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.

In about 50% of cases of burning mouth sensation no identifiable cause is apparent, these cases are termed (primary) BMS. Several theories of what causes BMS have been proposed, and these are supported by varying degrees of evidence, but none is proven.

As most people with BMS are postmenopausal women, one theory of the cause of BMS is of estrogen or progesterone deficit, but a strong statistical correlation has not been demonstrated. Another theory is that BMS is related to autoimmunity, as abnormal antinuclear antibody and rheumatoid factor can be found in the serum of more than 50% of persons with BMS, but these levels may also be seen in elderly people who do not have any of the symptoms of this condition. Whilst salivary flow rates are normal and there are no clinical signs of a dry mouth to explain a complaint of dry mouth, levels of salivary proteins and phosphate may be elevated and salivary pH or buffering capacity may be reduced.

Depression and anxiety are strongly associated with BMS. It is not known if depression is a cause or result of BMS, as depression may develop in any setting of constant unrelieved irritation, pain, and sleep disturbance. It is estimated that about 20% of BMS cases involve psychogenic factors, and some consider BMS a psychosomatic illness, caused by cancerophobia, concern about sexually transmitted infections, or hypochondriasis.

Chronic low-grade trauma due to parafunctional habits (e.g. rubbing the tongue against the teeth or pressing it against the palate), may be involved. BMS is more common in persons with Parkinson's disease, so it has been suggested that it is a disorder of reduced pain threshold and increased sensitivity. Often people with BMS have unusually raised taste sensitivity, termed hypergeusia ("super tasters"). Dysgeusia (usually a bitter or metallic taste) is present in about 60% of people with BMS, a factor which led to the concept of a defect in sensory peripheral neural mechanisms. Changes in the oral environment, such as changes in the composition of saliva, may induce neuropathy or interruption of nerve transduction. The onset of BMS is often spontaneous, although it may be gradual. There is sometimes a correlation with a major life event or stressful period in life. In women, the onset of BMS is most likely three to twelve years following menopause.

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.

Bacterial

- (Plaque-induced) gingivitis—A common periodontal (gum) disease is Gingivitis. Periodontal refers to the area the infection affects, which include the teeth, gums, and tissues surrounding the teeth. Bacteria cause inflammation of the gums which become red, swollen and can bleed easily. The bacteria along with mucus form a sticky colorless substance called plaque which harbours the bacteria. Plaque that is not removed by brushing and flossing hardens to form tartar that brushing doesn't clean. Smoking is a major risk factor. Treatment of gingivitis is dependent on how severe and how far the disease has progressed. If the disease is not too severe it is possible to treat it with chlorhexidine rinse and brushing with fluoride toothpaste to kill the bacteria and remove the plaque, but once the infection has progressed antibiotics may be needed to kill the bacteria.

- Periodontitis—When gingivitis is not treated it can advance to periodontitis, when the gums pull away from the teeth and form pockets that harbor the bacteria. Bacterial toxins and the body's natural defenses start to break down the bone and connective tissues. The tooth may eventually become loose and have to be removed.

- Scarlet fever is caused by streptococci species, and starts as tonsilitis and pharyngitis before involving the soft palate and the tongue. It usually occurs in children where a fever occurs and a rash develops on the skin. It is treated with penicillin and the prognosis is generally excellent.

Viral

- Herpes simplex (infection with herpes simplex virus, or HSV) is very common in the mouth and lips. This virus can cause blisters and sores around the mouth (herpetic gingivostomatitis) and lips (herpes labialis). HSV infections tend to recur periodically. Although many people get infected with the virus, only 10% actually develop the sores. The sores may last anywhere from 3–10 days and are very infectious. Some people have recurrences either in the same location or at a nearby site. Unless the individual has an impaired immune system, e.g., owing to HIV or cancer-related immune suppression, recurrent infections tend to be mild in nature and may be brought on by stress, sun, menstrual periods, trauma or physical stress.

- Mumps of the salivary glands is a viral infection of the parotid glands. This results in painful swelling at the sides of the mouth in both adults and children. The infection is quite contagious. Today mumps is prevented by getting vaccinated in infancy. There is no specific treatment for mumps except for hydration and painkillers. Sometimes mumps can cause inflammation of the brain, testicular swelling or hearing loss.

