Ulcers and Vesicles2

8/2/2019 Ulcers and Vesicles2

http://slidepdf.com/reader/full/ulcers-and-vesicles2 1/24

Ulcers and Vesicles

Ulcers are lesions of skin or mucosa in which the entire layer of epithelium is necrotic, missing or abraded

away. Most are painful. The lesion is generally gray centrally with an erythematous halo. While some ulcers

originate as vesicles or bullae, others begin initially as ulcers, never having passed through a vesiculobullous

stage. The configuration of the ulcer is highly germane to the diagnosis. Three configurations most often seen

are:

round or oval, shallow and symmetrical,

irregularly marginated, and

deep with rolled margins.

Additionally, these ulcers may occur as solitary lesions or in multiples. Although not foolproof, the following

table lists the most likely diagnoses for various ulcerative lesions:

Table 1 - Configuration of Ulcers

Round Shallow

Multiple

Herpes,

Varicella-Zoster,

Coxsackievirus,

Aphthous Ulcers

Focal

Aphthous Ulcer,Denture Ulcer

Irregular Shallow

Multiple

Agranulocytosis

Focal

TraumaticFocal

Deep, Rolled Margins

Squamous Cancer,

Granulomatous Infection,

Necrotizing Sialometaplasia

Most of the lesions listed above can be diagnosed on the basis of clinical features alone or with the aid of

laboratory studies that include culture, CBC or specific antibody titers. The viral ulcers all begin as vesicles



and are generally accompanied by fever. Each viral disease is diagnosed on the basis of lesion distribution.

Primary herpetic gingivostomatitis is characterized by fever, malaise, oral pain, gingival erythema with

ulceration and movable mucosal vesicles that pop to become ulcers and lymphadenopathy of cervical nodes.

The labial, buccal and sublingual mucous membranes are usually involved (Figure 1). Herpes labialis affects

either the upper or lower lips or sometimes both (Figure 2). The lesions represent recurrences from

awakening of trigeminal ganglion latent herpes virus infections. Classically, the lesions evolve as vesicles

with a tendency for clustering into groups that ulcerate, coalesce and after four to five days become crusted.

After 12 days, healing occurs and the virus is inactivated immunologically, only to recur at a future date. The

chief stimuli that reactivate the latent virus include intense sun exposure to the lips, emotional anxiety

episodes and trauma from stretching the lips. Recurrent intraoral herpes of the palatal gingiva is typified by

clusters of ulcers; a history of antecedent vesicles may be obtained from the patient (Figure 3). A history of

recurrent episodes is usually gleaned. Herpes infections are treated with acyclovir, analgesics and palliative

anesthetic mouth rinses.

Figure 1: Primary Herpetic Gingivo Stomatitis

Figure 2 Recurrent herpes Labialis

Figure 3 Recurrent intraoral herpes

In contrast to herpes simplex induced ulcers,

coxsackievirus ulcers do not regularly recur; unlike

herpes group viruses, coxsackies are not latent

within host neurons. In hand, foot and mouth

disease, ulcers are present anywhere in the mouth;

however, unlike primary herpes, the gingiva is

rarely or minimally affected. Characteristically,

intact vesicles are identifiable on the hands and feet.

The trunk is not involved. In another coxsackie

infection known as herpangina, the lesions are

limited to the oropharynx and soft palate. Other enteric viruses and coxsackies can cause mucosal ulcers that

resemble aphthae; yet unlike aphthae, the patients are febrile and suffer malaise. Coxsackie-induced ulcers are

widespread without a tendency for focal clustering. There are no antivirals available for coxsackievirus

infections. Anesthetic mouth rinses and analgesics can be prescribed as needed.

QuickTimeª and adecompressor

are needed to see this picture.







Recurrent aphthous stomatitis (RAS) is often mistaken for a herpes infection and many practitioners are

under the mistaken impression that the common canker sore is indeed a herpes virus induced lesion. In fact,

the etiology of RAS remains enigmatic. Immunologic mechanisms underlie the pathogenesis; however, the

instigating antigen that triggers the response remains unknown. Patients prone to develop RAS are usually

young and the lesions recur from monthly to once or twice

annually. The lesions never go through a vesicular stage. They

ulcerate from their inception and are found on loose movable

mucosa, with gingival or palatal involvement being very rare

(Figure 4). Patients with one to three ulcers can be treated with

silver nitrate impregnated sticks, electrocautery or laser therapy.

Multiple lesions are managed with tetracycline oral rinses and

palliative mouth rinses.

Figure 4 Recurrent Aphtous Stomatitis

Focal shallow ulcers may also represent aphthae, although trauma from a rubbing denture flange or even

cheek or lip biting can produce a shallow ulcer. Traumatic ulcers will heal in 10 days when the irritant iseliminated. When a suspected traumatic ulcer does not resolve after removal of an irritant, biopsy should be

performed to rule out cancer or a specific inflammatory lesion.

While most traumatic ulcers are oval, some show an irregular outline. When irregularly marginated

ulcers are observed and there is no history of a traumatic episode, agranulocytosis may be suspected.

