Orofacial

Background and Setting: Oral health influences general health that in turn improves the quality of life. It is a said to be a state where a person is free from oral infection and sores, tooth decay, oral and facial pain, oral and throat cancer, tooth loss, periodontal disease, and other disorders and diseases that restrict an individual from speaking, smiling, etc. and even affecting his psychological state.

Orofacial pain in its comprehensive cataloguing can affect up to 7% of the people.
The responsibility of early diagnosis and managing it lies on the doctors, dentists and those who belong to the minor care segment, like the oral physicians, pain physicians, and headache neurologists. Facial pain is usually chronic and similar to the other chronic pain and is commonly associated with a large number of co-morbidities and treating it would involve the treatment of associated conditions such as the anxiety, depression, and the presence of other chronic pain; which must be attended to; as a part of management. Though the majority of chronic pains are continuous, there are some that are intermittent. Most of the pain is intraoral, and among them; odontalgia and burning mouth syndrome are common; whereas many of the pain could manifest both intra and extra orally. Among the extra oral pain, the most common are the musculoskeletal pain, in relation to the muscles of mastication, which may be associated with disc problems.
Neuralgias include the trigeminal neuralgia, and the less common glossopharyngeal neuralgia, having welldefined care pathways. Trigeminal neuropathic pain may also be caused by trauma; and may be secondary to such conditions as infection, malignancies and auto-immune diseases. The condition is normally managed along the lines of other neuropathic pain; by using the commonly used drugs besides the psychological support. If the type of pain cannot be categorised as occurring due to any specific cause, then a diagnosis of insistent or chronic idiopathic facial pain is made and the treatment given, may include a combination of cognitive behavioural therapy and antidepressants. A multidisciplinary team should be the one normally managing the facial pain. In order to establish an accurate diagnosis a thorough knowledge of a wide spectrum of diagnostic characteristics of orofacial pain which includes the source and type of pain (psychogenic, somatic and neurogenic); period (acute or chronic); and how the pain originated (nociceptive, psychosomatic and neuropathic); and their differentiation. This article stresses on the most common painful conditions of oral mucosa, their clinical manifestations and treatment.
Pain is ‚An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage‛. [1] Pain of the oral mucosa is co-associated with multiple lesions of the oral mucosa, caused by local and systemic diseases. It is usually associated with a known cause of tissue damage, e.g. an erosion or mucosal ulcer, off which some may be caused by physicians, e.g., Medications, trauma following surgery, or after radiotherapy to the head and neck; and responds mostly to treatment; which disappears after healing. Chronic pain lasts much longer and continues for months or years after the causative factor has healed, and attempts to eliminate this pain is challenging. Patients with intermittent or persistent, painful sensations in the oral mucosa often represent a substantial clinical challenge with regard to diagnosis and management. [2] The oral cavity is thickly innervated as compared to the other parts of the body and has an elaborate sensorimotor presence in the central nervous system (CNS). This rich somatosensory supply controls the eating, swallowing, drinking, and speaking, and also a large number of oral sensations, including, pain. [3]

