Lichen Planus

Clinical

♦

This mucocutaneous disease is characterize d by bilateral, symmetrical white striations (striae of Wickham) superimposed upon an erythematous background. Most commonly this is seen in perimenopausal females on the buccal mucosa, tongue, or gingiva. In the erosive form, it presents as an erythematous lesion with faint peripheral striations

 

Microscopic

♦

A band-like infiltrate of lymphocytes obscuring the epithelial/connective tissue junction represents the seminal microscopic feature (Fig. 24.4). Spike-shaped rete ridges and dissolution of basal epithelial layer are also apparent

Fig. 24.4.

Band-like inflammatory infiltrates and spike-shaped rete ridges characterize lichen planus .

 

Immunofluorescence

♦

Should direct immunofluorescent testing be undertaken, granular deposition of fibrinogen is observed at the basement membrane level

 

Differential Diagnosis

♦

Lichenoid mucositis

• 
  
  Histologically this is similar to lichen planus but typically is not symmetrical. This may be due to a variety of stimuli – dental products, dental materials, and systemic medication

 

♦

Epithelial dysplasia with lichenoid inflammation

• 
  
  Epithelial alterations consistent with irreversible, precancerous change probably account for most cases of “malignant transformation” of lichen planus

 

Benign Mucous Membrane (Cicatricial) Pemphigoid

Clinical

♦

This immunologically mediated disease demonstrates generalized sloughing of epithelium leaving a bleeding erythematous base. The typical population is peri-/postmenopausal females. Often sloughing can be elicited with gauze or a gloved finger. Ocular and genital mucosal involvement may also be seen

 

Microscopic

♦

Subbasilar separation of the epithelium is characteristic of this condition (Fig. 24.5). A diffuse chronic inflammatory infiltrate of lymphocytes is seen with a smattering of neutrophils

Fig. 24.5.

Subbasilar separation of the epithelium with chronic inflammation.

 

Immunofluorescence

♦

Linear deposition of C3 and IgG along the basement membrane zone is seen in almost all cases in which direct immunofluorescence is performed

 

Differential Diagnosis

♦

Lichen planus

• 
  
  Can demonstrate separation but basal layer is lost. The lymphocytic infiltrate is typically more band-like

 

♦

Pemphigus vulgaris

• 
  
  Separation occurs above the basal layer, and Tzanck cells may be present

 

Pemphigus Vulgaris

Clinical

♦

Widespread sloughing and ulceration of mucosa are the typical manifestations. Young adult males and females are the commonly afflicted individuals. This can manifest primarily as gingival desquamation without cutaneous lesions

 

Microscopic

♦

Suprabasilar separation of the epithelium is seen, possibly with evidence of Tzanck cells. The inflammatory infiltrate is composed mostly of lymphocytes

 

Immunofluorescence

♦

Intraepithelial (desmosomal) deposition of C3 and IgG in a spider web pattern is characteristic of pemphigus when viewed with immunofluorescence (Fig. 24.6)

Fig. 24.6.

Direct immunofluorescence revealing IgG positivity in the desmosomal areas.

 

Differential Diagnosis

♦

Lichen planus, see above

 

♦

Cicatricial pemphigoid, see above

 

♦

Drug-induced pemphigus

• 
  
  Can be seen in particular with penicillamine

 

♦

Paraneoplastic pemphigus

• 
  
  Supra- and subbasilar splits are seen in patients with lymphoma and leukemia

 

Peripheral Ossifying Fibroma

Clinical

♦

This represents a reactive mesenchymal proliferation of periodontal ligament origin that retains the capacity to form bone or cementum-like product. Most commonly seen in the second to third decade, the peripheral ossifying fibroma demonstrates a female predilection. Occurring exclusively on the gingiva, it presents as a broad-based nodule that is typically ulcerated and asymptomatic

 

Microscopic

♦

The microscopic features include a cellular mesenchymal tissue with intermixed calcifications that can resemble bone or cementum (Fig. 24.7). It often extends to the base because of its origin in the periodontal ligament, resulting in recurrence

Fig. 24.7.

