Xerostomia, also known as dry mouth syndrome, can precipitate dysgeusia because normal salivary flow and concentration are necessary for taste. Injury to the glossopharyngeal nerve can result in dysgeusia. In addition, damage done to the pons, thalamus, and midbrain, all of which compose the gustatory pathway, can be potential factors. In a case study, 22% of patients who were experiencing a bladder obstruction were also suffering from dysgeusia. Dysgeusia was eliminated in 100% of these patients once the obstruction was removed. Although it is uncertain what the relationship between bladder relief and dysgeusia entails, it has been observed that the areas responsible for urinary system and taste in the pons and cerebral cortex in the brain are close in proximity.

Many of the causes for dysgeusia occur due to unknown reasons. A wide range of miscellaneous factors may contribute to this taste disorder, such as gastric reflux, lead poisoning, and diabetes mellitus. A minority of pine nuts can apparently cause taste disturbances, for reasons which are not entirely proven. Certain pesticides can have damaging effects on the taste buds and nerves in the mouth. These pesticides include organochloride compounds and carbamate pesticides. Damage to the peripheral nerves, along with injury to the chorda tympani branch of the facial nerve, also cause dysgeusia. A surgical risk for laryngoscopy and tonsillectomy include dysgeusia. Patients who suffer from the burning mouth syndrome, most likely menopausal women, are often suffering from dysgeusia as well.

There are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste. The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. Drugs that prevent the production of angiotensin II by inhibiting angiotensin converting enzyme, eprosartan for example, have been linked to dysgeusia. There are few case reports claiming calcium channel blockers like Amlodipine also cause dysguesia by blocking calcium sensitive taste buds.

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.

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

Dentin hypersensitivity is a relatively common condition. Due to differences in populations studied and methods of detection, the reported incidence ranges from 4-74%. Dentists may under-report dentin hypersensitivity due to difficulty in diagnosing and managing the condition. When questionnaires are used, the reported incidence is usually higher than when clinical examination is used. Overall, it is estimated to affect about 15% of the general population to some degree.

It can affect people of any age, although those aged 20–50 years are more likely to be affected. Females are slightly more likely to develop dentin hypersensitivity compared to males. The condition is most commonly associated with the maxillary and mandibular canine and bicuspid teeth on the facial (buccal) aspect, especially in areas of periodontal attachment loss.

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.

The main cause of DH is gingival recession (receding gums) with exposure of root surfaces, loss of the cementum layer and smear layer, and tooth wear. Receding gums can be a sign of long-term trauma from excessive or forceful toothbrushing, or brushing with an abrasive toothpaste (dental abrasion), or a sign of chronic periodontitis (gum disease). Other less common causes are acid erosion (e.g. related to gastroesophageal reflux disease, bulimia or excessive consumption of acidic foods and drinks), and periodontal root planing. Dental bleaching is another known cause of hypersensitivity. Other causes include smoking tobacco, which can wear down enamel and gum tissue, cracked teeth or grinding of teeth (bruxism).

Dentine contains many thousands of microscopic tubular structures that radiate outwards from the pulp; these dentinal tubules are typically 0.5–2 micrometres in diameter. Changes in the flow of the plasma-like biological fluid present in the dentinal tubules can trigger mechanoreceptors present on nerves located at the pulpal aspect, thereby eliciting a pain response. This hydrodynamic flow can be increased by cold, air pressure, drying, sugar, sour (dehydrating chemicals), or forces acting onto the tooth. Hot or cold food or drinks, and physical pressure are typical triggers in those individuals with teeth sensitivity.

Most experts on this topic state that the pain of DH is in reality a normal, physiologic response of the nerves in a healthy, non-inflamed dental pulp in the situation where the insulating layers of gingiva and cementum have been lost; i.e., dentin hypersensitivity is not a true form of allodynia or hyperalgesia. To contradict this view, not all exposed dentin surfaces cause DH. Others suggest that due to the presence of patent dentinal tubules in areas of hypersensitive dentin, there may be increased irritation to the pulp, causing a degree of reversible inflammation.

Also termed "lip dermatitis", eczematous cheilitis is a diverse group of disorders which often have an unknown cause. Chronic eczematous reactions account for the majority of chronic cheilitis cases.

It is divided into endogenous (due to an inherent characteristic of the individual), and exogenous (where it is caused by an external agent). The main cause of endogenous eczematous cheilitis is atopic cheilitis (atopic dermatitis), and the main causes of exogenous eczematous cheilitis is irritant contact cheilitis ("e.g.", caused by a lip-licking habit) and allergic contact cheilitis. The latter is characterized by a dryness, fissuring, edema, and crusting. It affects females more commonly than males, in a ratio of about 9:1.

