Local damage and inflammation that interferes with the taste buds or local nervous system such as that stemming from radiation therapy, glossitis, tobacco use, and denture use also cause ageusia. Other known causes include loss of taste sensitivity from aging (causing a difficulty detecting salty or bitter taste), anxiety disorder, cancer, renal failure and liver failure.

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.

Deficiency of vitamin B (niacin) and zinc can cause problems with the endocrine system, which may cause taste loss or alteration. Disorders of the endocrine system, such as Cushing's syndrome, hypothyroidism and diabetes mellitus, can cause similar problems. Ageusia can also be caused by medicinal side-effects from antirheumatic drugs such as penicillamine, antiproliferative drugs such as cisplatin, ACE inhibitors, and other drugs including azelastine, clarithromycin, terbinafine, and zopiclone.

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.

A longitudinal study on pregnant females found that 76% of pregnant females experienced significant changes in gustation and olfaction perception. This was found to be caused and linked to their pregnancy. The study concluded that 67% of the pregnant females had reported a higher level of sensitivity to smell, 17% suffered from an olfactory distortion and 14% suffered from phantosmia; these distortions were very minimal towards the last stages of pregnancy and in the majority were not present post partum. Furthermore, 26% of these participants also claimed that they also experienced an increased sensitivity to foods that were bitter and a decreased sensitivity to salt. These findings suggest that pregnant females experience distorted smell and taste perception during pregnancy. It has also been found that 75% of women alter their diets during pregnancy. Further research is being conducted to determine the mechanism behind food cravings during pregnancy.

The frequency of phantosmia is rare in comparison with the frequency of parosmia. Parosmia has been estimated to be in 10-60% of patients with olfactory dysfunction and from studies, it has been shown that it can last anywhere from 3 months to 22 years. Smell and taste problems result in over 200,000 visits to physicians annually in the US. Lately, it has been thought that phantosmia might co-occur with Parkinson's disease. However, its potential to be a premotor biomarker for Parkinson's is still up for debate as not all patients with Parkinson's disease have olfactory disorders

Phantosmia is most likely to occur in women between the ages of 15 and 30 years. The time of the first hallucination(s) lasts from anywhere from five to twenty minutes. It has also been found that the second hallucination will occur approximately a month later in the same manner as the first. Over time, the length of the hallucination will begin to increase.

Aside from physiologic causes of xerostomia, iatrogenic effects of medications are the most common cause. A medication which is known to cause xerostomia may be termed "xerogenic". Over 500 medications produce xerostomia as a side effect (see table). Sixty-three percent of the top 200 most commonly prescribed drugs in the United States are xerogenic. The likelihood of xerostomia increases in relation to the total number of medications taken, whether the individual medications are xerogenic or not. The sensation of dryness usually starts shortly after starting the offending medication or after increasing the dose. Anticholinergic, sympathomimetic, or diuretic drugs are usually responsible.

Xerostomia is a very common symptom. A conservative estimate of prevalence is about 20% in the general population, with increased prevalences in females (up to 30%) and the elderly (up to 50%).

Smell disorders can result in the inability to detect environmental dangers such as gas leaks, toxins, or smoke. In addition to safety, nutritional and eating habits can also be affected. There is a loss of appetite because of unpleasant flavor and fear of failing to recognize and consuming spoiled food. A decreased or distorted sense of smell therefore results in a decreased quality of life. Distortions are believed to have a greater negative impact on people than the complete loss of smell because they are constantly reminded of the disorder and the distortions have a greater effect on eating habits.

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

A temporary loss of smell can be caused by a blocked nose or infection. In contrast, a permanent loss of smell may be caused by death of olfactory receptor neurons in the nose or by brain injury in which there is damage to the olfactory nerve or damage to brain areas that process smell (see olfactory system). The lack of the sense of smell at birth, usually due to genetic factors, is referred to as "congenital anosmia." Family members of the patient suffering from congenital anosmia are often found with similar histories; this suggests that the anosmia may follow an autosomal dominant pattern. Anosmia may very occasionally be an early sign of a degenerative brain disease such as Parkinson's disease and Alzheimer's disease.

Another specific cause of permanent loss could be from damage to olfactory receptor neurons because of use of certain types of nasal spray; i.e., those that cause vasoconstriction of the nasal microcirculation. To avoid such damage and the subsequent risk of loss of smell, vasoconstricting nasal sprays should be used only when absolutely necessary and then for only a short amount of time. Non-vasoconstricting sprays, such as those used to treat allergy-related congestion, are safe to use for prescribed periods of time. Anosmia can also be caused by nasal polyps. These polyps are found in people with allergies, histories of sinusitis & family history. Individuals with cystic fibrosis often develop nasal polyps.

