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.

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.

Erythroplakia has an unknown cause but researchers presume it to be similar to the causes of squamous cell carcinoma. Carcinoma is found in almost 40% of erythroplakia. It is mostly found in elderly men around the ages of 65 - 74. It is commonly associated with smoking.

Alcohol and tobacco use have been described as risk factors.

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.

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.

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.

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.

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.

A study in Sweden showed that 21.5% of smokers and 3% of nonsmokers (genetic pigmentation or unknown cause) had lesions that could be classified as an oral melanin pigmentation. A gingival melanin index in 4 degrees was established. Already with a consumption of 1-3 cigarettes a day 9.3% of all 20.333 examined showed a smoker's melanosis. Pipe smokers had smoker's melanosis in 16.8%. One year after the start of cigarette smoking a clinically visible smoker's melanosis could be seen in 12.3% of women, and 17% among men.

In cigarette smokers who quit smoking, the number of individuals with smoker's melanosis becomes slowly less frequent after 2–3 months, but can still be seen in a few former smokers three years after smoking stop.

Although clinically visible genetic melanin pigmentations in the mouth are present in several ethnic groups all over the world, more mucosal areas will be melanin-pigmentet if tobacco products are used. Smoker's melanosis is found in India, Italy, Japan, Nigeria, Sweden, Turkey, USA, and several other countries.

Smoker's melanosis is expected to be found also in other tissue surfaces exposed to tobacco and tobacco smoke, for instance lips and in skin of the fingers holding the cigarette. Future studies will also show if the use of tobacco exaggerates the pigmentation of skin.

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.

Treatment involves biopsy of the lesion to identify extent of dysplasia. Complete excision of the lesion is sometimes advised depending on the histopathology found in the biopsy. Even in these cases, recurrence of the erythroplakia is common and, thus, long-term monitoring is needed.

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.

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.

STK is extremely common among smokeless tobacco users. Given the association with smokeless tobacco use, this condition tends to occur in adults. A national USA survey estimated an overall prevalence of 1.5% of all types of smokeless tobacco lesions, with males affected more commonly than females.

The oral lesion itself is benign and self-limiting, however this may not necessarily be the case for the underlying cause of immunocompromise. For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease).

Smoking or the use of nicotine-containing drugs is the cause to Smoker's melanosis. Also tar-components (benzopyrenes) are known to stimulate melanocytes to melanin production, and other unknown toxic agents in tobacco may also be the cause. These chemical agents have a polycyclic, chain-like structure. Environmental tobacco smoke from parents is causing smoker's melanosis in their children Swedish snuff causes a small elevation of oral melanin pigmented individuals from 3.0% to 4.7%. Nicotine tablets have shown to stimulate to melanin pigmentation of the oral mucosa.

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.

Usually this lesion is reversible if the tobacco habit is stopped completely, even after many years of use. In one report, 98% of lesions disappeared within 2 weeks of stopping tobacco use. The risk of the lesion developing into oral cancer (generally squamous cell carcinoma and its variant verrucous carcinoma) is relatively low. Indeed, veruccous carcinoma is sometimes term snuff dipper's cancer. In most reported cases, malignant transformation has occurring in individuals with a very long history of chewing tobacco or who use dry snuff.

Smokeless tobacco use is also accompanied by increased risk of other oral conditions such as dental caries (tooth decay), periodontitis (gum disease), attrition (tooth wear) and staining.

Hairy leukoplakia is one of the most common oral manifestations of HIV/AIDS, along with oral candidiasis. It is the most common HIV/AIDS related condition caused by EBV, although EBV associated lymphomas may also occur. OHL mainly occurs in adult males, less commonly in adult females and rarely in children. The incidence rises as the CD4 count falls, and the appearance of OHL may signifiy progression of HIV to AIDS. A study from 2001 reported a significant decrease in the incidence of some oral manifestations of AIDS (including OHL and necrotizing ulcerative periodontitis), which was attributed to the use of HAART, whilst the incidence other HIV associated oral lesions did not alter significantly.

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.

There are many oral and maxillofacial pathologies which are not fully understood.

- Burning mouth syndrome (BMS) is a disorder where there is a burning sensation in the mouth that has no identifiable medical or dental cause. The disorder can affect anyone but tends to occur most often in middle aged women. BMS has been hypothesized to be linked to a variety of factors such as the menopause, dry mouth (xerostomia) and allergies. BMS usually lasts for several years before disappearing for unknown reasons. Other features of this disorder include anxiety, depression and social isolation. There is no cure for this disorder and treatment includes use of hydrating agents, pain medications, vitamin supplements or the usage of antidepressants.

- Aphthous stomatitis is a condition where ulcers (canker sores) appear on the inside of the mouth, lips and on tongue. Most small canker sores disappear within 10–14 days. Canker sores are most common in young and middle aged individuals. Sometimes individuals with allergies are more prone to these sores. Besides an awkward sensation, these sores can also cause pain or tingling or a burning sensation. Unlike herpes sores, canker sores are always found inside the mouth and are usually less painful. Good oral hygiene does help but sometime one may have to use a topical corticosteroid.

- Migratory stomatitis is a condition that involves the tongue and other oral mucosa. The common migratory glossitis (geographic tongue) affects the anterior two thirds of the dorsal and lateral tongue mucosa of 1% to 2.5% of the population, with one report of up to 12.7% of the population. The tongue is often fissured, especially. in elderly individuals. In the American population, a lower prevalence was reported among Mexican Americans (compared with Caucasians and African Americans) and cigarette smokers. When other oral mucosa, beside the dorsal and lateral tongue, are involved, the term migratory stomatitis (or ectopic geographic tongue) is preferred. In this condition, lesions infrequently involve also the ventral tongue and buccal or labial mucosa. They are rarely reported on the soft palate and floor of the mouth.

The incidence of the disease is higher in people from certain parts of the world including South-East Asia, South Africa and the Middle East.

This phenomenon is fairly common, with one in every 800 adults showing evidence of active lesions at any one time. It is more common in people who are experiencing stress or psychological conditions. The prevalence in females is double the prevalence in males, and it is two or three times more prevalent in people over the age of thirty-five.

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.