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4 CE credits This course was written for dentists, dental hygienists, and assistants.

Demystifying Recurrent Oral Ulc茅rations A Peer-Reviewed Publication Written by Michelle Hurlbutt, RDH, BS and Lane Thomsen, DDS, MS

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Go Green, Go Online to take your course This course has been made possible through an unrestricted edutaiional grant from Tom's of Maine. The cost of this CE course is 559.00 for 4 CE credits. Caniellation/ftefund Polity: Any participant who is not 100% satisfied with this course can fequest a fuli refund by conlaning the Academy of Dental Therapeutics and Stomatology in writing.

Educational Objectives Upon completion of this course, the clinician will be able to do the following: 1. Explain the etiology of oral ulcérations. 2. Describe the clinical features and symptoms of aphthous ulcers. 3. Conduct a differential diagnosis for recurrent oral ulcérations. 4. Outline the topical and systemic medications used in the treatment of recurrent aphthous ulcérations and other palliative care and recommendations for patients.

include Behçet's disease, inflammatory bowel disease, Sweet's syndrome, HIV infection, lupus, neutropenia. Mouth and Genital Ulcers with Inflamed Cartilage Syndrome (MAGlCj syndrome, mucous membrane pemphigoid, pemphigus vulgaris and erythema multiforme. It is essential that the clinician understands the etiological factors and can perform a differential diagnosis for RAU to treat the patient appropriately.

Signs and Symptoms of Recurring Aphthous Uicers Minor aphthous ulcers

Abstract Oral irritations and ulcérations occur frequently in the general population. Recurrent aphthous ulcers (RAU) are the most common. There are three types of RAU — minor, major and herpetiform, the most common being minor aphthae. The exact etiology of RAU is not known. Systemic and local factors, as well as infectious agents, have been proposed. Certain medications and foods are associated with oral ulcérations, and chemicals such as sodium lauryl sulfate (SLS) contained in dentifrices have also been implicated. RAU also occur in more serious systemic diseases and where appropriate patients should be referred for screening and medical care. Treatment of recurrent aphthous ulcers is palliative, based on the severity of the lesions. Both topical and systemic medications are available. Nutritional and oral hygiene advice should also be given, and if patients are sensitive to SLS, a low-dose SLS or SLS-free dentifrice should be recommended.

Minor aphthous ulcers are small and cause the least discomfort. They are most prevalent in people 10-40 years of age. Usual locations include the floor of the mouth, buccal and labial mucosa, tip of the tongue, and ventral surface of the tongue. They are rare on the dorsum of the tongue and on keratinized mucosa. Patients may become aware of them when a tingling or burning sensation occurs. Within two days, a raised erythematous (red) papule or white spot appears. This ulcerates, resulting in a pseudomembranous grayish or yellowish center within the lesion. Minor aphthae are round or oval and measure up to 4 mm in diameter. They usually heal uneventfully seven to ten days after thefirstsigns appear. Recurrence may take weeks or years.''"' Figure 1. Minor aphthous ulcer

Introduction/Overview Oral irritations and ulcérations occur frequently in the general population and result in varying degrees of pain and debilitation for patients. Recurrent aphthous ulcers (RAU), also known as "canker sores," are the most common.' RAU occur in approximately 2Ü% of the population, with greater prevalence in upper socioeconomic groups and nonsmokers.' There are three types of RAU: minor, major and herpetifoim. The most common are minor aphthae, accounting for at least 80% of all cases.'-' Major aphthae account for approximately 10% of cases, and herpetiform less than 10%,'-^ Usually patients only have one type.' The second most common source of recurring oral ulcérations is the herpes simplex virus (HSV-l). Oral ulcérations also result from infection by other viruses, including the HIV, Coxsackie and ECHO viruses. Fungal and bacterial infections associated with oral ulcers are rarer and require extra consideration with respect to immunocompromised status.^ Other uicerative conditions include oral squamous cell carcinoma (SCC) and trauma-related lesions (thermal, chemical or physical). Prescribed medications are also associated with the development of oral ulcers. Extensive mucositis and stomatitis are seen in patients following head and neck radiation and chemotherapy. Systemic conditions involving oral ulcérations

Major aphthous uicers Major aphthae (Sutton's ulcers) are more severe than minor aph thae — larger, slower to heal and more painful — and can lead to adjacent and facial edema. They are found in all regions of oral mucosa, including keratinized mucosa, and are often larger than a centimeter in size. While they typically heal in ten to forty days, in extreme cases healing can take months while new ulcers are developing. Major RAU heal with scarring. If long-lasting and frequently recurring, they can result in morbidity and poor quality of life, with poor nutrition and stress."'" Herpetiform aphthous uicers Herpetiform ulcers occur as multiple lesions, up to 100 at a time, and can range from <1 mm to 3 mm in diameter each. Herpetiform RAU also coalesce into larger irregular lesions. Healing

Figure 2. Major aphthous ulcer

Figure 3, Herpetiform aphthous ulcers

drome often presents with classic RAU in addition to fever, erytbematous skin lesions and neutrophil disorder. '" Gastrointestinal diseases associated with R.A,U include celiac disease and Crobn's disease. Ceüac disease (also known as celiac sprue or gluten-sensitive enteropathy) is cbaracterized by nutrient malabsorption and improves as gluten is withdrawn from the diet. The most common oral symptom is RAU. A recent study revealed that as many as 42% of celiac disease patients screened bad oral soft tissue ulcérations, compared with 2% of the control group.'" With Crobn's disease, RAU are tbe common oral manifestation; in a prospective study of 792 patients, RAU occurred in 10.6%) of patients witb tbe mcidence sligbtly bigber than witb ulcerative colitis.-" Oral ulcers bave been seen in 25%-45% of systemic lupus erythematosis (SLE) patients. "' SLE-related lesions are more apt to be on tbe bard palate and often improve witb tbe treatment of otber systemic and cutaneous SLE manifestations." Other conditions associated witb oral ulcérations include (but are not limited to) mucous membrane pempbigoid, pemphigus vulgaris, Reiter's syndrome and erythema multiforme.

Immunologie factors usually occurs in seven to ten days, without any scarring. Herpetifonn ulcers do not exhibit a vesicle stage and are not infectious.

