Some have suggested that surgery is not an appropriate for treatment for AFP, however the frequent failure medical treatment to relieve pain has occasionally lead surgeons to attempt surgical treatments. Surgery may give a temporary remission from pain, but rarely is there a long term cure achieved via these measures. Sometimes the pain may be increased or simply migrate to an adjacent area following a surgical procedure. Descriptions of procedures such as removal of a portion of the affected branch of the trigeminal nerve, or direct injections of a caustic substance (e.g. phenol, glycerol, alcohol) into the nerve have been reported. Proponents of the so-called "Neuralgia inducing cavitational necrosis" suggest surgical exploration of the bone marrow surrounding the intra-bony course of the affected nerve to discover diseased marrow.

Psychosocial interventions for AFP include cognitive behavioral therapy and biofeedback. A systematic review reported that there was weak evidence to support the use of these treatments to improve long-term outcomes in chronic orofacial pain, however these results were based primarily upon temporomandibular joint dysfunction and burning mouth syndrome rather than ATP and AO.

Psychosocial interventions assume 2 models of chronic facial pain, namely "inactivity" and "over activity". The former is where people with pain become conditioned to avoid physical activity as a result of exacerbating their pain. These negative thoughts and behaviors in fact prolong and intensify their symptoms. Some psychosocial interventions work on this fear-avoidance behaviour to improve functioning and thereby alleviate symptoms. The over activity model involves factors such as anxiety, depression or anger acting to increase pain by triggering autonomic, visceral and skeletal activity.

Treatment of people believed to have ATN or TN is usually begun with medication. The long-time first drug of choice for facial neuralgia has been carbamazepine, an anti-seizure agent. Due to the significant side-effects and hazards of this drug, others have recently come into common use as alternatives. These include oxcarbazepine, lamotrigine, and gabapentin. A positive patient response to one of these medications might be considered as supporting evidence for the diagnosis, which is otherwise made from medical history and pain presentation. There are no present medical tests to conclusively confirm TN or ATN.

If the anti-seizure drugs are found ineffective, one of the tricyclic antidepressant medications such as amitriptyline or nortriptyline, may be used. The tricyclic antidepressants are known to have dual action against both depression and neuropathic pain. Other drugs which may also be tried, either individually or in combination with an anti-seizure agent, include baclofen, pregabalin, anti-seizure drugs (to calm nerve endings), muscle relaxants, and opioid drugs such as oxycodone or an oxycodone/paracetamol combination.

For some people with ATN opioids may represent the only viable medical option which preserves quality of life and personal functioning. Although there is considerable controversy in public policy and practice in this branch of medicine, practice guidelines have long been available and published.

Medication is the main method of managing pain in TMD, mostly because there is little if any evidence of the effectiveness of surgical or dental interventions. Many drugs have been used to treat TMD pain, such as analgesics (pain killers), benzodiazepines (e.g. clonazepam, prazepam, diazepam), anticonvulsants (e.g. gabapentin), muscle relaxants (e.g. cyclobenzaprine), and others. Analgesics that have been studied in TMD include non-steroidal anti-inflammatory drugs (e.g. piroxicam, diclofenac, naproxen) and cyclo-oxygenase-2 inhibitors (e.g. celecoxib). Topical methyl salicylate and topical capsaicin have also been used. Other drugs that have been described for use in TMD include glucosamine hydrochloride/chondroitin sulphate and propranolol. Despite many randomized control trials being conducted on these commonly used medications for TMD a systematic review carried out in 2010 concluded that there was insufficient evidence to support or not to support the use of these drugs in TMD. Low-doses of anti-muscarinic tricyclic antidepressants such as amitriptyline, or nortriptyline have also been described. In a subset of people with TMD who are not helped by either noninvasive and invasive treatments, long term use of opiate analgesics has been suggested, although these drugs carry a risk of drug dependence and other side effects. Examples include morphine, fentanyl, oxycodone, tramadol, hydrocodone, and methadone.

