Approximately one half of drug-related taste distortions are caused by a zinc deficiency. Many medications are known to chelate, or bind, zinc, preventing the element from functioning properly. Due to the causal relationship of insufficient zinc levels to taste disorders, research has been conducted to test the efficacy of zinc supplementation as a possible treatment for dysgeusia. In a randomized clinical trial, fifty patients suffering from idiopathic dysgeusia were given either zinc or a lactose placebo. The patients prescribed the zinc reported experiencing improved taste function and less severe symptoms compared to the control group, suggesting that zinc may be a beneficial treatment. The efficacy of zinc, however, has been ambiguous in the past. In a second study, 94% of patients who were provided with zinc supplementation did not experience any improvement in their condition. This ambiguity is most likely due to small sample sizes and the wide range of causes of dysgeusia. A recommended daily oral dose of 25–100 mg appears to be an effective treatment for taste dysfunction provided that there are low levels of zinc in the blood serum. There is not a sufficient amount of evidence to determine whether or not zinc supplementation is able to treat dysgeusia when low zinc concentrations are not detected in the blood.

It has been reported that approximately 68% of cancer patients undergoing chemotherapy experience disturbances in sensory perception such as dysgeusia. In a pilot study involving twelve lung cancer patients, chemotherapy drugs were infused with zinc in order to test its potential as a treatment. The results indicated that, after two weeks, no taste disturbances were reported by the patients who received the zinc-supplemented treatment while most of the patients in the control group who did not receive the zinc reported taste alterations. A multi-institutional study involving a larger sample size of 169 patients, however, indicated that zinc-infused chemotherapy did not have an effect on the development of taste disorders in cancer patients. An excess amount of zinc in the body can have negative effects on the immune system, and physicians must use caution when administering zinc to immunocompromised cancer patients. Because taste disorders can have detrimental effects on a patient's quality of life, more research needs to be conducted concerning possible treatments such as zinc supplementation.

If a cause can be identified for a burning sensation in the mouth, then treatment of this underlying factor is recommended. If symptom persist despite treatment a diagnosis of BMS is confirmed. BMS has been traditionally treated by reassurance and with antidepressants, anxiolytics or anticonvulsants. A 2016 Cochrane review of treatment for burning mouth syndrome concluded that strong evidence of an effective treatment was not available. Other treatments which have been used include atypical antipsychotics, histamine receptor antagonists, and dopamine agonists.

BMS is benign (importantly, it is not a symptom of oral cancer), but as a cause of chronic pain which is poorly controlled, it can detriment quality of life, and may become a fixation which cannot be ignored, thus interfering with work and other daily activities. Two thirds of people with BMS have a spontaneous partial recovery six to seven years after the initial onset, but in others the condition is permanent. Recovery is often preceded by a change in the character of the symptom from constant to intermittent. No clinical factors predicting recovery have been noted.

If there is an identifiable cause for the burning sensation (i.e. primary BMS), then psychologic dysfunctions such as anxiety and depression often disappear if the symptom is successfully treated.

At-home treatments include desensitizing toothpastes or dentifrices, potassium salts, mouthwashes and chewing gums.

A variety of toothpastes are marketed for dentin hypersensitivity, including compounds such as strontium chloride, strontium acetate, arginine, calcium carbonate, hydroxyapatite and calcium sodium phosphosilicate. Desensitizing chewing gums and mouthwashes are also marketed.

Potassium-containing toothpastes are common; however, the mechanism by which they may reduce hypersensitivity is unclear. Animal research has demonstrated that potassium ions placed in deep dentin cavities cause nerve depolarization and prevent re-polarization. It is not known if this effect would occur with the twice-daily, transient and small increase in potassium ions in saliva that brushing with potassium-containing toothpaste creates. In individuals with dentin hypersensitivity associated with exposed root surfaces, brushing twice daily with toothpaste containing 5% potassium nitrate for six to eight weeks reduces reported sensitivity to tactile, thermal and air blast stimuli. However, meta analysis reported that these individuals' subjective report of sensitivity did not significantly change after six to eight weeks of using the potassium nitrate toothpaste.

Desensitizing toothpastes containing potassium nitrate have been used since the 1980s while toothpastes with potassium chloride or potassium citrate have been available since at least 2000. It is believed that potassium ions diffuse along the dentinal tubules to inactivate intradental nerves. However, , this has not been confirmed in intact human teeth and the desensitizing mechanism of potassium-containing toothpastes remains uncertain. Since 2000, several trials have shown that potassium-containing toothpastes can be effective in reducing dentin hypersensitivity, although rinsing the mouth after brushing may reduce their efficacy.