Etiology of Oral Ulcérations The exact etiology of RAU is not known. Systemic and local factors, as well as intectious agents, have been proposed. Medications including nonsteroidai anti-inflammatory drugs (NSAlDs); hypertensive medications such as ACE inhibitors, beta-btockers with alpha-blocking activity and calcium channel blockers; and cyclosporine, interferons, penicillin, sulfonamidesandnicorandil haveal! been implicated in oral ulcérations."'"'•''•"••''•"'•'^

Systemic Factors and Conditions Genetic factors More tban 40% of patients witb RAU may bave a family history of these ulcers.'" Patients witb a positive family bistory tend to develop oral ulcers at an earlier age and have more symptoms tban do otber individuals.-^'" Genetically specific antigens, called human leukocyte antigen (HLA) subtypes, bave been identified in patients witb RAU; bowever, no definitive association bas been sbown.-^-^*

Syndromes and conditions Systemic conditions associated witb RAU include Behçet's disease, MAGIC disease, Sweet'.s syndrome, inflammatory intestinal diseases and immunological factors. Behçet's disease is cbaracterized by recurrent oral, ocular and genital ulcers and mcludes vascular, central nervous system and gastrointestinal involvement. Of patients with Bebçet's disease, 99% experience oral apbthae.-^ MAGIC disease includes oral and genital ulcers and cartilage inflammation.-" Sweet's

Some studies have suggested that RAU is a result of an abnormal immune response. Increased concentrations of neutrophils in the ulcerative pbase of the lesion suggest an active role in the pathogenesis or healing of Ri\U. *'" Mast cells are able to release a variety of mediators, including cytokines and proteinases, and have been sbown to be 63% more numerous in RAU than in heaithy mucosa. '' A decreased ratio of CD4 to CD8 T-lymphocytes has also been reported. '' Further research is needed to better understand tbe relationship of RAU to immunoregulation.

HematinJc deficiencies The prevalence of iron, folie acid and B12 deficiencies and tbeir role in RAU is not well understood. In recent studies, patients with RAU were found to have more bematinic deficiencies than did tbe control group, with low-serum vitamin B12 being the most common deficiency."'''

Neutropenia Neutropenia is cbaracterized by an abnormally low count {<1,500 cells/mm-*) of neutropbils in tbe peripbera! blood. It is often associated with clinical AIDS and lower CD4 cell counts, and the risk for bacterial infection is a concern.'" Neutropenic ulcérations are often severe and can appear on the keratinized and nonkeratinized tissue, and if the neutrophil count is not restored to normal, resolution is not as successful. '''^"

Hormonal Tbe appearance of RAU may coincide with tbe menstrual cycle in a minority of women, but studies are contradictory.""''- In a review of the literature, no association could be determined from existing studies between RAU and the premenstrual pjeriod, pregnancy or menopause.^'

Stress Early studies associated R.MJ' with anxiety and emotional stress."'*' Higher incidences of RAU have been found among patients suffering from psychological disorders'*' and in patients with genetic defects linked to increased anxiety traits.'"' Clinical assessment should at least consider the role of stress in the appearance of RAU. Bacterial and Viral Factors Bacterial agents A recent study using DNA sequencing found 93 bacteria! species in RAU,"'' with only three species or phylotypes common to both the RAU and control groups. Prevotella was found only in RAU samples, and the RAU group showed greater bacterial diversity. In early studies, streptococci were implicated as a possible cause for RAU,'"* but further study has not been able to confirm this relationship/'' Helicohacter pylori has been found in up to 72% of RAU,~" but a link to RAU is considered unlikely."' Tuberculosis and syphilis have also been found to be associated with oral uleerations in rare cases.'^ Viral agents Viruses may play a role in oral ulcération by eliciting an immune response. Viruses associated with oral uleerations include human herpes virus-8 (HHV-8), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human papilioma virus (HPV) and herpes simplex virus (HSV-1). Some of these viruses may be solely responsible for oral ulcération, while others require a co infection of two or more viruses to induce ulcération."' Oral manifestations of measles have been seen in 20% of patients affected.''''•"' HIV results in oral uleerations including (but not limited to) RAU. Severe episodes of RAU are seen in HIV-infected patients. Unlike RAU that affect the general population, Ri^U in HIV-infected patients tend to be liirger, last longer (weeks or months in some cases) and be more resistant to treatment.'''-'''

Local Factors and Conditions

Food hypersensitivities Histamine release to food antigens has been reported in RAU patients."' RAU patients have reported a correlation between the onset of lesions and the consumption of walnuts, tomatoes and strawberries. Subsequent testing of these patients failed to identify any significant causation relationship between food hypersensitivity and RAU. However, this study did not utilize skin prick tests or patch tests to determine hypersensitivity.''"^ One study using patch tests reported that, in RAL patients testing positive to benzoic acid and cinnamaidehydc, a more than 80% decrease in the frequency of RAU was found with avoidance of the allergen,''' and in other studies specific food avoidance resulted in similar results.'''''"' Sodium lauryl sulfate (SLS) Sodium lauryl sulfate (SLS) has been implicated as a factor in the development of RAU. SLS is the most frequentK used detergent and surfactant in commercially available dentifrices and mouthwashes. SLS-susceptible (or sensitive) individuals were found to have severe skin reactions and irritation to four commercial dentifrices containing SLS, indicating that such individuals should avoid these products."'' It has been proposed that SLS may denature the mucosal mucin layer, which then exposes the oral epithelium to irritating agents and allergens, making the patient more susceptible to RAU.'"•'''* This undesirable effect is not due to any increased oral retention of SLS, as the contact time of retained SLS is minimal.'''' Studies reveal that use of dentifrices with 0.5%, 1.0% and 1.5% SLS resulted in significantly more epithelial desquamation than is seen with SLS-freedentifrices.'"'' Premenopausal women react more to SLS-containing dentifrices than do their postmenopausa! counterparts.^- In one study, the incidence of RAU was reduced by 81% when an SLS-free dentifrice was used instead of an SLS-containing dentifrice;'' however, a second study found no difference in the frequency or severity of RAU in people using SLS-containing versus SLS-free dentifrice.'' In a 6-week test, xerostomic patients showed no increase in RAU when using a dentifrice containing 1% SLS. ' ^

Trauma Patients predisposed to RAU develop lesions at sites of trauma."^ It is important to note that not all trauma leads to RAU, and many patients with RAU do not develop lesions after trauma.''' A recent population-based study of American adults did not find any significant association of trauma, such as cheek or lip bite, with RAU.""