Agranulocytic ulcers are often large and may be multifocal. When located on the alveolar ridge or gingiva,

sequestration of the bone underlying the ulcer may occur. Agranulocytosis may be idiopathic; yet, in most

instances of oral ulcers secondary to decreased neutrophils, the ulcers are encountered by patients taking

anticancer chemotherapeutic agents. Indeed, the occurrence of oral ulcers in a patient undergoingchemotherapy is a sign of dangerous drug toxicity that may quickly predispose to secondary infection or

death. When oral ulcers are encountered, consultation with the patient's treating physician should be

undertaken immediately.

Focal deep ulcers with rolled margins are indicative of cancer or granulomatous inflammation from

mycobacteria or deep invasive fungi. A single large ulcer in the soft palate could represent a salivary tumor,

yet may also be a manifestation of minor salivary gland necrosis, a lesion often mistaken for cancer both

clinically and microscopically and referred to as necrotizing sialometaplasia. All deep ulcers with rolled

borders should be biopsied to reach a definitive diagnosis.

Bullous/Erosive Lesions

Mucosal lesions that evolve through desquamation of all or a portion of the surface epithelium are

immunologic diseases that lead to erosions and bulla formation. In reality, intact bullae are rarely seen in the

mouth, because blisters are easily broken, leaving broad areas of desquamation or erosion. Both humoral

(immunoglobulin) and T-cell mediated immune mechanisms underlie these processes. Histopathologic

diagnosis is augmented by immunofluorescence studies; therefore, biopsy should include the procurement of





a formalin fixed specimen, as well as an unfixed sample to be placed in immunofluorescence transport media

to allow frozen sections and immunostaining. Four more common bullous/erosive oral diseases can be

grouped according to clinical features and site predilection (Table 2):

Table 2 - Common bullous/erosive lesions

Buccal mucosa with associated white stria

erosive lichen planus

Gingival and ocular erosions

mucous membrane pemphigoid

Soft palate erosions

pemphigus vulgaris

Hemorrhagic lesions of the lips

erythema multiforme

The most frequently encountered oral erosive/desquamative disease is erosive lichen planus. In the erosive

form of the disease, mucosal burning pain or a feeling of rawness is the chief complaint. Cutaneous lesions, if

present, are usually located on the forearms and ankles as pruritic, scaly keratotic plaques overlying a

violacious base. The oral lesions are red and ulcerated (Figure 5). They are usually localized to the buccalmucosa and mandibular vestibule, although other sites, particularly the gingiva, may be involved. White lacy

foci usually accompany the red and erosive lesions, being "Stria of Wickham". The disease has no known

etiology in the majority of cases; however, in some patients, medications cause the disease, which is then

referred to as a lichenoid drug eruption. The chief drugs include antimalarials, antihypertensives and gold

salts. Lichen planus-like lesions are sometimes associated with cinnamon and outdated corroding dental

amalgams that are in direct contact with the lesions. Most cases, however, are idiopathic and patients tend to

have lesions throughout their lives. The severity of symptoms is often accentuated by stress and anxiety.

Biopsy should be performed to confirm the diagnosis and immunofluorescence studies disclose the presence

of fibrinogen along the basement membrane. Topical steroids are the treatment of choice, reserving short-term

systemic steroids for more severe episodes.

Figure 5 Erosive lichen planus

After lichen planus, mucous membrane pemphigoid is the second

most common oral bullous/desquamative disease.

Postmenopausal - f-females are predilected 5:1 to males and





the lesions always affect the attached gingiva (Figure 6). Extragingival lesions occur anywhere in the mouth,

yet are not seen in the absence of gingival desquamation. About 10% of patients will manifest conjunctival

lesions (ocular, cicatricial pemphigoid). Skin lesions are not observed, except in one variant in which patients

may have bullae of the face and scalp. Immunofluorescent staining shows deposition of complement and

immunoglobulins along the basement membrane. Topical steroids occluded with a soft acrylic splint that

extends over the attached gingiva offers the best method of control. The disease persists for many years and

the etiology is unknown.

Figure 6: Mucous Membrane Pemphigoid

While pemphigus vulgaris is potentially a fatal

autoimmune disease, it is quite rare. Oral lesions may

precede skin bullae by up to six months and the oral

lesions may be the first sign of the disease. Once skin

involvement occurs, there is a potential for septicemia

and fluid/electrolyte imbalance, both of which maycause death. Oral lesions are extremely painful and

may occur anywhere, although the soft palate is the

most common. Biopsy is required for definitive diagnosis and immunofluorescent staining shows pericellular

staining with complement and immunoglobulins, yielding a fishnet appearance. Systemic steroids are usually

required to contain this incurable, yet controllable disease.

Of all the oral bullous/desquamative diseases, only erythema multiforme (EM) has an identifiable etiology.