Physiology of Pain
Noxious stimuli in the orofacial region depolarize the high threshold free nerve endings: Aδ (thinly myelinated) and C-fibers (unmyelinated); that may further be sensitised and excited by a large number of chemicals such as prostaglandins, histamine, bradykinin, substance P, etc. The fibers transmit the nociceptive stimuli along the trigeminal pathway to primarily synapse with the second-order neurons (nociceptive specific and/or wide dynamic) located in the caudalis nucleus of the trigeminal spinal tract within the brain stem. These signals are subjected to modulation here. It undergoes further modulation when the second-order fibers cross the midline, and climb the synapse in the thalamus, and plays a role in the perception of pain. Finally, the noxious impulse is directed to the somatic sensory areas of the cerebral cortex, where determination and discrimination of the nociceptive stimulus are intensified. This stimulus under the influence of cognitive behavioural and affective motivational factors: past experiences etc., is interpreted; hence, pain is understood as a complex mixture of sensory, cognitive and affective process, making it "personal experience" for each. [2] Oral mucosal pain may also manifest in the absence of any visible pathology or reason as in the case of a previous trauma and is termed idiopathic pain.
Pain is a multidimensional subjective experience, and more than just tissue damage, it contributes to the patient's expression and rating of pain response. Patients state that their oral pain is unbearable, yet may present with only very mild or clinically, barely evident mucosal changes. On the other hand patients with severe, extensive mucosal lesions report minimal oral pain and can function normally. The reaction of different people exposed to the same stimuli to pain is different, and it has been seen that some people are less sensitive to pain than others, which can further be elaborated by a recent scientific discovery.
Nature Medicine has cited a major new discovery into the molecular mechanisms of pain. A "pain gene" that explains why certain individuals are less sensitive to acute pain and less likely to develop chronic pain has been unearthed. The relevant gene that is affected is called GCH1, which encodes for GTP cyclohydrolase an enzyme. This enzyme initiates the production of a chemical called tetrahydrobiopterin or BH4. They found that a pathway that produces BH4 was significantly activated during painstates. When the researchers' inhibited BH4 production in experimental models the pain was relieved; whereas the administration of BH4 produced pain. The authors also identified a connection between people carrying a mutation in the human gene responsible for BH4 production and reduced pain sensitivity. Twenty to twenty-five percent of the population have at least one copy of this pain protective form of the gene where as 3% of those who carry 2 copies of the gene undergo a significantly less pain after for, e.g., A disc surgery; than those having a single copy. Administering inhibitors of GTP cyclohydrolase (the critical enzyme in BH4 production) to reduce the elevated BH4 levels in pain conditions, could mimic the effects of the pain protective function of the gene and lead to a disease;-modifying the pain therapy. Therefore this data also suggests that individuals who say they feel less pain are not just stoics but genuinely have inherited molecular machinery that reduces their perception of pain. This difference results, not from personality or culture, but real differences in the biology of the sensory nervous system. [5]  reported chronic widespread pain, 8% chronic fatigue and 9% had the irritable bowel syndrome. Of these, 9% reported more than one of these pains. A German population study and another one from Netherlands using strictly defined criteria by headache neurologists found that the trigeminal neuralgia is commoner than persistent idiopathic facial pain, but both were rare with a lifetime prevalence (0.3%) of trigeminal neuralgia versus 0.03% for persistent idiopathic facial pain. Koopman et al. found an incidence rate of 38.7 per 100,000 people. The diagnosis was validated by pain experts as they found up to 48% had been misdiagnosed by the primary care physicians. Trigeminal neuralgia and cluster headaches were the most common types and the temperomandibular pain and muscle disorder-type pain (TMD) were also found to be common; population-based studies among adults reported that approximately 10-15% have these disorders. When making a diagnosis, it is useful to make the distinction if the diagnosis is definite, possible or even probable; as this allows for a change in diagnosis, once number of facts comes to light. Type and causes of non-dental chronic orofacial pain Benoliel et al. showed in their clinic population of 328 patients, that, chronic orofacial pain could be defined in the same way as a chronic daily headache but stresses that chronic oro-facial pain includes a very heterogeneous group of symptoms. Conditions that can result in neuropathy include autoimmune disorders, for e.g. Systemic sclerosis, trauma, Sjogren's syndrome, multiple sclerosis, sarcoidosis, rare vascular malformations, Lyme disease, neoplasia anywhere along the trigeminal nerve and infections such as syphilis, leprosy and viral, syphilis. (Table 1 and Table 2) [5] DIAGNOSTICS OF ORAL MUCOSAL PAIN Diagnostic evaluation of patients with oral mucosal pain requires a careful and thorough medical and dental history, physical examination and the review of systems and functioning of the oral mucosa and surrounding structures with special examination of the temporomandibular joint (TMJ) and muscles; and the cranial and cervical muscles and nerves.
In the case of pain, it has been found that the history taking is most important part of the diagnostic procedure based on which the diagnosis and treatment are planned. They include information about: • Origin of pain, • Time • Location and intensity, • Type of tissue affected by pain and its etiology. [1] (Table 2) An acute type of pain occurs in relation to the accidental injury, inflammation, or following surgery. Most conditions manifesting an acute pain can be treated, and usually, subside when healing of the tissue has taken place. Chronic pain remains for a longer period even after the apparent tissue has healed; and attempts to lessen pain are often futile. The chronic pain may also cause practical and physical alterations within the CNS. It is important that acute pain does not turn into a chronic pain condition which would impair the quality of life and result in depression.
[3] For the purpose of proper treatment, it is important to determine the duration of pain and distinguish acute pain from chronic. (Table 3)

Dental pain
The most common cause of lower face pain is related to the teeth and their neighbouring structures. Given the high occurrence of chronic dental pain, it needs to be kept in mind while considering patients with other chronic pain especially those who report an alteration in their symptoms which does not arise from the main diseasse. (Discussed in Part II)

Temporomandibular disorders (TMD)
The TMJ pain may be musculoskeletal with its pain being felt in the retromolar area. TMD has been researched by dentists with a specific interest in facial pain. The Research Diagnostic Criteria (RDC) for TMD was published in 1992 has been used as a source for research globally. This will be discussed in Part II of this article.