Fungal

- Oral candidiasis is by far the most common fungal infection that occurs in the mouth. It usually occurs in immunocompromised individuals. Individuals who have undergone a transplant, HIV, cancer or use corticosteroids commonly develop candida of the mouth and oral cavity. Other risk factors are dentures and tongue piercing. The typical signs are a white patch that may be associated with burning, soreness, irritation or a white cheesy like appearance. Once the diagnosis is made, candida can be treated with a variety of anti fungal drugs.

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.

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.

Daily oral muscle physical therapy, or the administration of antidepressants have been reported as effective therapy for occlusal dysesthesia patients. Tooth grinding, and the replacement or removal of all dental work should be avoided in patients with occlusal dysesthesia, despite the frequent requests for further surgery often made by these patients.

Antidepressants are also often prescribed for scalp dysesthesia.

Prakash et al. found that many patients suffering from burning mouth syndrome (BMS), one variant of occlusal dysesthesia, also report painful sensations in other parts of the body. Many of the patients suffering from BMS met the classification of restless leg syndrome (RLS). About half of these patients also had a family history of RLS. These results suggest that some BMS symptoms may be caused by the same pathway as RLS in some patients, indicating that dopaminergic drugs regularly used to treat RLS may be effective in treating BMS as well.

Amelogenesis imperfecta hypomaturation type with taurodontism are often confused. Amelogenesis imperfecta of the hypomaturation type with taurodontism (AIHHT) has no hair or bone changes which helps to differentiate between TDO cases and AIHHT. Polymerase chain reaction also known as PCR is used to amply pieces of DNA and observed for the 141 base pair allele as a result of a deletion of four nucleotides in exon 3 of the DLX-3 gene. Additionally, the current research shows that there is heavy reliance on the physical characteristics in the differentiation of TDO verses AIHHT and the severity and prevalence of their expression. For instance, taurodontism is severely expressed in TDO, but mildly expressed in AIHHT. Currently, researchers are trying to identify the reason for the alteration in the DLX-3 and DLX-7 genes that are responsible for AIHHT versus TDO.

A single copy of the abnormal gene from one parent is able to cause the disease; this is called autosomal dominance. A mutation in the DLX3 gene has been confirmed as the cause of TDO. The onset of TDO begins with a 4 base pair deletion on chromosome 17q21, causing a mutation, specifically frameshift, and the termination codon to be the cause of the lack of complete maturation of the tooth enamel; this mutation is also responsible for the osseous defects in the bone. DLX-3 is expressed in the placenta and is significantly important during embryonic development in regards to hard bone tissue which is present in the teeth, skull, and long bones such as in the arms and legs. During normal tooth development, DLX 3 shifts from predominant expression in the inner enamel epithelium; the outer layer does not express DLX 3. In TDO cases, the DLX-3 is present on the outer enamel epithelium and leads to the dental abnormalities seen in this disease. Improper expression of DLX-3 causes the tooth enamel to be thinner, which leads to attrition and is most often the cause of dental abscess seen in TDO persons.

During osseous, connective tissue, and dermal cell differentiation, DLX 3 in TDO is also responsible for upper cranial thickness, calvaria, osteosclerosis of the long bones, long narrow head (dolichocephaly), abnormally thin brittle nails, and premature closing of fibrous joints. Consequently, 95% of people with TDO that are 16 years old or younger show skeletal abnormalities before full maturation takes place. Lack of mastoid pneumatization by mastoid cells occurs in 82% of the cases and is rarely prevalent outside of TDO diagnosis. Mastoid pneumatization occurs at about 6 months of ages and acts to minimize pressure fluctuations in the Eustachian tubes of the ear. The mastoid lies posterior to the lower jawbone (mandible) and distal to the ear. The Eustachian tube connects the middle ear to the back of the nose, and acts to create a specific pressure in the ear canal that causes vibrations to the eardrum; if adequate pressure is not attained, muffled, dull hearing results. In addition to the mastoid pneumatization assisting the Eustachian tubes for normal hearing, lack of mastoid pneumatization causes inflammation of the ear, general irritation, and does not allow enough air in to assist with mucus flowing out. It is not completely understood why gene mutations occur, but it is known that genetic mutations that cause disease are acquired from either or both parents at fertilization.