The disease may affect skin, oral, ocular and genital mucosa as a result of allergy to sulfa drugs. Antibiotic

sulfas and hypoglycemic sulfonylurea compounds are the chief precipitators. In allergic patients, lesions develop in one to two

days. On the skin they may appear as bull's eye target lesions with a

red center surrounded by a pale halo with an outer erythematous

ring or they may be bullous. Oral lesions classically involve the lips

as hemorrhagic ulcers and bullae, while intraoral lesions of a similar

nature occur as well (Figure 7). When oral, ocular, genital and skin

lesions occur together, the disease is referred to as erythema

multiforme major, or Steven's-Johnson syndrome. The histology is

nonspecific; importantly, immunostaining discloses the presence of perivascular immune complexes with

complement fixation. Some cases are recurrent and are associated with the formation of immune complexes to

herpes virus. In these instances, the EM outbreak is preceded by either recurrent orolabial or genital herpes

lesions. Sulfa-associated EM can be managed by withdrawal of the drug and prescription of systemic

prednisone. Postherpetic EM can be prevented by prescribing daily acyclovir.

Figure 7 Erythema multiform

The decision to prescribe topical versus systemic steroids for oral erosive diseases is generally based upon the







extent and severity of disease. Severe erosions with extensive lesions and significant pain usually warrant a

seven to 10 day course of prednisone or Medrol. Less severe disease or maintenance therapy is usually

managed with topical fluocinonide or clobetasol gels applied to lesional areas four to six times daily for seven

days and then retreated as needed.

Erythematous Lesions

Erythema of the mucous membranes connotes an inflammatory reaction. Red lesions of the oral cavity may

therefore represent infections, irritations or allergic reactions. Early carcinomatous transformation may appear

red because the precancerous changes are accompanied by an inflammatory response in the underlying

connective tissue. Location and configuration are of utmost consideration in the differential diagnosis of red

mucosal lesions. In this context, red lesions are grouped as follows (Table 3):

Table 3 - Red Lesions

Diffuse hard palate

Erythematous (atrophic) candidiasis

Multifocal circinate, tongue, buccal mucosa/lips

Benign migratory glossitis,

Erythema migrans

Focal velvety patch, soft palate, oral floor, ventral tongue

Erythroplakia,

Chemical injury mucositis

Multifocal velvety patches

Erythematous candidiasis,

Multiple erythroplakias,

Allergic stomatitis

Perhaps the most common oral red lesion is erythematous candidiasis. In HIV infected patients the lesions can

occur anywhere in the mouth. The most common form is localized to the hard palate in patients with old, ill-

fitting dentures (Figure 8). The diagnosis can often, yet not always, be confirmed with a smear positive for

mycelia using a PAS stain. Even when a smear is negative, topical nystatin treatment should be undertaken

along with a soft reline. Once the erythema has resolved, a permanent reline, rebase or new denture can be

fabricated. The fiery red appearance has been attributed to an allergic reaction to candida antigens and the

organisms may actually accumulate within the pores of denture acrylic.



Figure 8 Erythematous Candidiasis

Red lesions with a circinate (C-shaped) pattern

with a white rim and a history of resolution

followed by recurrence at another site are benign

lesions of unknown etiology. Benign migratory

glossitis or geographic tongue affects the dorsal

tongue and occasionally the lateral and ventral

tongue (Figure 9). The filiform papillae are shed,

leaving a bald red focus with reddened fungiform

papillae. Pain is uncommon. The extraglossal counterpart is erythema migrans or erythema areata

migrans. No treatment is needed and the diagnosis is usually made clinically.

Figure 9 Benign Migratory Glossitis

A focal red lesion of oral mucosa with no history of migration and no

identifiable etiology should arouse suspicion of precancer, particularly

among tobacco users. Such lesions are common on the soft palate and

floor of the mouth, being termed erythroplakias. Erythroplakic lesions

may also have a white keratotic component that gives them the

appellation speckled erythroplakias or speckled leukoplakias (Figure

10). Red plaques have a high probability of harboring premalignant

cells (dysplasia, carcinoma-in-situ, early invasive squamous cellcarcinoma). Hence, all require immediate biopsy.

Figure 10 Erythroplakia with ulcerations

Multifocal erythematous lesions are seen in the

aforementioned bullous erosive diseases,

candidiasis and multifocal field cancerization.

Clinical diagnosis is impossible, necessitating

biopsy.

White Lesions - 1









White mucosal lesions are due to increased thickness of the epithelium (hyperorthokeratosis,

hyperparakeratosis, acanthosis), the presence of ulceration with a gray-white pseudomembrane or surface

mycelia from a candida infection. Clinically, white lesions may be categorized as follows (Table 4):

Table 4 - White Lesions

Flat smooth corrugated or verrucous plaques

Leukoplakias

Lace-like or striated

Lichen planus,

Lupusery thematosus,

Hairy leukoplakia

Oval shallow with a red halo

Various ulcerative diseases (see section above)

