Aphthous stomatitis

Aphthous stomatitis is a common condition characterized by the

Aphthous stomatitis
repeated formation of benign and non-contagious mouth ulcers
(aphthae) in otherwise healthy individuals. The informal term canker Synonyms Recurrent aphthous stomatitis,
sores is also used, mainly in North America, although this may also recurring oral aphthae, recurrent
refer to any mouth ulcer. aphthous ulceration

The cause is not completely understood, but involves aT cell-mediated

immune response triggered by a variety of factors. Different
individuals have different triggers, which may include nutritional
deficiencies, local trauma, stress, hormonal influences, allergies, or
genetic predisposition.

These ulcers occur periodically and heal completely between attacks.

In the majority of cases, the individual ulcers last about 7–10 days, and
ulceration episodes occur 3–6 times per year. Most appear on the non-
keratinizing epithelial surfaces in the mouth (i.e. anywhere except the
attached gingiva, the hard palate and the dorsum of the tongue),
although the more severe forms, which are less common, may also
involve keratinizing epithelial surfaces. Symptoms range from a minor
nuisance to interfering with eating and drinking. The severe forms may
be debilitating, even causing weight loss due tomalnutrition.

The condition is very common, affecting about 20% of the general Canker sore on the lower lip
population to some degree.[1] The onset is often during childhood or Specialty Oral medicine, dermatology
adolescence, and the condition usually lasts for several years before
Frequency ~20% of people to some degree[1]
gradually disappearing. There is no cure, and treatments aim to
manage pain, reduce healing time and reduce the frequency of episodes of ulceration. The term is from Greek: αφθα aphtha meaning
"mouth ulcer".

Contents
Signs and symptoms
Causes
Immunity
Mucosal barrier
Antigenic sensitivity
Systemic disease
Diagnosis
Classification
Treatment
Medication
Other
Prognosis
Epidemiology
History, society and culture
 References
External links

Signs and symptoms

Persons with aphthous stomatitis have no detectable systemic
symptoms or signs (i.e., outside the mouth).[2] Generally, symptoms
may include prodromal sensations such as burning, itching, or stinging,
which may precede the appearance of any lesion by some hours; and
pain, which is often out of proportion to the extent of the ulceration and
is worsened by physical contact, especially with certain foods and
drinks (e.g., if they are acidic or abrasive). Pain is worst in the days
immediately following the initial formation of the ulcer, and then
recedes as healing progresses.[3] If there are lesions on the tongue, or
certain parts of the lips, speaking and chewing can be uncomfortable,
and ulcers on the soft palate, back of the throat, or esophagus can cause
painful swallowing.[3] Signs are limited to the lesions themselves. Aphthous ulcers on the labial mucosa (lower lip is
retracted). Note erythematous "halo" surrounding
Ulceration episodes usually occur about 3–6 times per year.[4] ulcer.
However, severe disease is characterized by virtually constant
ulceration (new lesions developing before old ones have healed) and
may cause debilitating chronic pain and interfere with comfortable eating. In severe cases, this prevents adequate nutrient intake
leading to malnutrition and weight loss.[3]

Aphthous ulcers typically begin as erythematous macules (reddened, flat area of mucosa) which develop into ulcers that are covered
with a yellow-grey fibrinous membrane that can be scraped away. A reddish "halo" surrounds the ulcer.[5] The size, number, location,
healing time, and periodicity between episodes of ulcer formation are all dependent upon the subtype of aphthous stomatitis.

Causes
The cause is not entirely clear,[2] but is thought to be multifactorial.[6] It has even been suggested that aphthous stomatitis is not a
single entity but rather a group of conditions with different causes.[2] Multiple research studies have attempted to identify a causative
organism, but aphthous stomatitis appears to be non-contagious, non-infectious, and not sexually transmissible.[2] The mucosal
destruction is thought to be the result of a T cell (T lymphocyte) mediated immune response which involves the generation of
interleukins and tumor necrosis factor alpha (TNF-α).[6] Mast cells and macrophages are also involved, secreting TNF-α along with
the T cells. When early aphthous ulcers are biopsied, the histologic appearance shows a dense inflammatory infiltrate, 80% of which
is made up of T cells.[5] Persons with aphthous stomatitis also have circulating lymphocytes which react with
peptides 91–105 of heat
shock protein 65–60,[2] and the ratio of CD4+ T cells to CD8+ T cells in the peripheral blood of individuals with aphthous stomatitis
is decreased.[5]