Non-dental pain
There may be other causes of oral pain that are not related to teeth. These include oral mucosal lesions such as (RAU) recurrent oral ulcerations, blistering conditions, and lichen planus that cause 4 chronic pain but whose manifestations are very standard and diagnosis is easy. Another common cause of oral pain is the salivary stone that causes sporadic pain of relatively low intensity, and which commonly occurs when eating; or at the thought of food.
Pain may sometimes be due to nerve damage, and in some cases, it remains impossible to determine the cause of the pain. To solve the confusing nomenclature regarding the oral pain, recently, a group of experts from the international community suggested the use of the term ' insistent dento-alveolar pain disorders' to include all conditions that cause persistent pain without the presence of any local disease (other names include phantom tooth pain or atypical odontalgia). When it has been attempted to understand the patients' experience of pain, some common excuses have emerged e.g. complex description of the pain, difficult to obtain a clear history, and presence of well localised deep pain. [6] Atypical odontalgia In a typical odontalgia, the location of the pain is adjacent to the dentoalveolar structure; either in relation to existing teeth or at a site where they have been extracted. [7] It may arise either before or after the dental treatment. The pain may be itinerant and may be a dull, throbbing; continuous pain which may exacerbate. It is provoked when touched even lightly. Baad-Hansen postulated that it is most likely to be a neuropathic pain that has different features from TMD. Treatment • Drugs for the same may be both topical and systemic. If the pain is localized to a peripheral origin, the diagnostic block gives an ambiguous response; but whenever there is a decrease in pain, a topical drug may be used, and a neurosensory stent can be fabricated. [    There is little data on the prognosis.

Somatic pain
Somatic pain results from the toxic excitement of normal neural structures that innervate the affected areas and pain may be either superficial or deep somatic. Superficial somatic pain has a bright and stimulating quality, is primarily involved in acute painful conditions and usually does not exhibit any diagnostic difficulty. Numerous local and systemic factors can cause damage and consequently acute inflammatory reaction in the oral mucosa with the release of inflammatory substances, act, causing pain. The nature of painful symptoms depends on the type of stimuli, the extent and location of the injury, the injured tissue reactivity and stage of inflammation. Pain due to inflammation occurs mainly due to the action of histamine and bradykinins; substances that are released during inflammation; stimulate nociceptors and reduce their threshold. These substances together increase the local vasodilatation and capillary permeability, causing edema that mechanically stimulates receptors and causes pain. As the threshold of pain decreases, nociceptors become more sensitive to stimuli. As a result, stimulus-induced primary hyperalgesia and spontaneous pain occur which has been classified as superficial somatic pain or mucogingival pain and occurs in the damaged oral mucosa. In contrast, deep somatic pain arises from damaged deeper body structure; has a dull, deep, depressing quality, and frequently exhibits CNS secondary excitatory effects such as referred pain to other sites and local autonomic effects (e.g., .odontogenic pain, musculoskeletal pain), [2]

Mucositis vs Stomatitis
The terms stomatitis and oral mucositis are often used as synonyms, but their processes are not identical. Stomatitis is any inflammatory condition of oral mucosa as a consequence of local infections or injuries or underlying systemic diseases. Mucositis on the other hand and oral tissue damage can be a grave problem for patients undergoing anticancer therapy.
Oral Mucositis is the term used to describe inflammation of oral mucosa as a result of chemotherapeutic agents or ionising radiation. Mucositis can differ considerably with the dose and type of therapy. The pathophysiology of oral mucositis is said to be multiple. Mucositis is said to occur in 75-80% of patients who needs to undergo high-dose chemotherapy before hematopoietic cell transplantation and in patients subjected to 22% of 1236 cycles of chemotherapy.

