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2021Course#4

Writtenby:Sarah Aguirre, DDS, MS

ReleaseDate:November1,2021

8:30amEST

LastDaytoTakeCourseFreeofCharge:

November30,20214:30pmEST

CourseReviewedby:Christine Harrington,

DDS, MS

Oral UlcerationsCourseFormat:Supervisedself‐instruction

About the AuthorSarah Aguirre, DDS, MS

Neither I nor my immediate family have any financial interests that would create a conflict of interest or restrict my judgement with regard to the content of this course.

PURPOSELearning Objectives:

1. The difference in clinical presentation and treatment of aphthous ulcerations vs. recurrent herpes.

2. Treatment options for various forms of oral ulcerations.3. Which diseases and conditions can present with oral

ulcerations.4. How to clinically differentiate between different presentations

of oral ulceration.5. Which clinical situations involving oral ulceration warrant a

referral for biopsy.6. Test his or her knowledge by reviewing the True or False

Questions

Sarah Aguirre graduated from the Arthur A. Dugoni School ofDentistry in San Francisco, California. She completed a residencyin Oral and Maxillofacial Pathology at The Ohio State UniversityCollege of Dentistry. Currently she is an Assistant Professor atThe University of Tennessee Health Science Center College ofDentistry.

INTRODUCTIONOral ulcerations are relatively common lesions that can have a widerange of etiologies, from traumatic to infectious to autoimmune toidiopathic. The management of oral ulcerations varies accordingly withthe cause of the ulceration. Consequently, accurate diagnosis of oralulcerations is paramount in ensuring the correct treatment,recommendations, and follow-up are provided for affected patients. Thedental clinician should be familiar with following diseases and conditionshave presentations that may involve oral ulceration.

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Introduction

Oral ulcerations are a relatively common lesions that can have a wide range of etiologies, from traumatic to infectious to autoimmune to idiopathic. The management of oral ulcerations varies accordingly with the cause of the ulceration. Consequently, accurate diagnosis of oral ulcerations is paramount in ensuring the correct treatment, recommendations, and follow-up are provided for affected patients. The dental clinician should be familiar with following diseases and conditions have presentations that may involve oral ulceration.

Traumatic Ulceration

Ulcerations resulting from physical trauma are the most common type of ulceration found in the oral cavity. Traumatic ulcerations may arise from acute or chronic injury to the oral mucosa. Biting a cheek or a tongue, abrasion from a sharp tooth or restoration, or damage from hard or sharp food are all common injuries that may result in a traumatic ulcer. (See Figure 1) Most traumatic ulcers heal within a few days, however others may persist for extended periods of time, depending on the size and depth of injury and whether or not the cause of injury is still present.

Lesions present as well circumscribed erythematous areas with a central yellowish pseudo-membrane. The ulcer often has rolled white borders which blend with the surrounding mucosa.

If a patient presents with a long-standing ulceration of suspected traumatic etiology, it may be a histopathologically unique variant of traumatic ulceration known as an eosinophilic ulceration, or traumatic granuloma. This variant can may last from 1 week to 8 months and is most often reported on the tongue, although buccal mucosa, floor of mouth, gingiva, lip, and palate are all possible locations. It has been observed that eosinophilic ulcerations often resolve following incisional biopsy.

A similar lesion is seen sublingually in infants, resulting from chronic trauma from adjacent anterior primary teeth. This specific presentation of ulceration, often associated with nursing, is termed Riga-Fede disease.

Treatment for any ulceration of suspected traumatic origin should include removal of the traumatizing factor, if still present, and follow up with the patient in two weeks to assess healing. Incisional biopsy is recommended for oral ulcerations persisting without signs of resolution after two weeks, provided the suspected source of trauma has been removed. Eosinophilic ulceration or secondary infection with Candida albicans may delay healing of a traumatic ulcer, however microscopic evaluation is necessary to exclude other causes of persistent ulceration, including infectious and neoplastic.

Treatment for ulcerations in Riga-Fede disease of infants may include smoothing the incisal edges of the offending teeth, applying composite over the edges of the teeth, constructing a protective shield, cessation of nursing, or even removal of the teeth. Primary teeth should be retained if possible.

