OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

The cause of the condition is unknown. The disease is characterized by non-caseating granulomatous inflammation. That is, the granulomas do not undergo the caseating ("cheese-like") necrosis typical of the granulomas of tuberculosis.

There is disagreement as to whether OFG represents an early form of Crohn's disease or sarcoidosis, or whether it is a distinct, but similar clinical entity. Crohn's disease can affect any part of gastrointestinal tract, from mouth to anus. When it involves the mouth alone, some authors refer to this as "oral Crohn's disease", distinguishing it from OFG, and others suggest that OFG is the same condition as Crohn's disease when it presents in the oral cavity.

OFG may represent a delayed hypersensitivity reaction, but the causative antigen(s) is not identified or varies form one individual to the next. Suspected sources of antigens include metals, e.g. cobalt, or additives and preservatives in foods, including benzoates, benzoic acid, cinnamaldehyde, metabisulfates, butylated hydroxyanisole, dodecyl gallate, tartrazine, or menthol, Examples of foods which may contain these substances include margarine, cinnamon, eggs, chocolate or peppermint oil.

Some suggest that infection with atypical mycobacteria could be involved, (paratuberculosis), and that OFG is a reaction to mycobacterial stress protein mSP65 acting as an antigen.

In response to an antigen, a chronic, submucosal, T cell mediated inflammatory response occurs, which involves cytokines (e.g. tumor necrosis factor alpha), protease-activated receptors, matrix metalloproteinases and cyclooxygenases. The granulomas in OFG form in the lamina propria, and may form adjacent to or within lymphatic vessels. This is thought to cause obstruction of lymphatic drainage and lymphedema which is manifest as swelling clinically.

There may be a genetic predisposition to the condition. People who develop OFG often have a history of atopy, such as childhood asthma or eczema.

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.

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).

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.

AC is caused by chronic and excessive exposure to ultraviolet radiation in sunlight.

Risk factors include:

- Outdoor lifestyle: e.g. farmers, sailors, fishermen, windsurfers, mountaineers, golfers, etc. This has given rise to synonyms for this condition such as "sailor's lip" and "farmer's lip". The prevalence in agricultural workers in a semi-arid region of Brazil is reported to be 16.7%.

- Light skin complexion: the condition typically affects individuals with lighter skin tones, particularly Caucasians living in tropical regions. In one report, 96% of persons with AC had phenotype II according to the Fitzpatrick scale.

- Age: AC typically affects older individuals, and rarely those under the age of 45.

- Gender: the condition affects males more commonly than females. Sometimes this ratio is reported as high as 10:1.

Additional factors may also play a role, including tobacco use, lip irritation, poor oral hygiene, and ill-fitting dentures.

Malnutrition (improper dietary intake) or malabsorption (poor absorption of nutrients into the body) can lead to nutritional deficiency states, several of which can lead to stomatitis. For example, deficiencies of iron, vitamin B2 (riboflavin), vitamin B3 (niacin), vitamin B6 (pyridoxine), vitamin B9 (folic acid) or vitamin B12 (cobalamine) may all manifest as stomatitis. Iron is necessary for the upregulation of transcriptional elements for cell replication and repair. Lack of iron can cause genetic downregulation of these elements, leading to ineffective repair and regeneration of epithelial cells, especially in the mouth and lips. Many disorders which cause malabsorption can cause deficiencies, which in turn causes stomatitis. Examples include tropical sprue.

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.

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.

To prevent AC from developing, protective measures could be undertaken such as avoiding mid-day sun, or use of a broad-brimmed hat, lip balm with anti UVA and UVB ingredients (e.g. para-aminobenzoic acid), or sun blocking agents (e.g. zinc oxide, titanium oxide) prior to sun exposure.

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.

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.

Many conditions can cause glossitis via malnutrition or malabsorption, which creates the nutritional deficiencies described above, although other mechanisms may be involved in some of those conditions listed.

- Alcoholism

- Sprue (celiac disease, or tropical sprue), secondary to nutritional deficiencies

- Crohn’s disease

- Whipple disease

- Glucagonoma syndrome

- Cowden disease

- Acquired immunodeficiency syndrome (AIDS)

- Carcinoid syndrome

- Kwashiorkor amyloidosis

- Veganism and other specialized diets,

- Poor hydration and low saliva in the mouth, which allows bacteria to grow more readily

- Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma

- Tongue piercing Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament

- Exposure to irritants such as tobacco, alcohol, hot foods, or spices

- Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors)

- Administration of ganglion blockers (e.g., Tubocurarine, Mecamylamine).

- Oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris

- Heredity

- Albuterol (bronchodilator medicine)

- Schizophrenia

A painful tongue may be an indication of an underlying serious medical condition and nearly always merits assessment by a physician or dental surgeon.

Good oral hygiene (thorough tooth brushing and flossing and regular professional cleaning and examination) may be helpful to prevent these disorders. Drinking plenty of water and the production of enough saliva, aid in the reduction of bacterial growth. Minimizing irritants or injury in the mouth when possible can aid in the prevention of glossitis. Avoiding excessive use of any food or substance that irritates the mouth or tongue may also help.

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.

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.

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

Many infections can cause oral ulceration (see table). The most common are herpes simplex virus (herpes labialis, primary herpetic gingivostomatitis), varicella zoster (chicken pox, shingles), and coxsackie A virus (hand, foot and mouth disease). Human immunodeficiency virus (HIV) creates immunodeficiencies which allow opportunistic infections or neoplasms to proliferate. Bacterial processes leading to ulceration can be caused by "Mycobacterium tuberculosis" (tuberculosis) and "Treponema pallidum" (syphilis).

Opportunistic activity by combinations of otherwise normal bacterial flora, such as aerobic streptococci, "Neisseria", "Actinomyces", spirochetes, and "Bacteroides" species can prolong the ulcerative process. Fungal causes include "Coccidioides immitis" (valley fever), "Cryptococcus neoformans" (cryptococcosis), and "Blastomyces dermatitidis" ("North American Blastomycosis"). Entamoeba histolytica, a parasitic protozoan, is sometimes known to cause mouth ulcers through formation of cysts.

The cause is unknown, but it may be partly a genetic trait. Aging and environmental factors may also contribute to the appearance.

Plasma cell gingivits and plasma cell cheilitis are thought to be hypersensitivity reactions to some antigen. Possible sources of antigens include ingredients in toothpastes, chewing gum, mints, pepper, or foods. Specifically, cinnamonaldehyde and cinnamon flavoring are often to blame. However, the exact cause in most is unknown.

Tobacco smoking or chewing is the most common causative factor, with more than 80% of persons with leukoplakia having a positive smoking history. Smokers are much more likely to suffer from leukoplakia than non-smokers. The size and number of leukoplakia lesions in an individual is also correlated with the level of smoking and how long the habit has lasted for. Other sources argue that there is no evidence for a direct causative link between smoking and oral leukoplakia. Cigarette smoking may produce a diffuse leukoplakia of the buccal mucosa, lips, tongue and rarely the floor of mouth. Reverse smoking, where the lit end of the cigarette is held in the mouth is also associated with mucosal changes. Tobacco chewing, e.g. betel leaf and areca nut, called paan, tends to produce a distinctive white patch in a buccal sulcus termed "tobacco pouch keratosis". In the majority of persons, cessation triggers shrinkage or disappearance of the lesion, usually within the first year after stopping.

It is a relatively common condition, with an estimated prevalence of 6.8%–11% amongst children. Males are more commonly affected. The condition may be seen at any age, but generally affects older people more frequently. The condition also generally becomes more accentuated with age. The prevalence of the condition increases significantly with age, occurring in 40% of the population after the age of 40.

Although the synergistic effect of alcohol with smoking in the development of oral cancer is beyond doubt, there is no clear evidence that alcohol is involved in the development of leukoplakia, but it does appear to have some influence. Excessive use of a high alcohol containing mouth wash (> 25%) may cause a grey plaque to form on the buccal mucosa, but these lesions are not considered true leukoplakia.

BMS is fairly common worldwide, (however, other sources describe it as rare), and affects up to five individuals per 100,000 general population. People with BMS are more likely to be middle aged or elderly, and females are three to seven times more likely to have BMS than males. Some report a female to male ratio of as much as 33 to 1. BMS is reported in about 10-40% of women seeking medical treatment for menopausal symptoms, and BMS occurs in about 14% of postmenopausal women. Males and younger individuals of both sexes are sometimes affected.

Asian and Native American people have considerably higher risk of BMS.