Several drugs may cause AC as a side effect, by various mechanisms, such as creating drug-induced xerostomia. Various examples include isotretinoin, indinavir, and sorafenib. Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primary hypervitaminosis A, which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine, methamphetamines, heroin, and hallucinogens.

This is a rare inflammatory condition of the minor salivary glands, usually in the lower lip, which appears swollen and everted. There may also be ulceration, crusting, abscesses, and sinus tracts. It is an acquired disorder, but the cause is uncertain. Suspected causes include sunlight, tobacco, syphilis, poor oral hygiene and genetic factors. The openings of the minor salivary gland ducts become inflamed and dilated, and there may be mucopurulent discharge from the ducts. A previous classification suggested dividing cheilitis into 3 types based on severity, with the later stages involving secondary infection with bacteria, and increased ulceration, suppuration and swelling: Type 1, Simple; Type 2, Superficial suppurative ("Baelz's disease"); and Type 3, Deep suppurative ("cheilitis glandularis epostemetosa"). Cheilitis glandularis usually occurs in middle-aged and elderly males, and it carries a risk of malignant transformation to squamous cell carcinoma (18% to 35%). Preventative treatment such as vermilionectomy ("lip shave") is therefore the treatment of choice.

Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa. Other disorders may cause lip enlargement (e.g. orofacial granulomatosis), which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC. Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications, or conditions such as Sjögren's syndrome. Conversely, conditions which cause drooling or sialorrhoea (excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC. This is due to relative macroglossia, an apparently large tongue in a small mouth, which may constantly stick out of the mouth causing maceration of the corners of the mouth with saliva. Inflammatory bowel diseases (such as Crohn's disease or ulcerative colitis) can be associated with angular cheilitis. In Crohn's, it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth. Glucagonomas are rare pancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome. Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis, and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis. Angular cheilitis may be present in human immunodeficiency virus infection, neutropenia, or diabetes. Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants. Other conditions possibly associated include plasma cell gingivitis, Melkersson-Rosenthal syndrome, or sideropenic dysphagia (also called Plummer-Vinson syndrome or Paterson-Brown-Kelly syndrome).

Allergic contact stomatitis (also termed "allergic gingivostomatitis" or "allergic contact gingivostomatitis") is a type IV (delayed) hypersensitivity reaction that occurs in susceptible atopic individuals when allergens penetrate the skin or mucosa.

Allergens, which may be different for different individuals, combine with epithelial-derived proteins, forming haptens which bind with Langerhans cells in the mucosa, which in turn present the antigen on their surface to T lymphocytes, sensitizing them to that antigen and causing them to produce many specific clones. The second time that specific antigen is encountered, an inflammatory reaction is triggered at the site of exposure. Allergic contact stomatitis is less common than allergic contact dermatitis because the mouth is coated in saliva, which washes away antigens and acts as a barrier. The oral mucosa is also more vascular (has a better blood supply) than skin, meaning that any antigens are more quickly removed from the area by the circulation. Finally, there is substantially less keratin in oral mucosa, meaning that there is less likelihood that haptens will form.

Allergic contact stomatitis appears as non-specific inflammation, so it may be mistaken for chronic physical irritation. There may be burning or soreness of the mouth and ulceration. Chronic exposure to the allergen may result in a lichenoid lesion. Plasma cell gingivitis may also occur, which may be accompanied by glossitis and cheilitis.

Allergens that may cause allergic contact stomatitis in some individuals include cinnamaldehyde, Balsam of Peru, peppermint, mercury, gold, pyrophosphates, zinc citrate, free acrylic monomer, nickel, fluoride, and sodium lauryl sulfate. These allergens may originate from many sources, including various foods and drink, chewing gum, toothpaste, mouthwash, dental floss, dental fillings, dentures, orthodontic bands or wires, and many other sources. If the substance containing the allergen comes into contact with the lips, allergic contact cheilitis can occur, together with allergic contact stomatitis.

The diagnosis is confirmed by patch test, and management is by avoidance of exposure to the allergen.

In contrast to cutaneous LP, which is self limited, lichen planus lesions in the mouth may persist for many years, and tend to be difficult to treat, with relapses being common. Atrophic/erosive lichen planus is associated with a small risk of cancerous transformation, and so people with OLP tend to be monitored closely over time to detect any potential change early. Sometimes OLP can become secondarily infected with Candida organisms.

Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster virus, adenovirus, and cytomegalovirus. 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.

In some instances, recurrent mouth ulcers may be a manifestation of an allergic reaction. 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. Where dietary allergens are responsible, mouth ulcers usually develop within about 12–24 hours of exposure.