There is no association between aphthous stomatitis and other autoimmune diseases, which often accompany each other; common
autoantibodies are not detected, the condition tends to resolve spontaneously with advancing age rather than worsen, and usually
serum immunoglobulins are at normal levels.[2]

Evidence for the T cell-mediated mechanism of mucosal destruction is strong, but the exact triggers for this process are unknown and
are thought to be multiple and varied from one person to the next. This suggests that there are a number of possible triggers, each of
which is capable of producing the disease in different subgroups. In other words, different subgroups appear to have different causes
for the condition. These can be considered in three general groups, namely primary immuno-dysregulation, decrease of the mucosal
barrier and states of heightened antigenic sensitivity (see below).[5] Risk factors in aphthous stomatitis are also sometimes considered
as either host-related or environmental.[7]
Immunity
At least 40% of people with aphthous stomatitis have a positive family history, suggesting that some people are genetically
predisposed to suffering with oral ulceration.[6] HLA-B12, HLA-B51, HLA-Cw7, HLA-A2, HLA-A11, and HLA-DR2 are examples
of human leukocyte antigen types associated with aphthous stomatitis.[2][5] However, these HLA types are inconsistently associated
with the condition, and also vary according to ethnicity.[8] People who have a positive family history of aphthous stomatitis tend to
[8]
develop a more severe form of the condition, and at an earlier age than is typical.

Stress has effects on the immune system, which may explain why some cases directly correlate with stress. It is often stated that in
studies of sufferers who are students, ulceration is exacerbated during examination periods and lessened during periods of
vacation.[2][5] Alternatively, it has been suggested that oral parafunctional activities such as lip or cheek chewing become more
[8]
pronounced during periods of stress, and hence the mucosa is subjected to more minor trauma.

Aphthous-like ulceration also occurs in conditions involving systemic immuno-dysregulation, e.g. cyclic neutropenia and human
immunodeficiency virus infection. In cyclic neutropenia, more severe oral ulceration occurs during periods of severe immuno-
dysregulation, and resolution of the underlying neutropenia prevents the cycle of ulceration. The relative increase in percentage of
[5]
CD8+ T cells, caused by a reduction in numbers of CD4+ T cells may be implicated in RAS-type ulceration in HIV infection.

Mucosal barrier
The thickness of the mucosa may be an important factor in aphthous stomatitis. Usually, ulcers form on the thinner, non-keratinizing
mucosal surfaces in the mouth. Factors which decrease the thickness of mucosa increase the frequency of occurrence, and factors
[5]
which increase the thickness of the mucosa correlate with decreased ulceration.

The nutritional deficiencies associated with aphthous stomatitis (Vitamin B12, folate, and iron) can all cause a decrease in the
thickness of the oral mucosa (atrophy).[5]

Local trauma is also associated with aphthous stomatitis, and it is known that trauma can decrease the mucosal barrier. Trauma could
occur during injections of local anesthetic in the mouth, or otherwise during dental treatments, frictional trauma from a sharp surface
[8]
in the mouth such as broken tooth, or from tooth brushing.

Hormonal factors are capable of altering the mucosal barrier

. In one study, a small group of females with apthous stomatitis had fewer
occurrences of aphthous ulcers during the luteal phase of the menstrual cycle or with use of the contraceptive pill.[2][5] This phase is
associated with a fall in progestogen levels, mucosal proliferation and keratinization. This subgroup often experiences remission
during pregnancy. However, other studies report no correlation between aphthous stomatitis and menstrual period, pregnancy or
menopause.[8]