In a recent in vitro study of reconstructed human oral mucosa, a dual biological effect was demonstrated with SLS. " Progressive desquamation and cell death prevailed at concentrations of SLS ranging from >0.15% to 1,5%. Compared to previous studies that supported the destructive effects of SLS,"'^ this study observed a protective mucosal effect induced by a low SLS concentration (Ü.Ü15%). Based on this in vitro study and existing data, more studies are indicated to develop less-irritating products for patient home care.

Squamous cell carcinoma Oral squamous cell carcinoma (SCC) is often asymptomatic until advanced. One presentation of SCC is as an ulcer that does not heal. It is essential to consider this, given the morbidity and mortality associated with oral cancer.

Other chemicals Chemicals have been implicated in oral uleerations, Painful hydrogen peroxide burns appearing as focal areas of ulcération have been reported.•'' Gingival irritation and sensitivity are side effects of tooth bleaching and are resolved a few

days following discontinuation of use."""' A high-alcohol oromuco.sal spray was shown to cause painful oral ulcers that resolved when use was discontinued.'^- High-alcohol mouthwashes have also been associated with oral ulcérations, but the appearance of the associated ulcers is not typical of RAU.^' l-'Iavoring, preservatives and coloring agents are common allergens in dentifrices and may cause contact stomatitis on the oral mucosa.**"' Tartar control toothpastes with pyrophosphates may also contribute to irritation, ulcérations and gingival sensitivity in

Differential Diagnosis A medical and dental history, intraoral and perioral examination, and examination of the cervical lymph nodes are all required. It is worthwhile to review the history with the patient and ask specific questions related to possible etiologies (Table 2). Patients may wrongly assume that other problems are unrelated, not worth mentioning or too embarrassing, and therefore may not note them on the medical history form. Table 2. Patient history review questions for oral ulcérations

Table 1. Etiological factors of oral ulcérations Systemic



Inflammatory bowel disease


• • •

Crohn's disease


Celiac disease


Ulcerative colitis


Drug reactions


Hematinic deficiencies

Hydrogen/carbamide peroxide


Food additive sensitivities





Immunologie factors



Behçet's disease


MAGIC disease

Herpes simplex, human and zoster

Sweet's syndrome

Epstein-Barr virus


Human papilloma virus

Mucous membrane pemphigoid


Pemphigus vulgaris

ECHO virus

Erythema multiforme

Coxsackie virus

Lichen planus







Inverse relationshijp to smoking


Tobacco There is an inverse relationship between tobacco use. including smokeless tobacco, and RAU. In smokeless tobacco, this negative association may be related to increased keratinization of the oral mucosa, especially in the area where the tobacco is held,'*' It has been suggested that nicotine may affect the immune response. In a case study of nonsmokers suffering from RAU, chewable nicotine (2 8 mg) gum tablets were administered for one month. In all cases there was remission, but after treatment was discontinued the RAU reappeared.**'^

How long have you had this ulcer? Have you had this before? When? How many? Where? Has anything changed recently? Have you stopped smoking recently? Have you changed your toothpaste? What are you using? Do you notice the ulcers after eating certain foods? Do you get ulcers on otherareasof your skin or body? Do you have inflammatory bowel disease? Is there anything else you feel you should add?

In many cases, the medical history and examinations described above may be all that is required for a definitive diagnosis of RAU. Also ascertain if the patient recently stopped smoking, as this results in an increased incidence of RAU.**" This is not to suggest that patients should resume tobacco habits. The most common ulcers to be mistaken for RAU are recurring intraoral herpes lesions. Recurring intraoral herpes lesions are similar to RAU but have important differences. If recurrences are common and the appearance is one of multiple tiny vesicles, typically < 1 mm in diameter, and the lesions are located on keratinized tissue (attached gingivae, hard palate) or the vermilion border, the diagnosis is likely recurrent herpetic lesions."" The vesicles may also rupture and coalesce. If a red halo is present, it is scalloped, not smooth as in RAU.'*' Recurrent herpes lesions may also be accompanied by malaise, fever, joint pain and cervical lymphadenopathy. Fever is rare with RAU and would suggest a different diagnosis, Trauma-induced ulcers may mimic RAU in appearance, however usually they can be linked to a traumatic incident such as lip-biting (Figure 5). If the patient has genital and/or ocular ulcers and lesions as well as RAU, this is suggestive of Behçet's disease, and for 67% of patients oral aphthae are the first sign and symptom.^-''' Genital and oral ulcers, when also involving inflammation of cartilage, are suggestive of MAGIC syndrome.'" RAU and ocular lesions are also found in benign mucous membrane pemphigoid (Figure 6)- A patient with skin lesions may require investigation for a variety of conditions, including Sweet's syndrome, pemphigus vulgaris (Figure 7), and fungal and bacterial infections. Careful clicitation of the medical history (particularly concerning diarrhea) may suggest investigation for inflammatory bowel disease, if it is not already diagnosed. Of RAU patients, 5% have been found to suffer from celiac disease.''' '''' Oral symptoms precede intestinal symptoms in about 60% of the cases of Crohn's disease."

Figure 4. Intraoral herpes lesions

Figure 5. Trauma-induced ulcer following lip biting

Single lesions that do not heal within 2 weeks (includ ing following removal of a traumatic irritant}, particularly if there is no previous history of similar lesions, should be viewed with suspicion. The differential diagnosis must include squamous cell carcinoma (SCC), and a definitive biopsy may be required (Figure 8). Patients with long-lasting RAU that are particularly severe and refuse to heal are suspect for HIV infection or another immunocompromised condition, RAU in these patients are more severe, are of long duration, heal poorly and are debilitating.""" In cases of frequent or severe outbreaks of RAU, a referral for systemic disease and vitamin deficiency screening should be given, if such conditions were not previously diagnosed. Sensitivity screening may also be considered to rule out reac tions to foods and chemicals such as SLS.

Palliative Care There is no definitive cure for aphthous ulcers. Palliative can: can be provided to relieve pain, promote healing and prevent secondary infection. Various topical and systemic medications are available.

