<<

2016 self-study course four course The Ohio State University College of is a recognized provider for ADA CERP credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to the Commission for Continuing Education Provider Recognition at www.ada.org/cerp. The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education. This continuing education activity has been planned and implemented in accordance with the standards of the ADA Continuing Education Recognition Program (ADA CERP) through joint efforts between The Ohio State University College of Dentistry Office of Continuing Dental Education ABOUT this and the Sterilization Monitoring Service (SMS).

COURSE… FREQUENTLY asked

QUESTIONS… . Read and READ the MATERIALS. Q: Who can earn FREE CE credits? review the course materials. . COMPLETE the TEST. Answer the A: EVERYONE - All dental professionals eight question test. A total of 6/8 in your office may earn free CE questions must be answered credits. Each person must read the correctly for credit. course materials and submit an contact online answer form independently. . SUBMIT the ANSWER FORM ONLINE. You MUST submit your answers ONLINE at: Q: What if I did not receive a confirmation ID? us http://dentistry.osu.edu/sms-continuing-education A: Once you have fully completed your . RECORD or PRINT THE answer form and click “submit” you phone CONFIRMATION ID This unique ID will be directed to a page with a is displayed upon successful unique confirmation ID. 614-292-6737 submission of your answer form. Q: Where can I find my SMS number?

ABOUT your A: Your SMS number can be found in

toll free FREE CE… the upper right hand corner of your 1-888-476-7678 monthly reports, or, imprinted on the back of your test envelopes. The SMS number is the account number for . TWO CREDIT HOURS are issued your office only, and is the same for fax for successful completion of this everyone in the office. self-study course for the OSDB 614-292-8752 2015-2016 biennium totals. Q: How often are these courses available? . CERTIFICATE of COMPLETION is used to document your CE credit A: FOUR TIMES PER YEAR (8 CE credits.) e-mail and is mailed to your office. [email protected] . ALLOW 2 WEEKS for processing and mailing of your certificate. . The Ohio State University College of web Dentistry is an American Dental Association (ADA) Continuing dentistry.osu.edu/sms Education Recognized Provider (CERP). Page 1 Oral Ulcerations

2016 Learning Objectives: course 1. The difference in clinical presentation and treatment of aphthous ulcerations vs. recurrent herpes. 2. Treatment options for various forms of oral ulcerations. four 3. Which 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 . 6. Test his or her knowledge by reviewing the True or False Questions

This is a OSDB Category B – Supervised self-instruction course.

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

release date November 1, 2016 (7:30 AM EST)

last day to take the course at no charge November 30, 2016 (4:00 PM EST)

last day course is available for credit December 31, 2018

Page 2

If a patient presents with a long-standing Introduction ulceration of suspected traumatic etiology, it may be a histopathologically unique variant of Oral ulcerations are a relatively common lesions traumatic ulceration known as an eosinophilic that can have a wide range of etiologies, from ulceration, or traumatic granuloma. This variant traumatic to infectious to autoimmune to idiopathic. can may last from 1 week to 8 months and is The management of oral ulcerations varies most often reported on the , although accordingly with the cause of the ulceration. buccal mucosa, floor of , gingiva, , and Consequently, accurate diagnosis of oral are all possible locations. It has been ulcerations is paramount in ensuring the correct observed that eosinophilic ulcerations often treatment, recommendations, and follow-up are resolve following incisional biopsy. provided for affected patients. The dental clinician should be familiar with following diseases and A similar is seen sublingually in infants, conditions have presentations that may involve oral resulting from chronic trauma from adjacent ulceration. anterior primary teeth. This specific presentation of ulceration, often associated with nursing, is termed Riga-Fede . Traumatic Ulceration Treatment for any ulceration of suspected Oral ulcerations are a relatively common lesions traumatic origin should include removal of the that can have a wide range of etiologies, from traumatizing factor, if still present, and follow up traumatic to infectious to autoimmune to idiopathic. with the patient in two weeks to assess healing. The management of oral ulcerations varies Incisional biopsy is recommended for oral accordingly with the cause of the ulceration. ulcerations persisting without signs of resolution Consequently, accurate diagnosis of oral after two weeks, provided the suspected source ulcerations is paramount in ensuring the correct of trauma has been removed. Eosinophilic treatment, recommendations, and follow-up are ulceration or secondary with Candida provided for affected patients. The dental clinician may delay healing of a traumatic , however should be familiar with following diseases and microscopic evaluation is necessary to exclude conditions have presentations that may involve oral other causes of persistent ulceration, including ulceration. infectious and neoplastic.

