228

The primary disease processes that give rise to swellingsand tumors of the oral cavity include cysts, mucousextravasation and retention in the minor salivaryglands, foci of granulation tissue and inflammation,abscesses and connective-tissue proliferations that arewell defined or encapsulated, as well as infiltrative sar-comas. Figure 23–1 is a representation of the processesthat cause soft-tissue tumefactions in the mouth. Bothepithelial and connective-tissue disease processes canpresent as masses. Benign and malignant surface epithe-lial tumors are discussed in the Chapters 15 and 20,respectively. From a clinical perspective the three mostimportant defining characteristics of any soft-tissueswelling are location, coloration, and palpable nature.

As for location, certain diseases tend to occur in spe-cific sites to the exclusion of others. Table 23–1 lists themost common lesions according to site. This is not tosay that these sites are exclusive, since many lesions canin fact occur anywhere in the mouth; rather, this tabu-lation catalogues the most likely lesions for that site interms of overall prevalence. Coloration is dependentupon the tissues present in the mass and the depth of thelesion. Table 23–2 lists the most frequently encounteredcolorations observed with soft-tissue masses and indi-

cates the lesions that most often present with a givencoloration. In general, yellow-appearing lesions arecomprised of lymphoid tissue or adipose tissue, red

Cyst

Abscess

Sarcoma

Tumor

Granuloma

Carcinoma

Figure 23–1 Schematic diagram showing the various pathologicprocesses that can manifest as a submucosal or subcutaneous mass.

Molecular and pathologic

correlates of disease, 229

Clinical features of oral

swellings, 231

Traumatic fibroma, 231

Inflammatory fibrous

(denture) hyperplasia, 232

Mucous extravasation

phenomenon (mucocele), 232

Mucous retention cyst, 232

Reactive gingival

tumefactions, 233

Peripheral odontogenic cysts

and tumors, 234

Diffuse gingival

enlargements, 234

Varix, 234

Pulsatile labial artery, 235

Parulis, 236

Specific granulomas, 236

Ectopic lymphoid tissue and

benign lymphoepithelial

cysts, 237

Amyloidosis, 237

Mesenchymal neoplasms, 238

Aggressive proliferations, 240

Squamous cell carcinoma, 240

Salivary gland tumors, 240

Sarcomas and lymphomas,

241

Clinical features of facial

tumors and swelling, 241

Odontogenic infections, 242

Soft-tissue emphysema, 242

Seborrheic keratosis, 242

Melanocytic lesions, 242

Mesenchymal neoplasms,

243

Basal cell carcinoma, 243

Squamous cell carcinoma,

244

Suggested reading, 244

23 Swellings and Tumors ofthe Oral Cavity and FaceL. Roy Eversole, DDS, MSD, MA, and Sol Silverman, Jr, MA, DDS

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swellings are vascular, blue swellings are mucinous orvenous, and brown swellings contain melanin or bloodpigments. Lesions with normal mucosal pink colorationare generally composed of fibrous tissues or some othertissues lying deeper in the connective tissues.

Table 23–3 groups swellings according to their pal-pation characteristics. Firm movable masses are usuallyneoplasms or granulomas; soft movable masses are fattyor myxoid tumors; fluctuant masses are cysts, mucoce-les or mucous-duct retention cysts and abscesses; andindurated fixed masses are probably malignant and mayrepresent carcinomas, salivary adenocarcinomas, lym-phomas, and sarcomas.

In terms of frequency, the majority of oral mucosalmasses are reactive proliferations, such as fibroushyperplasias, pyogenic granulomas, and mucousextravasation reactions. Mesenchymal and salivary neo-plasms are uncommon, and lymphomas and sarcomasare rare causes of oral swelling. Indeed, the probabilitythat a mucosal mass is a reactive or hyperplastic processis probably 50-fold compared to a true neoplasticprocess. In most instances, biopsy is necessary to arriveat a definitive diagnosis. Aspiration or incision anddrainage may be performed as a diagnostic procedurewhen the mass is consistant with an abscess.

Molecular and pathologic correlates of disease

The molecular aspects or oral soft-tissue swellings arepoorly understood and have not received much attentionin the experimental literature. Conversely, the underlyingpathologic processes associated with the various lesions

that produce tumefaction in the oral cavity are welldefined in the oral and maxillofacial pathology literature.

As an overview of pathologic mechanisms, basic con-cepts are briefly presented here. The common masses thatrepresent hyperplasias evolve as a consequence of irrita-tion to the mucosal tissues by a dental appliance or bytrauma, often the consquence of biting. The injured tis-sues respond to chronic and sometimes acute injury byproliferation of cells. The most commonly encounteredhyperplasias are those involving fibroblasts. Injury toconnective tissue results in fibroblastic proliferation of abenign nature, followed by collagen fibrillogenesis. Manyfibrous hyperplasias are comprised of loose collagen andare soft to palpation, such as denture-induced fibroushyperplasia and the common traumatic fibromas of thetongue and labial and buccal mucosae. In the gingiva, theperiodontal tissues may be the targets of injury, particu-larly from irritants that may become entrapped in the gin-gival sulcus. Calculus, food particles, and foreign objectsmay be introduced into the sulcus, where they irritate the