Topical medications

Figure 6a. Intraoral ulcer associated with benign mucous membrane pemphigoid

Figure 6b. Ocular lesion associated with benign mucous membrane pemphigoid

If patients have skin, ocular, genital or other non-oral mucosa! lesions, the diagnosis is unlikely to be RAU unless there are coincidental one-time unrelated lesions. Similarly, the diagnosis is unlikely to be RAU if fever is present.

Pain-relieving topical gels that can be dabbed on the lesion include 2% lidocaine and 20% benzocaine-based products (Colgate* Orábase*, Orajei* Ultra, Anbesol"). Lidocaine mouth rinse or spray can also be used. Topical pain-relieving barrier agents that have been shown to promote healing include octylcyanoacryiate (Soothe-N-SeaF")'''' and 5% anJex anox paste (AphthasoP).""' "" 5% amlexanox paste can reduce the severity of ulcers if applied two to four times daily in the initial phase of ulcer development. Rinses that form a bioadherent protective mucosal coating are available (Rincinol", Gelciair®); these are useful if lesions are widespread. Topical corticosteroids are available in varying potencies. Topical hydrocortisone hemisuccinate pellets (2.5 mg) can bo used for nonsevere cases.'"- Triamcinolone acetonlde paste (Kenalog in Orábase'") is a medium-potency prescription topical corticosteroid that helps to reduce pain, inflammation and ulcération when applied two or three times daily for five days. An alternative is fluocinonide dental paste (Lidex in Orábase).'"' Four to five days' use of tetracycline or minocycline rinse four times daily has also been found to be helpful in treating RAU. Tetracycline rinse can be made using a 250 mg capsule dissolved in 180 cc water."" These rinses should no: be used in young children because ot the risk of intrinsic stain ing in developing teeth should the child swallow the rinse. For severe RAU, higher potency anesthetic rinses, topical corticosteroids, tetracycline and/or systemic medications arc needed, Palliative rinses combining equal parts 2% lidocaine, a bioadhesive coating agent (such as kaopectate) and an antihistamine are effective. Fietamethasone mouth rinse is more effective than are hydrocortisone and triamcinolone rinses. However, there is a risk of opportunistic candidal infections.


Figure 7a. Oral ulcérations in a pemphigus patient

Table 3. Topicai medications Mild and moderate RAU 2% lidocaine

Hydrocortisone hemi succinate

20% benzocaine

Triamcinalone acetonide




Tetracyctine/minocyline rinses




Zinc lozenges Severe RAU

Figure 7b. Skin lesions in pemphigus patient

Combination rinses

á-interferon rinse

Betamethasone rinse Table 4, Additional care


Figure 8. Squamous cell carcinoma


Elimination of food allergens

Non-spicy food and drink

Elimination of gluten (Celiac's)

Adeguate fluid intake

Reduced dose SLS dentifrice

Oral Hygiene

SLS-free dentifrice

Ultra soft toothbrush

Eiimination of other chemicals

Adjunctive rinsing

Drug reactions — discontinue drugs

Remove sharp points

become pregnant, as it is a potent teratogen. Other systemic medications have also been used. Altemative therapies, such as bee propolis (500mg/day), show promise in reducing the number of recurrences of RAU. "^ Courtesy of Denis P. Lynch, DDS, PhD

tind a greater risk for adrenal suppression with long-term use.'"' If long-term use of topical corticosteroids is necessary, antifungal lozenges or mouth rinses may be required to help prevent candidiasis. Aná-Ínterferon rinse — an imniunomodulator — may also be effective in treating severe cases of R.AU. ' ""

Systemic medications Systemic medications may be required for the most severe cases. I'rednisone (60 mg} four times daily for five to seven days is effective; its use should be avoided in HIV-infected and other immunocompromised patients. If prednisone is used for longer than seven days, slow tapering off is required due to adrenal suppression. For focally severe resistant ulcers, a local triamcinalone injection into the lesion may help.'"' For refractory cases, thaJidomide (200 mg four times daily for four weeks), dapsone. colchicine and pentoxifylline may he helpful.'"'*•'*'•"" Cotchicine administered three times daily (0.5 mg) over two months has been found to decrease the number of ulcers and to reduce pain,'"'"' Thalidomide must never be used in pregnant women or women who may


Nutrition and oral hygiene Aphthae make eating and drinking painful. Patients should avoid hard or crunchy foods and snacks, spicy and salty foods, hot drinks, and acidic drinks (such as orange juice). Using a straw or sipping liquid slowly will help, as will eating soft, bland foods. Patients must drink an adequate amount of fluid."'' Sipping cold, nonacidic drinks may also help soothe lesions. Maintaining oral hygiene, in addition to its usual benefits, helps prevent secondary infection. Patients should use an ultrasoft toothbrush. Adjunctive use of chiorhexidine giuconate or cetylpyndmum chloride mouth rinse helps reduce the bacterial load and plaque while patients are having difficulty brushing." ^ Twice-daily rinsing with 0.12% chiorhexidine giuconate can increase the number of days without ulcers, although it has not been found to influence the incidence or severity of RAU. If vitamin deficiencies are present, supplements can be given. RAU patients have been shown to respond to Bl 2 replacement therapy."" Sharp areas on the dentition or restorations should be smoothed to help prevent trauma if a lesion is present and to help reduce pain during eating and drinking. While discontinuation of medications associated with oral ulcers is indicated to prevent oral ulcers, such discontinuation

may be medically contraindicated if an alternative is not available. In tbese cases, aggressive management and palliative care of oral ulcération is essential.

Sensitivities Strict elimination diets for food sensitivities have shown significant improvement and/or resolution of persistent lesions in 40'/n-80% of patients, but patient dropout rates in tbese studies raise concerns about compliance."''"'*"'' Also of note is that 89% of celiac disease patients bave been found to have no RAU after one year on a gluten-free diet.'-" SLS-related sensitivities may be dose-related ratber tban absolute. For patients witb sucb sensitivities, use of SLS-free oral care products or those with reduced SLS is recommended.'''

Summary Oral ulcérations are a common condition, with RAU being tbe most common. It is important to be able to perform an accurate differential diagnosis to ensure tbat tbe patient receives the appropriate treatment. RAU include minor, major and berpetiform variants that differ in size, location, duration, and level of discomfort or pain. Possible etiologies include systemic and local conditions as well as food and chemical sensitivities. RAU are treated palliatively with a variety of topical and systemic medications, tbe selection of whicb is based on the individual patient's needs and on the severity of the ulcération. In cases where allergic responses to food or food additives are involved, tbe patient sbouid avoid those foods. Patients who bave suspected or confirmed SLS sensitivity sbouid use a dentifrice containing eitber no SLS or a low level of SLS.