Aphthous stomatitis is common in people who smoke,[6] and there is also a correlation between habit duration and severity of the
condition.[9] Tobacco use is associated with an increase in keratinization of the oral mucosa.[5] In extreme forms, this may manifest
as leukoplakia or stomatitis nicotina (smoker's keratosis). This increased keratinization may mechanically reinforce the mucosa and
reduce the tendency of ulcers to form after minor trauma, or present a more substantial barrier to microbes and antigens, but this is
unclear. Nicotine is also known to stimulate production of adrenal steroids and reduce production of TNF-α, interleukin-1 and
interleukin-6.[8] Smokeless tobacco products also seem to protect against aphthous stomatitis.[9] Cessation of smoking is known to
sometimes precede the onset of aphthous stomatitis in people previously unaffected, or exacerbate the condition in those who were
already experiencing aphthous ulceration.[2] Despite this correlation, starting smoking again does not usually lessen the condition.
[10]

Antigenic sensitivity
Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster
virus, adenovirus, and cytomegalovirus.[5] Some people with aphthous stomatitis may show herpes virus within the epithelium of the
mucosa, but without any productive infection. In some persons, attacks of ulceration occur at the same time as asymptomatic viral
shedding and elevated viral titres.[5]
In some instances, recurrent mouth ulcers may be a manifestation of an allergic reaction.[11] Possible allergens include certain foods
(e.g., chocolate, coffee, strawberries, eggs, nuts, tomatoes, cheese, citrus fruits, benzoates, cinnamaldehyde, and highly acidic foods),
toothpastes, and mouthwashes.[7][11] Where dietary allergens are responsible, mouth ulcers usually develop within about 12–24 hours
of exposure.[7]

Sodium lauryl sulphate (SLS), a detergent present in some brands of toothpaste and other oral healthcare products, may produce oral
ulceration in some individuals.[2] It has been shown that aphthous stomatitis is more common in people using toothpastes containing
SLS, and that some reduction in ulceration occurs when a SLS-free toothpaste is used.[8] Some have argued that since SLS is almost
[8]
ubiquitously used in oral hygiene products, there is unlikely to be a true predisposition for aphthous stomatitis caused by SLS.

Systemic disease
Aphthous-like ulceration may occur in association with several systemic disorders
Systemic disorders associated with
(see table). These ulcers are clinically and histopathologically identical to the
aphthous-like ulceration[5]
lesions of aphthous stomatitis, but this type of oral ulceration is not considered to
be true aphthous stomatitis by some sources.[6][12] Some of these conditions may Behçet's disease
cause ulceration on other mucosal surfaces in addition to the mouth such as the
Celiac disease
conjunctiva or the genital mucous membranes. Resolution of the systemic
[5]
condition often leads to decreased frequency and severity of the oral ulceration. Cyclic neutropenia

Nutritional deficiencies
Behçet's disease is a triad of mouth ulcers, genital ulcers and anterior uveitis.[7]
The main feature of Behçet's disease is aphthous-like ulceration, but this is usually IgA deficiency
more severe than seen in aphthous stomatitis without a systemic cause, and
Immunocompromised states, e.g.
typically resembles major or herpetiforme ulceration or both.[6][13] Aphthous-like HIV/AIDS
ulceration is the first sign of the disease in 25–75% of cases.[5] Behçet's is more
Inflammatory bowel disease
common in individuals whose ethnic origin is from regions along the Silk Road
(between the Mediterranean and the Far East).[14] It tends to be rare in other MAGIC syndrome

countries such as the United States and the United Kingdom.[7] MAGIC syndrome PFAPA syndrome
is a possible variant of Behçet disease, and is associated with aphthous-like
Reactive arthritis
ulceration. The name stands for "mouth and genital ulcers with inflamed cartilage"
(relapsing polychondritis).[8] Sweet's syndrome

Ulcus vulvae acutum

PFAPA syndrome is a rare condition that tends to occur in children.[8] The name
stands for "periodic fever, aphthae, pharyngitis (sore throat) and cervical adenitis"
(inflammation of the lymph nodes in the neck). The fevers occur periodically about every 3–5 weeks. The condition appears to
[13]
improve with tonsillectomy or immunosuppression, suggesting an immunologic cause.