The most common causes of allergic contact cheilitis is lip cosmetics, including lipsticks and lip balm, followed by toothpastes. A lipstick allergy can be difficult to diagnose in some cases as it is possible that cheilitis can develop without the person even wearing lipstick. Instead, small exposure such as kissing someone who is wearing lipstick is enough to cause the condition.

Allergy to Balsam of Peru can manifest as cheilitis. Allergies to metal, wood, or other components can cause cheilitis reactions in musicians, especially players of woodwind and brass instruments, "e.g.", the so-called "clarinetist's cheilitis", or "flutist's cheilitis". "Pigmented contact cheilitis" is one type of allergic cheilitis in which a brown-black discoloration of the lips develops. Patch testing is used to identify the substance triggering allergic contact cheilitis.

The aetiology of dental abrasion can be due to a single stimuli or, as in most cases, multi-factorial. The most common cause of dental abrasion, is the combination of mechanical and chemical wear.

Tooth brushing is the most common cause of dental abrasion, which is found to develop along the gingival margin, due to vigorous brushing in this area. The type of toothbrush, the technique used and the force applied when brushing can influence the occurrence and severity of resulting abrasion. Further, brushing for extended periods of time (exceeding 2-3 min) in some cases, when combined with medium/hard bristled toothbrushes can cause abrasive lesions.

Different toothbrush types are more inclined to cause abrasion, such as those with medium or hard bristles. The bristles combined with forceful brushing techniques applied can roughen the tooth surface and cause abrasion as well as aggravating the gums. Repetitive irritation to the gingival margin can eventually cause recession of the gums. When the gums recede, the root surface is exposed which is more susceptible to abrasion.

Comparatively, electric toothbrushes have less abrasive tendencies.

Types of toothpastes can also damage enamel and dentine due to the abrasive properties. Specific ingredients are used in toothpaste to target removal of the bio-film and extrinsic staining however in some cases can contribute to the pastes being abrasive.

Whitening toothpastes are found to be one of the most abrasive types of toothpastes, according to the RDA Scale, detailed below. In-home and clinical whitening have been proven to increase the likelihood of an individual experiencing dental abrasion. It is believed that dental abrasion due to the whitening process is caused by a combination of both mechanical and chemical irritants, for example, using whitening toothpaste and at home bleaching kits together. However, if an individual is regimented in their after-whitening care then they can avoid loss of dentine minerals and in turn abrasion can be avoided. (that contribute to developing abrasion).

Another factor that can contribute to abrasion is alteration of pH levels in the saliva. This can be sugary/ acidic foods and liquids. The reasoning behind this is that an increase in acidity of saliva can induce demineralization and therefore compromising the tooth structure to abrasive factors such as tooth brushing or normal wear from mastication. When the tooth structure is compromised, this is where the mineral content of the saliva can create shallow depressions in the enamel and thus, when brushed can cause irreparable damage on tooth surface. The dental abrasion process can be further stimulated and accelerated through the effects of dental Acid erosion.

Succinyl choline, phenothiazines and tricyclic antidepressants causes trismus as a secondary effect. Trismus can be seen as an extra-pyramidal side-effect of metoclopromide, phenothiazines and other medications.

Most blinded conscious provocation studies have failed to show a correlation between exposure and symptoms, leading to the suggestion that psychological mechanisms play a role in causing or exacerbating EHS symptoms. In 2010, Rubin et al. published a follow-up to their 2005 review, bringing the totals to 46 double-blind experiments and 1175 individuals with self-diagnosed hypersensitivity. Both reviews found no robust evidence to support the hypothesis that electromagnetic exposure causes EHS, as have other studies. They also concluded that the studies supported the role of the nocebo effect in triggering acute symptoms in those with EHS.

Some other types of studies suggest evidence for symptoms at non-thermal levels of electromagnetic exposure. A review in 2010 of ten studies on neurobehavioral and cancer outcomes near cell phone base stations found eight with increased prevalence, including sleep disturbance and headaches. Since 1962, the microwave auditory effect or tinnitus has been shown from radio frequency exposure at levels below significant heating. Studies during the 1960s in Europe and Russia claimed to show effects on humans, especially the nervous system, from low energy RF radiation; the studies were disputed at the time.

Other studies on sensitivity have looked at therapeutic procedures using non-thermal electromagnetic exposure, genetic factors, an alteration in mast cells, oxidative stress, protein expression and voltage-gated calcium channels. Mercury release from dental amalgam and heavy metal toxicity have also been implicated in exposure effects and symptoms. Another line of study has been the nature of hyper-sensitivity or intolerance and the range of environmental exposures which may be related to it. Some 80% of people with self-diagnosed electromagnetic intolerance also claim intolerance to low levels of chemical exposure.

One proposed hypothesis for the cause of multiple chemical sensitivity is immune system dysfunction after being sensitized by a chemical exposure.

Fractures, particularly those of the mandible and fractures of zygomatic arch and zygomatic arch complex, accidental incorporation of foreign bodies due to external traumatic injury.