Ulcerations resulting from physical trauma are the Treatment for ulcerations in Riga-Fede disease most common type of ulceration found in the oral of infants may include smoothing the incisal cavity. Traumatic ulcerations may arise from edges of the offending teeth, applying composite or chronic to the . Biting a over the edges of the teeth, constructing a or a tongue, from a sharp tooth or protective shield, cessation of nursing, or even restoration, or damage from hard or sharp food are removal of the teeth. Primary teeth should be all common that may result in a traumatic retained if possible. ulcer. (See Figure 1) Most traumatic heal within a few days, however others may persist for extended periods of time, depending on the size Apththous and depth of injury and whether or not the cause of (Aphthous Ulcers) injury is still present. Two commonly encountered, and most often Lesions present as well circumscribed confused, oral ulcerations are those caused by erythematous areas with a central yellowish (HSV) and recurrent pseudo-membrane. Rolled white borders . Clinical distinction between surrounding the ulceration are common in these two conditions is important because traumatic ulcers. management differs, and some treatments for aphthous ulcers may actually exacerbate a HSV infection. Page 3

Recurrent aphthous stomatitis (RAS) affects 5 – etiology in the majority of cases, treatment is 25% of the population. RAS is idiopathic in origin, aimed at alleviating symptoms and shortening with many proposed contributing factors to its the duration of the ulcers. Many patients with etiology. Genetic predisposition, autoimmunity, minor RAS do well with no treatment or with food , nutritional deficiencies, hormonal over-the-counter or protective barrier alterations, chemical irritants, and anxiety, bioadhesives. For patients with more involved and microbial agents have all been suggested as disease, topical to shorten lesion having some role in RAS. However, none of the duration and relieve symptoms are the treatment suggested etiologies have been confirmed as of choice. Numerous topical corticosteroids are definitely causing RAS. Several systemic disorders available for use, including 0.05% augmented are known to be associated with aphthous-like betamethasone dipropionate gel or 0.05% ulcerations (see Table 1) and should be ruled out if gel, which are effective for localized the patient has additional accompanying ulcerations. For more diffuse or herpetiform symptoms. Aphthous stomatitis has three ulcerations, a rinse, such as recognized clinical variations: minor, major, and (0.5 mg/5 mL) may be more herpetiform. successful. Major aphthae may require a more potent topical corticosteroid, such as 0.05% Minor aphthous ulcerations are the most common propionate gel. Efficacy of any of the presentation, seen in over 80% of patients with topical corticosteroids is largely dependent on RAS. They usually present as one to five contact time with the ulceration. Accordingly, use ulcerations, nearly exclusively on non-keratinized of gels versus creams is important in the (moveable) mucosa. The ulcerations are hydrophilic oral environment and application by composed of a yellow-white pseudo-membrane the patient at least 4-6 times a day is advised. surrounded by an erythematous halo 2-10 mm in Systemic side effects are not seen with diameter. associated with the lesion is appropriate use of topical corticosteroids; normally disproportionately greater than the size of however, patients may be at a greater risk of the lesion. (See Figure 2 & 3) developing an oral yeast infection while using the . Major aphthous ulcerations are observed in about 10% of patients with RAS, and may require Systemic corticosteroid use is reserved for therapeutic intervention more often compared with resistant cases in which must minor aphthae. (See Figure 4) be supplemented in order to gain control over the disease process. Once under control, systemic The herpetiform variant has the greatest number of treatment should be discontinued and RAS lesions per episode and the most frequent managed topically due to the adverse side recurrences. It is the form that is most often effects of prolonged systemic corticosteroid use. mistaken for a HSV infection. Numerous 1-3 mm While there are abundant alternative treatments ulcerations present predominantly on non- to corticosteroids available, caution should be keratinized mucosa, with reports of as many as exercised before making any recommendations 100 individual lesions at one time. These to patients since sufficient, high-quality evidence ulcerations may coalesce into larger, irregular to support their therapeutic value is often lacking. ulcerations. Low-level laser therapy at the site of ulceration has been shown to be effective at reducing both Unlike primary infection with HSV, RAS is not the pain and duration of aphthous ulcerations; associated with , or chills. however, such treatment for every episode of Aphthous ulcerations are never preceded by RAS is impractical for most patients. 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 Page 4