Neuropathic Pain without Visible Mucosal Lesion
Patients, who have no evident clinical lesions or pathological changes of oral mucosa and suffer pain, are the most difficult patients for treatment. In such cases, pain initiating from a structural anomaly in one or more elements of the nervous system that innervate the affected area; is therefore termed as neuropathic pain. The most common neuropathic pain syndromes in the orofacial region include trigeminal neuralgia; traumatic neuropathy; trigeminal neuroma; postherpetic neuralgia; diabetic neuropathy; cancer-related neuropathy, neuropathy induced by acquired immunodeficiency syndrome or AIDS; and chronic continuous trigeminal nociceptor neuropathy (with and without sympathetic mediation), Acute herpetic neuralgia (AHN) and postherpetic one commonly involve one of three divisions of the trigeminal nerve and involvement of the mouth is due to the maxilla and mandibular branch involvement. Virus reactivation in Varicella Zoster Virus (VZV) infection cause occurrence of vesicles on affected oral mucosa and skin which are innervated by an affected branch of the trigeminal nerve. Pain is always unilateral, recurrent, together with 8 lancinating episodes; and is described as burning or itching; well-localized to the affected site; frequently associated with hyperesthesia and hyperalgesia. The most common complication of HZ is post-herpetic neuralgia. [2]

Neuropathic Pain
Neuropathic pain occurs due to structural abnormalities [9] in one or more components of the nervous system that innervate the affected area. It can arise extemporaneously in the absenteeism of any obvious harmful stimulation and is usually described as a burning pain.
Neuropathic pain together with paraesthesia is seen along a distinct nerve distribution [10]. The severity of the pain is compared to the degree of stimulation, and even the slightest touch may result in intense pain. Neuropathic pain may be  spasmodic (paroxysmal) and   continuous, (

  
An example of a continuous neuropathic disorder is atypical odontalgia (AO), also known as phantom tooth pain. Continuous neuropathic disorders have an unremitting, constant pain of variable intensity. The pain is burning and may be accompanied by paraesthesia or dysesthesia. AO refers to persistent pain in apparently normal teeth and surrounding alveolar bone, or at extraction sites from which teeth have been removed because of pain, (Table 5).

Trigeminal neuralgia
The International Association for the Study of Pain (IASP) has defined the trigeminal neuralgia "as sudden usually unilateral severe brief, stabbing, recurrent pain; shown to have a significant impact on quality of life‛. TN is caused by a disturbance in the lower two branches of the trigeminal nerve [11]. The trigger zone for the same may be localised close to teeth, and sometimes the patients may be subjected to unwanted treatments due to this. TN is often misdiagnosed as TMD especially in cases where the TMD is unilateral; due to its relative frequency. The reason for the misdiagnosis may be due to its varied presentation and due to the reduced intensity of the burning or dull pain after the initial lancinating attack, which may be apparent in more than 50% of the cases. These have been labelled as type 2 or TN with concomitant pain. Neurosurgeons state a different outcome, in these individuals. Of the trigeminal autonomic cephalalgias SUNA (short unilateral neuralgiform pain with autonomic symptoms) needs to be reflected as a likely differential; being present in the lower face. [5]The most prominent feature of trigeminal neuralgia is the existence of trigger points often located in the skin of the lips, cheeks or gums and when touched may provoke a painful stimulus. Onset is frequently triggered by mechanical stimulation such as talking, chewing, or touch. Attacks can last from seconds to a few minutes.
Benign tumours, multiple sclerosis and A-V malformations need to be considered in the symptomatic causes of TN. Imaging is now mandatory as a part of the routine practice whereas some centres practice qualitative sensory testing.

Treatment
 Initial drugs such as carbamazepine or oxcarbazepine   Second-line drugs namely the lamotrigine and baclofen.   Surgery, if the patient suffers side effects or has poor pain control. Not much data is available on the outcome of surgical treatment though.   Microvascular decompression that is non-destructive and which gives the longest pain-free interval (70% pain free at 10 years) has also been recommended.   Other procedures include the ablative procedure such as balloon 9 compression or Gamma knife and radiofrequency thermocoagulation glycerol rhizotomy, which gives the patient 50% pain relief for four years; but patients, may have sensory changes which may hinder the quality of life. [3]