Botulinum toxin solution ("Botox") is sometimes used to treat TMD. Injection of botox into the lateral pterygoid muscle has been investigated in multiple randomized control trials, and there is evidence that it is of benefit in TMD. It is theorized that spasm of lateral pterygoid causes anterior disc displacement. Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction. The effects usually last for a period of months before they wear off. Complications include the creation of a "fixed" expression due to diffusion of the solution and subsequent involvement of the muscles of facial expression, which lasts until the effects of the botox wear off. Injections of local anesthetic, sometimes combined with steroids, into the muscles (e.g. the temoralis muscle or its tendon) are also sometimes used. Local anesthetics may provide temporary pain relief, and steroids inhibit pro-inflammatory cytokines. Steroids and other medications are sometimes injected directly into the joint (See Intra-articular injections).

If drug treatment is found to be ineffective or causes disabling side effects, one of several neurosurgical procedures may be considered. The available procedures are believed to be less effective with type II (atypical) trigeminal neuralgia than with type I (typical or "classic") TN. Among present procedures, the most effective and long lasting has been found to be microvascular decompression (MVD), which seeks to relieve direct compression of the trigeminal nerve by separating and padding blood vessels in the vicinity of the emergence of this nerve from the brain stem, below the cranium.

Choice of a surgical procedure is made by the doctor and patient in consultation, based on the patient's pain presentation and health and the doctor's medical experience. Some neurosurgeons resist the application of MVD or other surgeries to atypical trigeminal neuralgia, in light of a widespread perception that ATN pain is less responsive to these procedures. However, recent papers suggest that in cases where pain initially presents as type I TN, surgery may be effective even after the pain has evolved into type II.

Acupuncture is sometimes used for TMD. There is limited evidence that acupuncture is an effective symptomatic treatment for TMD. A short term reduction in muscular pain of muscular origin can usually be observed after acupuncture in TMD, and this is more than is seen with placebo. There are no reported adverse events of acupuncture when used for TMD, and some suggest that acupuncture is best employed as an adjuvent to other treatments in TMD. However, some suggest that acupuncture may be no more effective than sham acupuncture, that many of the studies investigating acupuncture and TMD suffer from significant risk of bias, and that the long term efficacy of acupuncture for TMD is unknown.

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.

The evidence for surgical therapy is poor. Surgery is normally recommended only after medication has proved ineffective, or if side effects of medication are intolerable. While there may be pain relief after surgery, there is also a considerable risk of side effects, such as facial numbness after the procedure. Microvascular decompression appears to result in the longest pain relief. Percutaneous radiofrequency thermorhizotomy may also be effective as may stereotactic radiosurgery; however the effectiveness decreases with time.

Surgical procedures can be separated into non-destructive and destructive:

A trial of the anticonvulsant drug carbamazepine is common for patients diagnosed with GN. For patients who do not tolerate or respond to carbamazepine, alternative drugs include oxcarbazepine, gabapentin, phenytoin, lamotrigine, and baclofen. In addition, tricyclics (e.g., amitriptyline) and pregabalin are useful in other types of neuropathic pain.

All destructive procedures will cause facial numbness, post relief, as well as pain relief.

- Percutaneous techniques which all involve a needle or catheter entering the face up to the origin where the nerve splits into three divisions and then damaging this area, purposely, to produce numbness but also stop pain signals. These techniques are proven effective especially in those where other interventions have failed or in those who are medically unfit for surgery such as the elderly.

- Balloon compression - inflation of a balloon at this point causing damage and stopping pain signals.

- Glycerol injection- deposition of a corrosive liquid called glycerol at this point causes damage to the nerve to hinder pain signals.

- Radiofrequency thermocoagulation rhizotomy - application of a heated needle to damage the nerve at this point.

- Stereotactic radiosurgery is a form of radiation therapy that focuses high-power energy on a small area of the body

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.

There are many causes of toothache and its diagnosis is a specialist topic, meaning that attendance at a dentist is usually required. Since many cases of toothache are inflammatory in nature, over the counter non-steroidal anti-inflammatory drugs (NSAIDs) may help (unless contraindicated, such as with a peptic ulcer). Generally, NSAIDs are as effective as aspirin alone or in combination with codeine. However, simple analgesics may have little effect on some causes of toothache, and the severe pain can drive individuals to exceed the maximum dose. For example, when acetaminophen (paracetamol) is taken for toothache, an accidental overdose is more likely to occur when compared to people who are taking acetaminophen for other reasons. Another risk in persons with toothache is a painful chemical burn of the oral mucosa caused by holding a caustic substance such as aspirin tablets and toothache remedies containing eugenol (such as clove oil) against the gum. Although the logic of placing a tablet against the painful tooth is understandable, an aspirin tablet needs to be swallowed to have any pain-killing effect. Caustic toothache remedies require careful application to the tooth only, without coming into excessive contact with the soft tissues of the mouth.