Dysesthesia (or dysaesthesia) comes from the Greek word "dys", meaning "not-normal" and "aesthesis", which means "sensation" (abnormal sensation). It is defined as an unpleasant, abnormal sense of touch. It often presents as pain but may also present as an inappropriate, but not discomforting, sensation. It is caused by lesions of the nervous system, peripheral or central, and it involves sensations, whether spontaneous or evoked, such as burning, wetness, itching, electric shock, and pins and needles. Dysesthesia can include sensations in any bodily tissue, including most often the mouth, scalp, skin, or legs.

It is sometimes described as feeling like acid under the skin. Burning dysesthesia might accurately reflect an acidotic state in the synapses and perineural space. Some ion channels will open to a low pH, and the acid sensing ion channel has been shown to open at body temperature, in a model of nerve injury pain. Inappropriate, spontaneous firing in pain receptors has also been implicated as a cause of dysesthesia.

Patients suffering from dysesthesia can become incapacitated with pain, despite no apparent damage to the skin or other tissue. Patients suffering from dysesthesia also often suffer from psychological disorders.

This disease is more common in women and an association with the gene FLT4 has been described. FLT4 codes for VEGFR-3, which is implicated in development of the lymphatic system.

Milroy's disease is also known as primary or hereditary lymphedema type 1A or early onset lymphedema.

It is a very rare disease with only about 200 cases reported in the medical literature. Milroy's disease is an autosomal dominant condition caused by a mutation in the FLT4 gene which encodes of the vascular endothelial growth factor receptor 3 (VEGFR-3) gene located on the long arm (q) on chromosome 5 (5q35.3).

In contrast to Milroy's disease (early onset lymphedema type 1A,) which typically has its onset of swelling and edema at birth or during early infancy, hereditary lymphedema type II, known as Meige disease, has its onset around the time of puberty. Meige disease is also an autosomal dominant disease. It has been linked to a mutations in the ‘forkhead’ family transcription factor (FOXC2) gene located on the long arm of chromosome 16 (16q24.3). About 2000 cases have been identified. A third type of hereditary lymphedema, that has an onset after the age of 35 is known as lymph-edema tarda.

As many as 90% of Americans and 92% of teenagers use antiperspirants or deodorants. In 2014, the global market for deodorants was estimated at 13.00 billion USD with a compound annual growth rate of 5.62% between 2015 and 2020.

Body odor may be reduced or prevented or even aggravated by using deodorants, antiperspirants, disinfectants, underarm liners, triclosan, special soaps or foams with antiseptic plant extracts such as ribwort and liquorice, chlorophyllin ointments and sprays topically, and chlorophyllin supplements internally. Although body odor is commonly associated with hygiene practices, its presentation can be affected by changes in diet as well as the other factors.

Vaginal intraepithelial neoplasia (VAIN) is a condition that describes premalignant histological findings in the vagina characterized by dysplastic changes.

The disorder is rare and generally has no symptoms. VAIN can be detected by the presence of abnormal cells in a Papanicolaou test (Pap smear).

Like cervical intraepithelial neoplasia, VAIN comes in three stages, VAIN 1, 2, and 3. In VAIN 1, a third of the thickness of the cells in the vaginal skin are abnormal, while in VAIN 3, the full thickness is affected. VAIN 3 is also known as carcinoma in-situ, or stage 0 vaginal cancer.

Infection with certain types of the human papillomavirus ("high-risk types") may be associated with up to 80% of cases of VAIN. Vaccinating girls with HPV vaccine before initial sexual contact has been shown to reduce incidence of VAIN.

One study found that most cases of VAIN were located in the upper third of the vagina, and were multifocal. In the same study, 65 and 10% patients with VAIN also had cervical intraepithelial neoplasia and vulvar intraepithelial neoplasia, respectively.

In another study, most cases of VAIN went into remission after a single treatment, but about 5% of the cases studied progressed into a more serious condition despite treatment.

Acrocephalosyndactylia (or acrocephalosyndactyly) is the common presentation of craniosynostosis and syndactyly.

Basophilia as an isolated finding is uncommon. However it is a common feature of myeloproliferative disorders and particularly prominent in chronic myelogenous leukemia.