Treatment: fracture reduction, removal of foreign bodies with antibiotic coverage

Many chemicals have been reported to trigger MCS symptoms. Substances with strong scents are the most commonly reported triggers. These include a variety of cleaning agents, pesticides, perfumes, vehicle exhaust, the products used in barber shops and beauty salons, new carpeting, new furniture, chlorine and fluoride in drinking water, fresh ink, and less commonly wood smoke and secondhand tobacco smoke. Food items reported as triggers include tartrazine (a.k.a. FD&C Yellow #5 or E102), and other azo dyes (in the absence of an allergy), caffeine, and monosodium glutamate.

Otodental syndrome, also known as otodental dysplasia, is an exceptionally rare disease that is distinguished by a specific phenotype known as globodontia, that in rare cases can be associated with eye coloboma and high frequency hearing loss. Globodontia is an abnormal condition that can occur in both the primary and secondary dentition, except for the incisors which are normal in shape and size. This is demonstrated by significant enlargement of the canine and molar teeth. The premolars are either reduced in size or are absent. In some cases, the defects affecting the teeth, eye and ear can be either individual or combined. When these conditions are combined with eye coloboma, the condition is also known as oculo-otodental syndrome. The first known case of otodental syndrome was found in Hungary in a mother and her son by Denes and Csiba in 1969. Prevalence is less than 1 out of every 1 million individuals.

The cause of otodental syndrome is considered to be genetic. It is an autosomal dominant inheritance and is variable in its expressivity. Haploinsufficiency in the fibroblast growth factor 3 (FGF3) gene (11q13) has been reported in patients with otodental syndrome and is thought to cause the phenotype. Both males and females are equally affected. Individuals diagnosed with otodental syndrome can be of any age; age is not a relevant factor.

Currently there are no specific genetic treatments for otodental syndrome. Dental and orthodontic management are the recommended course of action.

Otodental syndrome is a rare condition that is genetically inherited in an autosomal dominant manner. Although there is no specific biological mechanism for otodental syndrome, what is recognized is that there is a genetic mutation, known as haploinsufficiency, that occurs in the fibroblast growth factor 3 (FGF3) gene (11q13). This is the alleged cause of the physical abnormalities and symptoms associated with otodental syndrome. Although in individuals with signs of ocular coloboma, a microdeletion in the Fas-associated death domain (FADD) gene (11q13.3) was also found to be responsible. There is variable penetrance and variable gene expression within these genetic mutations. Individuals with sensorineural hearing loss are believed to have a local lesion in the auditory segment of the inner ear, known as the cochlea. The biological mechanism for this is currently unknown as well.

"Relative dentin abrasivity" ("RDA") is a standardised measurement of the abrasive effect that the components of the toothpaste have on a tooth.

The RDA scale was developed by the American Dental Association (ADA). The RDA scale compares toothpaste abrasivity to standard abrasive materials and measures the depth of cut at an average of 1 millimetre per 100,000 brush strokes onto dentine. This comparison generates abrasive values for the dentifrices that would be safe for daily use. In vitro dental studies showed a positive correlation between the highest RDAs and greater dentin wear.

Since 1998, the RDA value is set by the standards DIN EN ISO 11609. Currently, the claim on products such as toothpaste are not regulated by law, however a dentifrice is required to have a level lower than 250 to be considered safe and before being given the ADA seal of approval. The values obtained depend on the size, quantity and surface structure of abrasive used in toothpastes.

While the RDA score has been shown to have a statistically significant correlation to the presence of abrasion, it is not the only contributing factor to consider. Other factors such as the amount of pressure used whilst brushing, the type, thickness and dispersion of bristle in the toothbrush and the time spent brushing are other factors that contribute to dental abrasion.

Intermittent hair–follicle dystrophy is a disorder of the hair follicle leading to increased fragility of the shaft, with no identifiable biochemical disturbance, also with an unknown prevalence.

The prevalence of migraine and vertigo is 1.6 times higher in 200 dizziness clinic patients than in 200 age- and sex-matched controls from an orthopaedic clinic. Among the patients with unclassified or idiopathic vertigo, the prevalence of migraine was shown to be elevated. In another study, migraine patients reported 2.5 times more vertigo and also 2.5 more dizzy spells during headache-free periods than the controls.

MAV may occur at any age with a female:male ratio of between 1.5 and 5:1. Familial occurrence is not uncommon. In most patients, migraine headaches begin earlier in life than MAV with years of headache-free periods before MAV manifests.

In a diary study, the 1-month prevalence of MAV was 16%, frequency of MAV was higher and duration longer on days with headache, and MAV was a risk factor for co-morbid anxiety.