Herpes Simplex Virus Recurrent herpes occurs with reactivation of the latent herpes virus. Factors that may induce Oral cavity infection by HSV is most commonly due reactivation include light, physical or to infection with HSV-1, although infrequent cases emotional stress, fatigue, heat, cold, hormonal may be caused by HSV-2. HSV-1 is transmitted changes associated with or through infected or active perioral lesions. In pregnancy, allergy, trauma, dental treatment, developing areas, nearly 100% of the population is fever, , and old age. exposed by 15 years of age. Developed areas see Accompanying symptoms, such as those seen in a much lower rate of exposure, with only 50% to a primary HSV infection, are generally not 60% of the population being exposed by adulthood. present with a secondary infection. Recurrence Infection with HSV can either be primary or may occur along any epithelial surface supplied recurrent (secondary). After initial infection with by the involved , but the most frequent HSV, the virus is taken up by sensory nerves and site of recurrence is along the vermillion border establishes latency in a sensory nerve ganglion, and surrounding skin. This presentation is often the for HSV-1. The virus termed , commonly referred to as may then become re-activated at a later time. cold sores or fever . Patients are often Primary infection occurs when a previously aware of prodromal symptoms which may unexposed individual is infected with the virus. include tingling, burning, warmth, , or Most primary HSV occur at a young age pain in the area preceding vesicle formation. and are usually ; however, when Antiviral medication, topical and/or systemic, is symptoms do occur, they can be quite debilitating. most effective if initiated during the prodromal Symptoms have an abrupt onset and frequently stage. When HSV recurs intraorally, it is almost include fever (103˚ F to 105˚ F), chills, , always restricted to the attached mucosa (hard anterior , nausea, palate and attached gingiva). This is a helpful anorexia, irritability, and painful oral ulcerations. feature when distinguishing recurrent intraoral These symptoms range from mild to severe and herpes from recurrent aphthous ulcerations. appear 3 to 9 days after initial exposure. Oral Recurrent intraoral herpes is usually far less ulcerations first appear as pinpoint vesicles on both symptomatic than a primary infection, and many attached and moveable mucosa, which quickly patients do not require any treatment. For those rupture into small red lesions. These then may who do require treatment, rinses coalesce and form larger areas of ulceration have been show to exert antiviral activity and covered by a yellow-white pseudomembrane. The may even have some synergistic effects with gingiva will be enlarged, erythematous, and painful. acyclovir. Untreated, the intraoral ulcerations will Perioral involvement is not uncommon. Depending resolve within 7 to 10 days. on the severity, primary HSV infection can last from 5 days up to 2 weeks. Antiviral medication Recurrence of HSV in immunocompromised administered within the first 3 symptomatic days is patients can develop into severe disease, with beneficial in reducing the clinical course of the large, persistent ulcerations on both moveable infection (See Table 2 for dosing information). and attached mucosa. These patients may Acyclovir is the most commonly used antiviral require intravenous antiviral therapy and agent, but has the disadvantage of requiring the management of their underlying immune patient to take the drug 5 times a day. Newer dysfunction. such as valacyclovir and offer increased bioavailability and a subsequently more convenient dosing schedule, with a very similar safety profile to acyclovir. Topical 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) Page 5

acetaminophen or NSAIDs may be warranted for pain control. A (Zostavax) is FDA approved for adults 50 years of age and The varicella zoster virus (VZV or HHV-3) is older and has shown to decrease the responsible for two diseases: varicella, or of shingles by 50% to 70% as well as decrease , in childhood; and herpes zoster, or post-herpetic incidence by 67%. shingles, as a reoccurrence in adulthood.

