eMedicine Specialties > Dermatology > Diseases of the Oral Mucosa

Aphthous Stomatitis

Author: Jeffrey M Casiglia, DMD, DMSc, Lecturer, Harvard School of Dental Medicine; Private Practice, Salem, Massachusetts
Coauthor(s): Ginat W Mirowski, MD, DMD, Adjunct Associate Professor, Departments of Oral Pathology, Medicine, and Radiology, Indiana University School Medicine; Christy L Nebesio, MD, Dermatologist
Contributor Information and Disclosures

Updated: Feb 6, 2009

Introduction

Background

Recurrent aphthous ulcers (RAUs), or canker sores, are among the most common oral mucosal lesions physicians and dentists observe. Recurrent aphthous ulcer is a disorder of unknown etiology that can cause clinically significant morbidity. One or several discrete, shallow, painful ulcers are visible on the unattached mucous membranes. Individual ulcers typically last 7-10 days. Larger ulcers may last several weeks to months and can scar when healing.

Although the process in idiopathic disease is usually self-limiting, in some individuals, the ulcer activity can be almost continuous. Similar ulcers can be noted in the genital region. Behçet syndrome, systemic lupus erythematosus, and inflammatory bowel disease are systemic diseases associated with oral recurrent aphthous ulcers.

Pathophysiology

The classic categorization of recurrent aphthous ulcer is division into 3 clinical forms: recurrent aphthous ulcer minor, recurrent aphthous ulcer major, and herpetiform recurrent aphthous ulcer. Recurrent aphthous ulcer affects the following nonkeratinized or poorly keratinized surfaces of the oral mucosa:

  • Labial and buccal mucosa
  • Maxillary and mandibular sulci
  • Unattached gingiva
  • Soft palate
  • Tonsillar fauces
  • Floor of the mouth
  • Ventral surface of the tongue

Recurrent aphthous ulcer minor

Recurrent aphthous ulcer minor is the most common form, accounting for 80% of all cases. Discrete, painful, shallow, recurrent ulcers smaller than 1 cm in diameter characterize this form. At any time, one or more ulcers can be present. Lesions heal without scarring within 7-10 days. The periodicity varies between individuals, with some having longer ulcer-free episodes and some never being free from ulcers.

Recurrent aphthous ulcer major

Recurrent aphthous ulcer is formerly known as periadenitis mucosa necrotica recurrens. This form is less common than the others and is characterized by oval ulcers greater than 1 cm in diameter. In this relatively severe form, many major aphthae may be present simultaneously. Ulcers are large and deep, may have irregular borders, and may coalesce. Upon healing, which may take as long as 6 weeks, ulcers can leave scarring, and severe distortion of oral and pharyngeal mucosa may occur.

Herpetiform recurrent aphthous ulcer

This least common form (5-10% of cases) has the smallest of the aphthae, commonly no larger than 1 mm in diameter. The aphthae tend to occur in clusters that may consist of tens or hundreds of minute ulcers. Clusters may be small and localized, or they may be distributed throughout the soft mucosa of the oral cavity.

Frequency

United States

  • Recurrent aphthous ulcers are the most common oral mucosal disease in North America. They affect 20% of the population, with the incidence rising to more than 50% in certain groups of students in professional schools. Children from high socioeconomic groups may be affected more than those from low socioeconomic groups.1

International

  • Recurrent aphthous ulcers occur worldwide and are reported on every populated continent. Recurrent aphthous ulcers affect 2-66% of the international population.2

Mortality/Morbidity

  • Unless recurrent aphthous ulcer is associated with a systemic disease, such as Behçet syndrome or inflammatory bowel disease, it rarely leads to clinically significant morbidity or mortality.

Sex

  • In children and in some adult communities who are affected, the incidence of recurrent aphthous ulcer is higher in female individuals than in male individuals.

Age

  • Recurrent aphthous ulcer minor is the most common form of childhood recurrent aphthous ulcer. Approximately 1% of American children may have recurrent aphthous ulcers, with onset before age 5 years. The percentage of patients who are affected decreases after the third decade.
  • Recurrent aphthous ulcer major has a typical onset after puberty and can persist for the remainder of an individual's life, although after late adulthood episodes become much less common.
  • Herpetiform recurrent aphthous ulcer first occurs in the second decade of life; the majority of persons have onset when younger than 30 years. The frequency and the severity of episodes may increase during the third and fourth decades and then decrease with advancing age.