References 1 I

3 4 5 6 7 8


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19 Sculiy C, Feiix DH, Orai medicine - Update for the dentai practitioner. Aphthous and other commie uicets.Br Dent J. 2005:199:259-64. 20 Ship il. Inheritance of aphthous ulcers of the mouth, J Dent Res, 1965; 44:837-44. 21 Ship jA. Recurrent aphthous stomatitis: An update. Oral Surg Oral Med Oral Pathol. 1996, 22 Lake Rl, Thomas SJ, Martin NG, Genetic láaors in the aetiology af mouth ulcers. Genet, Epidemioi 1997:14 (Suppl):17-33, 23 Challacombe SJ, Batchelor JR, Kennedy LA, Lehner T HLA antigens in recurrent oral ulcérations Arch Dematol. 1977:113:17-19. 24 Shohat-ZabarskíR,KaideronS,KleinT,WeinbergerA,TikvaRAvivR.CloseassociationofHLA-B51ii' persons with recurrent aphthous stomatitis. Orai Surg Oral Med Oral Pathol. 1992:74(4) :455-8. 25 LehnerT. Oral ulcération and Behçet's syndrome. Gut. 1977:18:491-511. 26 Porter SR, Scully C, Pedersen A, Recurrent aphthous stomatitis. Crit Rev Orai Biol Med 1998:9(31:306-21. 27 Notaril K, Kobayashi S, Kondoh K, Shindoh M, Ferguson MM, Fukuda H, A case of Sweet's syndrome (acute febrile neutrophilic dermatosis) with palatal ulcération. Oral Surg Oral Med Oral Pathol Or¿: RadiolEndod. 2000:89:477-9. 28 Campisi G, Di Liberto C, lacono G, Compiiato D, D¡ Prima L, étal. Oral pathology in untreated coeliai disease. Aliment Pharmacnl Ther, 2007:26(11-12):1529-36. 29 Burgan SZ, Sawair FA, Amarir ZO, Hematciogic status in patients with rKurrent aphthou'. stomatitis in todan. Saudi Med ). 2OO6:27(3):381 - 4 . 30 Urman JD, Lowenstein MB, Abeies M, Weinstein A. Oral mucosal ulcération In systemic iupu'. erythematosus. Arthritis Rheum, 1978:21(1):58-61, 31 McCauliffe DP Cutaneous Lupus Erythematosus. Semin Cutan Med Surg, 2001:20(1): 14-26. 32 Dagaiis f. Bagg 1, Walkei D. Spontaneous migration and chemotactic aaivity of neutroph,i polymorphonuclear leukocyles in recurrent aphthous ulcération. Oral Surg Oral Med Oral Pathr,i 1987:64(3):298-30l. 33 Wray D, Charon J. Polymorphonuclear neutrophil function in recurrent aphthous stomatitis, J Oral Paihol Med. 1991:20:392-4, 34 Natah SS, Hayrinen-immonen R, Heitanen J, Malstrom M, líonttinen YT Quantitative assessmeni of mast cells in recurrent aphthous ulcers (RAU), J Oral Pathoi Med. 1998:27:124-9. 3.Í Bachtiar EW, Cornain S, Siregar B. Raharjo TW. Decreased CD4+/CD8+ ratio in major types of recurrent aphthous ulcers: comparing major to minor types of ulcers. AsianfeeJ Allergy Immunol. 1998:16:75-9, 36 Burgan SZ, Sawair FA, Amarin ZO. Hématologie status in patients with recurrent aphthou'.. stomatitis in Jordan. Saudi Med J. 2O06:27(3):381-4. 37 Koybasi S, Parlak AH, Serin [, Yiimaz F, Sedn D. Recurrent aphthous stomatitis: investigation u' possible etioloqtc faaors. Am J Otolaryngal. 2OO6:27(4):229-32. 38 Levine AM, Ervin CM, Gange SJ, Anastos K, Young M, et al, Neutropenia in huma^ immunodeficiency virus infection: Data from the women's interagency HIV study. Arch intem Med 2OO6:166(4):405-10. 39 Porter SR, Scully C, Standen GR, Autoimmune neutropenia manifesting as recunent oral uiceration Orai Surg Oral Med Orai Pathol. 1994:78(2).! 78-80. 40 Luzzi GA, Jones B). Treatment of neutropenic oral ulcération in human immunodeficiency viru'. infection with G-CSE Oral Surg Oral Med Oral Pathol. 1996:81(l):53-4. 41 Dolby AE. Recurieni Mikulia's oral apthae. Their relationship to the menstmal cycle, Br Dent • 1968:124:359-60. 42 Segal AL, Katcher AH, Brightman VI, Miller MF Recurrent herpes labialis, recurrent aphthous ulcer^ and the menstrual cycie. J Dent Res. 1974:53(4) :797-803. 43 McCartan BE, Sullivan A, The association of menstrual cycle, pregnancy, and menopause m\\ recurrent oral aphthous stomatitis: A review and criiigue. Obstet Gynecoi. 1992:80(3):455-8. 44 Ship I, Morris AL, Durocher RT, Burket LW. Recurrent aphthous ulcérations in a professional schod student population. Oral Surg Oral Med Orai Pathoi. l%1:14(l):30-9. 45 Soto-Ara/a M, Rojas AG, fsguep A, Association between psychoiogical disordersand the presence of orai lichen pianus, burning mouth syndrome and recurrent aphthous stomatitis. Med Orai 2004;9(l):1-746 Victoria JMN, Correia-Silva J, Pimenta FJ, Kalapothakis E, Gomez, RS. Serotonin transporter gene polymorphism (5-HTTLPR) in patients with recurrent aphthous stomatitis, J Oral Pathol Mei! 2005:34:494-7. 47 Marchini L, Campos MS, Sila AM, Paulino LC, Nobrega FG. Sanerial diversity in aphthous ulcer. Oral Microbiol immunoL 2007:22:225-31. 48 Barile MF, Grayowski MD, Driscoil EJ, Riggs DB. L Form of bacteria isolated from recurrent aphthou^ stomatitis iesions. Orai Surg Orai Med Oral Pathol, 1963:16(1 l):1395-14OO. 49 RiggiD MR Lennon A, Ghodratnama F, Wray D. Lack of association between Streptococcus oralisand recurrent aphthous stomatitis. J Oral Pathol Med. 2000:29:26-32. 50 Birek C, Grandhi R, McNeill K, Singer D, Ficarra G, Bowden G, Detection of Helicobacter pylori in orai aphthous ulcers. ) Orai Pathoi Med. 1999,28:197-203. 51 lamaroon A, Chaimano S, Linpisam S, Pongsiriwet S, Phomphutkul K. Deteaion of Heiiobactoi pylori in recurrent aphthous ulcération by nested PCR, J Oral Sei. 2003:45 (2): 107-10. 52 Scully C, Felix DH. Oral medicine - Update for the dentai practitioner. Aphthousand other common ulcers. Br Dent J. 2005:199:259-64. 53 Lin SS, Chou MY, Ho CC, KaoCT, Isai CH,Wang L. Yang CC. Stuííy of the viral infections and cytokine^ associated with recurrent aphthous ulcération. Microbes Infect. 2005:7(4):635-44. 54 Guelmann KJ, Stavropolous F, Heft M. Gingival and other oral manifestations in measles vim infection. J Clin Periodontol. 2003:30:665-8. 55 Czerninski R, Katz J, Schlesinger M. Preliminary evidence for an association of measles vim antigen and CD46 virus with recurrent aphthous uiceration. Arch Dermotol, 2000:136:801-3. 56 Muzyka BC, Glick M. Major aphthcus ulcers in patients with HiV disease, Orai Surg Orai Med Orai Pathol 1994:77(21:116-20. 57 Youie M, Clartour J, Farthing C, et al.Treatment of resistant aphthous ulcération with thalidomirii