There are no specific symptoms associated with claims of EHS and reported symptoms range widely between individuals. They include headache, fatigue, stress, sleep disturbances, skin prickling, burning sensations and rashes, pain and ache in muscles and many other health problems. In severe cases such symptoms can be a real and sometimes disabling problem for the affected person, causing psychological distress. There is no scientific basis to link such symptoms to electromagnetic field exposure.

The prevalence of some reported symptoms is geographically or culturally dependent and does not imply "a causal relationship between symptoms and attributed exposure". Many such reported symptoms overlap with other syndromes known as symptom-based conditions, functional somatic syndromes, and IEI (idiopathic environmental intolerance).

Those reporting electromagnetic hypersensitivity will usually describe different levels of susceptibility to electric fields, magnetic fields, and various frequencies of electromagnetic waves. Devices implicated include fluorescent and low-energy lights, mobile, cordless/portable phones, and WiFi. A 2001 survey found that people self-diagnosing as EHS related their symptoms most frequently to mobile phone base stations (74%), followed by mobile phones (36%), cordless phones (29%), and power lines (27%). Surveys of electromagnetic hypersensitivity sufferers have not been able to find any consistent pattern to these symptoms.

CGPD occurs most often in children of African descent before puberty though reports of this disease occurring in Asian and Caucasian children have also been described.

In examining the published studies on opioid-induced hyperalgesia (OIH), Reznikov "et al" criticize the methodologies employed on both humans and animals as being far-removed from the typical regimen and dosages of pain patients in the real world. They also note that some OIH studies were performed on drug addicts in methadone rehabilitation programs, and that such results are very difficult to generalize and apply to medical patients in chronic pain. In contrast, a study of 224 chronic pain patients receiving 'commonly-used' doses of oral opioids, in more typical clinical scenarios, found that the opioid-treated patients actually experienced no difference in pain sensitivity when compared to patients on non-opioid treatments. The authors conclude that opioid-induced hyperalgesia may not be an issue of any significance for normal, medically-treated chronic pain patients at all.

Opioid-induced hyperalgesia has also been criticized as overdiagnosed among chronic pain patients, due to poor differential practice in distinguishing it from the much more common phenomenon of opioid tolerance. The misdiagnosis of common opioid tolerance (OT) as opioid-induced hyperalgesia (OIH) can be problematic as the clinical actions suggested by each condition can be contrary to each other. Patients misdiagnosed with OIH may have their opioid dose mistakenly decreased (in the attempt to counter OIH) at times when it is actually appropriate for their dose to be increased or rotated (as a counter to opioid tolerance).

The suggestion that chronic pain patients who are diagnosed as experiencing opioid-induced hyperalgesia ought to be completely withdrawn from opioid therapy has also been met with criticism. This is not only because of the uncertainties surrounding the diagnosis of OIH in the first place, but because of the viability of rotating the patient between different opioid analgesics over time. Opioid rotation is considered a valid alternative to the reduction or cessation of opioid therapy, and multiple studies demonstrate the rotation of opioids to be a safe and effective protocol.

CGPD is known to be a temporary skin disease with a benign course. The skin papules typically resolve after a few months to a few years. After CGPD resolves, the skin may return to normal without scarring or may have small atrophic depressions with collagen loss, milia, or small pit-like scars.

Opioid-induced hyperalgesia or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia is a phenomenon associated with the long-term use of opioids such as morphine, hydrocodone, oxycodone, and methadone. Over time, individuals taking opioids can develop an increasing sensitivity to noxious stimuli, even evolving a painful response to previously non-noxious stimuli (allodynia). Some studies on animals have also demonstrated this effect occurring after only a single high dose of opioids.

Tolerance, another condition that can arise from prolonged exposure to opioids, can often be mistaken for opioid-induced hyperalgesia and vice-versa, as the clinical presentation can appear similar. Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation to receive the same level of effect to treat pain, they are nevertheless caused by two distinct mechanisms. The similar net effect makes the two phenomena difficult to distinguish in a clinical setting. Under chronic opioid treatment, a particular individual's requirement for dose escalation may be due to tolerance, opioid-induced hyperalgesia, or a combination of both. In tolerance, there is a lower sensitivity to opioids, which occurs via two major theories: decreased receptor activation (desensitization of antinociceptive mechanisms), and opioid receptor down-regulation (internalization of membrane receptors). In opioid-induced hyperalgesia, sensitization of pronociceptive mechanisms occurs, resulting in a decrease in the pain threshold, or allodyna. Identifying the development of hyperalgesia is of great clinical importance since patients receiving opioids to relieve pain may paradoxically experience more pain as a result of treatment. Whereas increasing the dose of opioid can be an effective way to overcome tolerance, doing so to compensate for opioid-induced hyperalgesia may worsen the patient's condition by increasing sensitivity to pain while escalating physical dependence.

The phenomenon is common among palliative care patients following a too rapid escalation of opioid dosage.

In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.