Apththous Stomatitis (Aphthous Ulcers)

Two commonly encountered, and most often confused, oral ulcerations are those caused by herpes simplex virus (HSV) and recurrent aphthous stomatitis. Clinical distinction between these two conditions is important because management differs, and some treatments for aphthous ulcers may actually exacerbate an HSV infection.

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Recurrent aphthous stomatitis (RAS) affects 5 –25% of the population. RAS is idiopathic in origin, with many proposed contributing factors to its etiology. Genetic predisposition, autoimmunity, food allergy, nutritional deficiencies, hormonal alterations, chemical irritants, stress and anxiety, and microbial agents have all been suggested as having some role in RAS. However, none of the suggested etiologies have been confirmed as definitely causing RAS. Several systemic disorders are known to be associated with aphthous-like ulcerations (see Table 1) and should be ruled out if the patient has additional accompanying symptoms. Aphthous stomatitis has three recognized clinical variations: minor, major, and herpetiform.

Minor aphthous ulcerations are the most common presentation, seen in over 80% of patients with RAS. They usually present as one to five ulcerations, nearly exclusively on non-keratinized (moveable) mucosa. The ulcerations are composed of a yellow-white pseudo-membrane surrounded by an erythematous halo 2-10 mm in diameter. Pain associated with the lesion is normally disproportionately greater than the size of the lesion. (See Figure 2 & 3)

Major aphthous ulcerations are observed in about 10% of patients with RAS, and may require therapeutic intervention more often, compared with minor aphthae. (See Figure 4)

The herpetiform variant has the greatest number of lesions per episode and the most frequent recurrences. It is the form that is most often mistaken for a HSV infection. Numerous 1-3 mm ulcerations present predominantly on non-keratinized mucosa, with reports of as many as 100 individual lesions at one time. These ulcerations may coalesce into larger, irregular ulcerations.

Unlike primary infection with HSV, RAS is not associated with lymphadenopathy, fever or chills. Aphthous ulcerations are never preceded by vesicles, which can be another important distinction from HSV.

Some patients are aware of a trigger for their aphthae and can avoid those particular foods or substances. However, because of the unclear

etiology in the majority of cases, treatment is aimed at alleviating symptoms and shortening the duration of the ulcers. Many patients with minor RAS do well with no treatment or with over-the-counter anesthetics or protective barrier bioadhesives. For patients with more involved disease, topical corticosteroids to shorten lesion duration and relieve symptoms are the treatment of choice. Numerous topical corticosteroids are available for use, including 0.05% augmented betamethasone dipropionate gel or 0.05% fluocinonide gel, which are effective for localized ulcerations. For more diffuse or herpetiform ulcerations, a corticosteroid rinse, such as dexamethasone (0.5 mg/5 mL) may be more successful. Major aphthae may require a more potent topical corticosteroid, such as 0.05% clobetasol propionate gel. Efficacy of any of the topical corticosteroids is largely dependent on contact time with the ulceration. Accordingly, use of gels versus creams is important in the hydrophilic oral environment and application by the patient at least 4-6 times a day is advised. Systemic side effects are not seen with appropriate use of topical corticosteroids; however, patients may be at a greater risk of developing an oral yeast infection while using the medication.

Systemic corticosteroid use is reserved for resistant cases in which topical medication must be supplemented in order to gain control over the disease process. Once under control, systemic treatment should be discontinued and RAS should be managed topically, due to the adverse side effects of prolonged systemic corticosteroid use.

While there are abundant alternative treatments to corticosteroids available, caution should be exercised before making any recommendations to patients since sufficient, high-quality evidence to support their therapeutic value is often lacking. Low-level laser therapy at the site of ulceration has been shown to be effective at reducing both the pain and duration of aphthous ulcerations; however, such treatment for every episode of RAS is impractical for most patients.

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Herpes Simplex Virus

Oral cavity infection by HSV is most commonly due to infection with HSV-1, although infrequent cases may be caused by HSV-2. HSV-1 is transmitted through infected saliva or active perioral lesions. In developing areas, nearly 100% of the population is exposed by 15 years of age. Developed areas see a much lower rate of exposure, with only 50% to 60% of the population being exposed by adulthood. Infection with HSV can either be primary or recurrent (secondary). After initial infection with HSV, the virus is taken up by sensory nerves and establishes latency in a sensory nerve ganglion, often the trigeminal ganglion for HSV-1. The virus may then become re-activated at a later time.

Primary infection occurs when a previously unexposed individual is infected with the virus. Most primary HSV infections occur at a young age and are usually asymptomatic; however, when symptoms do occur, they can be quite debilitating. Symptoms have an abrupt onset and frequently include fever (103˚ F to 105˚ F), chills, malaise, anterior cervical lymphadenopathy, nausea, anorexia, irritability, and painful oral ulcerations. These symptoms range from mild to severe and appear 3 to 9 days after initial exposure. Oral ulcerations first appear as pinpoint vesicles on both attached and moveable mucosa, which quickly rupture into small red lesions. These then may coalesce and form larger areas of ulceration covered by a yellow-white pseudomembrane. The gingiva will be enlarged, erythematous, and painful. Perioral involvement is not uncommon. Depending on the severity, primary HSV infection can last from 5 days up to 2 weeks. Antiviral medication administered within the first 3 symptomatic days is beneficial in reducing the clinical course of the infection. Valacyclovir (Valtrex) is the drug of choice for an HSV infection (See Table 2 for dosing information). Topical anesthetic rinses or lozenges may be beneficial for patients experiencing severe pain from the oral ulcerations. Topical corticosteroids should not be used, as they may exacerbate the viral infection (See Figure 5).

Recurrent herpes occurs with reactivation of thelatent herpes virus. Factors that may induce reactivation include ultraviolet light, physical or emotional stress, fatigue, heat, cold, hormonal changes associated with menstruation or pregnancy, allergy, trauma, dental treatment, fever, systemic disease, and old age. Accompanying symptoms, such as those seen in a primary HSV infection, are generally not present with a secondary infection. Recurrence may occur along any epithelial surface supplied by the involved ganglion, but the most frequent site of recurrence is along the vermilion border and surrounding skin. This presentation is termed herpes labialis, commonly referred to as “cold sores” or “fever blisters.” Patients are often aware of prodromal symptoms which may include tingling, burning, warmth, erythema, or pain in the area preceding vesicle formation. Antiviral medication, topical and/or systemic, is most effective if initiated during the prodromal stage. When HSV recurs intraorally, it is almost always restricted to the attached mucosa (hard palate and attached gingiva). This is a helpful feature when distinguishing recurrent intraoral herpes from recurrent aphthous ulcerations. Recurrent intraoral herpes is usually far less symptomatic than a primary infection, and many patients do not require any treatment. For those who do require treatment, chlorhexidine rinses have been shown to exert some antiviral activity. Untreated, the intraoral ulcerations will resolve within 7 to 10 days.

Recurrence of HSV in immunocompromised patients can develop into severe disease, with large, persistent ulcerations on both moveable and attached mucosa. These patients may require intravenous antiviral therapy and management of their underlying immune dysfunction.

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Varicella Zoster Virus

The varicella zoster virus (VZV or HHV-3) is responsible for two diseases: varicella, or chickenpox, in childhood; and herpes zoster, or shingles, as a reoccurrence in adulthood.

The incidence of varicella has greatly decreased since the institution of universal varicella vaccination in the United States, however unvaccinated individuals are still susceptible. Symptoms begin with malaise, pharyngitis, and rhinitis. A characteristic pruritic (itchy) rash follows, beginning on the face and trunk and then spreading to the extremities. The rash consists of lesions that progress through several stages: erythema, vesicles, pustules, and then crusting. Perioral and oral manifestations are common and may precede skin lesions. Three to four millimeter white, opaque vesicles may begin on the vermilion border, palate, buccal mucosa or gingiva. These rupture to form 1 to 3 mm painless ulcerations that heal within 1 to 10 days, depending on the severity of the infection. Antiviral medication is generally not recommended for immunocompetent children with uncomplicated disease; rather, it is reserved for severe cases or individuals who are immunocompromised in some way.

Shingles results from a reactivation of VZV, which remains latent in the dorsal root ganglia. Reoccurrence is usually a singular event in adults over the age of 50. Herpes zoster has three phases: prodrome, acute, and chronic. The disease may be most noticeable to dental clinicians in the acute phase which can last 2 to 3 weeks. Involved skin develops clusters of vesicles on an erythematous base, which ulcerate and crust over. A striking unilateral appearance to the lesions is observed, with termination at the midline. Oral lesions may present on moveable or non-moveable mucosa with the same unilateral spread. Intraoral lesions are similar to those seen in varicella, with 1 to 4 mm vesicles that rupture into shallow ulcerations. Unlike varicella, teeth in the affected area may develop pulpal involvement that can lead to pulpal necrosis, pulpal calcification, or root resorption. Systemic antiviral therapy initiated within 72 hours of the first vesicle formation is effective at accelerating healing and reducing pain. Concurrent analgesic treatment with

acetaminophen or NSAIDs may be warranted for pain control. A shingles vaccine (Shingrix) is FDA approved for adults 50 years of age and older. Two doses of the vaccine, separated by 2 – 6 months) is more than 90% effective at preventing shingles and post-herpetic neuralgia.

Enteroviruses

Human enteroviruses are responsible for a variety of disease in young children worldwide. The virus is usually spread person-to-person, via contaminated water, or via contaminated objects. Most infections are asymptomatic; however symptomatic cases can be mild to quite severe. Three clinical presentations of enterovirus infection can exhibit oral ulcerations: herpangina, hand-foot-and-mouth disease, and acute lymphonodular pharyngitis. These are closely related conditions and some regard lymphonodular pharyngitis as a variant of herpangina. The severity of disease ranges with the strain of virus for all three presentations. While most strains produce a self-limiting disease that does not require therapy, some strains can produce significant complications and rare fatalities.

Symptoms associated with herpangina begin with sore throat, dysphagia, fever, rhinorrhea, anorexia, vomiting, diarrhea, myalgia, headache, and occasionally, cough. The majority of cases are mild or subclinical. Patients may develop 2 to 6 small, aphthous-like ulcerations on the soft palate or tonsillar pillars. Systemic symptoms resolve within a few days, while oral ulcerations may take up to 10 days to heal.

Hand-foot-and-mouth disease presents with similar systemic symptoms to herpangina. Its name aptly describes the location of vesicular lesions associated with this disease. Oral and hand lesions are most consistently seen, with the oral lesions usually preceding the cutaneous lesions. Cutaneous lesions develop as erythematous macules that proceed into vesicles that heal without crusting. While oral lesions are similar to those seen in herpangina, they are usually more numerous and are not restricted to the soft palate and tonsillar pillars. The intraoral lesions present as erythematous macules that

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rapidly ulcerate and are typically 2 to 7 mm in diameter.

Acute lymphonodular pharyngitis presents with sore throat, fever, and mild headache, which normally resolves within 4 to 14 days. Oral lesions manifest as 1 to 5 yellow to dark-pink nodules on the soft palate or tonsillar pillars. These lesions do not ulcerate and represent hyperplastic lymphoid aggregates that resolve within 10 days.

Tuberculosis

Tuberculosis is a chronic infections disease caused by the bacterial organism Mycobacterium tuberculosis. Over 2 billion people are estimated to be infected worldwide. Primary tuberculosis is the initial stage of the disease, which affects previously unexposed people. Pulmonary involvement characterizes primary tuberculosis, and usually only progresses to a localized fibro-calcified nodule at the original site of infection. Only 5% to 10% of people with primary tuberculosis progress to active disease, or secondary tuberculosis. Immunosuppressive medications, poor living conditions, diabetes, old age, and AIDS increase the risk of progression to secondary tuberculosis. Active infection can disseminate from the lungs to nearly any location in the body, including the oral cavity. While uncommon, oral lesions from disseminated secondary infection generally present on the tongue as a chronic, painless ulceration that may have a granular appearance. Such lesions are indistinguishable from other pathologic processes clinically, and therefore, require biopsy and microscopic examination for a definitive diagnosis.