In cyclic neutropenia, there is a reduction in the level of circulating neutrophils in the blood that occurs about every 21 days.
[13]
Opportunistic infectionscommonly occur and aphthous-like ulceration is worst during this time.

Hematinic deficiencies (vitamin B12, folic acid and iron), occurring singly or in combination,[7] and with or without any underlying
gastrointestinal disease, may be twice as common in people with RAS. However, iron and vitamin supplements only infrequently
improve the ulceration.[13] The relationship to vitamin B12 deficiency has been the subject of many studies. Although these studies
found that 0–42% of those with recurrent ulcers suffer from vitamin B12 deficiency, an association with deficiency is rare. Even in
the absence of deficiency, vitamin B12 supplementation may be helpful due to unclear mechanisms.[15] Hematinic deficiencies can
[6]
cause anemia, which is also associated with aphthous-like ulceration.

Gastrointestinal disorders are sometimes associated with aphthous-like stomatitis, e.g. most commonly Celiac disease, but also
inflammatory bowel diseasesuch as Crohn's disease or ulcerative colitis.[6] The link between gastrointestinal disorders and aphthous
stomatitis is probably related to nutritional deficiencies caused by malabsorption.[13] Less than 5% of people with RAS have Celiac
disease, which usually presents with severe malnutrition, anemia, abdominal pain, diarrhea and glossitis (inflammation of the
tongue).[8] Sometimes aphthous-like ulcerations can be the only sign of celiac disease.[8] Despite this association, a gluten-free diet
does not usually improve the oral ulceration.[13]

Other examples of systemic conditions associated with aphthous-like ulceration include reactive arthritis,[6] and recurrent erythema
multiforme.[6]

Diagnosis
Diagnosis is mostly based on the clinical appearance and the medical history.[2] The
most important diagnostic feature is a history of recurrent, self healing ulcers at
fairly regular intervals.[17] Although there are many causes of oral ulceration,
recurrent oral ulceration has relatively few causes, most commonly aphthous
stomatitis, but rarely Behçet's disease, erythema multiforme, ulceration associated
with gastrointestinal disease,[10][17] and recurrent intra-oral herpes simplex
infection. A systemic cause is more likely in adults who suddenly develop recurrent Photographic comparison of: 1) a
oral ulceration with no prior history.[13] canker sore – inside the mouth, 2)
herpes, 3) angular cheilitis, and 4)
Special investigations may be indicated to rule out other causes of oral ulceration. chapped lips.[16]
These include blood tests to exclude anemia, deficiencies of iron, folate or vitamin
B12 or celiac disease.[7] However, the nutritional deficiencies may be latent and the
peripheral blood picture may appear relatively normal.[7] Some suggest that screening
for celiac disease should form part of the routine work up for individuals complaining of
recurrent oral ulceration.[8] Many of the systemic diseases cause other symptoms apart
from oral ulceration, which is in contrast to aphthous stomatitis where there is isolated
oral ulceration. Patch testing may be indicated if allergies are suspected (e.g. a strong
relationship between certain foods and episodes of ulceration). Several drugs can cause
oral ulceration (e.g. nicorandil), and a trial substitution to an alternative drug may
highlight a causal relationship.[2]
Blood is often taken to assess the
Tissue biopsy is not usually required, unless to rule out other suspected conditions such hemoglobin, iron, folate and
as oral squamous cell carcinoma.[17] The histopathologic appearance is not vitamin B12 levels
pathognomonic (the microscopic appearance is not specific to the condition). Early
lesions have a central zone of ulceration covered by a fibrinous membrane. In the
connective tissue deep to the ulcer there is increased vascularity and a mixed
inflammatory infiltrate composed of lymphocytes, histiocytes and
polymorphonuclear leukocytes. The epithelium on the margins of the ulcer shows
spongiosis and there are many mononuclear cells in the basal third. There are also
lymphocytes and histiocytes in the connective tissue surrounding deeper blood
vessels near to the ulcer, described histologically as "perivascular cuffing".[5][17]