For the dentist, the goal of treatment generally is to relieve the pain, and wherever possible to preserve or restore function. The treatment depends on the cause of the toothache, and frequently a clinical decision regarding the current state and long-term prognosis of the affected tooth, as well as the individual's wishes and ability to cope with dental treatment, will influence the treatment choice. Often, administration of an intra-oral local anesthetic such as lidocaine and epinephrine is indicated in order to carry out pain-free treatment. Treatment may range from simple advice, removal of dental decay with a dental drill and subsequent placement of a filling, to root canal treatment, tooth extraction, or debridement.

Hyperalgesia is similar to other sorts of pain associated with nerve irritation or damage such as allodynia and neuropathic pain, and consequently may respond to standard treatment for these conditions, using various drugs such as SSRI or tricyclic antidepressants, Nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, gabapentin or pregabalin, NMDA antagonists, or atypical opioids such as tramadol. Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management. However, as with other forms of nerve dysfunction associated pain, treatment of hyperalgesia can be clinically challenging, and finding a suitable drug or drug combination that is effective for a particular patient may require trial and error. The use of a transcutaneous electrical nerve stimulation device has been shown to alleviate hyperalgesia.

A physician may recommend engaging in sexual activity less strenuously. Case series have found indomethacin and beta blockers to be successful in treating these headaches. Propranolol, Bellergal, and triptans have also been used with success. Anecdotal and indirect evidence suggests a trial of magnesium supplementation may improve symptoms (in subjects with known or suspected low Mg levels).

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.

In pulpitis, an important distinction in regard to treatment is whether the inflammation is reversible or irreversible. Treatment of reversible pulpitis is by removing or correcting the causative factor. Usually, the decay is removed, and a sedative dressing is used to encourage the pulp to return to a state of health, either as a base underneath a permanent filling or as a temporary filling intended to last for a period while the tooth is observed to see if pulpitis resolves. Irreversible pulpitis and its sequalae pulp necrosis and apical periodontitis require treatment with root canal therapy or tooth extraction, as the pulp acts as a nidus of infection, which will lead to a chronic infection if not removed. Generally, there is no difference in outcomes between whether the root canal treatment is completed in one or multiple appointments. The field of regenerative endodontics is now developing ways to clean the pulp chamber and regenerate the soft and hard tissues to either regrow or simulate pulp structure. This has proved especially helpful in children where the tooth root has not yet finished developing and root canal treatments have lower success rates.

Reversible/irreversible pulpitis is a distinct concept from whether the tooth is restorable or unrestorable, e.g. a tooth may only have reversible pulpitis, but has been structurally weakened by decay or trauma to the point that it is impossible to restore the tooth in the long term.

Anti-tumour necrosis factor α antagonists (e.g. infliximab)

Dietary restriction of a particular suspected or proven antigen may be involved in the management of OFG, such as cinnamon or benzoate-free diets.

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

There is no universally accepted treatment strategy, but, generally, treatments aim to prevent movement of the segments of the involved tooth so they do not move or flex independently during biting and grinding and so the crack is not propagated.

- Stabilization (core buildup) (a composite bonded restoration placed in the tooth or a band is placed around the tooth to minimize flexing)

- Crown restoration (to do the same as above but more permanently and predictably)

- Root Canal therapy (if pain persists after above)

- Extraction

Treatment with the steroid "prednisone" and the antiviral drug "acyclovir 800mg 5 times a day" is controversial, with some studies showing to achieve complete recovery in patients if started within the first three days of facial paralysis, with chances of recovery decreasing as treatment was delayed. Delay of treatment may result in permanent facial nerve paralysis. However, some studies demonstrate that even when steroids are started promptly, only 22% of all patient achieve full recovery of facial paralysis.