Table 23–1 Orofacial Soft-Tissue Swellings according to Site

Site Type of Lesion

IntraoralLips and buccal mucosa Fibroma, mucocele, mesenchymal tumor, salivary tumor, squamous cell carcinomaGingiva Parulis, pyogenic granuloma, peripheral fibroma, peripheral giant cell granuloma, peripheral ossifying

fibroma, gingival cyst, peripheral odontogenic tumors, squamous cell carcinomaPalate Abscess, torus, salivary gland tumorDorsolateral tongue Fibroma, granular cell tumor, pyogenic granuloma, squamous cell carcinomaVentral tongue and oral floor Mucocele, ranula, lymphoid aggregates, lymphoepithelial cyst, osteocartilagenous choristoma, squamous

cell carcinoma

Face and neck swellingsMasseteric region Cellulitis, space infection, jaw cysts and tumors, masseteric hypertrophyParotid region Sialadenitis, sialolithiasis, salivary neoplasm Submandibular region Lymphadenopathy, sialolithiasis, salivary neoplasmLateral neck Lymphadenopathy, mesenchymal neoplasm, branchial cleft cyst, metastatic carcinoma, lymphoma, carotid

body tumorAnterior neck Goiter, thyroid neoplasm, thyroglossal cystFace Seborrheic keratosis, basal cell carcinoma, adnexal skin tumors, squamous cell carcinoma, melanoma

Table 23–2 Masses with Coloration or Pigmentation

Color Soft-Tissue Mass

Blue–purple Hemangioma, varix, hematoma, peripheral giant cell granuloma, mucocele, Kaposi sarcoma

Red Hemangioma, pyogenic granuloma, Kaposi sarcoma

Brown Nevus, hematoma, seborrheic keratosis, Kaposi sarcoma, melanoma

Black MelanomaYellow–orange Lymphoid aggregates, lymphoepithelial cyst,

lipoma, granular cell tumor

230 C H A P T E R 2 3

fibrovascular connective tissues, periosteum, and perio-dontal ligament fibrous tissues. Proliferation of thefibrovascular connective tissue, along with inflammation,gives rise to pyogenic granulomas, whereas proliferationof the periosteal tissues, which contain osteoblasts andosteoclasts, gives rise to peripheral giant cell granulomas.When periodontal ligament fibroblasts proliferate, theyretain the potential to elaborate bone and cementum,thereby giving rise to peripheral ossifying fibromas.

Minor salivary glands are located everywhere in theoral cavity except on the anterior dorsal tongue and theattached gingiva. They are most easily damaged fromaccidental biting in the lower lip and sometimes in thebuccal mucosa, whereas injuries to the palatal andupper lip glands are rare. Therefore, severence of theminor gland ducts after an acute biting episode fre-quently leads to mucous extravasation into the connec-tive tissues of the lips and buccal mucosa. In thesemucoceles, the extravasated mucus becomes encapsu-lated, or walled-off, by fibrous and granulation tissues,giving the appearance of a cyst. Less commonly, mucousplugs form in the ducts of minor glands and cause reten-tion of mucus. The ducts undergo cystic dilation and areepithelial lined; such lesions are referred to as mucousretention cysts or sialocysts. Although rare, true salivarystones may arise in minor salivary ducts, and as theygrow, they result in an enlargement within the sub-mucosa that is movable and hard.

Acute infections of the soft tissues are uncommon;however, occasionally a foreign body, such as a small fishbone or material from a dental procedure may beimplanted into the soft tissues and cause an acute reac-tion. These submucosal fluctuant abscesses are moreoften seen on the tongue. Of course the most commonlocation for abscess in the oral cavity is the gingiva andvestibule. In such instances the abscess is a parulis fromodontogenic infection or a periodontal abscess arising ina periodontal pocket. Pulp vitality testing of adjacentteeth, periapical radiographs, periodontal probing, andaspiration are all important procedures when attemptingto establish a definitive diagnosis. For accurate culturesprocured for identifying causative microorganisms, apure suppurate is essential; this is to avoid contaminants.

Chronic foci of inflammation may also account forsubmucosal masses. Lymph nodes are located in the buc-cal mucosa and in health are not palpable. Sometimesthey become irritated or drain a local viral or bacterialinfection and become enlarged. This enlargement isreferred to as reactive lymphoid hyperplasia in whichboth T cells and germinal-center B cells undergo immune-mediated proliferation. Foreign bodies, in addition toacute infections, may induce granuloma formation.Recall that many foreign bodies can cause a giant cellreaction with accompanying chronically inflamed granu-lation tissue. Oral mucosal foreign body granulomas areseen with many dental materials, including amalgam anddental cements, handpiece oil (oil granulomas), and veg-etable particles (legume or pulse granulomas).

A group of idiopathic diseases, collectively known asorofacial granulomatosis, is histologically characterizedby multiple, often confluent foci of granulation tissuewith giant cell formation in the absence of foreign ma-terial or a specific infectious agent. These are termednoncaseating granulomas, because unlike the granulo-mas of tuberculosis, there is no focus of caseous necro-sis. Included in the orofacial granulomatosis group oflesions are Crohn disease, sarcoidosis, Melkersson-Rosenthal syndrome, and cheilitis granulomatosa (seeChapter 24). Submucosal masses comprised of granulo-mas also occur in response to infectious agents and areknown as specific granulomatous inflammatory lesions.Included here are such specific infections as tuberculosisand deep fungal infections, the most common of whichis histoplasmosis. The specific infectious granulomasare typically multinodular with an erythematous granu-lar surface. Wegener granulomatosis is a systemic dis-ease with multiple organ involvement that also mani-fests as a red granular swelling, usually confined to thefixed gingiva, so-called strawberry gums.

Swellings that diffusely involve the gingiva are theresult of pathologic leukocytic infiltrates, such as mightbe encountered in leukemia, proliferation of granula-tion tissue in instances of nonspecific hyperplastic gin-

Table 23–3 Masses according to Palpation Characteristic

Palpation Characteristic Mass

Soft, fluctuant Mucocele, ranulaDevelopmental cystsSialocystsGingival cystsParulisSpace infections and abscesses

Soft, nonfluctuant LipomaFibromaOrganized mucocele

Firm, movable Mesenchymal tumorsGranulomasSalivary adenomasAdnexal skin tumors

Firm, fixed Granular cell tumorSeborrheic keratosisKeratoacanthomaFibromatosis

Indurated, fixed Basal cell carcinomaSalivary adenocarcinomasSquamous cell carcinomaMelanomaSarcomasLymphomas

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givitis, and overproduction of collagen in cases of drug-induced gingival hyperplasia (eg, Dilantin, nifedipine,cyclosporine), or the rare hereditary condition, familialfibromatosis gingivae.

