There is strong evidence to show that chronic orofacial pain (including AFP) is associated with psychological factors. Sometimes stressful life events appear to precede the onset of AFP, such as bereavement or illness in a family member. Hypochondriasis, especially cancerophobia, is also often cited as being involved. Most people with AFP are "normal" people who have been under extreme stress, however other persons with AFP have neuroses or personality disorders, and a small minority have psychoses. Some have been separated from their parents as children.

Depression, anxiety and altered behavior are strongly correlated with AFP. It is argued whether this is a sole or contributing cause of AFP, or the emotional consequences of suffering with chronic, unrelieved pain. It has been suggested that over 50% of people with AFP have concomitant depression or hypochondria. Furthermore, about 80% of persons with psychogenic facial pain report other chronic pain conditions such as listed in the table.

AFP is sometimes described as being fairly common, and one estimated prevalence is about 1–2% of the general population. However, the IASP described PIFP as being rare, less common than trigeminal neuralgia (which has a prevalence of about 0.01–0.3% in the general population), and possessing no available epidemiologic data for estimated prevelence in the general population. The predominant age group is 30–50, and females are more often affected than males, with most reports stating that about 80% of people with AFP are female.

Occlusal factors as an etiologic factor in TMD is a controversial topic. Abnormalities of occlusion (problems with the bite) are often blamed for TMD but there is no evidence that these factors are involved. Occlusal abnormalities are incredibly common, and most people with occlusal abnormalities do not have TMD. Although occlusal features may affect observed electrical activity in masticatory muscles, there are no statistically significant differences in the number of occlusal abnormalities in people with TMD and in people without TMD. There is also no evidence for a causal link between orthodontic treatment and TMD. The modern, mainstream view is that the vast majority of people with TMD, occlusal factors are not related. Theories of occlusal factors in TMD are largely of historical interest. A causal relationship between occlusal factors and TMD was championed by Ramfjord in the 1960s. A small minority of dentists continue to prescribe occlusal adjustments in the belief that this will prevent or treat TMD despite the existence of systematic reviews of the subject which state that there is no evidence for such practices, and the vast majority of opinion being that no irreversible treatment should be carried out in TMD (see Occlusal adjustment).

TMD does not obviously run in families like a genetic disease. It has been suggested that a genetic predisposition for developing TMD (and chronic pain syndromes generally) could exist. This has been postulated to be explained by variations of the gene which codes for the enzyme catechol-O-methyl transferase (COMT) which may produce 3 different phenotypes with regards pain sensitivity. COMT (together with monoamine oxidase) is involved in breaking down catecholamines (e.g. dopamine, epinephrine, and norepinephrine). The variation of the COMT gene which produces less of this enzyme is associated with a high sensitivity to pain. Females with this variation, are at 2–3 times greater risk of developing TMD than females without this variant. However this theory is controversial since there is conflicting evidence.

ATN is usually attributed to inflammation or demyelination, with increased sensitivity of the trigeminal nerve. These effects are believed to be caused by infection, demyelinating diseases, or compression of the trigeminal nerve (by an impinging vein or artery, a tumor, or arteriovenous malformation) and are often confused with dental problems. An interesting aspect is that this form affects both men and women equally and can occur at any age, unlike typical trigeminal neuralgia, which is seen most commonly in women. Though TN and ATN most often present in the fifth decade, cases have been documented as early as infancy.

Both forms of facial neuralgia are relatively rare, with an incidence recently estimated between 12 and 24 new cases per hundred thousand population per year.

ATN often goes undiagnosed or misdiagnosed for extended periods, leading to a great deal of unexplained pain and anxiety. A National Patient Survey conducted by the US Trigeminal Neuralgia Association in the late 1990s indicated that the average facial neuralgia patient may see six different physicians before receiving a first definitive diagnosis. The first practitioner to see facial neuralgia patients is often a dentist who may lack deep training in facial neurology. Thus ATN may be misdiagnosed as Tempormandibular Joint Disorder.

