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.

The overall prevalence of lichen planus in the general population is about 0.1–4.0%. It generally occurs more commonly in females, in a ratio of 3:2, and most cases are diagnosed between the ages of 30 and 60, but it can occur at any age.

Oral lichen planus is relatively common, It is one of the most common mucosal diseases. The prevalence in the general population is about 1.27–2.0%, and it occurs more commonly in middle aged people. OLP in children is rare. About 50% of females with oral lichen planus were reported to have undiagnosed vulvar lichen planus.

The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.

Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".

Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.

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.

A 2003 survey of diseases of the foot in 16 European countries found onychomycosis to be the most frequent fungal foot infection and estimates its prevalence at 27%. Prevalence was observed to increase with age. In Canada, the prevalence was estimated to be 6.48%. Onychomycosis affects approximately one-third of diabetics and is 56% more frequent in people suffering from psoriasis.

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.

Following effective treatment recurrence is common (10–50%).

Nail fungus can be painful and cause permanent damage to nails. It may lead to other serious infections if the immune system is suppressed due to medication, diabetes or other conditions. The risk is most serious for people with diabetes and with immune systems weakened by leukemia or AIDS, or medication after organ transplant. Diabetics have vascular and nerve impairment, and are at risk of cellulitis, a potentially serious bacterial infection; any relatively minor injury to feet, including a nail fungal infection, can lead to more serious complications. Infection of the bone is another rare complication.

Leukoedema is common. It occurs in about 70-90% of black skinned adults and about 50% of black skinned children. The prevalence in white skinned people is considerably less, but reports range from less than 10% to more than 90%, probably varying depending upon the population studied, and the methods used in the study, e.g. examination conditions and the diagnostic criteria. The ethnic variation may be explained by genetic factors or simply because black skinned people have greater amount of melanin in the mucosa, making it appear darker (termed racial or physiologic pigmentation). This darker mucosa may make the edematous changes more noticeable, whereas in the mucosa of people with lighter skin types leukoedema gives a milder presentation.

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.

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)

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.

The cause of nicotine stomatitis is thought to be chemical or thermally induced keratosis. The chemicals in tobacco may act as irritants in this condition. Chronic heat exposure is also responsible. Pipe smoking produces more heat on the palate than any other forms of smoking. Long-term drinking of very hot beverages can also cause a similar condition. The severity of the changes correlates with the frequency of the habit. The prevalence depends on a society's use of consuming hot beverages and of smoking in its various forms.

A similar, but more pronounced palatal keratosis occurs with reverse smoking. This is where the lit end of the cigar or cigarette is held in the mouth, another form of smoking associated with high levels of heat in the mouth. This form of the condition is sometimes termed "reverse smoker's keratosis", and is a premalignant lesion. That is, the condition is associated with an increased risk of malignant transformation to oral squamous cell carcinoma (a type of oral cancer). Some sources do not distinguish between reverse smoker's keratosis and smoker's palate that is caused by heat. As such, these sources tend to state that stomatitis nicotina is a premalignant condition. Some reports show that there is an increased risk of tonsillar cancer, lung cancer and tumors of the posterior oral cavity in people who develop stomatitis nicotina.

The cause is unknown, but it is thought to be caused by intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin. Although leukoedema is thought to be a developmental condition, it may be more common and more pronounced in smokers, and becomes less noticeable when smoking is stopped. Smoking cannabis is known to be linked to this condition. It may also develop in areas subjecte to repeat subclinical irritation, caused by low grade irritants such as spices, oral debris or tobacco.

Lichen nitidus is a chronic inflammatory disease of unknown cause characterized by 1–2 mm, discrete and uniform, shiny, flat-topped, pale flesh-colored or reddish-brown papules that may appear as hypopigmented against dark skin. Occasionally, minimal scaling is present or can be induced by rubbing the surface of the papules. The disease usually affects children and young adults and is painless and usually nonpruritic, although protracted itching may occur in some cases. It is sometimes referred to by dermatologists as "mini lichen planus".

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.

Pemphigus foliaceus has been recognized in pet dogs, cats, and horses and is the most common autoimmune skin disease diagnosed in veterinary medicine. Pemphigus foliaceus in animals produces clusters of small vesicles that quickly evolve into pustules. Pustules may rupture, forming erosions or become crusted. Left untreated, pemphigus foliaceus in animals is life-threatening, leading to not only loss of condition but also secondary infection.

Pemphigus vulgaris is a very rare disorder described in pet dogs and cats. Paraneoplastic pemphigus has been identified in pet dogs.

The condition is uncommon. It occurs usually in elderly males who have a history of heavy pipe smoking, but it also can occur in cigar or cigarette smokers. The condition was once common, but has become more rare as habits such as pipe and cigar smoking have decreased in popularity.

Desquamative gingivitis (DG) is an erythematous (red), desquamatous (shedding) and ulcerated appearance of the gums. It is a descriptive term and can be caused by several different disorders.

The exact cause of VIN is unknown. Studies are being done to determine the cause of VIN. The following factors have been associated with VIN:

- HPV (Human Papilloma Virus)

- HSV-2 (Herpes simplex Virus - Type 2)

- Smoking

- Immunosuppression

- Chronic vulvar irritation

- Conditions such as Lichen Sclerosus

A papulosquamous disorder is a condition which presents with both papules and scales, or both scaly papules and plaques.

Examples include psoriasis, lichen planus, and pityriasis rosea.

The bacteria staphylococci are present in the majority of cases. Treatment with systemic antibiotics and coal tar shampoo can completely clear the condition when Staphylococcus aureus bacteria are found. Fungal infections such as tinea capitis are known to mimic the symptoms of the condition and can be cleared with antifungal treatment.

Generally, lichen nitidus is asymptomatic and self-limited; therefore, no treatment is required. However, if persistent pruritus is present, or the appearance “...interferes with daily activities or outlook...” topical glucocorticoids may be tried. If the disease process is symptomatic, generalized and extensive, oral glucocorticoids may be indicated. Other reported treatments include PUVA, UVA/UVB phototherapy, astemizole, acitretin, and etretinate.

When appears with sun/humidity; air conditioning (cool dry air) reduces swelling and discomfort.

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).

Erythroderma (also known as "Exfoliative dermatitis," "Dermatitis exfoliativa") is an inflammatory skin disease with erythema and scaling that affects nearly the entire cutaneous surface.

In ICD-10, a distinction is made between "exfoliative dermatitis" at L26, and "erythroderma" at L53.9.