As stated previously, true connective-tissue neoplasmsare uncommonly seen in the oral cavity as compared withreactive and inflammatory masses. They may derive fromany of the submucosal tissues, such as fibroblasts,lipocytes, nerve sheath, smooth muscle, skeletal muscle,vessels, osteoblasts, and chondroblasts. Sarcomas ofthese tissues are extremely rare. The proliferations con-tain cellular elements that are histogenically related to thenormal tissues from which they arise and are namedaccording to their histologic differentiation. The benignentities derived from mesenchymal or connective-tissuesare variably encapsulated or are at least well circum-scribed. A specific microscopic diagnosis is essential,since not all connective-tissue tumors behave in the sameway. Some are aggressive, such as myofibromatoses, andhave a tendency for local recurrence. Others are benignand have no tendency for recurrence after excision.

Minor salivary tumors also present as submucosalmasses (see Chapter 26). They are most commonlyfound in the palate and buccal mucosa, but can arise inany location where minor glands are located. Clinically,benign salivary gland tumors are nonulcerated andshow normal surface coloration, whereas the malignanttypes often exhibit surface telangiectasia, can be ulcer-ated, and are usually firm to palpation, owing to cellu-lar proliferation. As with connective-tissue tumors, thesalivary adenomas and adenocarcinomas are classifiedaccording to histologic patterns of differentiation.Recall that normal glands are comprised of ducts, acini,and myoepithelial cells. The various salivary-glandtumors are segregated and classified according to thepatterns of these various cell types. The common pleo-morphic adenoma is a lesion comprised of benign prolif-erations of ducts and myoepithelial cells. In the malignantcategory, adenoid cystic carcinoma and polymorphouslow-grade adenocarcinoma are composed of solid-tumor islands with additional foci of ductal formations.Mucoepidermoid carcinoma shows both acinar andductal cells with squamous (epidermoid) and mucousacinar cell differentiation. Mucoepidermoid carcinomasshow variations in cell patterns that allow for assign-ment into low- or high-grade subgroups that correlatewith good and poor prognosis, respectively.

Masses of the facial skin can also, as in the mouth,be represented by inflammatory, infectious, develop-mental, and neoplastic processes. Diffuse swellingsoccur in edematous states and in inflammatory condi-tions, such as dental-space infections, cellulitis, andallergic reactions. Focal masses are often the conse-quence of either benign or malignant tumors that arisefrom the surface epithelium, adnexal structures (hair

follicles, sweat glands, sebaceous glands), and the der-mal connective tissues. The most common focal cancer-ous swelling of the face is basal cell carcinoma. It hasbeen shown that these tumors, as well as those associ-ated with the basal cell nevus syndrome, harbor muta-tions in the “patched” gene, a membrane tumor sup-pressor involved in the sonic hedgehog morphogenpathway. Jaw keratocysts harbor these same mutations.

Clinical features of oral swellings

The clinical features for the more common mucosalswellings vary according to each specific entity. As hasalready been emphasized, it is crucial that the cliniciantake note of the location, coloration, surface texture, andpalpable nature of the mass before attempting to secure adefinitive diagnosis. If the lesion shows the features of anabscess, then diagnostic testing for odontogenic or perio-dontal origin must be performed by obtaining radio-graphs, pocket probing, pulp vitality testing, and identi-fying pyogenic suppuration. If no apparent infectioussource is uncovered, then biopsy may be the chief methodfor procurement of a definitive diagnosis. In the case ofdiffuse gingival enlargement, interrogation with regardto drug use is imperative. As in all cases of oral lesions,the clinician must obtain a thorough medical history,knowing that some swellings may be associated withsystemic diseases. When biopsy is to be undertaken, adecision must be made as to whether the biopsy will beincisional or excisional, a consideration based on boththe size of the lesion and the possibility of malignancy.If malignancy has a high priority in the differential diag-nosis, then incisional biopsy is indicated (see Chapter20). The lesional and diagnostic tissue lies deep in thesubmucosa, and therefore, an incisional biopsy must betaken to a significant depth within the tumefaction. Awedge or pie-shaped incisional biopsy is advisable inthese situations, to get an adequate specimen.

Traumatic fibroma

Focal fibrous hyperplasia as a consequence of traumaunderlies the pathogenesis of this common benign oraltumor. It is pink in color yet may have a white keratoticsurface if it is repeatedly irritated. Most fibromas areround, dome shaped sessile, soft masses (Figure 23–2).They vary greatly in size and are usually asymptomatic.The most common sites are the lips, commissures, buc-cal mucosa, and tongue. When traumatic fibromasoccur on the gingiva they are commonly referred to asperipheral fibromas. Some show unique histologic fea-tures and are designated gingival fibromas. Anothervariant that can occur anywhere in the mouth is the

232 C H A P T E R 2 3

giant cell fibroma, not to be confused with giant cellgranuloma, an aggressive lesion of the gingiva. Fibro-mas are treated by simple excision as well as trying toidentify and remove a possible causative irritant, whichis not often apparent.

Inflammatory fibrous (denture) hyperplasia

The irritation from an overextended denture flange canirritate the submucosal connective tissue. This tends tooccur under dentures when alveolar ridge resorption hascaused the denture to overseat. The irritating flangesinduce multinodular flabby masses along the maxillaryor mandibular vestibule (Figure 23–3). This so-calledepulis fissuratum, an older term for fibrous hyperplasiaassociated with denture irritation, was used in a descrip-tive sense because so many of these common lesions arelobulated, with intervening fissural depressions. Themost common locations are the anterior maxillary andmandibular vestibules, but they can be located anywhere

along the sites of denture compression and irritation.Recall that in the palatal vault denture hyperplasias arediffuse and papillary, a lesion termed inflammatory pap-illary hyperplasia.