Clinical

History

Recurrent aphthous ulcers consist of one or multiple round-to-ovoid, shallow, punched-out–appearing, painful oral ulcers that recur at intervals of a few days to a few months. To evaluate oral ulcers as recurrent aphthous ulcers, ascertain the following information:

  • Nature of the lesions (number, size, duration, recurrence)
    • The prodromal stage (when present) begins with a pricking or burning sensation on the mucosa.
    • The ulcers develop within 24-48 hours.
    • Pain lasts 3-4 days or until a thicker fibrinous cover develops or early epithelialization occurs.
    • Healing is complete in 7-10 days.
  • Age of the patient at onset
  • Cutaneous or mucosal changes
  • Symptoms of other organ system involvement
  • Current medications
  • Host factors associated with recurrent aphthous ulcer (see Causes)
    • With regard to genetic factors, a family history is evident in some cases.
    • Hematinic deficiency may play a role. Iron, folic acid, or vitamin B-6 and B-12 deficiencies are possible.
    • Immune dysregulation may play possibly play a role.
    • Physical or emotional stress is often reported by patients as associated with recurrent outbreaks.
  • Environmental factors associated with recurrent aphthous ulcer
    • Local, chemical, or physical trauma may initiate ulcer development in patients who are susceptible (pathergy).
    • Allergy or sensitivity to chemicals or food additives may stimulate an outbreak.
    • The role of microbial infection is debated.
  • HIV infection (associated with lesions)3
    • Aphthouslike oral ulcerations involving all 3 types of recurrent aphthous ulcers are observed. Approximately 66% of patients who are HIV positive have herpetiform and major recurrent aphthous ulcers.
    • Unlike in healthy individuals, these ulcerations may be present on both keratinized and nonkeratinized surfaces, making it even more critical to rule out opportunistic infections.
    • Ulcerations must be distinguished from those caused by HIV medications and fungal, viral, or bacterial infections. Biopsy is indicated.
  • Behçet syndrome (associated with lesions)4,5,6,7,8,9
    • This complex, multisystemic inflammatory disorder of unknown cause is characterized by recurrent oral aphthae and at least 2 of the following findings: genital aphthae, synovitis, cutaneous pustular vasculitis, posterior uveitis, or meningoencephalitis.
    • Oral aphthae of Behçet syndrome are clinically similar to those in recurrent aphthous ulcers but are accompanied by ocular and genital lesions.
    • The incidence is highest in Japan, Southeast Asia, the Middle East, and southern Europe and in persons aged 30-40 years.
    • Behçet syndrome is strongly associated with HLA-B51.
  • Gluten-sensitive enteropathy (also known as celiac sprue)10,11,12
    • Oral lesions occur in most cases of gluten-sensitive enteropathy (GSE) and can often precede abdominal symptoms.
    • Less than 5% of patients with recurrent aphthous ulcers have GSE, also known as celiac disease, or other minor mucosal abnormalities of the small intestine.
    • Bowel symptoms may not be present, but patients may have folate deficiency, and they sometimes have reticulin antibodies.

Physical

Regardless of the clinical form of recurrent aphthous ulcer, ulcers are confined to the nonkeratinized mucosa of the mouth, sparing the dorsum of the tongue, the attached gingiva, and the hard palate mucosae, that are keratinized. Although patients may have submandibular lymphadenopathy, fever is rare. Most patients are otherwise well.

  • Recurrent aphthous ulcer minor
    • Recurrent aphthous ulcer minor is characterized by discrete shallow ulcers smaller than 1 cm in diameter.
    • The ulcers are covered by a yellow-gray pseudomembrane (fibrinous exudate) and are surrounded by an erythematous halo.
  • Recurrent aphthous ulcer major
    • Recurrent aphthous ulcer major is characterized by oval ulcers that are larger (>1 cm in diameter) and deeper than those observed in recurrent aphthous ulcer minor.
    • The ulcers may coalesce and often have an irregular border.
  • Herpetiform recurrent aphthous ulcer
    • Herpetiform recurrent aphthous ulcer is characterized by crops of smaller ulcers; tens of ulcerations may be present in clusters.
    • The ulcers can coalesce to produce a widespread area of irregular ulceration.

Causes

Although the clinical characteristics of recurrent aphthous ulcer are well-defined, the precise etiology and the pathogenesis of recurrent aphthous ulcer remain unclear. Many possibilities have been investigated. Recurrent aphthous ulcer is a multifactorial condition, and it is likely that immune-mediated destruction of the epithelium is the common factor in recurrent aphthous ulcer pathogenesis. Host risk factors associated with recurrent aphthous ulcer are described below.