Conditions Associated with Increased Numbers of Blood Basophils

- Allergy or inflammation

1. Ulcerative colitis

2. Drug, food, inhalant hypersensitivity

3. Erythroderma, urticaria

4. Juvenile rheumatoid arthritis

- Endocrinopathy

1. Diabetes mellitus

2. Estrogen administration

3. Hypothyroidism (myxedema)

- Infection

1. Chicken pox

2. Influenza

3. Smallpox

4. Tuberculosis

- Iron deficiency

- Exposure to ionizing radiation

- Neoplasia

1. "Basophilic leukemia" (see text)

- Myeloproliferative neoplasms (especially chronic myelogenous leukemia; also polycythemia vera, primary myelofibrosis, essential thrombocythemia)

- Carcinoma

A survey of 10,000 American households revealed that the prevalence of diagnosed primary immunodeficiency approaches 1 in 1200. This figure does not take into account people with mild immune system defects who have not received a formal diagnosis.

Milder forms of primary immunodeficiency, such as selective immunoglobulin A deficiency, are fairly common, with random groups of people (such as otherwise healthy blood donors) having a rate of 1:600. Other disorders are distinctly more uncommon, with incidences between 1:100,000 and 1:2,000,000 being reported.

It has several different types:

- type 1 - Apert syndrome

- type 2 - Crouzon syndrome

- type 3 - Saethre-Chotzen syndrome

- type 5 - Pfeiffer syndrome

A related term, "acrocephalopolysyndactyly" (ACPS), refers to the inclusion of polydactyly to the presentation. It also has multiple types:

- type 1 - Noack syndrome; now classified with Pfeiffer syndrome

- type 2 - Carpenter syndrome

- type 3 - Sakati-Nyhan-Tisdale syndrome

- type 4 - Goodman syndrome; now classified with Carpenter syndrome

- type 5 - Pfeiffer syndrome

It has been suggested that the distinction between "acrocephalosyndactyly" versus "acrocephalopolysyndactyly" should be abandoned.

Milroy's disease (MD) is a familial disease characterized by lymphedema, commonly in the legs, caused by congenital abnormalities in the lymphatic system. Disruption of the normal drainage of lymph leads to fluid accumulation and hypertrophy of soft tissues. It is also known as Milroy disease, Nonne-Milroy-Meige syndrome and hereditary lymphedema.

It was named by Sir William Osler for William Milroy, a Canadian physician, who described a case in 1892, though it was first described by Rudolf Virchow in 1863.

By definition, primary immune deficiencies are due to genetic causes. They may result from a single genetic defect, but most are multifactorial. They may be caused by recessive or dominant inheritance. Some are latent, and require a certain environmental trigger to become manifest, like the presence in the environment of a reactive allergen. Other problems become apparent due to aging of bodily and cellular maintenance processes.

VKC is thought to be an allergic disorder in which IgE mediated mechanism play a role. Such patients often give family history of other atopic diseases such as hay fever, asthma or eczema, and their peripheral blood shows eosinophilia and increased serum IgE levels.

3-M syndrome is most often caused by a mutation in the gene CUL7, but can also be seen with mutations in the genes OBS1 and CCDC8 at lower frequencies. This is an inheritable disorder and can be passed down from parent to offspring in an autosomal recessive pattern. An individual must receive two copies of the mutated gene, one from each parent, in order to be have 3-M syndrome. An individual can be a carrier for the disorder if they inherit only one mutant copy of the gene, but will not present any of the symptoms associated with the disorder.

Since 3-M syndrome is a genetic condition there are no known methods to preventing this disorder. However, genetic testing on expecting parents and prenatal testing, which is a molecular test that screens for any problems in the heath of a fetus during pregnancy, may be available for families with a history of this disorder to determine the fetus' risk in inheriting this genetic disorder.

Vernal keratoconjunctivitis (VKC) or spring catarrh is a recurrent, bilateral, and self-limiting inflammation of conjunctiva, having a periodic seasonal incidence.

Non-blanching rash (NBR) is a medical term used to describe a skin rash that does not fade when pressed with, and viewed through, a glass.

It is a characteristic of both purpuric and petechial rashes. Individual purpura measure 3–10 mm (0.3–1 cm, - in), whereas petechiae measure less than 3 mm.

A non-blanching rash can be a symptom of bacterial meningitis, but this is not the exclusive cause.

Nodular fasciitis, also known as nodular pseudosarcomatous fasciitis, pseudosarcomatous fasciitis, and subcutaneous pseudosarcomatous fibromatosis, is a benign soft tissue lesion most commonly found in the superficial fascia. The lesion commonly occurs in the first three decades of life. Upper extremities and trunk are the most common affected anatomical sites. Previous history of trauma may be present. Clinically and histologically, nodular fasciitis may be mistaken for a sarcoma.