Peripheral ossifying fibroma is a gingival-based nodule exhibiting matrix (i.e., bone or cementum) production.

 

Peripheral Giant Cell Granuloma

Verruciform Xanthoma

Clinical

♦

This interesting entity represents a peculiar reactive proliferation of lipid-laden macrophages with a papillary surface configuration. Typically occurring on the gingiva or palatal mucosa in adults, it can appear red to yellow in coloration with a granular surface that may look like a volcano crater

 

Microscopic

♦

The histologic appearance is that of papillary proliferations of epithelium with brightly eosinophilic keratin beneath which the connective tissue papillae are filled with lipid-laden macrophages (Fig. 24.8). These cells will be confined to papillary lamina propria

Fig. 24.8.

The connective tissue papillae are filled with lipid-laden macrophages in verruciform xanthoma.

 

Traumatic Ulcerative Granuloma With Stromal Eosinophilia

Clinical

♦

This peculiar exuberant reactive process can mimic squamous cell carcinoma in its clinical presentation. Typically present on the dorsolateral tongue in adults, it manifests as an exophytic ulcerative mass usually of several weeks duration. This may be painful and persist even after multiple surgeries

 

Microscopic

♦

Surface ulceration is seen overlying a proliferation of inflamed granulation tissue with prominent, reactive endothelial cells (Fig. 24.9). Eosinophils and macrophages are prominent in the deeper aspects approximating and involving muscle

Fig. 24.9.

The ulcer bed in traumatic ulcerative granuloma with stromal eosinophilia can be extremely cellular and mistaken for a neoplastic process.

 

Differential Diagnosis

♦

Squamous cell carcinoma but only from a clinical perspective

 

♦

Lymphoma

• 
  
  Atypical lymphoid cells, clonal
  
  
• 
  
  Aside from NK/T-cell lymphomas , which may be polymorphous , most lymphomas are monomorphic infiltrates, contrasted to mixed infiltrate of traumatic ulcerative granuloma. Lymphoma will generally lack prominent eosinophils

 

Mucous Extravasation Phenomenon (Mucocele/Ranula)

Clinical

♦

This is a reactive lesion representing spillage of mucin into tissue due to duct damage. Typically young patients, first to second decade, represent the common population. Mucoceles occur most commonly in the lower lip, ranulae in the floor of mouth. The clinical appearance is that of a dome-shaped, fluid-filled lesion that may wax and wane with rupture. A “plunging ranula” presents as a central neck mass and may simulate thyroglossal duct cyst

 

Microscopic

♦

Pseudocystic accumulations of mucin surrounded by macrophages, a wall of compressed granulation tissue, and inflammation represent the salient diagnostic features (Fig. 24.10)

Fig. 24.10.

Disruption of salivary gland ducts results in mucin extravasation into connective tissue.

 

Necrotizing Sialometaplasia

Granular Cell Tumor

Clinical

♦

This is a benign , nonneoplastic proliferation of probable perineural sheath cells. Seventy percent occur on the tongue, primarily dorsum, as a deep mass with maintenance of surface architecture. These often represent long-standing processes

 

Microscopic

♦

Ill-defined collections of cells with granular cytoplasm, eccentric nuclei, and indistinct cytoplasmic boundaries constitute the primary histologic features (Fig. 24.11). Many cases have superimposed pseudoepitheliomatous hyperplasia, mimicking squamous cell carcinoma. Granular cell tumors tend not to recur, even with incomplete removal

Fig. 24.11.

Granular cell tumors are notorious for inducing pseudoepitheliomatous hyperplasia of the overlying epithelium.