The incidence of varicella has greatly decreased Enteroviruses since the institution of universal varicella vaccination in the , however Human enteroviruses are responsible for a unvaccinated individuals are still susceptible. variety of disease in young children worldwide. Symptoms begin with malaise, , and The virus is usually spread person-to-person, via rhinitis. A characteristic pruritic follows, contaminated water, or via contaminated objects. beginning on the face and trunk and then Most infections are asymptomatic; however spreading to the extremities. The rash consists of symptomatic cases can be mild to quite severe. lesions that progress through several stages: Three clinical presentations of enterovirus erythema, vesicles, pustules, and then crusting. infection can exhibit oral ulcerations: , Perioral and oral manifestations are common and hand-foot-and-mouth disease, and acute may precede skin lesions. Three to four millimeter lymphonodular pharyngitis. These are closely white, opaque vesicles may begin on the vermilion related conditions and some regard border, palate, buccal mucosa or gingiva. These lymphonodular pharyngitis as a variant of rupture to form 1 to 3 mm painless ulcerations that herpangina. The severity of disease ranges with heal within 1 to 10 days, depending on the severity the strain of virus for all three presentations. of the infection. Antiviral medication is generally not While most strains produce a self-limiting recommended for immunocompetent children with disease that does not require therapy, some uncomplicated disease; rather, it is reserved for strains can produce significant complications and severe cases or individuals who are rare fatalities. immunocompromised in some way. Symptoms associated with herpangina begin Shingles results from a reactivation of VZV, which with sore throat, , fever, rhinorrhea, remains latent in the dorsal root ganglia. anorexia, vomiting, , , , Reoccurrence is usually a singular event in adults and occasionally, cough. The majority of cases over the age of 50. Herpes zoster has three are mild or subclinical. Patients may develop 2 to phases: , acute, and chronic. The 6 small, aphthous-like ulcerations on the soft disease may be most noticeable to dental clinicians palate or tonsillar pillars. Systemic symptoms in the acute phase which can last 2 to 3 weeks. resolve within a few days, while oral ulcerations Involved skin develops clusters of vesicles on an may take up to 10 days to heal. erythematous base, which ulcerate and crust over. A striking unilateral appearance to the lesions is Hand-foot-and-mouth disease presents with observed, with termination at the midline. Oral similar systemic symptoms to herpangina. Its lesions may present on moveable or non-moveable name aptly describes the location of vesicular mucosa with the same unilateral spread. Intraoral lesions associated with this disease. Oral and lesions are similar to those seen in varicella, with 1 hand lesions are most consistently seen, with the to 4 mm vesicles that rupture into shallow oral lesions usually preceding the cutaneous ulcerations. Unlike varicella, teeth in the affected lesions. Cutaneous lesions develop as area may develop pulpal involvement that can lead erythematous macules that proceed into vesicles to pulpal , pulpal calcification, or root that heal without crusting. While oral lesions are resorption. Systemic antiviral therapy initiated similar to those seen in herpangina, they are within 72 hours of the first vesicle formation is usually more numerous and are not restricted to effective at accelerating healing and reducing pain. the and tonsillar pillars. The intraoral Concurrent treatment with lesions present as erythematous macules that Page 6 rapidly ulcerate and are typically 2 to 7 mm in may present in the acute, chronic, or diameter. disseminated form. Oral lesions may be observed in the rarest presentation, the Acute lymphonodular pharyngitis presents with disseminated form. Oral involvement of the sore throat, fever, and mild headache, which disseminated form appears as chronic ulceration, normally resolves within 4 to 14 days. Oral lesions most often reported on the tongue, palate and manifest as 1 to 5 yellow to dark-pink nodules on buccal mucosa. These ulcerations can appear the soft palate or tonsillar pillars. These lesions do clinically indistinguishable from squamous cell not ulcerate and represent hyperplastic lymphoid carcinoma and biopsy is necessary to establish a aggregates that resolve within 10 days. diagnoses. (See Figure 6 & 7)