Mucous extravasation phenomenon (mucocele)

Mucoceles are the result of minor salivary gland ductseverage with resultant escape of mucus into the sub-mucosal connective tissues. With no conduit for excre-tion, the mucus collects in the connective tissues, creat-ing a pseudocyst (they lack an epithelial lining) whichbecomes walled-off with granulation tissue and if notremoved, the wall becomes fibrotic. The duct severageis the consequence of biting, usually in the lower lip.Mucoceles rarely involve the upper lip yet may occur atany site where minor salivary glands are located.

The clinical presentation is that of a soft-tissue cystthat is soft and fluctuant (Figure 23–4). When superficialthey are faintly blue; if walled-off or fibrosed they mayfeel more solid and have normal mucosal coloration.Occasionally, the patient pops the lesion (with a pin or bybiting) and it resolves; however, it usually recurs. Moreoften, is the tendency to remain or even enlarge. Surgicalexcision of the cystic tissue should be accompanied byremoval of the underlying “feeder” minor glands. Largemucoceles in the floor of the mouth arise from severageof the sublingual or even the major submandibular ductand are referred to as ranulas. Some of these mucousextravasations extend deeply into the intrinsic muscles ofthe tongue and mylohyoid, so-called plunging ranulas.

Mucous retention cyst

True cysts of the minor salivary ducts are referred to asmucous retention cysts or sialocysts. These lesions mani-

Figure 23–3 Inflammatory fibrous hyperplasia under a mandibulardenture.

Figure 23–2 A, Clinical appearance of traumatic (irritation) fibroma;B, microscopic appearance of fibroma.

A

B

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fest the same clinical characteristics as the mucocele, beingsoft fluctuant bluish masses. Whereas some are probablytrue blind cysts lined by salivary ductal epithelium, othersare ductal dilatations that develop as a consequence ofductal obstruction or occlusion by mucous plugs. Theselatter retentive cysts tend to occur in the buccal mucosaof older adults. Treatment is complete excision.

Reactive gingival tumefactions

Four pathologically related proliferations are encoun-tered on the gingiva, usually arising in the interdental orgingival papilla region. All are reactions to irritationfrom calculus or particles that become wedged into thegingival sulcus (toothpick fragments, popcorn kernels,etc.). The host reacts to the irritant by hyperplasia of theendogenous tissues in the site, which include fibrovascu-lar connective tissues, periodontal ligament fibroblasts,and periosteal tissues. Proliferation of granulation tissuegives rise to pyogenic granulomas, which may fibrose toperipheral fibroma; periodontal ligament cells give riseto cells capable of osteogenesis and cementogenesis,causing the ossifying fibroma; periosteal progenitor cells,including osteoblasts and osteoclasts, proliferate, pro-ducing a lesion termed peripheral giant cell granuloma(Figure 23–5). The term peripheral is employed to dis-tinguish these common lesions from their less commoncounterparts that arise within the jaw bones. Pyogenicgranulomas and peripheral ossifying fibromas are com-mon in pregnancy.

Clinically either facial-buccal or lingual gingiva maybe involved and there may be a history of rapid growth.The pyogenic granuloma is usually red; fibromas andossifying fibromas are pale pink; and giant cell granulo-mas are bluish; and all can become ulcerated with a whitepseudomembranous surface (Figure 23–6, 23–7, and23–8). The peripheral giant cell granuloma is the moreaggressive of these lesions, often eroding underlying alve-olar bone and even causing root resorption (Figure 23–9).

Figure 23–4 A, Mucocele of the lower lip; B, photomicrograph show-ing pooling of mucin under the surface epithelium with minor gland lob-ules in the deeper connective tissue; C, ranula in the floor of the mouth.

B

A

C

Fibrovascularconnective

tissues

Pyogenicgranuloma

Peripheralfibroma

Peripheralossifyingfibroma

Peripheralgiant cell

granuloma

Periodontalligament

Periosteum

Figure 23–5 Diagram depicting the various reactive lesions of thegingiva.

Figure 23–6 A, Pyogenic granuloma with red coloration; B, photo-micrograph of pyogenic granuloma showing fibrovascular tissues.

A

B

234 C H A P T E R 2 3

eral odontogenic fibroma being the most common (Fig-ure 23–11). Rare peripheral odontogenic tumors thatappear as gingival masses include ameloblastoma,dentinogenic ghost-cell tumor, and calcifying epithelialodontogenic tumor.

Diffuse gingival enlargements

Gingival hyperplasias can be nonspecific, drug-induced,hormonally-related, granulomatous, or even neoplastic.Nonspecific gingival hyperplasias often have theappearance of multifocal pyogenic granulomas, beingsoft, hemorrhagic, and fiery red. There is a systemicunderlying hormonal influence in the pathogenesis ofhyperplastic gingivitis when the patient is a femaleentering puberty or gravid (Figure 23–12). Suchinstances are often referred to as puberty and pregnancygingivitis, respectively. The gingival lesions are typicallyassociated with formation of pseudopockets.

Drug-induced gingival hyperplasias are diffuse, andthe lesions may be of normal coral pink coloration orred and inflamed. Phenytoin, calcium channel blockers,and cyclosporine used in the treatment of seizure dis-orders, hypertension and cardiovascular disease, andimmunosuppression for organ transplantation, respec-tively, are all responsible (Figures 23–13 and 23–14).The fibrosis of cyclosporine enlargement is not limitedto the gingival tissues; indeed, renal, pulmonary, andretroperitoneal fibrosis are complications of this drug.These lesions do not resolve with drug withdrawal.