Diffuse widespread, buccal mucosa

Genokeratoses

Curdled milk-like plaques that may be rubbed away

Candidiasis

Idiopathic leukoplakias are white lesions of oral mucosa that do not rub away, have no readily apparent

etiologic factors other than tobacco use and do not correspond to a specific disease characterized by a white

appearance (Figure 11a, b). Often, white patches occur in the buccal mucosa in cheek chewers or under the

flange of ill-fitting dentures (Figure 12). Some oral pathologists classify such lesions as leukoplakias. They

simply represent a callous from irritation and here are referred to as frictional keratoses, because all are

characterized by a benign thickening of the keratin layer. Frictional keratoses are not known to progress to

cancer, while idiopathic leukoplakias have the potential for malignant transformation. An idiopathic keratosis

has a 20% chance of harboring premalignant cell changes and those in the floor of the mouth harbor a 40%

chance for such changes. Thus, all idiopathic leukoplakias warrant biopsy. The progression from benign

hyperpara or hyperorthokeratosis to cancer usually progresses through well defined stages (Table 5):

Table 5 - Stages from hyperkeratosis to cancer

Hyperkeratosis



No cytologic atypia on biopsy

Mild dysplasia

Atypical cells confined to basal layer

Moderate dysplasia

Atypical cells in lower half of epithelium

Severe dysplasia

Atypical cells in most of epithelium

Carcinoma-in-situ

Atypical cells in all layers of epithelium

Carcinoma

Invasion of connective tissue

Figure 11a leukoplakia Figure 11b leukoplakia



Figure 12 Denture Keratons

Most, yet not all, idiopathic leukoplakias are associated with







tobacco use. Malignant transformation in leukoplakia occurs more often with smoking rather than smokeless

tobacco (i.e.: snuff, chewing tobacco). Some of these white lesions have a corrugated, rough or granular

surface and tend to occur in older females; tobacco use is frequently not a factor (Figure 13). Such lesions

have specific verrucous features histologically and are referred to as proliferative verrucous leukoplakia

(PVL). This disease is problematical because surgical excision is usually not effective and recurrences are

common. Many cases eventually progress to squamous cell carcinoma or variant forms, with an exophytic

papillary appearance (verrucous carcinoma, papillary variant of squamous cancer). Laser surgery has become

a preferred method of treating these lesions and their recurrences.

Figure 13 Proliferative Verrulous Leukoplakia



White Lesions - 2

Lichen planus, lupus erythematosus and hairy leukoplakia are white lesions of oral mucosa that show a lacy

pattern or a fringe-like periphery. Lichen planus has already been discussed with erosive lesions. The

nonerosive form is characterized by asymptomatic white lesions most often located in the buccal mucosa and

vestibule bilaterally (Figure 14). The lacy pattern is characteristic and referred to as "Stria of Wickham". This

asymptomatic form is also known as the reticular form of lichen planus and requires no treatment. Many

reticular forms may progress to the painful erosive variant.

Figure 14 Lichen Planus

Lupus erythematosus is an autoimmune disease of skin and

internal organs, affecting primarily young women. When

oral lesions are present, they may mimic lichen planus.

Usually, the histology is suggestive; yet,

immunofluorescence is often helpful. Furthermore,

serologic tests for antinuclear antibodies (ANA) and anti-

DNA antibodies support the diagnosis. If such a diagnosis is

rendered, referral to an internist is recommended because





the oral lesions are only a manifestation of a more widespread, often serious disease.

Hairy leukoplakia occurs in HIV seropositive patients, although a few cases have been reported in patients

with other immunocompromised states. White lesions occur on the lateral tongue with vertically oriented stria

resembling "sage" hairs. Biopsy shows a benign parakeratosis and the diagnosis is confirmed by special stains

(DNA in situ hybridization) for the causative agent--Epstein Barr virus or Western blot for HIV positivity.

The lesions are asymptomatic and usually do not require any treatment, although they recede with acyclovir

therapy. This unusual form of leukoplakia serves as a precedent marker for AIDS.

White sponge nevus is an inherited genokeratosis that is a dominant trait, meaning that many family members

may be affected. The lesions are characteristically diffuse and bilateral, involving the entire buccal mucosa

(Figure 15). The lateral and ventral tongue may also be affected. The buccal mucosal lesions are thick and

show curtain-like folds. Histologically, the diagnosis is not always readily made and therefore the clinical

findings are important to secure a definitive diagnosis. Once the diagnosis is made, no treatment is necessary

because the lesions are asymptomatic and do not progress to carcinoma. Leukoedema is another diffuse white

lesion of the buccal mucosa that occurs in African Americans. Typically, the white appearance is lost when

the mucosa is stretched; biopsy is not required.

Figure 15 White Sponge Nevus

The pseudomembranous form of candidiasis is a white

lesion with unique features. The lesions are multiple and

papular or speckled, giving the appearance of curdled milk

(Figure 16). They can usually be rubbed away with gauze.

This fungal infection occurs after antibiotic therapy and is

common among diabetics and immunocompromisedpatients. In the latter, the underlying cause may be HIV

infection or leukemia, lymphoma or chemotherapy patients.

The clinical diagnosis is confirmed by taking a smear on a

glass slide, fixing it in alcohol and having it stained in the

oral pathology laboratory for the presence of hyphae.

Topical nystatin pastilles or clotrimazole troches are usually

effective, as are the systemic antifungals such

as ketaconazole or fluconazole. In the

immunocompromised patient, recurrence

after cessation of antifungals is common,

necessitating long-term therapy.

