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.

It is an uncommon condition, occurring with equal prevalence in males and females and at any age.

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.

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).

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).

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.

Geographic tongue is a common condition, affecting 2-3% of the adult general population, although other sources report a prevalence of up to 14%. It is one of the most common tongue disorders that occurs in children. The condition often starts in childhood, sometimes at an early age, but others report that the highest incidence occurs in the over 40 age group. Females are sometimes reported to be more commonly affected than males, in a 2:1 ratio, although others report that the gender distribution is equal.

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.

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.

Predisposing factors include smoking, denture wearing, use of corticosteroid sprays or inhalers and human immunodeficiency virus (HIV) infection. "Candida" species even in healthy people mainly colonizes the posterior dorsal tongue. Median rhombiod glossitis is thought to be a type of chronic atrophic (or erythematous) candidiasis. Microbiological culture of the lesion usually shows "Candida" mixed with bacteria.

The name "lie bumps" is a result of a myth that telling lies would cause them. However, very little has been written about this condition in scientific articles or textbooks and scientific studies have failed to produce a definite cause. Possible causes include: "stress, gastrointestinal upset, menstruation, acidic or sour food, smoking, and local trauma" (direct physical irritation) of the tongue. Lie bumps are often caused by the taste bud(s) splitting.

These bumps are small, white bumps on the base of the tongue. They are likely to be the result of transient lingual papillitis (TLP). This condition is limited to the upper (dorsal) surface of the tongue, affecting some of the tiny bumps on the tongue known as the fungiform papillae, what we commonly call the "taste buds."

TLP is a harmless problem. These bumps can become notably red or white and are quite tender for up to several days. While the cause of TLP is not known with certainty, most experts feel that local accidental trauma (rubbing, scraping or biting) is a major factor; however, contact reactions to things like certain foods have also been suggested. Lie bumps are not contagious and the discomfort is relatively minor. Typically these lesions heal within a few days with no treatment, though a doctor may refer a patient to an oral pathologist in prolonged cases.

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

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.

There are no specific treatments for this problem, other than using ice or numbing medicines to ease the pain.

Among individuals being treated in intensive care units, the mortality rate is about 30-50% when systemic candidiasis develops.

Several local and systemic factors can give a burning sensation in the mouth without any clinical signs, and therefore may be misdiagnosed as BMS. Some sources state that where there is an identifiable cause for a burning sensation, this can be termed "secondary BMS" to distinguish it from primary BMS. However, the accepted definitions of BMS hold that there are no identifiable causes for BMS, and where there are identifiable causes, the term BMS should not be used.

Some causes of a burning mouth sensation may be accompanied by clinical signs in the mouth or elsewhere on the body. For example, burning mouth pain may be a symptom of allergic contact stomatitis. This is a contact sensitivity (type IV hypersensitivity reaction) in the oral tissues to common substances such as sodium lauryl sulfate, cinnamaldehyde or dental materials. However, allergic contact stomatitis is accompanied by visible lesions and gives positive response with patch testing. Acute (short term) exposure to the allergen (the substance triggering the allergic response) causes non-specific inflammation and possibly mucosal ulceration. Chronic (long term) exposure to the allergen may appear as chronic inflammatory, lichenoid (lesions resembling oral lichen planus), or plasma cell gingivitis, which may be accompanied by glossitis and cheilitis. Apart from BMS itself, a full list of causes of an oral burning sensation is given below:

- Deficiency of iron, folic acid or various B vitamins (glossitis e.g. due to anemia), or zinc

- Neuropathy, e.g. following damage to the chorda tympani nerve.

- Hypothyroidism.

- Medications ("scalded mouth syndrome", unrelated to BMS) - protease inhibitors and angiotensin-converting-enzyme inhibitors (e.g. captopril).

- Type 2 diabetes

- True xerostomia, caused by hyposalivation e.g. Sjögren's syndrome

- Parafunctional activity, e.g. nocturnal bruxism or a tongue thrusting habit.

- Restriction of the tongue by poorly constructed dentures.

- Geographic tongue.

- Oral candidiasis.

- Herpetic infection (herpes simplex virus).

- Fissured tongue.

- Lichen planus.

- Allergies and contact sensitivities to foods, metals, and other substances (see table).

- Hiatal hernia.

- Human immunodeficiency virus.

- Multiple myeloma

Tongue lesions are very common. For example, in the United States one estimated point prevalence was 15.5% in adults. Tongue lesions are more common in persons who wear dentures and tobacco users. The most common tongue conditions are geographic tongue, followed by fissured tongue and hairy tongue.

Oral candidiasis is the most common fungal infection of the mouth, and it also represents the most common opportunistic oral infection in humans. In the Western Hemisphere, about 75% of females are affected at some time in their lives with a vaginal yeast infection.

Esophageal candidiasis is the most common esophageal infection in persons with AIDS and accounts for about 50% of all esophageal infections, often coexisting with other esophageal diseases. About two-thirds of people with AIDS and esophageal candidiasis also have oral candidiasis.

Candidal sepsis is rare. Candida is the fourth most common cause of bloodstream infections among hospital patients in the United States.

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.

Tongue diseases can be congenital or acquired, and are multiple in number. Considered according to a surgical sieve, some example conditions which can involve the tongue are discussed below. Glossitis is a general term for tongue inflammation, which can have various etiologies, e.g. infection.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Gingival cyst (or dental lamina cyst) is a type of cysts of the jaws that originates from the dental lamina and is found in the mouth parts. It is a superficial cyst in the alveolar mucosa. It can be seen inside the mouth as small and whistish bulge. Depending on the ages in which they develop, the cysts are classsfied into gingival cyst of newborn (or infant) and gingival cyst of adult. Structurally, the cyst is lined by thin epithelium and shows a lumen usually filled with desquamated keratin, occasionally containing inflammatory cells. The nodes are formes as a result of cystic degeneration of epithelial rests of the dental lamina (called the rests of Serres).

Gingival cyst was first described by a Czech physician Alois Epstein in 1880. In 1886, a German physician Heinrich Bohn described another type of cyst. Alfred Fromm introduced the classification of gingival cysts in 1967. According to him, gingival cysts of newborns can be further classsified based on their specific origin of the tissues as Epstein’s pearls, Bohn’s nodules and dental lamina cysts.

The cause of PVS is unknown; however, genetic factors and nutritional deficiencies may play a role. It is more common in women, particularly in middle age (peak age is over 50). In these patients, esophageal squamous cell carcinoma risk is increased; therefore, it is considered a premalignant process.

The condition is associated with koilonychia, glossitis, inflammation of the lips (cheilitis), and splenomegaly.

Esophageal web in Plummer-Vinson syndrome is found at upper end of esophagus(post cricoid region) and Schatzki ring may be found at the lower end of esophagus.