Familial fibromatosis gingivae is a rare disorder thatis inherited as an autosomal dominant trait. Theenlarged gingivae are firmly fibrotic and devoid of sig-nificant inflammatory erythema as a rule (Figure 23–15).Periodic gingivectomies are often requested by thepatient for esthetic as well as functional reasons.

Wegener granulomatosis is a multisystem immuno-pathologic disease that affects the lungs, kidneys, skin,and middle ear. The enlarged gingiva is red and granu-lar, often termed strawberry gums (Figure 23–16). Ahistopathologic diagnosis of Wegener granulomatosiswarrants a systemic workup to examine for other sitesof involvement. The serologic marker antineutrophilcytoplasmic antibody (ANCA) is of diagnostic impor-tance, being found in over 85% of cases.

Varix

Focal varices are most common in the lower lip and areprobably the consequence of trauma, such as lip biting,to the submucosal vessels. Venous channels proliferateand become dilatated. These lesions may be flat or, moreoften, raised blue or purple masses (Figure 23–17). Somewill blanch on diascopy (exerting direct pressure on the

Wide surgical excision is the treatment. Recurrenceoccurs in over 20% of the cases, which can be minimizedby adequate surgical excision coupled with root planing.

Peripheral odontogenic cysts and tumors

Although odontogenic tumors are encounted central inthe jaws, recall that the dental lamina arises from thealveolar mucosa, and odontogenic rests, which can giverise to neoplasms and cysts, are located in the gingiva.The most common entity is the gingival cyst of the adult,a lesion that appears as a nodule on the attached gingivaand may erode the underlying cortex (Figure 23–10).Benign odontogenic tumors also occur here, the periph-

S W E L L I N G S A N D T U M O R S O F T H E O R A L C A V I T Y A N D F A C E 235

lesion to detect blanching of vascular channels). Thosethat fail to blanch are often thrombosed. Treatment iselective. Injection with a sclerosing agent, such asSotradecol™, may be effective. Surgical excision andlaser ablation are common treatment options.

Pulsatile labial artery

The labial branch artery may develop a small aneurys-mal dilatation that appears as a nodule or linear elon-

gated mass of the lower lip. The lesion is usually of nor-mal color because the vessel is deep and surrounded bythe usual arterial muscularis coat. Sometimes pulsationscan be observed visibly; in others palpation is requiredto detect the pulsatile nature of this vascular anomaly. Ifthe patient elects to have the lesion removed, the

Figure 23–9 Radiograph showing saucerized zone of alveolar ridgeresorption from an overlying peripheral giant cell granuloma.

A

B

Figure 23–7 A, Peripheral ossifying fibroma is coral pink in color; B,photomicrograph of peripheral ossifying fibroma.

A

B

Figure 23–8 A, Peripheral giant cell granuloma; B, photomicrographdepicted the multifocal nature of giant cell granuloma extending to thebase of the cut margin.

236 C H A P T E R 2 3

mucosa should be incised and the vessel blunt dissected,followed by ligation and excision.

Parulis

Odontogenic infections that evolve into periapicalinflammatory lesions may perforate the cortex, withdrainage into the oral soft tissues. Focal drainage of anacute inflammatory process creates a tract that deliverssuppurative material into the gingival submucosa.These drainage tracts may occur anywhere from the freegingival margin down to the vestibule (Figure 23–18).This submucosal abscess, or parulis, is associated withan endodontically involved necrotic tooth. Radiographsand pulp vitalometry testing disclose the incriminatingtooth. If all teeth in the region of the parulis are vital,then the lesion may represent a focal periodontalabscess, and in such cases, a deep pocket is identifiableand probing causes exudation.

Specific granulomas

Granulomatous inflammation is characterized by gran-ulomas with multinucleated giant cells. This type of his-tologic reaction is seen in foreign body reactions, orofa-cial granulomatosis, and such specific infections astuberculosis and deep fungal infections. Specific granu-lomas occur most often in the tongue, vestibule, andbuccal mucosa, where they appear as submucosal nod-ules, some being multinodular. Foreign body reactionsare commonly found to contain fruit or vegetable ma-terial (pulse granulomas), dental materials, or oil fromhandpieces, thereby representing iatrogenic lesions.Granulomas that represent specific microbial infectionsare often red with a granular “strawberry” appearance.They are generally firm to palpation. Biopsy with spe-cific microbial stains usually allows the pathologist toidentify the genus of the microorganism. Orofacialgranulomatosis includes sarcoid, sarcoid-like diseases,and Crohn disease (see Chapter 24).

Figure 23–10 Gingival cyst. Figure 23–12 Nonspecific puberty-associated hyperplastic gingivitis.

Figure 23–11 Peripheral odontogenic fibroma appearing as a gingivalmass. Figure 23–13 Dilantin-induced gingival hyperplasia.

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Ectopic lymphoid tissue and benignlymphoepithelial cysts

Ectopic lymphoid tissue is commonly seen in the oralcavity where it appears as a yellow nodular or multi-nodular mass (Figure 23–19). The common sites are thefloor of the mouth and the soft palate. Many of theselymphoid aggregates emulate tonsilar tissue in thatepithelial lined crypts extend into the lymphoid tissueand some become impacted with keratin, exhibiting acystic appearance.

Amyloidosis

Amyloid is a pathologic fibrillar protein that accumu-lates within the connective tissues and is associated withcertain neoplasms. Chemically, there are over 15 sepa-rate varieties, yet only three are of clinical significance:amyloid light chain (AL) protein, derived from plasma-cell-generated immunoglobulin light chains; amyloid-associated (AA) protein, which is made in the liver, and

beta-2-microglobulin. Amyloid light chain protein isassociated with primary amyloidosis and becomesdeposited in tissues in patients with B lymphocyte pro-liferations, multiple myeloma being the most prevalent.Amyloid-associated protein is deposited in secondaryamyloidosis, such as inflammatory lesions and tubercu-losis, and beta-2 microglobulin is associated with long-term renal dialysis. In the oral cavity, these deposits areusually encountered on the tongue as multiple or, less

Figure 23–14 Gingival enlargement associated with a calcium chan-nel blocker.