Figure 16 Pseudomembranous Candidiasis







Pigmentations

Three primary pigments in oral mucosa include:

foreign metals or graphite tattoos,

melanin, and

hemosiderin.

Metals are traumatically introduced into the submucosa. Melanin pigments are synthesized by melanocytes

and hemosiderin pigment is the result of hemorrhage and degradation of red blood cell hemoglobin within the

submucosal connective tissues. These pigmentations may be flat or raised, focal or multifocal (Table 6):

Table 6 - Shapes of pigmentation lesions

Focal macules

Amalgam and graphite tattoos,

Melanotic macule,

Ephilis.

Focal nodules

Nevi,

Melanoma,

Hematoma.

Diffuse and multifocal

Peutz-Jehger syndrome,



Physiologic pigmentation,

Melanoma,

Addison's disease.

A focal pigmented blue or gray spot of the oral mucosa is usually an amalgam tattoo (Figure 17). Often, they

will show up as radio-opaque flecks on a dental film; however, if the metal particles are small, no

radiographic evidence can be observed. Biopsy is usually indicated in such instances, although follow-up to

ensure no increase in size may be pursued. Graphite tattoos result from jamming a lead pencil into the oral

tissues and are usually seen in the palate. These tattoos cause no harm and do not necessarily need to be

removed unless the diagnosis is in doubt. Melanotic macules and ephilis (freckle) tend to occur on the lower

lip, yet can also be found intraorally (Figure 18). They represent accumulation of melanin pigment in the

basal layer of the epithelium and do not progress to melanoma. They are usually brown. Early melanomas

may show this appearance; biopsy diagnosis is therefore mandatory.

Figure 17 Amalgam Tatoo Figure 18 Oral Pigmented Melanotic Macule



Nevi and melanoma may be flat; most are pigmented and raised. They may appear black or brown (Figure

19). Nevi are benign and, once excised, they do not tend to recur. Melanomas are extremely rare in the oral

cavity; when they occur, the anterior maxillary gingiva or alveolar ridge are the favored sites. The lesion may

be huge or a single, darkly painted nodule. Alternatively, some are red or pink with only scattered foci of

pigmentation. The adjacent mucosa often shows macular pigmentations with intervening foci of pale,

depigmented mucosa. Any lesion with the aforementioned features should be considered malignant melanoma

unless proven otherwise by biopsy.

Figure 19 Nevus

Racial or physiologic pigmentation is multifocal and

diffuse, involving the facial gingiva as well as other sites(Figure 20). African Americans and dark-skinned

Caucasians as well as Asians, may be affected. Such

changes are present for many years without any change in

size and are considered normal. Multiple foci of

pigmentation with a history of perioral distribution should

arouse suspicion of the Peutz-Jegher syndrome. The lesions

are brown or black and small, appearing as many dark

freckles. Similar lesions occur on the palms of the hands.







These lesions are an oral marker of benign intestinal polyposis and patients may give a history of bowel

disorder (upset stomach, diarrhea, constipation). Recent onset of cutaneous as well as diffuse or spotty oral

brown pigmentation may herald the onset of Addision's disease (adrenal insufficiency). As the adrenal cortex

becomes affected, steroid levels drop and the pituitary secretes ACTH, a hormone that has melanocyte

stimulating properties. Patients with Addison's disease are hypotensive and hypoglycemic.

Focal Nodular Swellings

Mucosal nodules are represented by proliferation of submucosal connective tissues, cysts or growths of

adnexa, such as salivary tissues or gingival odontogenic tissues. These growths may be due to granulation

tissue proliferation or hyperplasias of various connective tissues in response to irritation (reactive

proliferations), developmental cysts, mucoceles, benign neoplasms and malignant neoplasms. Certain entities

tend to occur in specific locations with the more commonly encountered lesions below (Table 7):

Table 7 - Locations of Mucosal Lesions

Gingiva/Sulcus

Reactive proliferations,

Dental abscess,

Peripheral odontogenic cysts,

Kaposi's sarcoma

Buccal Mucosa

Fibrous hyperplasia,Mesenchymal neoplasms,

Salivary tumors

Lips

Mucoceles,

Salivary tumors

Floor of the mouth

Mucoceles (ranulas),

Dermoid cyst

Lateral tongue

Carcinoma



Dorsal tongue

Fibrous hyperplasia (fibroma),

Connective tissue tumors

Palate

Tori,

Dental abscess,

Salivary gland tumors,

Kaposi's sarcoma

Most swellings of the gingiva are reactive proliferations that evolve in response to some irritant lodged in the

gingival sulcus. As a group, these reactive proliferations occur commonly during pregnancy. The pyogenic

granuloma is the most common and tends to appear fiery red, emanating from the interdental papilla (Figure

21). Peripheral fibroma, ossifying fibroma and giant cell granuloma are the other members of this group of

hyperplasias. All are treated by excision with root planing. Before jumping to the conclusion that a gingivalmass is reactive, pulp testing must be performed because the mass may represent a parulis associated with a

necrotic tooth (Figure 22). Periodontal probing should be performed and if a deep pocket exists and purulent

exudate is expressed, a periodontal abscess is the cause of the swelling. A red mass resembling pyogenic

granuloma in an HIV positive patient is most likely Kaposi's sarcoma, an

AIDS-associated malignancy of vascular endothelial cells.