This disorder is regarded by many medical professionals to comprise the most severe form of chronic pain known in medical practice. In some patients, pain may be unresponsive even to opioid drugs at any dose level that leaves the patient conscious. The disorder has thus acquired the unfortunate and possibly inflammatory nickname, "the suicide disease".

Symptoms of ATN may overlap with a pain disorder occurring in teeth called atypical odontalgia (literal meaning "unusual tooth pain"), with aching, burning, or stabs of pain localized to one or more teeth and adjacent jaw. The pain may seem to shift from one tooth to the next, after root canals or extractions. In desperate efforts to alleviate pain, some patients undergo multiple (but unneeded) root canals or extractions, even in the absence of suggestive X-ray evidence of dental abscess.

ATN symptoms may also be similar to those of post-herpetic neuralgia, which causes nerve inflammation when the latent herpes zoster virus of a previous case of chicken pox re-emerges in shingles. Fortunately, post-herpetic neuralgia is generally treated with medications that are also the first medications tried for ATN, which reduces the negative impact of misdiagnosis.

The subject of atypical trigeminal neuralgia is considered problematic even among experts. The term atypical TN is broad and due to the complexity of the condition, there are considerable issues with defining the condition further. Some medical practitioners no longer make a distinction between facial neuralgia (a nominal condition of inflammation) versus facial neuropathy (direct physical damage to a nerve).

Due to the variability and imprecision of their pain symptoms, ATN or atypical odontalgia patients may be misdiagnosed with atypical facial pain (AFP) or "hypochondriasis", both of which are considered problematic by many practitioners. The term "atypical facial pain" is sometimes assigned to pain which crosses the mid-line of the face or otherwise does not conform to expected boundaries of nerve distributions or characteristics of validated medical entities. As such, AFP is seen to comprise a diagnosis by reduction.

As noted in material published by the [US] National Pain Foundation: "atypical facial pain is a confusing term and should never be used to describe patients with trigeminal neuralgia or trigeminal neuropathic pain. Strictly speaking, AFP is classified as a "somatiform pain disorder"; this is a psychological diagnosis that should be confirmed by a skilled pain psychologist. Patients with the diagnosis of AFP have no identifiable underlying physical cause for the pain. The pain is usually constant, described as aching or burning, and often affects both sides of the face (this is almost never the case in patients with trigeminal neuralgia). The pain frequently involves areas of the head, face, and neck that are outside the sensory territories that are supplied by the trigeminal nerve. It is important to correctly identify patients with AFP since the treatment for this is strictly medical. Surgical procedures are not indicated for atypical facial pain."

The term "hypochondriasis" is closely related to "somatoform pain disorder" and "conversion disorder" in the Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric Association. As of July 2011, this axis of the DSM-IV is undergoing major revision for the DSM-V, with introduction of a new designation "Complex Somatic Symptom Disorder". However, it remains to be demonstrated that any of these "disorders" can reliably be diagnosed as a medical entity with a discrete and reliable course of therapy.

It is possible that there are triggers or aggravating factors that patients need to learn to recognize to help manage their health. Bright lights, sounds, stress, and poor diet are examples of additional stimuli that can contribute to the condition. The pain can cause nausea, so beyond the obvious need to treat the pain, it is important to be sure to try to get adequate rest and nutrition.

Depression is frequently co-morbid with neuralgia and neuropathic pain of all sorts, as a result of the negative effects that pain has on one's life. Depression and chronic pain may interact, with chronic pain often predisposing patients to depression, and depression operating to sap energy, disrupt sleep and heighten sensitivity and the sense of suffering. Dealing with depression should thus be considered equally important as finding direct relief from the pain.

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

These headaches are estimated to appear in roughly 1% of the population. They can occur with sexual activity at any age. It is more common in men than women, with studies putting the gender ratio between 1.2:1 and 3:1.

A variety of surgeries have been performed including microvascular decompression (MVD) of the fifth, ninth, and tenth nerves; as well as partial cutting of the nervus intermedius, geniculate ganglion, chorda tympani and/or the ninth and tenth cranial nerves.