Figure 23–15 Familial gingival hyperplasia.

Figure 23–16 The “strawberry gums” of Wegener granulomatosis.

Figure 23–17 A, Varix of the lip; B, photomicrograph of varix with anorganizing thrombus.

A

B

238 C H A P T E R 2 3

Figure 23–21 A, Nerve sheath tumor of the tongue; B, photomicro-graph of a neurilemoma showing nuclear palisading (Antoni type Atissue).

A

B

often, single nodules (Figure 23–20). The presence ofamyloid in oral biopsies is determined by Congo redstaining with subsequent demonstration of green bi-refringence under polarized light. The fluorochromethioflavin T also stains amyloid, yet is not specific.

Mesenchymal neoplasms

A variety of neoplasms arise from the submucosal con-nective tissues, and such tumors appear as nodularswellings. They may show distinct clinical features, suchas hemangioma and lymphangioma, or they may benondescript, simply presenting as pink, smooth-surfaced tumefactions. Hemangiomas and lymphan-giomas are considered to be developmental lesions,since these lesions often proliferate in infancy or child-hood, and may spontaneously resolve during teenageyears (see Chapter 25). Most mesenchymal tumors arefound in the tongue or buccal mucosa, but they canoccur anywhere in the mouth. The more common arenerve sheath tumors, including neurilemoma (shwan-noma) and neurofibroma (Figure 23–21). The granularcell tumor is generally considered to be a nerve sheathtumor as well (Schwann cell origin) and is most com-

monly found in the tongue, where it appears as a yellow,smooth-surfaced, firm plaque or nodule (Figure 23–22).

Lipomas are typically located in the buccal mucosa,appearing as soft, yellow, single or multinodular masses(Figure 22–23). Choristomas are benign growths thataberrantly arise in locations that do not harbor theprogenitor cells from which they arise. In the oral cav-

Figure 23–18 Parulis associated with periapical infection.

Figure 23–19 Ectopic lymphoid tissue in the oral floor.

Figure 23–20 Amyloidosis presenting as multiple tongue nodules.

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ity, chondroid (cartilaginous) choristomas are typicallyencountered as hard nodules in the submucosa of thetongue. Other benign mesenchymal neoplasms that areoccasionally encountered in the oral cavity are rhab-domyoma, leiomyoma, nodular fasciitis, solitaryfibrous tumor, and fibrous histiocytoma, to mention buta few (Figures 23–24 and 23–25). These specific entitiesare all treated by surgical excision, and have variabletendencies for recurrence.

A

B

Figure 23–22 A, Granular cell tumor of the tongue; B, photomicrographof granular cell tumor with overlying pseudoepitheliomatous hyperplasia.

Figure 23–23 Lipoma with yellow coloration of the buccal mucosa.

Figure 23–24 Submucosal tumor of the lip.

Figure 23–25 Photomicrograph of a well-defined mesenchymal neo-plasms, in this case a leiomyoma.

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Figure 23–27 A, Adenocarinoma of the minor salivary glands of thepalate, the most common site for oral salivary gland tumors. B, Retro-molar adenocarcinoma.

Aggressive proliferations

Certain mesenchymal proliferations are characterized byrapid growth and can reach large proportions; someactually invade adjacent soft and hard tissues despitetheir inability to metastasize. All are defined by theirmicroscopic appearance. These aggressive mesenchymaltumors often lie deep within the facial tissues, floor ofthe mouth, tongue, or neck, and are firm to palpation. Ifthere is any invasion of contiguous tissues, they are par-tially fixed, as assessed by palpation. Included in thisgroup are fibrous histiocytoma, aggressive juvenile fibro-matosis, hemangiopericytoma (some of which showmalignant behavior), and hemangioendothelioma. Openbiopsy or needle aspiration cytology are acceptable diag-nostic procedures. Wide excision is generally required.

Squamous cell carcinoma

Chapter 20 discusses oral malignant epithelial neo-plasms in detail. Late-stage tumors often present asindurated ulcerated masses, although some are non-ulcerated. Most squamous cell carcinomas are locatedin the tongue and lips and in the floor of the mouth (Fig-ure 23–26). For oral cancers in general, the more ante-rior the carcinoma is located in the mouth, the betterthe prognosis; the more posterior, the worse the prog-nosis. This may be attributable to delayed diagnosis(advanced stages), intrinsic cell proliferation differ-ences, or greater lymphatic drainage in those areas. Inci-sional biopsy is recommended for diagnosing thesetumefactive indurated lesions. Treatment planning iscomplex, with the more advanced-stage lesions requir-ing more aggressive treatment. Overall prognosis ispoor, with only about 50% surviving.

Salivary gland tumors

Chapter 26 discusses each of the histologic types of sali-vary gland tumors. Some types that are commonly foundin the major glands are rare or may never be found in theminor glands of the mouth, conversely, there are minorsalivary gland tumors that rarely arise in the majorglands. Intraoral minor gland tumors present as sub-mucosal masses and are as apt to be malignant as they areto be benign. The most common site is the palate, wherethe mass is off the midline, arising in the posterior aspectof the hard palate or at the hard–soft palate junction (Fig-ure 23–27). The buccal mucosa, upper lip, and ventraltongue are also common sites for these neoplasms. Thebenign tumors that occur in minor glands include thepleomorphic adenoma, monomorphic adenoma, andcanalicular adenoma, the latter arising almost exclusivelyin the upper lip, where it may be multifocal. Polymor-phous low-grade adenocarcinoma is a common malig-nant minor salivary gland tumor that almost never arisesin the major glands. Other adenocarcinomas arising inthe oral mucosa are mucoepidermoid carcinoma, adenoidcystic carcinoma, and adenocarcinoma not otherwisespecified. There are many other rare histologic types thatcan arise in either major or minor glands. Clinically, thebenign adenomas are typically smooth surfaced, nonul-

Figure 23–26 Squamous cell carcinoma of the lip.