Figure 21 Pyogenic Granuloma

Figure 22

Peralis

Focal fibrous hyperplasia is the most common buccal mucosa and lip

nodular swelling. These so-called traumatic fibromas are dome shaped,

smooth and of normal color (Figure 23). They merely represent a

hyperplasia of the connective tissue that results from trauma. Biopsy

should be performed to rule out a true neoplastic process. Specifically,

salivary gland tumors can arise in the buccal mucosa and lips, as can nerve sheath tumors, vascular tumors

and lipomas (Figure 24). When the mass is fluctuant or has a history of increasing and decreasing in size,

mucocele is the probable diagnosis. Mucoceles arise from traumatic severage of the minor salivary ducts with

resultant accumulation of mucous secretions in the connective tissues. Mucoceles are usually seen on the

lower lip, while salivary tumors tend to arise in the upper lip.




are needed to see this p



Figure 23 Focal

Fibrous Hyperplasia

Figure 24: Varix

While most swellings of the dorsal

tongue are traumatic fibromas or connective tissue tumors such as

granular cell tumor, angioma or nerve sheath tumor, the lateral border

is a frequent site for squamous cell carcinoma. The cancers appear as

nodules and are often ulcerated. Biopsy should be performed if they do

not resolve in 10 days. If the nodule is located at the lateral base of the tongue, the lesion is probably

hyperplastic lingual tonsilar tissue. Biopsy is indicated here if the swelling shows progressive enlargement.

Midline hard nodules of the palate are invariably tori. When a mass in the palate is off the midline, palatalabscess and salivary tumor are the chief considerations in the differential diagnosis. Palatal abscess is

confirmed when adjacent to a necrotic tooth with an apical radiolucency and incision yields pus. The most

common site in the mouth for salivary neoplasia is the palate. Pleomorphic adenoma is most common and

may be soft or firm (Figure 25). The odds for adenocarcinoma in the palate are as high as for pleomorphic

adenoma. All such masses must be biopsied. Pleomorphic adenomas are treated with simple excision, while

salivary malignancies usually require a partial maxillectomy with fabrication of an obturating maxillary

prosthesis. Nodules of the palate that are purple or red may represent Kaposi's sarcoma, a lesion associated

with AIDS (Figure 26).

Figure 25

Pleomorphic

Adenoma

Figure 26

Kaposi’s

Sarcoma

Multiple and Papillary Swellings

Multiple nodular swellings of the gingiva include leukemia, drug-induced hyperplasias and fibromatosis

gingiva, an inherited condition; multiple swellings of the sulcus are generally denture-induced hyperplasias


are needed to see this picture.QuickTimeª and a

decompressorare needed to see this picture.







and papillary swellings may be viral-induced papillomas, inflammatory papillary hyperplasia from denture

irritation or papillary forms of neoplasia (Table 8).

Table 8 - Multiple and Papillary Swellings

Diffuse, multifocal gingival enlargement

Dilantin,

Cyclosporin and calcium channel blocker-induced hyperplasia,

Leukemic infiltrate,

Fibromatosis gingivae

Multiple nodules, vestibule

Denture fibrous hyperplasia

Palatal papillary lesions

Denture papillomatosis

Focal papillary lesions

Papilloma,

Verruca,

Condyloma

Diffuse papillary lesions

Proliferative verrucous leukoplakia,

Verrucous carcinoma,

Papillary form of squamous cell carcinoma

Diffuse gingival enlargement occurs in patients taking specific drugs. These include dilantin, cyclosporin and

calcium channel blockers, all which stimulate gingival fibroblasts to undergo hyperplasia (Figures 27a, 27b).

Recall that dilantin is used to control grand mal epilepsy; cyclosporin is an immunosuppressive agent used in

transplant patients; calcium channel blockers are employed in the management of coronary heart disease and

hypertension. Hyperplasia is minimized by appropriate prophylaxis and home care. Once present,

gingivectomy is the only treatment and recurrence should be anticipated. In leukemia, malignant white cells

leave the circulation and may infiltrate the gingival tissues. Such patients are usually children who present

with pallor, malaise and often have petechia of the mucosa and skin. A complete blood count should be

performed in suspected cases. Lastly, a rare familial disease may be the underlying cause, fibromatosis

gingivae.



Figure 27 Dilantin or Cyclosporin Hyperplasia

Denture hyperplasia may occur in the vestibule or

palate. Ill-fitting dentures resting on resorbed

ridges impinge upon the sulcus, resulting in

physical irritation. This irritation will induce

hyperplasia of the submucosal fibroblasts,

resulting in multinodular swellings that may be

fissured (epulis fissuratum). These hyperplastic tissues must be excised before fabricating a new prosthesis.

When denture irritation occurs in the palate, usually a consequence of negative pressure, the palatal vault

undergoes papillary hyperplasia. The vault has the appearance of a cobblestone street as multiple small

papules arise and become confluent (Figure 28).

Neither of these lesions has any precancerous

potential.

Figure 28 Papillary Hyperplasia

Focal masses with a papillary surface occur in

viral-induced benign growth that represent the

oral counterpart of the common skin wart. The

papillomavirus group of viruses are responsible.

Papillomas are common on the lips, buccal

mucosa, soft palate and ventral tongue. When

multiple papillomas are seen, one should suspect orogenital transmission. Oral venereal warts are termed

condylomas (Figure 29). The vermilion border of the lip may be the site for the common wart (verrucavulgaris). These lesions may be spread from the hands and fingers to the lips.

Figure 29 Condyloma

Recall from the previous discussion on leukoplakias that a

verrucous form occurs, termed proliferative verrucous

leukoplakia. Such lesions begin as white plaques but may

progressively enlarge into diffuse multinodular and papillary

growths. Eventually, they may transform into verrucous

carcinomas or papillary variants of squamous cell carcinoma.

The former tend to be papillary and white, whereas the latter

may lose the white keratotic character.

Your answer was incorrect. CLOSE [X]

Focal masses with a papillary surface occur in viral-induced benign growths that represent the oral

counterpart of the common skin wart. The papillomavirus group of viruses are responsible. Papillomas are

common on the lips, buccal mucosa, soft palate and ventral tongue. When multiple papillomas are seen, one

should suspect orogenital transmission. Oral venereal warts are termed condylomas (Figure 29). The









vermilion border of the lip may be the site for the common wart (verruca vulgaris). These lesions may be

spread from the hands and fingers to the lips.

Summary

Since the dentist is on the front line of defense for the identification and treatment of lesions of the oral cavity,

we must be ready to accept the challenge. This presentation was designed to reacquaint the practicing dentist

with some of the most common soft tissue lesions that may be encountered in a dental practice. Soft tissue

mucosal diseases were conveniently grouped into seven different lesion forms for ease of identification.

Specific disease processes occurring under the general form categories were discussed relative to varying

etiopathognesis.

1) White stria accompanying red erosive lesions in the buccal mucosa is typical for:

pemphigoid

pemphigus

herpescandidiasis

lichen planus

2) White lesions of the lateral tongue with vertical striations may be a harbinger of:

diabetes

HIV infection

lichenplanus

cancer

When multiple papillomas are seen in the oral mucosa, the following lesion should be suspected:

condyloma

denture papillomatosis

verruca vulgaris

4) The treatment of choice for multiple aphthae is:

tetracycline oral suspension

topical steroids

penicillinerythromycin oral rinse

acyclovir

Recurrent aphthous stomatitis (RAS) is often mistaken for a herpes infection and many practitioners are under

the mistaken impression that the common canker sore is indeed a herpes virus induced lesion. In fact, the

etiology of RAS remains enigmatic. Immunologic mechanisms underlie the pathogenesis; however, the

instigating antigen that triggers the response remains unknown. Patients prone to develop RAS are usually

young and the lesions recur from monthly to once or twice annually. The lesions never go through a vesicular

stage. They ulcerate from their inception and are found on loose movable mucosa, with gingival or palatal



involvement being very rare (Figure 4). Patients with one to three ulcers can be treated with silver nitrate

impregnated sticks, electocautery or laser therapy. Multiple lesions are managed with tetracycline oral rinses

and palliative mouth rinses.

The most likely cause of a focal pigmented spot in the palate of long duration is:

graphite tattoo

melanoma

amalgam tattoo

melanotic macule

coxsackievirus infection

A focal pigmented blue or gray spot of the oral mucosa is usually an amalgam tattoo (Figure 17). Often, they

will show up as radio-opaque flecks on a dental film; however, if the metal particles are small, no

radiographic evidence can be observed. Biopsy is usually indicated in such instances, although follow-up to

ensure no increase in size may be pursued. Graphite tattoos result from jamming a lead pencil into the oral

tissues and are usually seen in the palate. These tattoos cause no harm and do not necessarily need to be

removed unless the diagnosis is in doubt. Melanotic macules and ephilis (freckle) tend to occur on the lower

lip, yet can also be found intraorally (Figure 18). They represent accumulation of melanin pigment in thebasal layer of the epithelium and do not progress to melanoma. They are usually brown. Early melanomas

may show this appearance; biopsy diagnosis is therefore mandatory.

The most common nodular mass of the buccal mucosa is:

Hemangioma

mucocele

nerve sheath tumor

Pyogenic granuloma

traumatic fibroma

Salivary gland tumors appear as masses, most frequently located in the:

tongue

gingiva

buccal mucosa

palate

Focal fibrous hyperplasia is the most common buccal mucosa and lip nodular swelling. These so-called

traumatic fibromas are dome shaped, smooth and of normal color (Figure 23). They merely represent a

hyperplasia of the connective tissue that results from trauma. Biopsy should be performed to rule out a trueneoplastic process. Specifically, salivary gland tumors can arise in the buccal mucosa and lips, as can nerve

sheath tumors, vascular tumors and lipomas (Figure 24). When the mass is fluctuant or has a history of

increasing and decreasing in size, mucocele is the probable diagnosis. Mucoceles arise from traumatic

severage of the minor salivary ducts with resultant accumulation of mucous secretions in the connective

tissues. Mucoceles are usually seen on the lower lip, while salivary tumors tend to arise in the upper lip.

Most of the oral bullous-desquamative-erosive diseases respond to:

steroids



penicillin

nystatin

calcium channel blockers

NSAIDs

Leukoplakias occurring in females who do not smoke and which show a rough or warty appearance are

termed:

candidiasis

frictional keratoses

lichen planus

verrucous carcinoma

proliferative verrucous leukoplakia

Leukoplakias in general have a _____ percent chance of precancerous change while those in the floor of the

mouth have a _____ percent chance.

5%, 90%

10%, 50%

20%, 40%

Gingival masses arising from the interdental papilla are usually:

sarcomas

salivary tumors

melanomas

reactive proliferations

Diffuse erythema of the hard palate in a denture wearer is most likely:

candidiasis

physical irritation

precancerous

Desquamative lesions of the gingiva and basement membrane immunofluorescent for immunoglobulins and

complement are classic features of:

mucous membrane pemphigoid

desquamative candidiasis

pemphigus vulgariserythema multiforme

coxsackievirus infection

Curdled milk multifocal white spots that rub away in a patient who recently was on a course of antibiotics are

typical for:

herpes simplex

leukoplakia



candidiasis


lupus erythematosis

All multifocal red lesions should be biopsied because:

precancerous change is likely

they cannot be diagnosed clinically

most are immunologic diseases that require biopsy for diagnosis

Multifocal erythematous lesions are seen in the aforementioned bullous erosive diseases, candidiasis and

multifocal field cancerization. Clinical diagnosis is impossible, necessitating biopsy.

A pigmented mass in the anterior alveolar ridge is suspicious for:

multiple myeloma

pigmented candidiasis

graphite tattoo

ephilis

malignant melanoma

A patient with fever, lymphadenopathy, mucosal and gingival vesiculoulcerative lesions suffers from:

varicella Zoster

hairy leukoplakia

recurrent herpes

primary herpes (primary herpetic stomatitis)

allergic stomatitis

Most of the lesions listed above can be diagnosed on the basis of clinical features alone or with the aid of

laboratory studies that include culture, CBC or specific antibody titers. The viral ulcers all begin as vesicles

and are generally accompanied by fever. Each viral disease is diagnosed on the basis of lesion distribution.

Primary herpetic gingivostomatitis is characterized by fever, malaise, oral pain, gingival erythema with

ulceration and movable mucosal vesicles that pop to become ulcers and lymphadenopathy of cervical nodes.

The labial, buccal and sublingual mucous membranes are usually involved (Figure 1). Herpes labialis affects

either the upper of lower lips or sometimes both (Figure 2). The lesions represent recurrences from awakening

of trigeminal ganglion latent herpes virus infections. Classically, the lesions evolve as vesicles with a

tendency for clustering into groups that ulcerate, coalesce and after four to five days become crusted. After 12

days, healing occurs and the virus is inactivated immunologically, only to recur at a future date. The chief stimuli that reactivate the latent virus include intense sun exposure to the lips, emotional anxiety episodes and

trauma from stretching the lips. Recurrent intraoral herpes of the palatal gingiva is typified by clusters of

ulcers; a history of antecedent vesicles may be obtained from the patient (Figure 3). A history of recurrent

episodes is usually gleaned. Herpes infections are treated with acyclovir, analgesics and palliative anesthetic

mouth rinses.

A focal erythematous velvety lesion in the soft palate of a smoker is at high risk for:



candidiasis


sarcoma

dysplasia

syphilis

A fluctuant mass of the lower lip is usually a _____, while a mass in the upper lip is more likely to be a _

____.

hemangioma, fibroma

mucocele, salivary tumor

fibroma, squamous cell carcinoma

mucocele, hemangioma

Focal fibrous hyperplasia is the most common buccal mucosa and lip nodular swelling. These so-called

traumatic fibromas are dome shaped, smooth and of normal color (Figure 23). They merely represent a

hyperplasia of the connective tissue that results from trauma. Biopsy should be performed to rule out a true

neoplastic process. Specifically, salivary gland tumors can arise in the buccal mucosa and lips, as can nerve

sheath tumors, vascular tumors and lipomas (Figure 24). When the mass is fluctuant or has a history of

increasing and decreasing in size, mucocele is the probable diagnosis. Mucoceles arise from traumatic

severage of the minor salivary ducts with resultant accumulation of mucous secretions in the connective

tissues. Mucoceles are usually seen on the lower lip, while salivary tumors tend to arise in the upper lip.

A febrile patient with oral hand and foot vesiculoulcerative lesions has:

rhabdovirus

coxsackievirus

varicella

herpes simplexHIV infection

http://www.adaceonline.org/index.aspx?sec=olce&sub=cmain&ce_id=1028&section_id=21





Documents

Ulcers and Vesicles2