Studies have found that mouthwashes containing potassium salts and fluorides can reduce dentine hypersensitivity, although rarely to any significant degree. , no controlled study of the effects of chewing gum containing potassium chloride has been made, although it has been reported as significantly reducing dentine hypersensitivity.

Nano-hydroxyapatite (nano-HAp) is considered one of the most biocompatible and bioactive materials, and has gained wide acceptance in dentistry in recent years. An increasing number of reports have shown that nano-hydroxyapatite shares characteristics with the natural building blocks of enamel having the potential, due to its particle size, to occlude exposed dentinal tubules helping to reduce hypersensitivity and enhancing teeth remineralization.

For this reason, the number of toothpastes and mouthwashes that already incorporate nano-hydroxyapatite as a desensitizing agent is increasing.

In-office treatments may be much more complex and they may include the application of dental sealants, having fillings put over the exposed root that is causing the sensitivity, or a recommendation to wear a specially made night guard or retainer if the problems are a result of teeth grinding.

Other possible treatments include fluorides are also used because they decrease permeability of dentin "in vitro". Also, potassium nitrate can be applied topically in an aqueous solution or an adhesive gel. Oxalate products are also used because they reduce dentin permeability and occlude tubules more consistently. However, while some studies have showed that oxalates reduced sensitivity, others reported that their effects did not differ significantly from those of a placebo. Nowadays, dentin hypersensitivity treatments use adhesives, which include varnishes, bonding agents and restorative materials because these materials offer improved desensitization.

Low-output lasers are also suggested for dentin hypersensitivity, including GaAlAs lasers and . They are thought to act by producing a transient reduction in action potential in C-fibers in the pulp, but Aδ-fibers are not affected.

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.

Treatment requires treating the underlying condition with dental treatments, physical therapy, and passive range of motion devices. Additionally, control of symptoms with pain medications (NSAIDs), muscle relaxants, and warm compresses may be used.

Splints have been used.

In order for successful treatment of abrasion to occur, the aetiology first needs to be identified. The most accurate way of doing so is completing a thorough medical, dental, social and diet history. All aspects needs to be investigated as in many cases the cause of abrasion can be multi-factorial. Once a definitive diagnosis is completed the appropriate treatment can commence.

Treatment for abrasion can present in varying difficulties depending on the current degree or progress caused by the abrasion. Abrasion often presents in conjunction with other dental conditions such as attrition, decay and erosion however the below treatment is for abrasion alone. Successful treatment focuses on the prevention and progression on the condition and modifies the current habit/s instigating the condition.

The current selection of dentifrice should also be critically analysed and changed to include a less abrasive and gentler paste such as sensitive toothpaste. A toothpaste containing increased fluoride will also help combat the increased sensitivity and risk to dental decay

Treatment in the dental chair may include a fluoride application or the placement of a restoration in more severe cases. If the lesion is small and confined to enamel or cementum, a restoration is not warranted, instead the eradication of rough edges should occur to reduce plaque retentive properties. However, in the case of dental decay, aesthetic concerns or defects close to the pulp a restoration may be completed. Further restorative work may be required when the lesion compromises the overall strength of the tooth or when the defect contributes to a periodontal problem the lesion may be restored.

Once abrasions has been diagnosed and treated it should be closely monitored to identify further progression or potential relief of symptoms.

A 2006 systematic review and a 2005 review by the UK Health Protection Agency each evaluated the evidence for various medical, psychological, behavioral, and alternative treatments for EHS and each found that the evidence-base was limited and not generalizable. The conclusion of the 2006 review stated: "The evidence base concerning treatment options for electromagnetic hypersensitivity is limited and more research is needed before any definitive clinical recommendations can be made. However, the best evidence currently available suggests that cognitive behavioural therapy is effective for patients who report being hypersensitive to weak electromagnetic fields."

As of 2005, WHO recommended that people presenting with claims of EHS be evaluated to determine if they have a medical condition that may be causing the symptoms the person is attributing to EHS, that they have a psychological evaluation, and that the person's environment be evaluated for issues like air or noise pollution that may be causing problems.

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.

Angular cheilitis (angular stomatitis) is inflammation of one or both of the corners (angles) of the mouth. It is a fairly common condition, and often affects elderly people.