A

B

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cerated nodules that are movable, unless located in thepalate, where the tumor is trapped between the palatalbone and mucosa. Malignant salivary gland tumors areindurated (low-grade mucoepidermoid carcinoma beingthe exception) and may show surface ulceration andtelangiectasia. Incisional biopsy is the diagnositic proce-dure of choice; fine-needle aspiration is also useful fordiagnosis. Primary treatment is surgical removal. Basedon the histologic type and surgical margins, postsurgicalradiation therapy can be used. Adenomatous hyperplasiais seen in the soft palate and floor of the mouth and rep-resents a benign nonneoplastic growth of normal salivarytissue (Figure 23–28).

Sarcomas and lymphomas

Malignant mesenchymal neoplasms are rarely encoun-tered in the oral soft tissues, being much more prevalentin the neck. Sarcomas can arise anywhere, and caseshave been reported in the tongue, buccal mucosa, andoral floor, being extremely rare in other locations (Fig-ure 23–29). Rhabdomyosarcoma, fibrosarcoma, andmalignant fibrous histiocytoma have been the more fre-quent sarcomas reported to arise in the oral cavity (Fig-ure 23–30). These malignancies account for less than5% of all oral cancers.

Whereas lymphomas are usually seen in the cervicallymph node chain, extranodal non-Hodgkin lym-phomas are encountered in the oral cavity. They are farmore common in the human immunodeficiency virus(HIV)-infected patient, where they tend to occur on thebuccal and palatal gingiva. The masses are firm, rapidlygrowing, often multinodular, and may show surfaceulceration. Microscopically they are usually high-gradelesions populated by monoclonal B lymphoblasts with adiffuse medium or large cell morphology. Patients withacquired immunodeficiency syndrome (AIDS) present-

ing with lymphoma generally succumb within 6 monthsof diagnosis. In the United States, HIV-associated lym-phomas account for approximately 25% of all lym-phomas reported each year (see Chapters 8 and 14).

Atypical lymphoproliferative lesions represent alymphoid infiltrative disease of the palate that invadesminor salivary tissue while leaving the extralobularducts relatively well preserved. These lesions appear asunilateral, soft, boggy, diffuse swellings at the hard–softpalate junction. Some are polyclonal B-cell lesions thatare probably reactive; others are monoclonal and likelyrepresent low-grade mucosa-associated lymphoid tissue(MALT) lymphomas. These lesions are responsive tolow-dose radiation therapy.

Clinical features of facial tumors and swellings

The swellings that are seen on the face can be clinicallydivided into two major types: those that are diffuse

Figure 23–28 Adenomatous hyperplasia of salivary glands in the lat-eral oral floor.

Figure 23–29 Rhabdomyosarcoma of the tongue is a massive, aggres-sive malignancy that is rare in the oral cavity.

Figure 23–30 Photomicrograph of a sarcoma showing a spindle celllesion (fibrosarcoma) with marked nuclear pleomorphism.

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Figure 23–32 Red nodular hemangioma (a nevus is also present as abrown macule).

and those that are focal nodules. As alluded to previ-ously, diffuse swellings are usually inflammatorylesions, such as edema, emphysema, space infection, orcellulites. Facial asymmetry also may be seen whenthere is an underlying central lesion of the maxillary ormandibular bone and, of course, such lesions are bonyhard. Radiographs are necessary diagnostic and evalu-ative tools.

Focal nodules of the face may be covered by normalskin or they may be verrucous, ulcerated, or pigmented.Most small facial nodules are sebaceous cysts, basal cellcarcinomas, nevi, and seborrheic keratoses, the lattertwo being pigmented. Less common are squamous can-cers, melanomas, and mesenchymal neoplasms.

Odontogenic infections

Buccal drainage from a periapical abscess can result in sig-nificant facial swelling, which may localize over themandible or, less frequently, below the zygoma. As theinfection progresses through the buccal plate, bacteria andthe host response to it result in purulent exudates. If thissuppurative process is confined to spaces bordered bymuscle and fascia, the diffuse swelling is soft or fluctuantand tender to palpation. Alternatively, if the infectiousprocess infiltrates into muscle and leukocytic infiltratesare interposed within the substance of the muscle itself,then the lesion becomes indurated, a process termed cel-lulitis. The clinical distinction between cellulitis and spaceinfection is germane to treatment, since the former cannotbe incised and drained, whereas the latter is amenable tosuch intervention. Of course, the incriminated tooth mustbe treated as well. Depending upon the status of the tooth,endodontic therapy or extraction must be performed, andantibiotic therapy is indicated in these examples of moreextensive spread of infection. In some instances, the

periosteum reacts to underlying odontogenic infection,giving rise to proliferative periostitis (Figure 23–31).

Soft-tissue emphysema

On rare occasion, air may be forcefully introducedbetween tissue planes. This may occur during maxillaryendodontic, periodontal, and oral surgery procedures inwhich compressed air is applied and separates the tissueplanes. The entrapped air causes a diffuse facial swellingthat is crepitant to palpation. A potentially lethal com-pliction is vascular air embolism, an event that usuallyoccurs shortly after the introduction of compressed airinto the tissues. Aspiration of the swollen area may beattempted with caution, making sure not to puncture amajor vessel in the process. Eventually, the trapped airis absorbed by the tissues.