 

Immunohistochemistry

♦

S100 protein+

 

Differential Diagnosis

♦

Squamous cell carcinoma

• 
  
  Lacks the subepithelial granular cells that accompany pseudoepitheliomatous hyperplasia. Rare on the dorsum of the tongue where granular cell tumor is common

 

Congenital Gingival Granular Cell Tumor (Congenital Epulis)

“Leukoplakia”

Epithelial Dysplasia/Carcinoma In Situ

Clinical

♦

As with other sites , the oral epithelium tends to demonstrate precursor lesions prior to frank invasion. Most classifications grade epithelial dysplasia to carcinoma in situ dependent upon the degree and thickness of epithelial involvement. This may present as a white patch, red patch (erythroplakia), or ulcer. Typically epithelial dysplasia/carcinoma in situ is seen in patients over 40 who are also smokers and drinkers. Females now represent approximately 50% of cases. Ventrolateral tongue, floor of mouth, and soft palate complex represent high-risk sites for these squamous cell carcinoma precursors

 

Microscopic

♦

The histologic features include nuclear enlargement, hyperchromatism, pleomorphism, loss of polarity, and architectural changes (i.e., formation of bulbous rete ridges ) (Fig. 24.12)

Fig. 24.12.

The most apparent atypical changes of severely dysplastic epithelium in the oral cavity may be limited to lower aspect of the epithelium.

 

♦

WHO classification of oral dysplasia:

• 
  
  Mild – lower one-third abnormalities
  
  
• 
  
  Moderate – lower one-half abnormalities
  
  
• 
  
  Severe – lower two-thirds abnormalities
  
  
• 
  
  Carcinoma in situ – full-thickness abnormalities

 

♦

The grade of dysplasia does correlate with risk of squamous cell carcinoma (i.e., the higher the grade, the greater the risk). It is generally considered that moderate dysplasia and higher represents high-grade dysplasia and should be reported as such. Reproducibility of grading oral dysplasia (both intra- and interobserver) is generally poor

 

Proliferative Verrucous Leukoplakia

Squamous Cell Carcinoma

Verrucous Carcinoma

Clinical

♦

This represents a low-grade, well-differentiated variant of squamous cell carcinoma. Usually seen over the age of 60, it is more commonly seen in smokeless tobacco users than smokers. Characterized by a large (>4 cm) papillary mass with a broad base, verrucous carcinoma is often snow white due to hyperkeratosis. Generally, it is seen on tongue, alveolar mucosa, and buccal mucosa and is often of long-standing duration. As it is usually nonmetastazing, neck dissection is not indicated

 

Microscopic

♦

Verrucous carcinoma varies from standard squamous cell carcinoma by exhibiting broad papillations of squamous epithelium exhibiting minimal atypia with deeply invaginated folds of parakeratin (“parakeratin plugging”) (Fig. 24.13). If cytologic atypia is present, the diagnosis of “verrucous”-type carcinoma should be doubted as it probably represents a papillary keratinizing well-differentiated squamous cell carcinoma. This malignancy has an excellent prognosis with a 95% 5-year survival rate

Fig. 24.13.

Verrucous carcinoma is a broad-based, hyperkeratotic tumor that infiltrates in a “pushing” fashion.

 

Differential Diagnosis

♦

Papillomas

• 
  
  Typically smaller, well-confined lesions with a pedunculated base

 

Sarcomatoid (Spindle Cell) Carcinoma

Clinical

♦

This represents a poorly differentiated variant of squamous cell carcinoma. Usually, sarcomatoid carcinoma manifests after age of 40 and can occur in a history of radiation or burns, particularly electrical. Usually, it occurs as a polypoid, ulcerated mass on posterior tongue or in oropharynx

 

Microscopic

♦

The microscopic appearance is that of an exuberant proliferation of anaplastic spindle-shaped cells that appear to “drop off” from atypical surface epithelium (Fig. 24.14)

Fig. 24.14.

Spindle cell carcinoma , surrounding a focus of malignant basaloid cells, simulates sarcoma.