Sodium lauryl sulphate (SLS), a detergent present in some brands of toothpaste and other oral healthcare products, may produce oral ulceration in some individuals. 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. Some have argued that since SLS is almost ubiquitously used in oral hygiene products, there is unlikely to be a true predisposition for aphthous stomatitis caused by SLS.

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 which increase the thickness of the mucosa correlate with decreased ulceration.

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

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 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. 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.

Aphthous stomatitis is common in people who smoke, and there is also a correlation between habit duration and severity of the condition. Tobacco use is associated with an increase in keratinization of the oral mucosa. 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. Smokeless tobacco products also seem to protect against aphthous stomatitis. 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. Despite this correlation, starting smoking again does not usually lessen the condition.

This is a common condition present in denture wearers. It appears as reddened but painless mucosa beneath the denture. 90% of cases are associated with Candidia species, and it is the most common form of oral candidiasis. Treatment is by antifungal medication and improved dental hygiene, such as not wearing the denture during sleep.

The cause of lichen planus is unknown, but it is not contagious and does not involve any known pathogen. It is thought to be a T cell mediated autoimmune reaction (where the body's immune system targets its own tissues). This autoimmune process triggers apoptosis of the epithelial cells. Several cytokines are involved in lichen planus, including tumor necrosis factor alpha, interferon gamma, interleukin-1 alpha, interleukin 6, and interleukin 8. This autoimmune, T cell mediated, process is thought to be in response to some antigenic change in the oral mucosa, but a specific antigen has not been identified.

Where a causal or triggering agent is identified, this is termed a lichenoid reaction rather than lichen planus. These may include:

- Drug reactions, with the most common inducers including gold salts, beta blockers, traditional antimalarials (e.g. quinine), thiazide diuretics, furosemide, spironolactone, metformin and penicillamine.

- Reactions to amalgam (metal alloys) fillings (or when they are removed/replaced),

- Graft-versus-host disease lesions, which chronic lichenoid lesions seen on the palms, soles, face and upper trunk after several months.

- Hepatitis, specifically hepatitis B and hepatitis C infection, and primary biliary cirrhosis.

It has been suggested that lichen planus may respond to stress, where lesions may present during times of stress. Lichen planus can be part of Grinspan's syndrome.

It has also been suggested that mercury exposure may contribute to lichen planus.

Also termed "cheilitis exfoliativa" or "tic de levres", is an uncommon inflammatory condition of the vermilion zone of the lips, which are painful and crusted. There is continuous production and desquamation (shedding) of thick, brown scales of keratin. The keratin layer of the epidermis of the lips experiences a faster growth and death rate than normal and desquamates. When these scales are removed, a normal appearing lip is revealed beneath, although there may be associated erythema and edema. The condition has not yet been attributed to any particular cause. Rarely are infections to blame. In some individuals, there is an association with stress, anxiety, depression or personality disorders. In one report, 87% of individuals had some form of psychiatric disturbance, and 47% had thyroid dysfunction, which in turn can cause psychiatric conditions like depression.

Some cases of exfoliative cheilitis are thought to represent factitious damage, termed "factitious cheilitis" or "artifactual cheilitis", and are related to repetitive lip picking or licking habits. This appears as crusting and ulceration caused by repetitive chewing and sucking of the lips. Some consider habitual lip licking or picking to be a form of nervous tic. This habit is sometimes termed "perlèche" (derived from the French word "pourlècher" meaning "to lick one’s lips"). Factitious cheilitis is significantly more common in young females.

Exfoliative cheilitis has also been linked to HIV/AIDS. Management consists mostly of keeping the lips moist and the application of topical corticosteroids ranging from hydrocortisone to clobetasol. There have also been reports of using topical tacrolimus ointment.

Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for "C. albicans", or that local epithelial alterations occur that facilitate colonization of candida species.

Malnutrition, whether by malabsorption, or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis, by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity. Some sources state that deficiencies of vitamin A or pyridoxine are also linked.

There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis. "In vitro" and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.

Oral ulceration is a common reason for people to seek medical or dental advice. A breach of the oral mucosa probably affects most people at various times during life. For a discussion of the epidemiology of aphthous stomatitis, see Aphthous stomatitis#Epidemiology.

Contact stomatitis (also known as "Contact lichenoid reaction," "Lichenoid amalgam reaction," and "Oral mucosal cinnamon reaction") is characterized by cutaneous lesions that may be located where the offending agent contacts the mucosa for a prolonged time.

Denture-related stomatitis is usually a harmless condition with no long term consequences. It usually resolves with simple measures such as improved denture hygiene or topical antifungal medication. In severely immunocompromised individuals (e.g. those with HIV), the infection may present a more serious threat.

Desquamative gingivitis is a descriptive clinical term, not a diagnosis. Dermatologic conditions cause about 75% of cases of desquamative gingivitis, and over 95% of the dermatologic cases are accounted for by either oral lichen planus or cicatricial pemphigoid. The exact cause of desquamative gingivitis cannot be determined about a third of cases.