Seborrheic keratosis

Sun exposure to the facial skin damages DNA and mayinduce proliferative responses in the surface epithelium.This exposure may result in the formation of seborrheickeratosis, a benign entity. This common lesion is usuallyseen on the forehead, temples, or malar regions of theface. The lesions are slightly tumefactive, brown incolor, and have an oily texture. They vary considerablyin size and are typically symmetrical, with smooth well-delineated borders. The differential diagnosis includesnevus and basal cell carcinoma. Most “seb Ks” can beremoved by shave biopsy or laser ablation.

Melanocytic lesions

The common nevi are discussed in more detail in Chap-ter 22 on pigmentations; not all nevi, however, are pig-

Figure 23–31 Cellulitis of the masseteric region from an abscessedmandibular molar.

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mented. They can occur anywhere on the facial skin andare present from early childhood, with no history of anychange or increase in size. In adults, they all representintradermal nevi. The pigmented nevi are symmetrical,round and nodular. The nonpigmented nevi simplyappear as nonproliferative nodules of normal skin col-oration. Treatment is deferred unless the patient wantsthem removed for esthetic reasons, or if they are near thehairline and become easily irritated. Should any long-standing nevus begin to increase in size, ulcerate, ordeepen in color, biopsy is recommended to rule out dys-plastic change in a preexisting nevus. Melanomas arealso discussed in Chapter 22.

Mesenchymal neoplasms

A variety of mesenchymal tumors can arise from the sub-cutaneous tissues of the facial skin. Hemangiomas appearred or purple when superficial (Figure 23–32), or theymay not be discolored when they are deep and intramus-cular (Figure 23–33). Neurilemomas, neurofibromas, andlipomas are relatively common connective-tissue tumorsthat appear as subcutanous masses (Figure 23–34).

Basal cell carcinoma

Basal cell carcinomas (BCC) are the most frequentlyoccurring malignancy in the United States, accountingfor more than one million new cases each year. Sunexposure is also a factor in the etiology of BCC, whichexplains why those with fair skin and less melanocyticprotection are more prone to the development of theseskin cancers. They may appear as pearly nodules withsurface telangiectasia, or they may present as nonheal-ing ulcers (Figure 23–35). The ulcerated basal cell carci-nomas usually develop rolled borders. It is common for

these skin cancers to be multifocal. They are more oftenseen on the upper face, helix of the ear, and scalp thanon the lower face and lips. Wide local excision isrequired for cure, and despite adequate surgery, somerecur, presumably owing to a field effect of dysplasticchange that many occur in many areas of the facial skin.Radiation therapy is also effective in controlling BCC.

Prognosis is good, since few BCCs metastasize. How-ever, they spread locally and insidiously, so if not diag-nosed and treated early, the treatment defect can be dis-figuring. Basal cell carcinoma does not arise in themucosal tissues of the mouth. Some interesting cases havebeen reported of BCC occurring in skin grafts that havebeen placed in the mouth for repair or closure purposes.

Variant benign tumors of skin appendages areknown as adnexal skin tumors. These lesions present as

Figure 23–33 Intramuscular hemangioma is not discolored.

Figure 23–34 Supraorbital subcutaneous lipoma.

Figure 23–35 Basal cell carcinoma of the facial skin.

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smooth-surfaced nodules, because the cells of origin liewithin the dermis. Most are benign and are treated bysimple excision.

Squamous cell carcinoma

Arising de novo or from preexisting actinic keratoses,squamous cancers of the facial skin have potential forboth regional node and distant metastases. The actinickeratoses are reddish-brown macules with a superficialscaley keratotic crust. They are typically found on theforehead, nose, cheeks, and lower lip. When carcino-matous change arises from these precancerous dys-plasias, the lesions become tumefactive, indurated, andulcerated (Figure 23–36). Ulcerated growths on the eye-lids, particular the lower lid, tend to arise from malig-nant transformation of the dermally situated sebaceousglands (sebaceous carcinoma). Regional nodes become

palpably enlarged when metastases evolve. Treatmentconsists of wide local excision and/or radiation therapy;management of the neck is contingent upon clinical orimaging findings of nodal disease. On the lips, squa-mous cell carcinoma is common, and BCC is rare (seeChapter 20).

Suggested reading

Desai P, Silver JG. Drug-induced gingival enlargements. J CanDent Assoc 1998;64:263–8.

Eversole LR, Rovin S. Diagnosis of gingival tumefactions. JPeriodontol 1973;44:429–35.

Katz AD, McAlpin C. Face and neck neurogenic neoplasms.Am J Surg 1993;166:421–3.

Manor Y, Merdinger O, Katz J, Taicher S. Unusual peripheralodontogenic tumors in the differential diagnosis of gingi-val swellings. J Clin Periodontol 1999;26:806–9.

Rees SR, Gibson J. Angioedema and swellings of the orofacialregion. Oral Dis 1997;3:39–42.

Rossiter JL, Hendrix RA, Tom LW, Potsic WP. Intramuscularhemangioma of the head and neck. Otolaryngol HeadNeck Surg 1993;108:18–26.

Som PM, Norton KI. Lesions that manifest as medial cheekand nasolabial fold masses. Radiology 1991;178:831–5.

Stewart CM, Watson RE, Eversole LR, et al. Oral granular celltumors: a clinicopathologic and immunocytochemicalstudy. Oral Surg Oral Med Oral Pathol 1988;65:427–35.

Tunkel DE, Baroody FM, Sherman ME. Fine-needle aspira-tion biopsy of cervicofacial masses in children. Arch Oto-laryngol Head Neck Surg 1995;121:533–6.

Van Dis ML. Swellings of the oral cavity. Dermatol Clin1996;14:355–70.

Figure 23–36 Squamous cell carcinoma.