Classification A patch test is sometimes carried

out. Areas of the skin on the back are
Aphthous stomatitis has been classified as a type of non-infectious stomatitis
stimulated with various common
(inflammation of the mouth).[17] One classification distinguishes "common simple allergens. The ones which cause an
aphthae", accounting for 95% of cases, with 3–6 attacks per year, rapid healing, inflammatory reaction may also be
minimal pain and restriction of ulceration to the mouth; and "complex aphthae", involved in recurrent oral ulceration
accounting for 5% of cases, where ulcers may be present on the genital mucosa in
addition to mouth, healing is slower and pain is more severe.[4] A more common
method of classifying aphthous stomatitis is into three variants, distinguished by the size, number and location of the lesions, the
healing time of individual ulcers and whether a scar is left after healing (see below).
Minor aphthous ulceration
This is the most common type of aphthous stomatitis, accounting for about 80–85% of all cases.[7] This subtype is termed minor
aphthous ulceration (MiAU),[2] or minor recurrent aphthous stomatitis (MiRAS). The lesions themselves may be referred to as minor
[7] and affect non-
aphthae or minor aphthous ulcers. These lesions are generally less than 10 mm in diameter (usually about 2–3 mm),
keratinized mucosal surfaces (i.e. the labial and buccal mucosa, lateral borders of the tongue and the floor of the mouth). Usually
several ulcers appear at the same time, but single ulcers are possible. Healing usually takes seven to ten days and leaves no scar.
-free period of variable length.[6]
Between episodes of ulceration, there is usually an ulcer

Major aphthous ulceration

This subtype makes up about 10% of all cases of aphthous stomatitis.[5] It is termed major aphthous ulceration (MaAU) or major
recurrent aphthous stomatitis (MaRAS). Major aphthous ulcers (major aphthae) are similar to minor aphthous ulcers, but are more
than 10 mm in diameter and the ulceration is deeper.[5][6] Because the lesions are larger, healing takes longer (about twenty to thirty
days), and may leave scars. Each episode of ulceration usually produces a greater number of ulcers, and the time between attacks is
less than seen in minor aphthous stomatitis.[5] Major aphthous ulceration usually affects non keratinized mucosal surfaces, but less
commonly keratinized mucosa may also be involved, such as the dorsum (top surface) of the tongue or the gingiva (gums).[8] The
soft palate or the fauces (back of the throat) may also be involved,[8] the latter being part of the oropharynx rather than the oral
[7]
cavity. Compared to minor aphthous ulceration, major aphthae tend to have an irregular outline.

Herpetiform ulceration
Herpetiform ulcers,[6] (also termed stomatitis herpetiformis,[18] or herpes-like ulcerations) is a subtype of aphthous stomatitis so
named because the lesions resemble a primary infection with herpes simplex virus (primary herpetic gingivostomatitis).[5] However,
herpetiform ulceration is not caused by herpes viruses. As with all types of aphthous stomatitis, it is not contagious. Unlike true
herpetic ulcers, herpetiforme ulcers are not preceded by vesicles (small, fluid filled blisters).[8] Herpetiforme ulcers are less than
1 mm in diameter and occur in variably sized crops up to one hundred at a time. Adjacent ulcers may merge to form larger,
continuous areas of ulceration. Healing occurs within fifteen days without scarring.[7] The ulceration may affect keratinized mucosal
surfaces in addition to non keratinized. Herpetiform ulceration is often extremely painful, and the lesions recur more frequently than
minor or major aphthous ulcers. Recurrence may be so frequent that ulceration is virtually continuous. It generally occurs in a slightly
older age group than the other subtypes,[8] and females are affected slightly more frequentlythan males.[2]

RAS type ulceration

Recurrent oral ulceration associated with systemic conditions is termed "RAS type ulceration", "RAS like ulceration", or "aphthous-
like ulcers".[2] Aphthous stomatitis occurs in individuals with no associated systemic disease.[6] Persons with certain systemic
diseases may be prone to oral ulceration, but this is secondary to the underlying medical condition (see the systemic disease
section).[6] This kind of ulceration is considered by some to be separate from true aphthous stomatitis.[6][12] However, this definition
is not strictly applied. For example, many sources refer to oral ulceration caused by anemia and/or nutritional deficiencies as
aphthous stomatitis, and some also considerBehçet's disease to be a variant.[5][7]