Tuberculosis Chronic Inflammatory Bowel Disease Tuberculosis is a chronic infections disease cause by the bacterial organism Mycobacterium Inflammatory bowel disease (IBD) is most tuberculosis. Over 2 billion people are estimated to prevalent in North America and North-Western infected worldwide. Primary tuberculosis is the Europe, although its incidence has been initial stage of the disease, which affects previously increasing worldwide. Crohn’s disease and unexposed people. Pulmonary involvement are both part of the group of characterizes primary tuberculosis, and usually IBD. Besides affecting the , only progresses to a localized fibro-calcified nodule IBD can manifest with extraintestinal symptoms at the original site of infection. Only 5% to 10% of throughout the body. Extraintestinal people with primary tuberculosis progress to active manifestations (EIM) are reported in 6% to 47% disease, or secondary tuberculosis. of patients with IBD. Oral lesions can be a Immunosuppressive medications, poor living component of the EIMs with varying incidence conditions, , old age, and AIDS increase reports of 5% to 50%. the risk of progression to secondary tuberculosis. Active infection can disseminate from the lungs to Crohn’s disease, or regional enteritis, can have nearly any location in the body, including the oral both specific and non-specific oral lesions. These cavity. While uncommon, oral lesions from oral manifestations can precede intestinal disseminated secondary infection generally present manifestations or be seen concurrently. Specific on the tongue as a chronic, painless ulceration that oral lesions associated with Crohn’s disease may have a granular appearance. Such lesions are include granulomatous nodules which give a indistinguishable from other pathologic processes “cobblestone” appearance the oral mucosa, clinically, and therefore, require biopsy and mucosal tags, swelling of the , and microscopic examination for a definitive diagnosis. 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 Caused by the fungal organism Histoplasma seen around 60 years of age. capsulatum, histoplasmosis is the most common systemic fungal infection in the United States. It is Non-specific oral lesions that may be present in endemic to humid areas with soil enriched by bird both Crohn’s disease and ulcerative colitis or bat droppings, such as the Ohio and Mississippi include aphthous stomatitis, angular , River valleys. Most infections are asymptomatic or , and . Of these, very mild and are cleared by healthy individuals aphthous stomatitis and pyostomatitis vegetans with the development of against the manifest as oral ulcerations. Pyostomatitis organism in a matter of weeks. Reports indicate up vegetans begins as yellowish, slightly elevated, to 90% of individuals living in endemic areas will linear, curved pustules on an erythematous oral have antibodies against H. capsulatum. Disease mucosa. The buccal and labial mucosa, soft Page 7 palate, and ventral tongue are the most commonly When manifested in the oral cavity, the mucosa affected sites. These lesions may rupture to form is fragile and easily forms vesicles or bullae ulcerations, which then may cause discomfort for which quickly rupture to form ulcerations. the patient. Other conditions in this category are associated Treatment and management of the underlying with reactions to certain medications, bowel disease is helpful for resolution of the oral malignancies, or have poorly understood manifestations. For patients with mild bowel etiologies. Because of the diverse and complex symptoms, or oral lesions preceding bowl nature of many of these disease processes, the symptoms, use of a potent topical steroid may be discussion will be limited to clinical presentation beneficial for selective treatment of the oral lesions. relevant to the dental clinician, the process of diagnoses, and treatment for these conditions. Wegener’s Granulomatosis Vulgaris Wegener’s granulomatosis is an uncommon necrotizing granulomatous disease of unknown , is a rare condition in which etiology that can occur anytime from childhood to are produced against the late adulthood and may involve nearly every organ desmosomal junctions that hold epithelial cells system in the body. Occasionally oral changes may together. Without treatment, this condition often be present, including ulcerations. Strawberry will result in death. Oral lesions are often the first is the most distinctive oral manifestation, presentation of the systemic condition, and have seen early in the disease process when present. earned the expression, “the first to show, and the The affected gingiva, most often buccal surfaces, last to go.” Pemphigus usually presents in have a hyperplastic, red, bumpy appearance. Oral adulthood, with an average age at diagnoses of ulcerations present at later stages of the disease 50 years. Intraoral vesicles are usually not seen and do not form a specific pattern unique to due to their fragility; instead, patients will present Wegener’s granulomatosis. Generally, the with superficial, ragged erosions and ulcerations ulcerations are deep and irregular. The non- with a pattern-less distribution on nearly any specific nature of these oral ulcerations indicates a location of the oral mucosa. If lateral pressure is biopsy for definitive diagnosis. placed on normal-appearing portion of the mucosa, a bulla can be induced, termed a positive Nikolsky sign. A biopsy of an area with Chronic Vesiculoulcerative intact submitted in both formalin, for Diseases light microscopy, and Michel’s solution, for direct immunofluorescence (DIF), is necessary to This group includes several distinct conditions that confirm the diagnosis of pemphigus vulgaris. may produce chronic vesiculoulcerative or Patients are usually referred to due ulcerative lesions of the oral mucosa: pemphigus to the involvement of the cutaneous skin. These vulgaris, paraneoplastic pemphigus, mucous patients should be managed by a physician with membrane , , experience in administration of long-term , and . systemic corticosteroids.