Amiodarone is a drug used in the treatment of arrhythmias of the heart. A clinical study performed demonstrated that the use of this drug induced anosmia in some patients. Although rare, there was a case in which a 66-year-old male was treated with Amiodarone for ventricular tachycardia. After the use of the drug he began experiencing olfactory disturbance, however after decreasing the dosage of Amiodarone, the severity of the anosmia decreased accordingly hence correlating the use of Amiodarone to the development of anosmia.

When untreated, the prognosis for ORS is generally poor. It is chronic, lasting many years or even decades with worsening of symptoms rather than spontaneous remission. Transformation to another psychiatric condition is unlikely, although very rarely what appears to be ORS may later manifest into schizophrenia, psychosis, mania, or major depressive disorder. The most significant risk is suicide.

When treated, the prognosis is better. In one review, the proportion of treated ORS cases which reported various outcomes were assessed. On average, the patients were followed for 21 months (range: 2 weeks to 10 years). With treatment, 30% recovered (i.e. no longer experienced ORS odor beliefs and thoughts of reference), 37% improved and in 33% there was a deterioration in the condition (including suicide) or no change from the pre-treatment status.

Cases have been reported from many different countries around the world. It is difficult to estimate the prevalence of ORS in the general population because data are limited and unreliable, and due to the delusional nature of the condition and the characteristic secrecy and shame.

For unknown reasons, males appear to be affected twice as commonly as females. High proportions of ORS patients are unemployed, single, and not socially active. The average age reported is around 20–21 years, with almost 60% of cases occurring in subjects under 20 in one report, although another review reported an older average age for both males (29) and females (40).

Anosmia can have a number of harmful effects. Patients with sudden onset anosmia may find food less appetizing, though congenital anosmics rarely complain about this, and none report a loss in weight. Loss of smell can also be dangerous because it hinders the detection of gas leaks, fire, and spoiled food. The common view of anosmia as trivial can make it more difficult for a patient to receive the same types of medical aid as someone who has lost other senses, such as hearing or sight.

Losing an established and sentimental smell memory (e.g. the smell of grass, of the grandparents' attic, of a particular book, of loved ones, or of oneself) has been known to cause feelings of depression.

Loss of olfaction may lead to the loss of libido, though this usually does not apply to congenital anosmics.

Often people who have congenital anosmia report that they pretended to be able to smell as children because they thought that smelling was something that older/mature people could do, or did not understand the concept of smelling but did not want to appear different from others. When children get older, they often realize and report to their parents that they do not actually possess a sense of smell, often to the surprise of their parents.

A study done on patients suffering from anosmia found that when testing both nostrils, there was no anosmia revealed; however, when testing each nostril individually, tests showed that the sense of smell was usually affected in only one of the nostrils as opposed to both. This demonstrated that unilateral anosmia is not uncommon in anosmia patients.

Hypogeusia is a reduced ability to taste things (to taste sweet, sour, bitter, or salty substances). The complete lack of taste is referred to as ageusia.

Causes of hypogeusia include the chemotherapy drug bleomycin, an antitumor antibiotic as well as zinc deficiency.

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

The pain of GN is sharp, shooting or burning and can last for hours. Painful attacks can be triggered by cold, noise, swallowing or touch, but triggers are usually unique to the sufferer. Other related symptoms that may be experienced include increased salivation, bitter taste, tinnitus and vertigo.

GN is rare, and only limited data is available regarding the incidence, prevalence, and risk factors associated with this condition. Middle-aged adults, however, seem to be predominantly affected, women more than men.

GN may be caused by compression of somatic sensory branch of cranial nerve VII which goes through the nervus intermedius. In sufferers of GN, signals sent along these nerves are altered and interpreted by the geniculate ganglion (a structure in the brain) as GN pain. GN may also develop following herpes zoster oticus (Ramsay Hunt syndrome), where cold sores occur on the ear drum or ear. This may also be associated with facial paresis (weakness), tinnitus, vertigo and deafness. Disorders of lacrimation, salivation and/or taste sometimes accompany the pain. There is a common association with herpes zoster.