Treatment
The vast majority of people with aphthous stomatitis have minor symptoms and do not require any specific therapy. The pain is often
tolerable with simple dietary modification during an episode of ulceration such as avoiding spicy and acidic foods and beverages.[3]
Many different topical and systemic medications have been proposed (see table), sometimes showing little or no evidence of
usefulness when formally investigated.[6] Some of the results of interventions for RAS may in truth represent a placebo effect.[13] No
[6]
therapy is curative, with treatment aiming to relieve pain, promote healing and reduce the frequency of episodes of ulceration.

Medication
The first line therapy for aphthous stomatitis is topical agents rather than systemic medication,[6] with topical corticosteroids being
the mainstay treatment.[2][13] Systemic treatment is usually reserved for severe disease due to the risk of adverse side effects
associated with many of these agents. A systematic review found that no single systemic intervention was found to be effective.[6]
[2]
Good oral hygiene is important to prevent secondary infection of the ulcers.

Occasionally, in females where ulceration is correlated to the menstrual cycle or to birth control pills, progestogen or a change in
birth control may be beneficial.[2] Use of nicotine replacement therapy for people who have developed oral ulceration after stopping
smoking has also been reported.[8] Starting smoking again does not usually lessen the condition.[10] Trauma can be reduced by
avoiding rough or sharp foodstuffs and by brushing teeth with care. If sodium lauryl sulfate is suspected to be the cause, avoidance of
products containing this chemical may be useful and prevent recurrence in some individuals.[19] Similarly patch testing may indicate
that food allergy is responsible, and the diet modified accordingly.[2] If investigations reveal deficiency states, correction of the
deficiency may result in resolution of the ulceration. For example, there is some evidence that vitamin B12 supplementation may
prevent recurrence in some individuals.[19]

Medications
Intended
Drug type Example(s)
action
Topical covering
Reduce pain Orabase (often combined withtriamcinolone).[20]
agents / barriers
Topical analgesics /
anesthetics / anti- Benzydamine hydrochloridemouthwash or spray,[13] Amlexanox
Reduce pain
inflammatory paste,[20][19] viscous lidocaine,[20] diclofenac in hyaluronan.[2]
agents
Hasten
healing
Doxycycline,[6] tetracycline,[6] minocycline,[20] chlorhexidine gluconate,[13]
Topical antiseptics (prevent
secondary triclosan.[13]
infection)
Topical mild
Reduce
potency
inflammation Hydrocortisone sodium succinate.[2]
corticosteroids
Topical moderate
Reduce Beclomethasone dipropionateaerosol,[2] fluocinonide,[13] clobetasol,[2]
potency
corticosteroids
inflammation betamethasone sodium phosphate,[2] dexamethasone.[20]

Various,
mostly Prednisolone,[6] colchicine,[6] pentoxifylline,[6] azathioprine, thalidomide,[6]
Medications by
mouth
modulating dapsone,[6] mycophenolate mofetil,[6] adalimumab,[13] vitamin B12,[6]
immune Clofazimine,[6] Levamisole,[6][13] Montelukast,[6] Sulodexide,[6]
response

Other
Surgical excision of aphthous ulcers has been described, but it is an ineffective and inappropriate treatment.[5] Silver nitrate has also
been used as a chemical cauterant.[13] Apart from the mainstream approaches detailed above, there are numerous treatments of
unproven effectiveness, ranging from herbal remedies to otherwise alternative treatments, including aloe vera, myrtus communis,
Rosa damascena, potassium alum, zinc sulfate, nicotine, polio virus vaccine and prostaglandin E2.[2]

Prognosis
By definition, there is no serious underlying medical condition, and most importantly, the ulcers do not represent oral cancer nor are
they infectious. However, aphthae are capable of causing significant discomfort. There is a spectrum of severity, with symptoms
ranging from a minor nuisance to disabling.[3] Due to pain during eating, weight loss may develop as a result of not eating in severe
[2]
cases of aphthous stomatitis. Usually, the condition lasts for several years before spontaneously disappearing in later life.
Epidemiology
Aphthous stomatitis affects between 5% and 66% of people, with about 20% of individuals in most populations having the condition
to some degree.[5][7] This makes it the most common disease of the oral mucosa.[17] Aphthous stomatitis occurs worldwide, but is
more common in developed countries.[2]