- Oral lichen planus

- Cicatricial pemphigoid or less commonly bullous pemphigoid

- Pemphigus vulgaris

- Linear immunoglobulin A disease

- Dermatitis herpetiformis

- Lupus erythematosus

- Chronic ulcerative stomatitis

- Chronic bacterial, fungal, and viral infections

- Reactions to medications, mouthwashes, and chewing gum

Rare causes include:

- Crohn’s disease

- Sarcoidosis

- Leukemia

- factitious (self inflicted) lesions

- Squamous cell carcinoma (can be mistaken for desquamative gingivitis)

Caused by various autoimmune diseases as well as allergies. Erosive lichen planus, mucous membrane pemphigoid, pemphigus vulgaris, and lupus erythematosus.

Rarely, allergic reactions of the mouth and lips may manifest as erosions; however, such reactions usually do not produce frank ulceration. An example of one common allergen is Balsam of Peru. If individuals allergic to this substance have oral exposure they may experience stomatitis and cheilitis (inflammation, rash, or painful erosion of the lips, oropharyngeal mucosa, or angles of their mouth). Balsam of Peru is used in foods and drinks for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties.

Erythema (redness) multiforme (EM) is usually a reaction of the skin and mucous membranes that occurs suddenly. It appears as a symmetrical rash and may include the mucous membrane lesions. This means that the body is sensitive to something that causes the skin and mucous membranes to react. The more common mild form is refer to as EM minor. It consists of a skin rash that involve no more than one mucosal surface. The sudden onset will progress rapidly as symmetrical lesions with circular color changes in some or all of the lesions. Rash will spread towards center or trunk of the body. Evenly distributed bumps on the skin become classic iris or target lesions. They have bright red borders and small white bumps in the center.

The cause of EM appears to be a highly sensitive reaction that can be triggered by a variety of causes. The causes can include bacterial, viral or chemical products, such as antibiotics – specifically penicillins or cephalosporins. This reaction is an allergic reaction and is in no way contagious.

Erythema multiforme minus is sometimes divided into papular and vesiulobullous forms.

The cause is unknown. Geographic tongue does not usually cause any symptoms, and in those cases where there are symptoms, an oral parafunctional habit may be a contributory factor. Persons with parafunctional habits related to the tongue may show scalloping on the sides of the tongue (crenated tongue). Some suggest that hormonal factors may be involved, because one reported case in a female appeared to vary in severity in correlation with oral contraceptive use. People with geographic tongue frequently claim that their condition worsens during periods of psychologic stress. Geographic tongue is inversely associated with smoking and tobacco use. Sometimes geographic tongue is said to run in families, and it is reported to be associated with several different genes, though studies show family association may also be caused by similar diets. Some have reported links with various human leukocyte antigens, such as increased incidence of HLA-DR5, HLA-DRW6 and HLA-Cw6 and decreased incidence in HLA-B51. Vitamin B2 deficiency (ariboflavinosis) can cause several signs in the mouth, possibly including geographic tongue, although other sources state that geographic tongue is not related to nutritional deficiency. Fissured tongue often occurs simultaneously with geographic tongue, and some consider fissured tongue to be an end stage of geographic tongue.

In the past, some research suggested that geographic tongue was associated with diabetes, seborrheic dermatitis and atopy, however newer research does not corroborate these findings. Others suggest allergy as a major factor, e.g. to nickel sulphate. Some studies have reported a link between geographic tongue and psoriasis, although 90% of children who are diagnosed with geographic tongue do not develop psoriasis. Again however, modern research studies do not support any link between psoriasis and geographic tongue. Lesions that are histologically indistinguishable from geographic tongue may also be diagnosed in reactive arthritis (arthritis, uveitis/conjunctivitis and urethritis).

Denture-related stomatitis is common and occurs worldwide. Usually the people affected are middle aged or elderly, with females being affected slightly more commonly than males. Prevalences of up to 70% have been reported in elderly care home residents. It is by far the most common type of oral candidiasis.

Autoimmune estrogen dermatitis presents as a cyclic skin disorder, that may appear eczematous, papular, bullous, or urticarial. with pruritus typically present, skin eruptions that may be chronic but which are exacerbated premenstrually or occur immediately following menses.

The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:

•UV-A and UV-B light seem to be the main provoking agents. This observation is supported by the fact that most patients live at high altitudes (>1000 m above sea level), and the condition improves in many patients when they move to lower altitudes. However, some patients who are affected already live at sea level.18,19,27 •Some authors are considering a food photosensitizer or a nutritional selective deficiency as a cause; however, no evidence proves this theory.27

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Because the eruption is transient and self-limiting, no treatment is indicated.