Post-traumatic trigeminal neuropathy/Peripheral painful, traumatic trigeminal neuropathy
A dental extraction, local anaesthetic, root canal filling, implants, and facial trauma can result in a nerve injury, with the injury being of varying degrees; and these conditions could be called as post-traumatic trigeminal neuropathy or peripheral painful, traumatic trigeminal neuropathy (PPTTN); proposed by Benoliel et al. He also found that only 50% had continuous pain, whereas others had daily pain that was of less than 4 hours duration; some even had very short attacks that were similar to TN like pain. Pain is often described as burning and stabbing; but patients with definite nerve injury such as lingual and inferior alveolar nerve, describe it as a feeling of pins and needles; fizzing and swollen sensations. Pain is elicited on being evoked, and in other cases, it may be spontaneous while some sensory changes can be identified on clinical testing; and somatosensory testing will often show evidence of hypoaesthesia or allodynia; most imaging is negative. Pain need not be a manifestation of all traumatic injuries; some manifest only sensory changes.

Treatment
 Although, the inferior alveolar nerve can be surgically repaired; most patients would require the guidelines for neuropathic pain to be adhered to. [5]

Anaesthesia Dolorosa/post-traumatic trigeminal neuropathy
There is a likely complication called as anaesthesia dolorosa, [12] encountered by the neurosurgeons while performing ablative procedures for TN most commonly at the level of the Gasserian Ganglion. When the cause is due to trauma e.g. fractures; the term used for the same is the post-traumatic trigeminal neuropathy Both of these conditions manifest within 3-6 months of the traumatic incident. The dissemination varies depending on the amount of the trauma, but in cases of the trigeminal neuralgia, it may extend to all the three divisions of the trigeminal nerve. The patients normally complain of hyperalgesia, hypoaesthesia; where the patient's experience "ants crawling over the face" experience, allodynia, and hypoalgesia. Management is difficult in cases where psychological anomalies coexist such as anger and depression. Trauma patients manifest symptoms that are often less severe and more localised.

Post herpetic neuralgia (PHN)
The condition is defined as pain remaining for over a month after the mucocutaneous lesions of Herpes zoster have healed. The pain of PHN is diffuse, dull, and aching, with a superficial allodynic sensation evoked by touch and clothes. Diagnosis is clinical and based on the presence or past presence of vesicles. A more difficult diagnostic problem is severe pain caused by VZ virus without lesions, developing along the course of the nerve (zoster sine herpete; zoster sine eruption). Diagnosis in these cases is based on clinical symptoms and serologic evidence of a rising antibody titer. (Table 5). [2]

Superior Laryngeal Neuralgia
Severe spasmodic pain experienced in the submandibular, throat or under the ear within minutes to hours following damage to the superior laryngeal nerve from a common viral infection, or a scarring following a surgical procedure for tonsils, or a repeated trauma to the larynx from swallowing, singing or even talking.

Treatment
• Similar to that as for TN. [2]

Peripheral Neuritis
Inflammation of the nerves following some invasive dental procedures, periapical inflammation or a misplaced dental implant associated with a nerve trunk may occur; and is typically asymptomatic.  Using a combination of drugs such as antidepressants and cognitive  behaviour therapy as a multidisciplinary approach.

Migraine Headache and Facial Migraine
A migraine is thought of as a unilateral headache that causes pain posterior to the neck, eye, and cranium [19]; but it may also be experienced in the lower part of the face, particularly in the teeth. A Migraine [20] is a neurovascular disorder of the brain in which neural events cause meningeal blood vessel dilation, causing further nociceptive activation of the trigeminovascular system. Treatment  Non pharmacological: Here the patients need to be convinced that the pain they are experiencing is not a dental pain. Relaxation techniques, hypnosis, etc.

Giant cell arteritis/Horton disease/Temporal arteritis
This is a pain that primarily affects the temple region and aggravates following any jaw movement [21], to become widespread, and involve the tongue, causing it to undergo cyanosis. Biopsy of the temporal artery has been used as the gold standard