Histoplasmosis

Caused by the fungal organism Histoplasma capsulatum, histoplasmosis is the most common systemic fungal infection in the United States. It is endemic to humid areas with soil enriched by bird or bat droppings, such as the Ohio and Mississippi River valleys. Most infections are asymptomatic or very mild and are cleared by healthy individuals with the development of antibodies against the organism in a matter of weeks. Reports indicate up to 90% of individuals living in endemic areas will have antibodies against H. capsulatum. Disease

may present in the acute, chronic, or disseminated form. Oral lesions may be observed in the rarest presentation, the disseminated form. Oral involvement of the disseminated form appears as chronic ulceration, most often reported on the tongue, palate and buccal mucosa. These ulcerations can appear clinically indistinguishable from squamous cell carcinoma and biopsy is necessary to establish a diagnoses. (See Figure 6 & 7)

Chronic Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is most prevalent in North America and North-Western Europe, although its incidence has been increasing worldwide. Crohn’s disease and ulcerative colitis are both part of the group of IBD. Besides affecting the gastrointestinal tract, IBD can manifest with extraintestinal symptoms throughout the body. Extraintestinal manifestations (EIM) are reported in 6% to 47% of patients with IBD. Oral lesions can be a component of the EIMs with varying incidence reports of 5% to 50%.

Crohn’s disease, or regional enteritis, can have both specific and non-specific oral lesions. These oral manifestations can precede intestinal manifestations or be seen concurrently. Specific oral lesions associated with Crohn’s disease include granulomatous nodules which give a “cobblestone” appearance the oral mucosa, mucosal tags, swelling of the lips, cheeks and face, and deep linear ulcerations, often in the mandibular labial vestibule. Crohn’s disease usually manifests in the teenage years, with most patient’s diagnosed with the condition before the age of 30; however, a second diagnostic peak is seen around 60 years of age.

Non-specific oral lesions that may be present in both Crohn’s disease and ulcerative colitis include aphthous stomatitis, angular cheilitis, pyostomatitis vegetans, and glossitis. Of these, aphthous stomatitis and pyostomatitis vegetans manifest as oral ulcerations. Pyostomatitis vegetans begins as yellowish, slightly elevated, linear, curved pustules on an erythematous oral mucosa. The buccal and labial mucosa, soft

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palate, and ventral tongue are the most commonly affected sites. These lesions may rupture to form ulcerations, which then may cause discomfort for the patient.

Treatment and management of the underlying bowel disease may be needed for resolution of the oral manifestations. For patients with mild bowel symptoms, or oral lesions preceding bowl symptoms, use of a potent topical steroid may be beneficial for selective treatment of the oral lesions.

Granulomatosis with Polyangiitis

Granulomatosis with polyangiitis, previously known as Wegener’s granulomatosis, is an uncommon necrotizing granulomatous disease of unknown etiology that can occur anytime from childhood to late adulthood. It may involve any organ system in the body. Occasionally it includes oral ulcerations. Strawberry gingivitis is the most distinctive oral manifestation, seen early in the disease process when present. The affected gingiva, most often buccal surfaces, have a hyperplastic, red, bumpy appearance. Oral ulcerations present at later stages of the disease and do not form a specific pattern unique to Wegener’s granulomatosis. Generally, the ulcerations are deep and irregular. Biopsy is needed for definitive diagnosis.

Chronic Vesiculoulcerative Diseases

This group includes several distinct conditions that may produce chronic vesiculoulcerative or ulcerative lesions of the oral mucosa: pemphigus vulgaris, paraneoplastic pemphigus, mucous membrane pemphigoid, bullous pemphigoid, erythema multiforme, and lichen planus.

Some, including pemphigus vulgaris and mucous membrane pemphigoid, result from the inappropriate production of antibodies (autoantibodies) directed against normal molecular structures in a person’s epithelium. This misdirected immune response damages the connective junctions holding epithelial cells together or to the underlying connective tissue.

When manifested in the oral cavity, the mucosa is fragile and easily forms vesicles or bullae which quickly rupture to form ulcerations.

Other conditions in this category are associated with reactions to certain medications, malignancies, or have poorly understood etiologies. Because of the diverse and complex nature of many of these disease processes, the discussion will be limited to clinical presentation relevant to the dental clinician, the process of diagnoses, and treatment for these conditions.

Pemphigus Vulgaris

Pemphigus vulgaris, is a rare condition in which autoantibodies are produced against the desmosomal junctions that hold epithelial cells together. Without treatment, this condition often will result in death. Oral lesions are often the first presentation of the systemic condition, and have earned the expression, “the first to show, and the last to go.” Pemphigus vulgaris usually presents in adulthood, with an average age at diagnosis of 50 years. Intraoral vesicles are usually not seen due to their fragility; instead, patients will present with superficial, ragged erosions and ulcerations with a pattern-less distribution on nearly any location of the oral mucosa. If lateral pressure is placed on normal-appearing portion of the mucosa, a bulla can be induced. This is called a positive Nikolsky sign. A biopsy of an area with intact epithelium submitted in both formalin, for light microscopy, and Michel’s solution, for direct immunofluorescence (DIF), is necessary to confirm the diagnosis of pemphigus vulgaris. Patients are usually referred to dermatology due to the involvement of the cutaneous skin. These patients should be managed by a physician with experience in administration of long-term systemic corticosteroids.

Paraneoplastic Pemphigus

With only 150 reported cases, paraneoplastic pemphigus, is a very rare condition that can occur in patients with a neoplasm, usually lymphoma or chronic lymphocytic leukemia. Paraneoplastic pemphigus has developed before the malignancy was identified in about one third

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of the cases. Lesions involving the oral cavity include diffuse, irregular ulceration of any area of the oral mucosa. The vermilion border may also be involved with severe hemorrhagic crusting, similar to that seen in erythema multiforme. Skin lesions and involvement of other mucosal surfaces, such as the eye and respiratory tract, are commonly involved. Accordingly, paraneoplastic pemphigus is a serious condition with a poor prognosis. Treatment consists of systemic corticosteroids and immunosuppressive agents. Although this may control the autoimmune disease, it often allows the malignancy to proliferate.

Mucous Membrane Pemphigoid

Clinically, mucous membrane pemphigoid (cicatricial pemphigoid) may appear like pemphigus vulgaris, however the molecular basis for the disease and disease course are very different. In mucous membrane pemphigoid, autoantibodies are produced against the hemidesmosomal junctions which anchor the epithelium to the underlying connective tissue. The average age of onset is 50 to 60 years and females are affected two times more frequently than males. Oral lesions are usually present and include intraoral vesicles and bullae that rupture to form large, irregular ulcerations, as well as a pattern on the gingiva known as desquamative gingivitis. Desquamative gingivitis is not specific to mucous membrane pemphigoid and may also be seen in lichen planus and pemphigus vulgaris. Biopsy of tissue with intact epithelium submitted in both formalin, for light microscopy, and Michel’s solution, for direct immunofluorescence (DIF), is necessary to make the diagnosis of mucous membrane pemphigoid. Once a diagnosis of mucous membrane pemphigoid is made, it is important to also refer the patient to an ophthalmologist. Unlike pemphigus vulgaris, mucous membrane pemphigoid is not life threatening if left untreated. However, the mucous membranes of the eye are involved, progressive scarring can lead to blindness. Depending on the disease presentation in an individual, the patient may be successfully managed with topical corticosteroids, or may require systemic corticosteroids and/or immunosuppressive agents. Aggressive treatment is indicated for progressive

ocular disease. Alternative treatments for those with mild-to-moderate disease may include the sulfa drug dapsone or tetracycline/minocycline and niacinamide. Good results have been seen in some patients using these alternative therapies; however, more studies are needed to confirm their use as a standard therapy.