 

Immunohistochemistry

♦

Cytokeratin 5/6+, vimentin+, p63+

 

Differential Diagnosis

♦

Spindle cell sarcomas

• 
  
  Cytokeratin−
  
  
• 
  
  Most superficial spindle cell malignancies in the oral cavity are carcinomas

 

Nonkeratinizing Papillary Squamous Cell Carcinoma

Clinical

♦

A relatively recent addition to the literature , this represents an exophytic variant of squamous cell carcinoma that is highly associated with HPV types 16 and 18. There is a predilection for oropharynx (tonsil, base of tongue) and hypopharynx. The prognosis is generally more favorable and probably relates to depth of stromal invasion more than size of exophytic component

 

Microscopic

♦

A branching papillary architecture is seen (Fig. 24.15). Brisk mitotic activity and notable cytologic atypia are commonly present with limited to no keratin production

Fig. 24.15.

Papillary squamous cell carcinoma has a predilection for the oropharynx, including the tonsil, and is associated with human papillomavirus.

 

Differential Diagnosis

♦

Squamous papilloma

• 
  
  Lacks the cytologic atypia and architectural complexity of papillary squamous cell carcinomas

 

Malignant Melanoma

Adenomatoid Hyperplasia

Amalgam Tattoo

Aphthous Stomatitis

Dermoid Cyst

Geographic Tongue (Erythema Migrans)

♦

An inflammatory condition of the tongue primarily characterized by superficial microabscesses, this may be associated with psoriasis in the minority of cases (Fig. 24.16)

Fig. 24.16.

Subcorneal abscess formation is prominent in geographic tongue.

 

Lingual Thyroid

Lymphoepithelial Cyst

Melanoacanthoma

Nicotine Stomatitis

Oral Focal Mucinosis

Palisaded, Encapsulated (Solitary, Circumscribed) Neuroma

♦

A discrete nodule usually less than 1 cm seen most frequently on lip vermilion and hard palate, the palisaded, encapsulated neuroma is characterized by well-demarcated proliferation of Schwann cells with faint palisaded arrangements and has axons present (Fig. 24.17)

Fig. 24.17.

Palisaded encapsulated neuroma is a circumscribed neural lesion and, thus, may be mistaken for schwannoma. Inset: Axonal proliferation distinguishes neuroma from nerve sheath tumor.

 

Salivary Duct Cyst

Smokeless Tobacco-Induced Keratosis

♦

This represents a somewhat unique lesion occurring as a corrugated white patch seen in the location of placement of tobacco that demonstrates superficial epithelial necrosis and an amorphous hyalinized material histologically (Fig. 24.18)

Fig. 24.18.

Smokeless tobacco-induced keratosis is notable for acellular, subepithelial hyalinization.

 

Nonodontogenic Cysts/Pseudocysts

Odontogenic Cysts

Dentigerous Cyst

Clinical

♦

This represents a developmental odontogenic cyst occurring around the crown of impacted tooth. It occurs most commonly in mandibular third molar region. The lining of this cyst can give rise to ameloblastoma, squamous cell carcinoma, or intraosseous mucoepidermoid carcinoma

 

Radiograph

♦

The radiographic presentation is that of a unilocular radiolucency around the crown of an impacted tooth

 

Microscopic

♦

Histologically, a bilayer of cuboidal cells or stratified squamous lining with myxomatous connective tissue containing small islands of odontogenic epithelium is seen (Fig. 24.19)

Fig. 24.19.

A bland lining of squamous cells with a loose connective tissue wall constitute the diagnostic features of a dentigerous cyst.

 

Odontogenic Keratocyst (Keratocystic Odontogenic Tumor)

Clinical

♦

This entity represents a peculiar keratinized odontogenic cyst arising from prefunctional dental lamina. The WHO currently classifies this as an odontogenic tumor rather than a cyst due to mutational characteristics. It is most common in the second to third decades and the posterior mandible. It can occur as multiple lesions, perhaps forming “daughter” cysts, making complete removal more difficult. This may be the feature that contributes to a 30% recurrence rate

 

♦

It is associated with the nevoid basal cell carcinoma syndrome (Gorlin–Goltz syndrome) that possesses the following characteristics:

• 
  
  Autosomal dominant, defect in ptch gene (chromosome 9)
  