Psychological and social support has found to play a key role in the management of chronic illnesses and chronic pain conditions, such as trigeminal neuralgia. Chronic pain can cause constant frustration to an individual as well as to those around them. As a result, there are many advocacy groups.

Aetiology of CTS is multifactorial, the causative factors include:

- previous restorative procedures.

- occlusal factors

- developmental conditions/anatomical considerations.

- trauma

- others, e.g, aging dentition or presence of lingual tongue studs.

Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure.

The trigeminal nerve is a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression.

Several theories exist to explain the possible causes of this pain syndrome. It was once believed that the nerve was compressed in the opening from the inside to the outside of the skull; but leading research indicates that it is an enlarged or lengthened blood vessel – most commonly the superior cerebellar artery – compressing or throbbing against the microvasculature of the trigeminal nerve near its connection with the pons. Such a compression can injure the nerve's protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve's ability to shut off the pain signals after the stimulation ends. This type of injury may rarely be caused by an aneurysm (an outpouching of a blood vessel); by an AVM (arteriovenous malformation); by a tumor; such as an arachnoid cyst or meningioma in the cerebellopontine angle; or by a traumatic event such as a car accident.

Short-term peripheral compression is often painless. Persistent compression results in local demyelination with no loss of axon potential continuity. Chronic nerve entrapment results in demyelination primarily, with progressive axonal degeneration subsequently. It is, "therefore widely accepted that trigeminal neuralgia is associated with demyelination of axons in the Gasserian ganglion, the dorsal root, or both." It has been suggested that this compression may be related to an aberrant branch of the superior cerebellar artery that lies on the trigeminal nerve. Further causes, besides an aneurysm, multiple sclerosis or cerebellopontine angle tumor, include: a posterior fossa tumor, any other expanding lesion or even brainstem diseases from strokes.

Trigeminal neuralgia is found in 3–4% of people with multiple sclerosis, according to data from seven studies. It has been theorized that this is due to damage to the spinal trigeminal complex. Trigeminal pain has a similar presentation in patients with and without MS.

Postherpetic neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is damaged.

When there is no [apparent] structural cause, the syndrome is called idiopathic.

Cracked tooth syndrome (abbreviated to CTS, and also termed cracked cusp syndrome, split tooth syndrome, or incomplete fracture of posterior teeth), is where a tooth has incompletely cracked but no part of the tooth has yet broken off. Sometimes it is described as a greenstick fracture. The symptoms are very variable, making it a notoriously difficult condition to diagnose.

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.

To relieve pain, some doctors suggest pressing the tongue against the roof of the mouth to warm the area, tilting the head back for 20 seconds, or drinking something warmer than whatever caused the headache. Some people report relief from breathing in through the mouth and out through the nose, thus passing warm air through the nasal passages.

Functional somatic syndromes may occur in 6 to 36% of the population.

For some patients, the headaches may be related to general exertion. About 40% of patients with sexual headaches in one study also experienced headaches from non-sexual exertion. A pressor response to exercise has been suggested as a mechanism. For other patients, the pain appears to be specifically activated by sexual excitement and contraction of facial and neck muscles.

Sporadic case studies have linked sexual headaches to the use of certain drugs, including amiodarone, pseudoephedrine, birth control pills, and cannabis. It may be secondary to another condition, such as reversible cerebral vasoconstriction syndrome. It is associated with migraines.

In general, chronic periodontal conditions do not cause any pain. Rather, it is acute inflammation which is responsible for the pain.

Toothache, also known as dental pain, is pain in the teeth and/or their supporting structures, caused by dental diseases or pain referred to the teeth by non-dental diseases.