Bullous Pemphigoid

Although bullous pemphigoid has resemblance to mucous membrane pemphigoid, it is a distinct condition that manifests primarily with cutaneous skin lesions. Oral mucosa is less often affected, with only 10% to 20% of patients exhibiting oral involvement. Shallow ulcerations with smooth, definite margins may be observed on the oral mucosa following the rupture of bullae. Treatment varies depending on the severity of the disease. Mild or localized disease may be controlled well with topical corticosteroids, whereas moderate to severe disease may require systemic immunosuppressive therapy. Biopsy of apparently uninvolved tissue with submission for both DIF and standard microscopic evaluation is needed to reach a definitive diagnosis.

Erythema Multiforme

Erythema multiforme is a poorly understood blistering, ulcerative process. It is thought to be immunologically mediated and associated with a precipitating trigger, such as infection or medication use. Herpes simplex and infection with Mycoplasma pneumoniae have both been implicated in triggering erythema multiforme. Drugs associated with erythema multiforme are most often antibiotics or analgesics. Onset is acute and usually observed in young adults in their 20’s and 30’s. Flu-like prodromal symptoms often present about 1 week prior to onset. Characteristic skin lesions resembling a bull’s eye or target can appear on the extremities. Mucosal sites including the oral cavity, conjunctival, genitourinary, and respiratory mucosa may also be affected, although oral mucosa is the most common. Oral lesions start as erythematous patches that necrose into large, shallow erosions and ulcerations with irregular

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borders. Hemorrhagic, crusted lips are commonly seen. The disease is self-limiting and resolves in 2 to 6 weeks, so supportive and palliative care is usually administered. About 20% of patients have recurrences.

Erosive Oral Lichen Planus

Lichen planus is a dermatologic disease that has several different clinical patterns. The disease usually presents in middle-aged adults with a 3 : 2 female-to-male predilection. The etiology of lichen planus is still unclear. The erosive form of oral lichen planus is often symptomatic and uncomfortable for patients. Erythematous, atrophic areas with central ulceration are set against a background of fine, white radiating striae. When limited to the gingiva, erosive lichen planus presents as desquamative gingivitis. In these cases, a biopsy with submission of tissue for DIF is necessary to distinguish it from mucous membrane pemphigoid.

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Tables

Table 1 Systemic Disorders Associated with Aphthous 

Ulcerations

Behçet syndrome

Celiac disease

Cyclic neutropenia

Nutritional deficiencies (B1, B2, B6, B12, folate, iron, zinc)

Immunoglobulin A (IgA) deficiency

Immunocompromised conditions, including human immunodeficiency 

virus (HIV) 

Inflammatory bowel disease

MAGIC syndrome (mouth and genital ulcers with inflamed cartilage)

PFAPA syndrome (periodic fever, aphthous stomatitis, pharyngitis, 

cervical adenitis)

Reactive arthritis

Sweet syndrome

Ulcus vulvae acutum

Table 2 Treatment of Orolabial HSV Infections

Pediatric Adult

Primary herpes 

(acute herpetic 

gingivostomatitis)

Valacyclovir 20 mg/kg q 12 h for 7 days, 

maximum dose 1000mg/dose

1 g p.o. stat, 1 g q 12 h for 10 

days

Recurrent herpes 

(secondary 

herpes)

Valacyclovir 2 g p.o. stat, 2 g 12 hours later 

(≥ 12 y.o.)

2 g p.o. stat, 2 g 12 hours 

later

Figure 1. Healing traumatic ulceration of right ventral tongue. Note that the white border blends with the surrounding mucosa.

Figure 2. Minor aphthae on maxillary labial mucosa, presenting as ulcers surrounded by an erythematous halo.

Figure 3. Minor aphthous ulcer on dorsal tongue

Figure 4. Major and minor aphthae near left commissure

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Figure 5. Primary herpetic gingivostomatitis

Figure 6. Ulceration of the right ventral tongue due to a disseminated histoplasmosis infection.

Figure 7. Carcinoma-in-situ with ulceration, right ventral tongue. Note that the white borders of this lesion are not blended as in a traumatic ulcer. Here, they are sharply defined.

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