  
• 
  
  Multiple basal cell carcinomas on non-or minimally sun-exposed skin
  
  
• 
  
  Palmar and plantar pits
  
  
• 
  
  Skeletal anomalies – bifid ribs, brachymetacarpalism, kyphoscoliosis, and calcified falx cerebri
  
  
• 
  
  Other tumors including medulloblastoma

 

Radiograph

♦

The common radiographic pattern is that of a multilocular radiolucency with possible expansion although it may be unilocular. The odontogenic keratocyst tends to demonstrate linear growth pattern within the jaw

 

Microscopic

♦

The odontogenic keratocyst demonstrates squamous epithelium with a luminal layer of corrugated parakeratin (Fig. 24.20). A uniform thickness of six to eight cell layers is apparent with a prominent basal layer with palisading nuclei

Fig. 24.20.

Odontogenic keratocysts are cytologically bland, locally aggressive cystic lesions.

 

Differential Diagnosis

♦

Keratinizing odontogenic cyst

• 
  
  This cyst demonstrates a luminal layer of orthokeratin, an indistinct basal layer and no association with the nevoid basal cell carcinoma syndrome

 

Calcifying Odontogenic Cyst (Gorlin Cyst)

Clinical

♦

This developmental odontogenic cyst may demonstrate questionable neoplastic potential. It is seen in the second to third decades and the anterior aspects of the jaws. It may also occur in an extraosseous fashion on the gingiva. It has a low recurrence rate of 10% and may be associated with ameloblastomas

 

Radiograph

♦

The Gorlin cyst appears as a unilocular or multilocular expansile radiolucency with intermixed calcifications and may be associated with an odontoma

 

Microscopic

♦

A lining of odontogenic epithelium is seen with a basal layer of columnar cells with palisading nuclei. Prominent in this epithelium is the presence of “ghost” cells, squamous cells with abundant cytoplasm and central voids lacking nuclei (Fig. 24.21). Variable amounts of odontogenic product, “dentinoid,” may also be present

Fig. 24.21.

“Ghost” cells, prematurely keratinizing epithelial cells without nuclei, are the hallmark of the calcifying odontogenic cyst .

 

Reactive/Nonneoplastic Disease

“Giant Cell” and Giant Cell-Rich Lesions

Central Giant Cell Granuloma

Clinical

♦

This represents a central lesion seen most commonly in females in the early second decade. It demonstrates a propensity to occur in the anterior mandible crossing the midline. Its etiology is unknown, and it exhibits a recurrence rate of 15%. Peripheral variant is seen most commonly on the mandibular gingiva or alveolar mucosa as a purplish, exophytic mass

 

Radiograph

♦

Typically, this occurs as a multilocular radiolucency although it can be unilocular. Expansion, tooth movement, and resorption are all possible sequelae

 

Microscopic

♦

Microscopically, the giant cell granuloma is characterized by a cellular spindle cell framework with clusters of multinucleated giant cells (osteoclasts), extravasated erythrocytes, and hemosiderin

 

Differential Diagnosis

♦

Giant cell lesions of the jaws constitute an area of confusion

• 
  
  Much has been written as to whether giant cell granulomas, giant cell tumors, and aneurysmal bone cysts represent the same lesion, entities on a continuum, or separate and distinct conditions

 

♦

The brown tumor of hyperparathyroidism is indistinguishable from the central giant cell granuloma , and, accordingly, this systemic disease must be excluded (Fig. 24.22)

Fig. 24.22.

Osteitis fibrosa cystica (“brown tumor”) results from hyperparathyroidism and is histologically indistinguishable from giant cell reparative granuloma. Inset: Reactive osteoid may be prominent.

 

Benign Neoplasms

Ameloblastoma

Clinical

♦

This is the most common epithelial odontogenic neoplasm, recapitulating the enamel organ. Ameloblastoma occurs most commonly in the third to fifth decades of life and presents as painless expansion usually in the posterior mandible. Typically aggressive, the ameloblastoma demonstrates up to a 90% recurrence rate with curettage and a 15–20% recurrence rate with resection. Rare examples of metastasis have been reported (malignant ameloblastoma). Peripheral variant represents an ameloblastoma occurring in an extraosseous location (Fig. 24.23)

Fig. 24.23.