  • Genetics
    • A family history of recurrent aphthous ulcers is evident in some patients. A familial connection includes a young age of onset and symptoms of increased severity.
    • Recurrent aphthous ulcer is highly correlated in identical twins.13
    • Associations between specific HLA haplotypes and recurrent aphthous ulcer have been investigated. No consistent association has been demonstrated, most likely because of the lack of any immunogenetic basis for recurrent aphthous ulcer. However, host susceptibility is clearly variable, with a polygenic inheritance pattern, and penetrance depends on other factors.
  • Hematinic deficiency
    • In several studies, hematinic (iron, folic acid, vitamins B-6 and B-12) deficiencies were twice as common in patients with recurrent aphthous ulcers than in control subjects. As many as 20% of patients with recurrent aphthous ulcer had a deficiency.
    • Serologic workup is warranted. Hemoglobin and RBC indices are not sufficient in all cases.
  • Immune dysregulation
    • At present, no unifying theory of the immunopathogenesis of recurrent aphthous ulcer exists, but immune dysregulation may play a significant role.
    • Cytotoxic action of lymphocytes and monocytes on the oral epithelium seems to cause the ulceration, but the trigger remains unclear.
    • Upon histologic analysis, recurrent aphthous ulcer consists of mucosal ulcerations with mixed inflammatory cell infiltrates. T-helper cells predominate in the preulcerative and healing phases, whereas T-suppressor cells predominate in the ulcerative phase.
    • Other findings associated with immune dysregulation include the following:
      • Reduced response of patients' lymphocytes to mitogens
      • Circulating immune complexes
      • Alterations in the activity of natural killer cells in various stages of disease14
      • Increased adherence of neutrophils
      • Reduced quantities and functionality of regulatory T cells in lesional tissue
      • Release of tumor necrosis factor-alpha (TNF-alpha)15
      • Significant involvement of mast cells in the pathogenesis of recurrent aphthous ulcer
      • Reduced cellular expression of heat shock protein 27 and interleukin 10  in aphthous lesions16,17
      • Elevated levels of salivary and serum cortisol, as well as increased anxiety18
  • Microbial infection
    • Researchers disagree about the role of microbes in the development of recurrent aphthous ulcers. Emphasis has been on a microbial agent as a primary pathogen or an antigenic stimulus.
    • Numerous studies have failed to provide strong evidence to support the role of herpes simplex virus, human herpesvirus, varicella-zoster virus, or cytomegalovirus in the development of aphthous ulcers.19,20
    • Recurrent aphthous ulcer formation may be a T-cell–mediated response to antigens of Streptococcus sanguis that cross-react with the mitochondrial heat shock proteins and induce oral mucosa damage.
    • Helicobacter pylori has been detected in lesional tissue of oral ulcers, but the frequency of serum immunoglobulin G antibodies to H pylori is not increased in recurrent aphthous ulcers, and the organisms have never proven causative.21,22,23,24,25

More on Aphthous Stomatitis

Overview: Aphthous Stomatitis
Differential Diagnoses & Workup: Aphthous Stomatitis
Treatment & Medication: Aphthous Stomatitis
Follow-up: Aphthous Stomatitis
References
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Further Reading

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Keywords

recurrent aphthous ulcers, aphthous stomatitis, canker sores, recurrent aphthous stomatitis, RAS, recurrent aphthous ulcers, RAU, periadenitis mucosa necrotica recurrens, RAU minor, RAU major, herpetiform RAU, Sutton's disease

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Contributor Information and Disclosures

Author

Jeffrey M Casiglia, DMD, DMSc, Lecturer, Harvard School of Dental Medicine; Private Practice, Salem, Massachusetts
Jeffrey M Casiglia, DMD, DMSc is a member of the following medical societies: American Academy of Oral Medicine and American Dental Association
Disclosure: Nothing to disclose.

Coauthor(s)

Ginat W Mirowski, MD, DMD, Adjunct Associate Professor, Departments of Oral Pathology, Medicine, and Radiology, Indiana University School Medicine
Ginat W Mirowski, MD, DMD is a member of the following medical societies: American Academy of Dermatology and American Medical Women's Association
Disclosure: Nothing to disclose.

Christy L Nebesio, MD, Dermatologist
Christy L Nebesio, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.

Medical Editor

David P Fivenson, MD, Associate Director, St Joseph Mercy Hospital Dermatology Program, Ann Arbor, Michigan
David P Fivenson, MD is a member of the following medical societies: American Academy of Dermatology, Medical Dermatology Society, Michigan Dermatological Society, Michigan State Medical Society, Photomedicine Society, Society for Investigative Dermatology, and Wound Healing Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Warren R Heymann, MD, Head, Division of Dermatology, Professor, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey
Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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