in patier(s positive for HIV antibody. Br Med J 198:298:432. 58 Wray D, Graykowski EA, Notkins AL. Role of mucosal injury in initiating recurreiii aphihous slomaIitis.BrMedJ.Î98î;2S3112):1569-?0. 59 Ross R Kitscher AH, Zegarelli EV. Piro 10, Silvers H. Relationship of mechanical trauma to recurrent aphthous stomalills. HY State Dent J. 1985:22:101-2. 60 Chanopadhyay A, Chatterjee S. Risk indiGtors for recurrent aphthous ulcers among adults in ttie US. Community Deri Oral Edpidemiol, 2007:35:152-9, til Wray 0, VlagopouioLslF; üiraganian RP Food allergens and basophil histamine release in recurrent aphthous stomatitis. Oral Surg Orai Med Oral Pathci. 1982:54(4):388-95. b} Eversole LR, Shopper TR Chambers DW. Effeas of suspected foodstuff chalienging agents in the aetiology of recurrent aphthous stomatitis. Oral Surg Orai Med Oral Pathoi. 1982;54O):33-8, 6Í Molan A, Lamey PJ, Miliigan KA, Forsyth A. Recurrent aphtfious ulcération and tood sensitivity, J Oral Palhol Med. 1991,20:4/3-5. 64 Wright A, Ryan FR Wiilingham SE, Holt S. Page AC, et al. Food allergy or intolerance in severe recurreni aphthous ulcération of the mauth Br Med J (Clin Res Ed), 1986; 292(6530:1237-8. 65 Hay KO, Reade PC. The use of ar elimination diet in the treatment of fKurrent aphthous ulcération of the orai cavity. Oral Surg Oral Med Oral Pathoi. 57¡5):504-7. 66 Sl(aareAB,KjaerheimV,ßarkvollliRöllaG.SkinreaaiDnsandirrttationpotentialoffourcommercial toothpasles.AdaOdortolScand, 1997;55[2):133-6, 6? Herlofson BB, Barkvoll P Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary study. AaaOdomolScand, 1994:52:257-9. 68 Chahine L, Sempson N, Wagoner C. Ttie effect of sodium lauryl sulfate on recurrerit aphthous ulcers: A clinical study CompendCort Educ Dent. 1997; 18(121:1238-40. 69 Fakhry-Smith S, Din C. Nathoo SA, Gaffar A, Clearance of sojium lauryl sulpha» from the oral cavity. J Clin Periodontol. 1997:24:313-7, ?0 Herlofson BB, Barvoll ?. Oisi mucosal desguamation caused by two toothpaste detergents in an experimental model. Eur J. Oral Sei. 19%;IO4:21-6. 71 Heriofson BB, Barkvoil R Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary studyAda Odortoi Stand. 1994;52:257-9. "' ' Herlofson BB, Barkvcll P Oral mucosal desquamation of pre- and postmencpausal vramen: A comparison of response to sodium lauryl sulphate in toothpastes. J Clin taiodontol. 1996;23[6): 567-71. 73 Ctiahine L, Sempson H. Wagoner C. The effect of sodium lauryl sulfate on recurrent aphthous ulcers: A cliniGl study. Compend Com Educ Dem. 1997:18(12) :1238-40. 74 HealyCM,PatersonM,loystor-BechalS,Wil1iamsDM,ThomhillMH.Theeffect of a sodium lauryl sulfate-free dentifrice on patients with recurrent oral ulcération. Oral Dis. 1999:5:39-43. 75 Rantanen I, Tenovuo J, Pienihakkinen K, et al. Effects of a betaine-contairirg toothpaste on subjeaive symptoms of dry mouth, a randomised clinical trial, J Contemp Dent Pract. 2003,(4)2:11-23. 76 Neppelberg E, Costea DE, Vintennyr OK, Johannessen AC. Dual effects of sodium lauryl sulphateon human oral epithelial structure. ExpDermatol. 2007:16:574-9. 71 5kaare AB, Rolla G, Barlivoll P The influence of triclosan, zinc or propylene glyco! on oral mucosa exposed to sodium lamyl sulphate. Eur J Oral 5ci. 1997:105:527-33. 78 Healy CM, Cruchley AT, Thornhilt MH, Williams DM. The effea of sodium lauryl sulphate, triclosan and zinc on the permeability of normal orai mucosa, Orai Dis. 2000:15:801 -07. 79 Shetty K. Hydrogen peroxide bums of the oral mucosa. Ann Pharm. 2OO6:4OÍ2):351. 80 Leonard RH, Garland GE, Eagle JC, Caplan DJ. Safety issues when using a 16% cartamide peroxide whitening solution, J Esthet Restorat Dem. 2002;1416):358-67. 81 Leonard H, Smith LR, Garland GEJiwana KK, Zaidel LA, et al. Evaluation of Side Effectsand Patients' Perceptions during Tooth Bleaching, ) bthet Restorat Dent. 2007:19(6); 355-64. 82 Scully C. Cannabis: Adverse effeas from an oromucosal spray. Br Dent J. 2007:203(6) :336-7, 83 Touyz \2, Hille JJ. A fruit-mouthv^ash chemical burn. Repon of a case. Oral Surg Oral Med Oral Pathoi. 1984;58(3):290-2. 84 Sainio EL, Kanerva L. Contact allergens In toothpastes and a review of their hypetsensitivity. Contaa Dermatitis. 1995,33(2): 100-5. 85 Sarsiey R£, Cottone JA. The effects of tartar-control toothpaste on the oral soft tissues. Oral Surg Oral Med Oral Pathoi. 1990:70(4]:529-36. 36 Dctattre VF. Factors contributing to adverse soft tissue reactions due to the use of tartaf control toothpastes: Report of a case and literature review, J Periodontol. 1999;70(7):803-07. 87 Bittoun R. Recurrent aphthous ulcers and nicotine. Med J Aust. 1991;154:471-2. 88 Grady D, Ernster BL, Stillman L, Greenspan J. Smokeless tobacco use p^vents aphthous stomatitis. Oral Surg Oral Med Oral Pathoi. 1992:74:463-5. 89 McRobbie H, Hajek F! Giiiison F. The relationship between smoking cessation and mouth ulcers. NictoineTobRes.2004;6(4):655-59. 90 Sciubba JJ. Herpes simplex and aphthous uleerations. Presentation, diagnosis and management. Gen Dent. 2005;5l:510-i7. 91 Tilliss TSI, McDoviiell J. Differential diagnosis: is it herpes or aphthous? J Cont Dent PracL 2002: 3(1): 92 Lehner T. Immunological aspects of recuftent oral ulcération and Sehçet's syndrome. J Oral Pathoi 1978;7:424-3O. 93 Lehnerl Oral ulcération and Behçet'ssyndrome. Gut. 1977:18:491-511. 94 Porter SR, Scully C, Pedersen A. Recurrent aptithous stomatitis. Crit Rev Oral Biol Med. 1998:9(3):306-21, ^S VelosoFT,SaleiroJV,Small-bowelctiangeslnrecun'ertuicerationofthemouth,HepatogastroenteroL 1987:34:36-7. 96 Ferguson R, Basu MK, Asgulth R Cooke WT. Jejunal mucosal abnormalities in patients with recurrent aphthous ulcération. Br Med ), 1976:1:11-3, •^7 Rehberger A, Puspok A, Staiimeister T, Jureck W. Crohn'sdisease masquerading as aphthotis ulcers. EurJDermatoL1998;8(4}:274-276.