Peripheral ameloblastoma resembles its intraosseous counterpart. Note overlying mucosa.

 

Radiograph

♦

Either an expansile unilocular or multilocular (soap bubble) radiolucency is the classic radiographic presentation. Perforation of the cortical plate is often seen

 

Microscopic

♦

Two histologic variants are typically seen. The unicystic ameloblastoma demonstrates cystic areas with luminal proliferation of the plexiform pattern of ameloblastoma. The conventional ameloblastoma may exhibit a variety of patterns including follicular, plexiform, acanthomatous, granular cell, basal cell, and desmoplastic (Fig. 24.24). Both are typically characterized by a peripheral layer of columnar cells with reverse polarization and nuclear palisading. Central zones of stellate cells with exaggerated intercellular spacing are seen in more solid areas although the conventional ameloblastoma can be predominantly cystic

Fig. 24.24.

Ameloblastoma may show prominent cystic change . Peripheral cells exhibit nuclear palisading with reverse polarization; the latter is not conspicuous in this example.

 

Squamous Odontogenic Tumor

Clinical

♦

This, too, is a benign epithelial odontogenic neoplasm that can mimic squamous cell carcinoma at the histologic level. Present in the third to fourth decades, it occurs in the posterior jaws as an expansile mass. Treated appropriately, it rarely recurs

 

Radiograph

♦

The characteristic appearance is that of a semilunar radiolucency arising in alveolar bone

 

Microscopic

♦

Islands of squamous epithelial cells without a prominent basal layer are the histologic signature. Although worrisome, no atypia, mitotic figures, or central keratinization is seen (Fig. 24.25). The islands may demonstrate central cystic degeneration

Fig. 24.25.

Squamous odontogenic tumors demonstrate islands of squamous epithelium without atypical features or mitoses.

 

Differential Diagnosis

♦

Squamous cell carcinoma

• 
  
  Should demonstrate pleomorphism, mitoses, and keratinization, all of which are lacking in squamous odontogenic tumor

 

♦

Ameloblastoma, acanthomatous type

• 
  
  Prominent palisading arrangement of basal cell layer is the distinguishing characteristic

 

Ameloblastic Fibroma

Clinical

♦

This represents a mixed odontogenic tumor with coexistent epithelial and mesenchymal components. It occurs in the first and second decades, with the majority in the posterior mandible impeding the eruption of the permanent first molar. Even with appropriate surgery, a 10–20% recurrence rate is seen

 

Radiograph

♦

Radiographically, a unilocular or multilocular radiolucency associated with an impacted tooth is the typical presentation

 

Microscopic

♦

A bilayer of odontogenic epithelium embedded within cellular myxomatous mesenchymal tissue constitutes the diagnostic features (Fig. 24.26)

Fig. 24.26.

Bilayers of ameloblastic cells embedded in a myxomatous mesenchymal framework characterize ameloblastic fibroma.

 

Malignant Neoplasms

Ameloblastic Carcinoma

Clinical

♦

This is an odontogenic epithelial malignancy with ameloblastic differentiation. It occurs most commonly in the fourth decade with a mandibular predilection. It metastasizes preferentially to the lungs and demonstrates a <50% 5-year survival rate

 

Radiograph

♦

It manifests as an ill-defined, lytic lesion with a variable growth rate

 

Microscopic

♦

The microscopic appearance is that of an epithelial proliferation with peripheral cells demonstrating columnar morphology with reverse polarization (Fig. 24.27). Prominent pleomorphism and mitotic activity are usually seen

Fig. 24.27.

Cellular pleomorphism , as seen here, distinguishes ameloblastic carcinoma from ameloblastoma.

 

Metastatic Disease

Clinical

♦

Carcinomas of the breast, lung, prostate, and renal origin represent the most common metastases to the jaws. Fully one-third of patients are unaware of primary tumor at time of diagnosis. These often present with pain and/or paresthesia

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