Treatment apparently has no effect on the recovery of hearing loss. Diazepam is sometimes used to treat the vertigo.

Also called myofunctional therapy, the basic treatment aims of orofacial myofunctional therapist is to reeducate the movement of muscles, restore correct swallowing patterns, and establish adequate labial-lingual postures. An interdisciplinary nature of treatment is always desirable to reach functional goals in terms of swallowing, speech, and other esthetic factors. A team approach has been shown to be effective in correcting orofacial myofunctional disorders. The teams include an orthodontist, dental hygienist, certified orofacial myologist, general dentist, otorhinolaryngologist, and a speech-language pathologist.

This is the condition where the pulp is irreversibly damaged. The pulp can not recover from the insult and damage. For example, decay that has reached the pulp of the tooth introduces bacteria into the pulp. The pulp is still alive, but the introduction of bacteria into the pulp will not allow the pulp to heal and it will ultimately result in necrosis, or death, of the pulp tissue.

Symptoms associated with irreversible pulpitis may include dull aching, pain from hot or cold (though cold may actually provide relief) lingering pain after removal of a stimulus, spontaneous pain, or referred pain.

Clinical signs may include reduced response to electronic pulp testing and painful response to thermal stimuli. Today electronic pulp testers are rarely used for diagnosis of the reversibility of pulpitis due to their unreliable nature. Instead they should only be used to test the vitality of teeth.

The pulp of a tooth with irreversible pulpitis may not be left alone to heal. That is at least the general viewpoint of the dental profession, and not every dentist would agree that a dead tooth must be treated. No statistics are known but it is possible to have a trouble-free tooth after irreversible pulpitis, albeit a dead tooth. The tooth may be endodontically treated whereby the pulp is removed and replaced by gutta percha. An alternative is extraction of the tooth. This may be required if there is insufficient coronal tissue remaining for restoration once the root canal therapy has been completed.

Because Cherubism changes and improves over time the treatment should be individually determined. Generally moderate cases are watched until they subside or progress into the more severe range. Severe cases may require surgery to eliminate bulk cysts and fibrous growth of the maxilla and mandible. Surgical bone grafting of the cranial facial bones may be successful on some patients. Surgery is preferred for patients ages 5 to 15. Special consideration should be taken when operating on the face to avoid the marginal mandibular branch of the facial nerve as well as the zygomatic branch of the facial nerve. Unintentional damage to these nerves can decrease muscle strength in the face and mandible region. Orthodontic treatment is generally required to avoid permanent dental problems arising from malocclusive bite, misplaced, and unerupted permanent teeth. Orthodontic treatment may be used to erupt permanent teeth that have been unable to descend due to lesions and cysts being in their path of eruption. Patients with orbital issues of diplopia, eye proptosis, and visual loss will require ophthalmologic treatment.

Botulinum toxin is highly effective in the treatment of hemifacial spasm. It has a success rate equal to that of surgery, but repeated injections may be required every 3 to 6 months. The injections are administered as an outpatient or office procedure. Whilst side effects occur, these are never permanent. Repeated injections over the years remain highly effective. Whilst the toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery. Patients with HFS should be offered a number of treatment options. Very mild cases or those who are reluctant to have surgery or Botulinum toxin injections can be offered medical treatment, sometimes as a temporary measure. In young and fit patients microsurgical decompression and Botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, Botulinum toxin injection is the treatment of first choice. Imaging procedures should be done in all unusual cases of hemifacial spasm and when surgery is contemplated. Patients with hemifacial spasm were shown to have decreased sweating after botulinum toxin injections. This was first observed in 1993 by Khalaf Bushara and David Park. This was the first demonstration of nonmuscular use of BTX-A. Bushara further showed the efficacy of botulinum toxin in treating hyperhidrosis (excessive sweating). BTX-A was later approved for the treatment of excessive underarm sweating. This is technically known as severe primary axillary hyperhidrosis – excessive underarm sweating with an unknown cause which cannot be managed by topical agents (see focal hyperhidrosis).

Mild cases of hemifacial spasm may be managed with sedation or carbamazepine (an anticonvulsant drug). Microsurgical decompression and botulinum toxin injections are the current main treatments used for hemifacial spasm.