98 Muzyka BC, Glick M, Major aphthous ulcers in patients with HIV disease- Oral Surg Oial Med Oral Pathoi. 1994:77.116-20. 99 Gaffar A, Narang U, Kutcher M, et al. Oral ñrst aid in the 21st century. Supplement to Compendium of Continuing Education in Dentistry 2OOl:22(32):l-33. 100 Greer RO, Lindenmuth JE, Juarez T, Khandwala A. A double-blind study of topically applied 5% amlexanox in the treatment of aphthous ulcers. J Oral Maxillofac Surg, 1993:51:243-9. 101 Binnie WH, Curro FA, Khandwala A, Vanlnwegan RG. Amlexanox oral paste: a novel treatment that accelerates the healing of aphthous uicers, Compend Cont Educ Dent 1997:18:1116-8,1120-2. 102 Scully C, Felii DH. Oral medicine—Update for the dental practitioner. Aphthous and other common ulcers. Br Dent J. 2005:199:259-64. 103 Marinopoulos S. Apthous ulcers. Available at: organ_system/heent/fulLaphthoüS_ulcers.html. Accessed January 12,2008. 104 Ibid. 105 Scully C, Felix DH. Oral medicine - Update for the dental practitioner. Aphthousand other common ulcers, Br Dem J. 2005:199:259-64. 106 AltenburgA,Abdel-NaserMB,SeeberH,AbdalliihM,ZouboulisCC.Praaicalaspectsofmanagement ofrecuirentaphthousstomatitis. J Eur AcadDermatolVenereol. 2007:21(81:1019-26. 107 ScullyC,GorskyM,Lozada-NurF,Thediagnosisand management of recurrentaphthousstomatitis, A consensus approach. J Am Dent Assoc. 2003:134(2):20O-7. 108 Marinopoulos S. Apthous ulcers. Available at: or9an_system/heent/full_aphthous_uicers,html. Accessed January 12,2008. 109 Elsen D, Lynch DP Selecting topical and systemic agents for recurreni aphthous stomatitis. Cutis. 2001:68(3):201-6. 110 Jacobson JM, Greenspan JS, Spritzler J, et al. Tlialidomide for the treatment of oral aphthous ulcers in patients with human immunodeficiency virus infection. Nationai Institute of Alleigy and Infectious Diseases AiDS Clinical Trials Group. H EngI J Med: 1997:33611).487-93. 111 Gatot A, Tovi F. Colchicine therapy in recurrent oral ulcers. Arch Dermatol. 1984:120:994, 112 Katz J, Langevitz R Shemer J, Barak S, Livneh A. Prevention of recurrent aphthous stomatitis with colchicine: Anopentrial.JAmAcadDemiaioL 1994:31:459-61. 113 Samet N, Laurent C, Susaria SM, Samet-Rubinsteen N. The effect of bee propolis on recunrn! apthous stomatitis: a pilot study. Gin Oral Invest. 2007:11:143-7 114 ScullyCFelixDH. Oral medicine-Updateforthedental practitioner. Aphthousandothercommon ulcers. Br Dent J. 2005:199:259-64. 115 Ibid. 116 Volkov I, Rudoy I, Abu-Rabia U, Masalha T, Masaiha R. Case report: Recurrent aphthous stomatitis responds to vitamin B12 treatment. Can Fam Physician. 2005 June;Sl:844-45. 11/ Wright A, Ryan Fí Wiilingham SE, Holt S, Page AC, Hindle MO, Franklin CD. Food aliergy or intolerance in severe recurrent aphthous ulcération of the mouth. Br Med J (Clin Res Ed) 1986:292(6530:1237-38118 Nolan A, Lamey P¡, Milllgan KA, Forsyth A, Recurrent aphthous ulcération and food sensitivity. J Oral Pathoi Med. 1991:20:4/3-75. 119 Hay KD, fieade PC. The use of an elimination diet in the treatment of recurrent aphthous ulcération of the orai cavity. Oral Surg Oral Med Oral Pathoi. 57(5):S04-O7 120 Campisi G, Di liberto C, laconoG, Compilato D, Di Prima L, et al. Oral pathology in untreated coeliac disease. Aliment PharmacolTher,2007:26(1l-l2):l529-36. 121 Marinopoulos S. Apthous ulcers, Availabie at: hnp://www.hopl(inS' organ_system/heent/full_aphthous_ulcers.(itml. Accessed January 12,2008.

Author Profiles Michelle Hurlbutt, RDH, BS. Assistant Professor, Department of Dental Hygiene, School of Dentistry, Loma Linda University.

LaneThomsen, DDS, MS. Chairperson, Department of Oral Diagnosis, Radioiogy and Pathology, School of Dentistry, Loma Linda University.

Disclaimer The authors of this course have no commercial ties with the sponsors or the providers of the unrestricted educational grant for this course.

Reader Feedback We encourage your comments on this or any ADTS course. For your convenience, an online feedback form is available at

Questions 1. The most common oral ulcers a. b. c. d.

Rccurrenl herpes lesions Recurrent aphthous ulcers HlV-related none of the above

2. Recurrent aphthous ulcers occur in approximately 20 percent of [hf population, a. Tnie h. False 3. The second most common source of recurring oral ulcérations is . a. tbe berpes zoster vims b. tbe C^oxsackie virus c. sypbilis d. tbe herpes simplex virus

5. Minor aphthous ulcers are common on the dorsum of the tongue and on keratinized mucosa. a. True b. False fl. Minor aphthous ulcers present clinically with _. a. vesicles b. pseudomembranous grayisb or yellowish centers c. grey borders d. al! of ibe above a. b. c. d.

12. Neutropenic ulcérations are mild and appear only on nonkeratinized tissue. a. True b. False 13. Helieobacter pylori has been found to be definitively assoeiated with recurrent aphthous ulcers. a. True b. False

4. Systemic conditions involving oral ulcérations include . a. inflammatory bowel disease b. Bebçet's disease c. HIV infection d. all of tbe above

7. Major aphthae

11. The most common hematinic deficiency seen in patients with recurrent aphthous ulcers has been found to be . a. vitamin B6 b. vitamin Bl 2 c. vitamin C d. none of the above


beal without scarring occur in 5 percent of the population are also known as Sutton's ulcers all of tbe above

14. A recent population-based study of American adults found . a. a significant association of trauma with RAU b. no significant association of trauma with R.M' c. all smokers develop RAU d. aandc 15. Histamine release to food antigens has been reported in RAU patients. a. True b. False 16. Sodium lauryl sulfate {SLS) has been implieated as a factor in the development of RAU. a. True b. False

17. Use of dentifrices with 0.5 percent, 1.0 percent and 1.5 percent SLS in studies resulted in . a. significantly less epitbelial desquamation than is seen witb SLS-fi'ee dentifrices b. significantly more epitbeiial desquamation tban is seen witb SLS-free dentifrices c. no differences in tbe amount of epithelial desquamation seen compared to with SLSfree dentifrices d. oral malodor reduction

8. Herpetiform ulcers. a. occur as multiple lesions b. can range from <1 mm to 3 mm in diameter c. coalesce d. all of the above

18. O n e in vitro study found a proteetive mucosat effect induced by a low SLS concentration. a. True b. False

of patients 9. M o r e than with R A U m a y have a family history of these ulcers. a. 10 percent b. 20 percent c. 30 percent d. 40 percent

19. Common allergens in dentifrices that may cause contact stomatitis on the oral mucosa include . a. flavorings b. preservatives c. coloring agents d. all of tbe above

11). In one study, as many as 32 percent of celiac disease patients screened had oral soft tissue ulcérations. a. True b. False

20. Oral ulcérations and ocular lesions are found in . a. benign mucous membrane pemphigoid b. Behçet's disease c. MAGIC syndrome d. atloftbeabove


21. Oral ulcérations and skin lesions nrv found in .. a. pemphigus vulgans b. Sweetener syndrome c. fungal and bacterial infections d. aandc 22. In eases of severe outbreaks of RAU, a referral for systemic disease and vitamin deficiency screening should be given. a. True b. False 23. Recurrent aphthüu.s uleers can be treated witb topical and systemie medications. a. True b. False 24. Five pereent amlexanox can reduce the severity of ulcers if applied in the initial phase of ulcer development. a. one to two times daily b. two to four times daily c. two to tbree times weekly d. none of tbe above 25. Pain-relieving topieal gels containing can be dabbed on oral ulcérations. a. ]%bdocaineanii 10%ben2ocaine b. 2% lidocaine and 1 S% benzocaine c. 2% lidocaine and 20% benzocaine d. 20% lidocaine and 2% benzocaine 26. Klong-term use of topical cortieosteroids is necessary, antifungal agents may be required to help prevent candidiasis. a. True b. False 27. For severe refraetory cases of recurrent aphthous ulcers,

may be belpíul. a. colcbicine b. tlialidomide c. dapsone d. all of tbe above 28. Discontinuation of medications assoeiated witb oral uleers is always indicated. a. True b. False 29. For patients with sensitivities to



a. use ofSLS-free oral care products is recommended b. use of oral care products with reduced SLS is recommended c. use of oral care products witb cirmamaldebydiinstead is recommended d. aandb 30. T b e selection of wbich medication to use to treat a patient's recurrent aphthous ulcers is based a. b. c. d.

tbeseverityoftheulcer random selection that patient's individual needs aandc

Demystifying RecurrentOral Ulcérations  
Demystifying RecurrentOral Ulcérations  

Educational Objectives Upon completion of this course, the clinician will be able to do the following: 1. Explain the etiology of oral ulcér...