Some, including pemphigus vulgaris and mucous Paraneoplastic Pemphigus membrane pemphigoid, result from the inappropriate production of antibodies With only 150 reported cases, paraneoplastic (autoantibodies) directed against normal molecular pemphigus, is a very rare condition that can structures in a person’s epithelium. This occur in patients with a neoplasm, usually misdirected damages the or chronic lymphocytic leukemia. connective junctions holding epithelial cells Paraneoplastic pemphigus has developed before together or to the underlying . the malignancy was identified in about one third Page 8 of the cases. Lesions involving the oral cavity ocular disease. Alternative treatments for those include diffuse, irregular ulceration of any area of with mild-to-moderate disease may include the the oral mucosa. The vermillion border may also be sulfa drug or / involved with severe hemorrhagic crusting, similar and niacinamide. Good results have been seen to that seen in erythema multiforme. Skin lesions in some patients using these alternative and involvement of other mucosal surfaces, such therapies; however, more studies are needed to as the eye and respiratory tract, are commonly confirm their use as a standard therapy. involved. Accordingly, paraneoplastic pemphigus is a serious condition with a poor prognosis. Bullous Pemphigoid Treatment consists of systemic corticosteroids and immunosuppressive agents. Although this may control the autoimmune disease, it often allows the Although bullous pemphigoid has resemblance malignancy to proliferate. to pemphigoid, it is a distinct condition that manifests primarily with cutaneous skin lesions. Oral mucosa is less often affected, Mucous Membrane Pemphigoid with only 10% to 20% of patients exhibiting oral involvement. Shallow ulcerations with smooth, Clinically, mucous membrane pemphigoid definite margins may be observed on the oral (cicatricial pemphigoid) may appear like mucosa following the rupture of bullae. pemphigus vulgaris, however the molecular basis Treatment varies depending on the severity of for the disease and disease course are very disease. Mild or localized disease may be different. In mucous membrane pemphigoid, controlled well with topical corticosteroids, autoantibodies are produced against the whereas moderate to severe disease may hemidesmosomal junctions which anchor the require systemic immunosuppressive therapy. epithelium to the underlying connective tissue. The Biopsy of apparently uninvolved tissue with average age of onset is 50 to 60 years and female submission for both DIF and standard are affected two times more frequently than males. microscopic evaluation is needed to reach a Oral lesions are usually pr0esent and include definitive diagnosis. intraoral vesicles and bullae that rupture to form large, irregular ulcerations, as well as a pattern on Erythema Multiforme the gingiva known as . Desquamative gingivitis is not specific to mucous membrane pemphigoid and may also be seen in Erythema multiforme is a poorly understood lichen planus and pemphigus vulgaris. Biopsy of blistering, ulcerative process. It is thought to be tissue with intact epithelium submitted in both immunologically mediated and associated with a formalin, for light microscopy, and Michel’s precipitating trigger, such as infection or solution, for direct immunofluorescence (DIF), is medication use. Herpes simplex and infection necessary to make the diagnosis of mucous with Mycoplasma pneumoniae have both been membrane pemphigoid. Once a diagnosis of implicated in triggering erythema multiforme. mucous membrane pemphigoid is made, it is Drugs associated with erythema multiforme are important to also refer the patient to an most often antibiotics or . Onset is ophthalmologist. Unlike pemphigus vulgaris, acute and usually observed in young adults in mucous membrane pemphigoid is not life their 20’s and 30’s. Flu-like prodromal symptoms threatening if left untreated; however, the mucous often present about 1 week prior to onset. membranes of the eye can be involved and Characteristic skin lesions resembling a bull’s progressive resulting from the disease may eye or target can appear on the extremities. eventually lead to blindness. Depending on the Mucosal sites including the oral cavity, disease presentation in an individual, the patient conjunctival, genitourinary, and respiratory may be successfully managed with topical mucosa may also be affected, although oral corticosteroids, or may require systemic mucosa is the most common. Oral lesions start corticosteroids and/or immunosuppressive agents. as erythematous patches that necrosis into large, Aggressive treatment is indicated for progressive shallow erosions and ulcerations with irregular Page 9 borders. Hemorrhagic, crusted lips are commonly seen. The disease is self-limiting 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 from mucous membrane pemphigoid.