Common causes include inflammation of the pulp, usually in response to tooth decay, dental trauma, or other factors, dentin hypersensitivity (short, sharp pain, usually associated with exposed root surfaces), apical periodontitis (inflammation of the periodontal ligament and alveolar bone around the root apex), dental abscesses (localized collections of pus, such as apical abscess, pericoronal abscess, and periodontal abscess), alveolar osteitis ("dry socket", a possible complication of tooth extraction, with loss of the blood clot and exposure of bone), acute necrotizing ulcerative gingivitis (a gum infection, also called "trenchmouth"), temporomandibular disorder and others.

Pulpitis is classified as reversible when the pain is mild to moderate and lasts for a short time after a stimulus (for instance, cold or sweet); or irreversible when the pain is severe, spontaneous, and lasts a long time after a stimulus. Left untreated, pulpitis may become irreversible, then progress to pulp necrosis (death of the pulp) and apical periodontitis. Abscesses usually cause throbbing pain. The apical abscess usually occurs after pulp necrosis, the pericoronal abscess is usually associated with acute pericoronitis of a lower wisdom tooth, and periodontal abscesses usually represent a complication of chronic periodontitis (gum disease). Much less commonly, non-dental conditions can cause toothache, such as maxillary sinusitis, which can cause pain in the upper back teeth, or angina pectoris, which can cause pain in the lower teeth.

Toothache is the most common type of orofacial pain and, when severe, it is considered a dental emergency, since there may be a significant impact on sleep, eating, and other daily activities. It is one of the most common reasons for emergency dental appointments. Correct diagnosis can sometimes be challenging. The treatment of a toothache depends upon the exact cause, and may involve a filling, root canal treatment, extraction, drainage of pus, or other remedial action. The relief of toothache is considered one of the main responsibilities of dentists. In 2013, 223 million cases of tooth pain occurred as a result of dental caries in permanent teeth and 53 million cases occurred in baby teeth. Historically, the demand for treatment of toothache is thought to have led to the emergence of dental surgery as the first specialty of medicine.

OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

Neuralgia-inducing cavitational osteonecrosis (NICO) is a controversial diagnosis whereby a putative jawbone cavitation causes chronic facial neuralgia; this is different from osteonecrosis of the jaw.. In NICO the pain is said to result from the degenerating nerve ("neuralagia"). The condition is probably rare, if it does exist.

Also called Ratner's bone cavity, a neuralgia-inducing cavitational osteonecrosis was first described in dental literature by G V Black in 1920. Several decades later, oral pathologist Jerry E Bouquot took especial interest in NICO.

The diagnostic criteria for NICO are imprecise, and the research offered to support it is flawed. The diagnosis is popular among holistic dentists who attempt to treat NICO by surgically removing the dead bone they say is causing the pain.

It has been rejected as quackery by some dentists and maxillofacial surgeons. In its position statement, dated 1996, the American Association of Endodontists asserted that although NICO occur and are treatable in toothless areas, NICO occurrence and treatment at endodontically treated teeth is generally implausible, that the diagnosis ought to be a last resort, and that routine extraction of endodontically treated teeth is misguided.

Another theory into the cause of cold-stimulus headaches is explained by increased blood flow to the brain through the anterior cerebral artery, which supplies oxygenated blood to most medial portions of the frontal lobes and superior medial parietal lobes. This increase in blood volume and resulting increase in size in this artery is thought to bring on the pain associated with a cold-stimulus headache.

When the anterior cerebral artery constricts, reining in the response to this increased blood volume, the pain disappears. The dilation, then quick constriction, of this blood vessel may be a type of self-defense for the brain.

This inflow of blood cannot be cleared as quickly as it is coming in during the cold-stimulus headache, so the blood flow could raise the pressure inside the skull and induce pain that way. As the intracranial pressure and temperature in the brain rise the blood vessel contracts, and the pressure in the brain is reduced before reaching dangerous levels.

Treatment may involve investigation, reassurance and explanation, and possibly specialist treatment such as antidepressants or cognitive behavioral therapy.

Hyperalgesia ( or ; 'hyper' from Greek ὑπέρ (huper, “over”), '-algesia' from Greek algos, ἄλγος (pain)) is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Prostaglandins E and F are largely responsible for sensitizing the nociceptors. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.