Within nations, it is more common in higher socioeconomic groups.[2] Males and females are affected in an equal ratio, and the peak
age of onset between 10 and 19 years.[6] About 80% of people with aphthous stomatitis first developed the condition before the age
of 30.[5] There have been reports of ethnic variation. For example, in the United States, aphthous stomatitis may be three times more
[13]
common in white-skinned people than black-skinned people.

History, society and culture

"Aphthous affectations" and "aphthous ulcerations" of the mouth are mentioned several times in the treatise "Of the Epidemics" (part
of the Hippocratic corpus, in the 4th century BC),[21] although it seems likely that this was oral ulceration as a manifestation of some
infectious disease, since they are described as occurring inepidemic-like patterns, with concurrent symptoms such as fever
.

Aphthous stomatitis was once thought to be a form of recurrent herpes simplex virus infection, and some clinicians still refer to the
[22]
condition as "herpes" despite this cause having been disproven.

The informal term "canker sore" is sometimes used, mainly in North America,[23] either to describe this condition generally, or to
refer to the individual ulcers of this condition,[24] or mouth ulcers of any cause unrelated to this condition. The origin of the word
"canker" is thought to have been influenced by Latin, Old English, Middle English and Old North French.[25] In Latin, cancer
translates to "malignant tumor" or literally "crab" (related to the likening of sectioned tumors to the limbs of a crab). The closely
related word in Middle English and Old North French, chancre, now more usually applied to syphilis, is also thought to be
involved.[25] Despite this etymology, aphthous stomatitis is not a form of cancer but rather entirely benign.

An aphtha (plural aphthae) is a non specific term that refers to an ulcer of the mouth. The word is derived from the Greek word
aphtha meaning "eruption" or "ulcer".[8] The lesions of several other oral conditions are sometimes described as aphthae, including
Bednar's aphthae (infected, traumatic ulcers on the hard palate in infants),[26] oral candidiasis, and foot-and-mouth disease. When
used without qualification,aphthae commonly refers to lesions of recurrent aphthous stomatitis. Since the word aphtha is often taken
to be synonymous with ulcer, it has been suggested that the term "aphthous ulcer" is redundant, but it remains in common use.[27]
Stomatitis is also a non-specific term referring to any inflammatory process in the mouth, with or without oral ulceration.[28] It may
describe many different conditions apart from aphthous stomatitis such asangular stomatitis.

The current most widely used medical term is "recurrent aphthous stomatitis" or simply "aphthous stomatitis".[3] Historically, many
different terms have been used to refer to recurrent aphthous stomatitis or its sub-types, and some are still in use. Mikulicz' aphthae is
a synonym of minor RAS,[8] named after Jan Mikulicz-Radecki. Synonyms for major RAS include Sutton's ulcers (named after
Richard Lightburn Sutton), Sutton's disease,[29] Sutton's syndrome and pariadenitis mucosa necrotica recurrens.[2][8] Synonyms for
[5][12]
aphthous stomatitis as a whole include (recurrent) oral aphthae, (recurrent) aphthous ulceration and (oral) aphthosis.

In traditional Chinese medicine, claimed treatments for aphthae focus on clearing heat and nourishingYin.[30]

Rembrandt Gentle White toothpaste did not contain sodium lauryl sulfate, and was specifically marketed as being for the benefit of
"canker sore sufferers". When the manufacturer Johnson & Johnson discontinued the product in 2014, it caused a backlash of anger
eBay.[31][32]
from long term customers, and the toothpaste began to sell for many times the original price on the auction website

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External links
Classification ICD-10: K12.0 · D
ICD-9-CM: 528.2 ·
Aphthous stomatitis at Curlie (based on DMOZ)
MeSH: D013281
External MedlinePlus:
resources 000998 ·
eMedicine: ent/700
derm/486 ped/2672

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