Diagnostic criteria:

A. Pain paroxysms of intermittent occurrence, lasting for seconds or minutes, in the depth of the ear

B. Presence of a trigger area in the posterior wall of the auditory canal

C. Not attributed to another disorder

Causes can be remembered by mnemonic HERNIA:

- Hereditary factors: the disease runs in families

- Endocrine imbalance: the disease tends to start at puberty and mostly involves females

- Racial factors: whites are more susceptible than natives of equatorial Africa

- Nutritional deficiency: vitamins A or D, or iron

- Infection: "Klebsiella ozaenae", diphtheroids, "Proteus vulgaris", "E. coli", etc.

- Autoimmune factors: viral infection or some other unidentified insult may trigger antigenicity of the nasal mucosa.

Rumination disorder was initially documented

as affecting newborns,

infants, children

and individuals with mental and functional disabilities (the cognitively handicapped).

It has since been recognized to occur in both males and females of all ages and cognitive abilities.

Among the latter, it is described with almost equal prevalence among infants (6–10% of the population) and institutionalized adults (8–10%).

In infants, it typically occurs within the first 3–12 months of age.

The occurrence of rumination syndrome within the general population has not been defined. Rumination is sometimes described as rare, but has also been described as not rare, but rather rarely recognized.

The disorder has a female predominance. The typical age of adolescent onset is 12.9, give or take 0.4 years (±), with males affected sooner than females (11.0 ± 0.8 for males versus 13.8 ± 0.5 for females).

There is little evidence concerning the impact of hereditary influence in rumination syndrome. However, case reports involving entire families with rumination exist.

Specific infections, such as syphilis, lupus, leprosy and rhinoscleroma, may cause destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from long-standing purulent sinusitis or radiotherapy of the nose, or as a complication of surgery of the turbinates. The United Kingdom National Health Service has stated that "Most cases of atrophic rhinitis in the UK occur when the turbinates are damaged or removed during surgery". Some authors refer to as Atrophic rhinitis secondary to sinus surgery as the empty nose syndrome.

The cause of rumination syndrome is unknown. However, studies have drawn a correlation between hypothesized causes and the history of patients with the disorder. In infants and the cognitively impaired, the disease has normally been attributed to over-stimulation and under-stimulation from parents and caregivers, causing the individual to seek self-gratification and self-stimulus due to the lack or abundance of external stimuli. The disorder has also commonly been attributed to a bout of illness, a period of stress in the individual's recent past, and to changes in medication.

In adults and adolescents, hypothesized causes generally fall into one of either category: habit-induced, and trauma-induced. Habit-induced individuals generally have a history of bulimia nervosa or of intentional regurgitation (magicians and professional regurgitators, for example), which though initially self-induced, forms a subconscious habit that can continue to manifest itself outside the control of the affected individual. Trauma-induced individuals describe an emotional or physical injury (such as recent surgery, psychological distress, concussions, deaths in the family, etc.), which preceded the onset of rumination, often by several months.

Ramsay Hunt syndrome type 2 refers to shingles of the geniculate ganglion. After initial infection, varicella zoster virus lies dormant in nerve cells in the body, where it is kept in check by the immune system. Given the opportunity, for example during an illness that suppresses the immune system, the virus travels to the end of the nerve cell, where it causes the symptoms described above.

The affected ganglion is responsible for the movements of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth. The syndrome specifically refers to the combination of this entity with weakness of the muscles activated by the facial nerve. In isolation, the latter is called Bell's Palsy.

However, as with shingles, the lack of lesions does not definitely exclude the existence of a herpes infection. Even before the eruption of vesicles, varicella zoster virus can be detected from the skin of the ear.

Oral galvanism is a phenomenon that can occur when two or more dissimilar metals in dental restorations which are bathed in saliva, or a single metal in contact with two electrolytes such as saliva and pulp fluid tissue, produce an electric current. When associated with pain, the term galvanic pain has been used.

While there seems to be little dispute that the presence of dissimilar metals can cause an electric current and can, in some cases, cause a metallic taste in the mouth, some discomfort, and also possibly lead to premature corrosion of the metallic restorations, there is controversy over other claimed effects. Those other claimed effects include oral discomfort, skin irritation, and headaches . Many scientific studies dispute these claims.

This galvanism is said by some to be able to affect immune levels and the trigeminal nerve, causing a variety of other symptoms, such as insomnia, vertigo, and memory loss. The condition is claimed to be idiopathic, depending on the individual’s state of health, and to have varying effects on oral microbial communities. It was first proposed in 1878.

Oral galvanism is sometimes treated by replacing metallic amalgam restorations with ceramic or polymer restorations.