There are many possible causes, including nutritional deficiencies (iron, B vitamins, folate), contact allergy, infection ("Candida albicans", "Staphylococcus aureus" or β-hemolytic streptococci) and edentulism (often with overclosure of the mouth and concomitant denture-related stomatitis), and others.

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.

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.

There is currently no specified treatment for individuals suffering from otodental syndrome. Considering that there are many possible genetic and phenotypic associations with the condition, treatment is provided based on each individual circumstance. It is recommended that those affected seek ear, nose & throat specialists, dental health specialists, and facial oral health specialists immediately; in order to determine potential treatment options.

Common treatment methods given are:

- Dental treatment/management – which can be complex, interdisciplinary and requires a regular follow up. Tooth extraction(s)and if needed, medications may be administered for pain, anxiety, and anti-inflammation. The affected individual is usually placed on a strict and preventative dental regiment in order to maintain appropriate oral hygiene and health.

- Endodontic treatment – individuals consult with an endodontist to analyze the individuals dental pulp. Typically endodontic treatment proves to be difficult due to duplicated pulp canals within the affected teeth. There may be a need for multiple extractions as well. Dental prosthesis and/or dental implants may be necessary for individuals that lack proper oral function, appearance, and comfort.

- Orthodontic treatment – given the predicament of the size and location of the affected oral area, molars and canines, orthodontic treatment is generally required in order treat any problems associated with the individuals bite pattern and tooth appearance.

- Hearing aids – in some cases affected individuals will suffer from hearing imparities and it may be necessary for hearing aid use.

The functional prognosis is mostly good with those that suffer from otodental syndrome. Appropriate dental treatment, hearing aids, and visitation to necessary specialists are recommended. Quality of life may be affected by psychological and functional aspects. It is also recommended that genetic counseling be given to families that have or may have this condition.

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.

Treatment of opioid tolerance and Opioid-Induced Hyperalgesia (OIH) differs but it may be difficult to differentiate these two conditions in a clinical setting where most pain assessments are done through simple scale scores. The treatment for OIH may be challenging because an inadequate number of quality studies exists possibly due to the complexity in diagnosis of OIH and challenges in working with patients on chronic opioids. Currently there is no single best treatment method for OIH and clinicians are advised to choose an appropriate therapy based on the unique clinical scenario and history of each patient.

One general treatment option is to reduce or discontinue the dose of opioid to see if OIH is improved. Opioid sparing or opioid switching, which is replacing the current opioid with another pharmacological agent such as morphine or methadone, has been reported to be effective in some studies but this may also increase the sensitivity to pain according to some case reports. Ketamine, a NMDA antagonist, has been shown to prevent the extended use of opioid in post-operative hyperalgesia when it is infused in a small amount perioperatively along with the opioid but there are also studies that show ketamine being ineffective in modulating hyperalgesia. Addition of the NSAID, especially some COX-2 inhibitors, or acetaminophen is also suggested as a possible treatment option.

Two small randomized controlled trials (RCTs) and one larger RCT (86 subjects) tested glutamine in the prevention of platinum treatment-induced neuropathy and showed promise. As of September 2013 a larger, placebo-controlled trial is running.

A 2013 systematic review of the use of acetyl-L-carnitine, glutamine, vitamin E, glutathione, vitamin B6, omega-3 fatty acids, magnesium, calcium, alpha lipoic acid and n-acetyl cysteine as anti-CIPN adjuvants concluded that "currently no agent has shown solid beneficial evidence to be recommended for the treatment or prophylaxis of CIPN."

Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. However, their use is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children. The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies have found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others found incomplete resolution or prolonged symptoms. Topical azelaic acid has also been used successfully to treat CGPD.

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.

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.

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

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.

In a study of patients receiving oxaliplatin treatment, only 4 percent of those also receiving intravenous calcium and magnesium (ca/mg) before and after each oxaliplatin dose had to discontinue treatment due to neurotoxicity, compared to 33 percent who were receiving intravenous placebo; onset of neuropathy was also significantly delayed in the ca/mg patients, and only 22 percent of the ca/mg patients had long-term CIPN of grade 2 or worse compared with 41 percent of those on placebo. Overall, trials of ca/mg infusion suggest there are no serious harmful side effects and it may be an effective preventative therapy — the number of patients so far studied is small, however, and confident conclusions cannot be drawn.