Page 10

Tables

Table 1 Systemic Disorders Associated with Aphthous Ulcerations Behçet syndrome Celiac disease

Nutritional deficiencies (B1, B2, B6, B 12, , iron, ) Immunoglobulin A (IgA) deficiency Immunocompromised conditions, including human virus (HIV) Inflammatory bowel disease MAGIC syndrome (mouth and genital ulcers with inflamed cartilage) PFAPA syndrome (periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis) Sweet syndrome Ulcus vulvae acutum

Table 2 Treatment of Orolabial HSV Infections Pediatric Adult Primary herpes Acyclovir 75 mg/kg/day p.o. 5 400 mg p.o. 5 times/day x 5 (acute herpetic times/day (max 1 g/day) x 7 days gingivostomatitis) days Valacyclovir 1 g p.o. b.i.d. x 7 days, or 2 g 2 g p.o. stat, 2 g 12 hours p.o. b.i.d. x 1 day (if ≥ 12 y.o.) later Famciclovir 500 mg p.o. b.i.d. x 7 days (≥ 500 mg p.o. b.i.d. x 7 days 18 y.o.) Recurrent herpes Acyclovir 400 mg p.o. 5 times/day x 5 400 mg p.o. 5 times/day x 5 (secondary days days herpes) Valacyclovir 2 g p.o. stat, 2 g 12 hours later 2 g p.o. stat, 2 g 12 hours (≥ 12 y.o.) later Famciclovir 1.5 g p.o. x 1 day (≥ 18 y.o.) 1.5 g p.o. x 1 day

Page 11 Figure 1. Healing traumatic ulceration of Figure 2. Minor aphthae on maxillary labial mucosa right ventral tongue

Figure 3. Minor aphthous ulcer on dorsal Figure 4. Major and minor aphthae near left tongue commisure Figure 5. Primary herpetic gingivostomatitis

Figure 6. Ulceration of right ventral tongue due to disseminated Histoplasmosis

Figure 7. Carcinoma in situ with ulceration, right ventral tongue James, S. H., & Whitley, R. J. (2010). Treatment REFERENCES AND of infections in pediatric RESOURCES patients: current status and future needs. Clinical

Pharmacology and Therapeutics, 88(5), 720–4. Altenburg, A., El-Haj, N., Micheli, C., Puttkammer, https://doi.org/10.1038/clpt.2010.192 M., Abdel-Naser, M. B., & Zouboulis, C. C. (2014). The treatment of chronic recurrent oral Koh, W. M., Bogich, T., Siegel, K., Jin, J., Chong, aphthous ulcers. Deutsches Arzteblatt E. Y., Tan, C. Y., … Cook, A. R. (2016). The International, 111(40), 665–73. Epidemiology of Hand, Foot and Mouth Disease https://doi.org/10.3238/arztebl.2014.0665 in Asia: A Systematic Review and Analysis. The Pediatric Infectious Disease Journal, 35(10), Arduino, P. G., & Porter, S. R. (2007). Herpes e285-300. Simplex Virus Type 1 infection: overview on https://doi.org/10.1097/INF.0000000000001242 relevant clinico-pathological features*. Journal of Oral Pathology & Medicine, 37(2), 107–121. Lankarani, K. B., Sivandzadeh, G. R., & https://doi.org/10.1111/j.1600-0714.2007.00586.x Hassanpour, S. (2013). Oral manifestation in inflammatory bowel disease: a review. World Arduino, P., & Porter, S. (2006). Oral and perioral Journal of Gastroenterology, 19(46), 8571–9. herpes simplex virus type 1 (HSV-1) infection: https://doi.org/10.3748/wjg.v19.i46.8571 review of its management*. Oral Diseases, 12(3), 254–270. https://doi.org/10.1111/j.1601- Messadi, D. V., & Younai, F. (2010). Aphthous 0825.2006.01202.x ulcers. Dermatologic Therapy, 23(3), 281–290. https://doi.org/10.1111/j.1529-8019.2010.01324.x Belenguer-Guallar, I., Jiménez-Soriano, Y., & Claramunt-Lozano, A. (2014). Treatment of Mohan, R. P. S., Verma, S., Singh, U., & Agarwal, recurrent aphthous stomatitis. A literature review. N. (2013). Acute primary herpetic Journal of Clinical and Experimental Dentistry, gingivostomatitis. BMJ Case Reports, 2013. 6(2), e168-74. https://doi.org/10.4317/jced.51401 https://doi.org/10.1136/bcr-2013-200074