Neck-Tongue Syndrome
A rare type of pain is the neck-tongue syndrome (NTS) where cervical spine involvement is misdiagnosed or unrecognised source of oro-facial pain; which manifests as paraesthesia in the tongue. The syndrome is characterised by ipsilateral paraesthesia (numbness) of the tongue together with unilateral paroxysmal neck pain. The neck rotates the same side as the sensory sign; is the triggering factor for the syndrome. The tongue manifestations arise from sensory fibers, including proprioceptive afferents originating in the lingual nerve, which joins the dorsal roots of C2 by way of the hypoglossal nerve. Neck and Tongue symptoms dissipate in approximately 60 seconds.
The typical presentation of symptoms is brought on by a sudden axial rotation of the head and may be associated with pathologic findings in the region of the first two cervical vertebrae. Tumours, malformations, and degenerative processes may result in compression and irritation of the C2 root. NTS has been reported over a wide age range for which there is no clear sex or age predilection. Cases arise before 20 years of age. The communication of the hypoglossal nerve with the sympathetic trunk, the vagus, and the first and second cervical and lingual nerves explains the sensory signs in the oropharyngeal area. Since the trigeminal nerve is not anatomically close to the hypoglossal nerve or the upper cervical roots involvement; it may play no role.

•
Conservative management includes avoidance of neck trauma and the use of anti-inflammatory agents and drugs to ease neuropathic pain which has been effective. [2]

Mucogingival Pain with Recognised Oral Lesions
Over a third of acute oro-facial pain is caused due to bacterial infections, local injuries and inflammation as well as underlying systemic diseases. [22] Oral infections Some bacterial, fungal and viral infections may cause blisters, vesicles, erosions and ulcers that result in mucosal pain. The predominant diseases and their management are described in Table 7.
The oral cavity plays a key role in the life strategy of several viruses. A recent case report has stated that HSV-1 can be responsible for BMS-like symptoms. These patients have been found to have a high titre of the virus in saliva, and the disappearance of the pain on antiviral treatment. plasmacytoma, and metastatic diseases; are mostly diagnosed by radiological and laboratory findings; in some cases, the systemic disease may manifest in the form of oral pain. (e.g. Jaw pain in angina pectoris), Craniofacial pain -site being the throat, mandible, TMJ, ear, neck and teeth aches may sometimes be the only manifestation of an acute myocardial infarction (AMI) and cardiac ischemia. Jaw pain induced by cardiac ischemia tends to occur bilaterally as opposed to the pain of odontogenic origin, which rarely crosses the midline. Therefore, craniofacial pain due to cardiac ischemia should be considered in the differential diagnosis of orofacial and dental pain. Any failure to recognise it can put the patient's life at risk. Hence the patients with more medically complicated orofacial pain would require a multidisciplinary treatment.

Referred Pain
Referred pain to the oro-facial region is an important clinical consideration. The location of pain, therefore, will not always correspond to its source. The pathophysiology for this has been proposed as the convergence of different primary afferent fibers from different sites on the same second-order neuron in the brainstem nucleus.

Differential Diagnostics Of Oro-Facial Pain
Obtaining a medical history from each patient with oro-facial pain should be a routine procedure in the dental office. It gives the dentist an insight into the past and presents physical health of the patient, and this information is of great importance regarding diagnosis and treatment of oro-facial pain. [5] Because of the complexity of anatomy and the diversity of causes, patients with oral pain represent a diagnostic and therapeutic challenge to dental professionals. Dentists encounter 10-50% of patients with pain, on a daily and increasing frequency. This makes the role of the dentists extremely important in the treatment of oro-facial pain. [2] Patients may experience more than one pain diagnosis and may also have an underlying psychiatric or personality disorder which will influence the chronic pain and which may change the presentation and severity.
When problems arise in the pain area, the patients are unsure about the speciality of the practitioner who would solve their problem.
The health care specialists including the dentists are only familiar with the oro-dental pain and are not with the pain that is bio-psychosocial and are also unsure about the drugs they need to prescribe. Hence as Hals et al. pointed out; what is needed is a multi-professional team to handle such pain. A recent study on the chronic orofacial pain patients in the UK; their healthcare ‚journey‛ showed that the patients had attended a number of health care settings, seen specialists and only 24% were satisfied with the treatment provided, whereas the study from Germany showed a poor response rate of 45% on 34,242 patients that showed that patients were incompetently treated, though standard guidelines were adhered to. Thirty% even had a treatment, focus on the psychology, [4] but wrongly, all were approached similarly. [3]

Differential Diagnostics of Oro-facial Pain in Elderly
Older people often have a variety of simultaneous health problems, although ageing does not necessarily mean disease and many take a variety of medications, often making it difficult for a dentist to make a definitive diagnosis of oral pain. Differential diagnosis of oral pain in the elderly should include: