root of the tongue along with the clinical history will narrowthe differential quickly. Within the jaws, recognition of whether the lesion isprimarily odontogenic or nonodontogenic will eliminate a diverse list ofentities. Tables 1 and 2 provide a tabular guide to this differential approach.

References

[1] SeikalyH, JhaN,McGawT, et al. Submandibular gland transfer: a newmethod for prevent-

ing radiation induced xerostomia. Laryngoscope 2001;111:347–52.

[2] MassineRE,Durning SJ, Koroscil TM. Lingual thyroid carcinoma: a case report and review

of the literature. Thyroid 2001;11(12):1191–6.

[3] Fugitt B, Puckett ML, Quigley MM, et al. Necrotizing fasciitis. Radiographics 2004;24(5):

1472–6.

136 MOSIER

[4] McGurk M, Escudier MP, Brown JE. Modern management of salivary calculi. Br J Surg

2005;92:107–12.

[5] Tiemann M, Teymoortash A, Schrader C, et al. Chronic sclerosing sialadenitis of the sub-

mandibular gland is mainly due to a T lymphocyte immune reaction. Mod Pathol 2002;

15(8):845–52.

[6] Miller MB, Rao VM, Tom BM. Cystic masses of the head and neck: pitfalls in CT andMR

Interpretation. AJR 1992;159:601–7.

[7] Macdonald AJ, Salzman KL, Harnsberger HR. Giant Ranula of the neck: differentiation

from cystic Hygroma. AJNR Am J Neuroradiol 2003;24:757–61.

[8] Kittredge RD, Finby N. The many facets of lymphangioma. Am J Roentgenology 1965;

95(1):56–66.

[9] Goetsch E. Hygroma colli cysticum and hygroma axillare: pathologic and clinical study and

report of twelve cases. Arch Surg 1938;36:394–479.

[10] Thompson JE, Keiller VH. Lymphangioma of the neck. Ann Surg 1923;77(4):385–96.

[11] Koeller KK, Alamo L, Adair CF, et al. Congenital cystic masses of the neck: radiologic-

pathologic correlation. Radiographics 1999;19:121–46.

[12] Batsakis JG, Rice DH. The pathology of head and neck tumors: Vasoformative tumors,

part 9A. Head Neck 1981;3(3):231–9.

[13] Leipzig B, Rabuzzi DD. Recurrent massive cystic lymphangioma. Otolaryngology 1978;

86(5):758–60.

[14] Siegel MJ, Glazer HS, St. Amour TE, et al. Lymphangiomas in children: MR imaging.

Radiology 1989;170:467–70.

[15] KingRC, Smith BR, Burk JL.Dermoid cyst in the floor of themouth: review of the literature

and case reports. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1994;78(5):567–76.

[16] Fuchshuber S, Grevers G, Issing WJ. Dermoid cyst of the floor of the mouth-a case report.

Eur Arch Otorhinolaryngol 2002;259:60–2.

[17] Mulliken JB, Glowacki J. Hemangiomas and vascular malformations: a classification based

on endothelial characteristics. Plast Reconstr Surg 1982;69:412–22.

[18] Fletcher DM. Distinctive soft tissue tumors of the head and neck. Mod Pathol 2002;15(3):

324–30.

[19] CheukW, Chan JKC. Salivary gland tumours. In: Fletcher CDM, editor. Diagnostic histo-

pathology of tumours. London: Churchill Livingstone; 2000. p. 231–311.

[20] Choi DS, Na DG, Byun HS, et al. Salivary gland tumors: evaluation with two-phase

helical CT. Radiology 2000;214:231–6.

[21] Yousem DM, Kraut MA, Challan AA. Major salivary gland imaging. Radiology 2000;216:

19–29.

[22] Shapiro SD, Abramovitch K, Van Dis ML, et al. Neurofibromatosis: oral and radiographic

manifestations. Oral Surg Oral Med Oral Pathol 1984;58(4):493–8.

[23] Flickinger FW, Lozano RL, Yuh WTC, et al. Neurilemoma of the tongue: MR findings.

J Comput Assist Tomogr 1989;13:886–8.

[24] De Bree R, Westerveld G-J, Smeele LE. Submandibular approach for excision of large

schwannoma in the base of the tongue. Eur Arch Otorhinolaryngol 2000;257:283–6.

[25] Rosenberg TJ, Ruggiero S. Osteonecrosis of the jaws associated with the use of bisphosph-

onates. J Oral Maxillofac Surg 2003;61(Suppl 1):60.

[26] Migliorati CA. Bisphosphonates and oral cavity avascular bone necrosis. J Clin Oncol 2003;

21:4253–4.

[27] Ruggiero SL, Fantasia J, Carlson E. Bisphosphonate-related osteonecrosis of the jaw: back-

ground and guidelines for diagnosis, staging and management. Oral Surg Oral Med Oral

Pathol Oral Radiol Endod 2006;102(4):433–41.

[28] Bianchi SD, Scoletta M, Cassione FB, et al. Computerized tomographic findings in

bisphosphonate-associated osteonecrosis of the jaw in patients with cancer. Oral Surg

Oral Med Oral Pathol Oral Radiol Endod 2007;104(2):249–58.


[29] Regezi JA. Odontogenic cysts, odontogenic tumors, fibroosseous and giant cell lesions of the

jaws. Mod Pathol 2002;15(3):331–41.

[30] Speight PM, Carlos R.Maxillofacial fibro-osseous lesions. Curr Diag Path 2006;12(1):1–10.

[31] YonestuK, Bianchi JG, TroulisMJ, et al. Unusual appearance of odontogenic keratocyst of

the mandible: case report. AJNR Am J Neuroradiol 2001;22:1887–9.

[32] Dungee BL, Sakai O, Pitsey R, et al. Radiologic and pathologic characteristics of benign and

malignant lesions of the mandible. Radiographics 2006;26:1751–68.

[33] Seper L, Burger H, Vormoor J, et al. Aggressive fibromatosis involving the mandible- case

report and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod

2005;99(1):30–8.

non oncologic imaging of the oral cavity and jaws

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