Chang, P.-C., Chen, S.-C., & Chen, K.-T. (2016). Muhvić-Urek, M., Tomac-Stojmenović, M., & The Current Status of the Disease Caused by Mijandrušić-Sinčić, B. (2016). Oral pathology in Enterovirus 71 Infections: Epidemiology, inflammatory bowel disease. World Journal of Pathogenesis, Molecular Epidemiology, and Gastroenterology, 22(25), 5655–67. Vaccine Development. International Journal of https://doi.org/10.3748/wjg.v22.i25.5655 Environmental Research and Public Health, 13(9). https://doi.org/10.3390/ijerph13090890 Neville, Damm, Allen, & Chi. (2016). Oral and Maxillofacial Pathology (Fourth Edi). Elsevier. Chauvin, P. J., & Ajar, A. H. (2002). Acute herpetic gingivostomatitis in adults: a review of 13 Omaña-Cepeda, C., Martínez-Valverde, A., del cases, including diagnosis and management. Mar Sabater-Recolons, M., Jané-Salas, E., Marí- Journal (Canadian Dental Association), 68(4), Roig, A., & López-López, J. (2016). A literature 247–51. Retrieved from review and case report of hand, foot and mouth http://www.ncbi.nlm.nih.gov/pubmed/12626280 disease in an immunocompetent adult. BMC Research Notes, 9, 165. Dhanrajani, P., & Cropley, P. W. (2015). Oral https://doi.org/10.1186/s13104-016-1973-y eosinophilic or traumatic ulcer: A case report and brief review. National Journal of Maxillofacial Tarakji, B., Gazal, G., Al-Maweri, S. A., Surgery, 6(2), 237–40. Azzeghaiby, S. N., & Alaizari, N. (2015). https://doi.org/10.4103/0975-5950.183854 Guideline for the diagnosis and treatment of recurrent aphthous stomatitis for dental practitioners. Journal of International Oral Health : JIOH, 7(5), 74–80. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/26028911 Page

14 REFERENCES AND RESOURCES, CONTINUED

Tidwell, E., Hutson, B., Burkhart, N., Gutmann, J. L., & Ellis, C. D. (1999). Herpes zoster of the third branch: a case report and review of the literature. International Endodontic Journal, 32(1), 61–66. https://doi.org/10.1046/j.1365-2591.1999.00187.x

Vale, F. A., Moreira, M. S., de Almeida, F. C. S., & Ramalho, K. M. (2015). Low-level laser therapy in the treatment of recurrent aphthous ulcers: a systematic review. TheScientificWorldJournal, 2015, 150412. https://doi.org/10.1155/2015/150412

EDUCATIONAL LINKS

1. http://www.oooojournal.net/ 2. http://www.joomr.org/

ABOUT THE AUTHOR

SARAH AGUIRRE, DDS

SARAH AGUIRRE GRADUATED FROM ARTHUR A. DUGUONI SCHOOL OF DENTISTRY IN SAN FRANCISCO, CALIFORNIA. SHE IS CURRENTLY A FIRST YEAR RESIDENT IN THE ORAL AND MAXILLOFACIAL PATHOLOGY PROGRAM AT THE OHIO STATE UNIVERSITY COLLEGE OF DENTISTRY. HER FUTURE CAREER PLANS INCLUDE SUPPORTING A BIOPSY SERVICE AS WELL AS TREATING AND MANAGING PATIENTS WITH ORAL DISEASE. DR. AGUIRRE CAN BE REACHED AT [email protected]

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

Page 15 post-test instructions - answer each question ONLINE - press “submit” - record your confirmation id - deadline is November 30, 2016 (4:00 PM EST)

Aphthous ulcers are the most common type 1 T F of oral ulceration

In order to be effective, antiviral therapy 2 T F should be initiated within the first 72 hours of a herpes simplex outbreak

Both the attached and unattached oral 3 T F mucosa are common sites for aphthous ulcers

A biopsy should be taken of any non-healing 4 T F oral ulceration

A deep, linear ulceration in the labial D i r e c t o r mandibular vestibule of a 13-year-old John R. Kalmar, DMD, PhD 5 T F patient may indicate the development of [email protected] ulcerative colitis Program Assistant Herpes zoster may present with vesicular Nick Kotlar, BS 6 T F lesions only on one side of a patient’s face [email protected] and oral mucosa Senior Lab Preparator Maitrayee Pariya Topical corticosteroids are an appropriate [email protected] 7 T F treatment for recurrent herpes

If a patient presents with a long-standing

ulcerations on the ventral surface of the tongue,

8 T F trauma, fungal infection, bacterial infection, and malignancy should be included in the differential diagnoses Page 16