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Zeroing in on the cause of your patient's facial pain.

The overlapping characteristics of facial pain can make it difficult to pinpoint the cause. This article, with a handy at-a-glance table, can help.

Facial pain is a common complaint: Up to 22% of adults in the United States experience orofacial pain during any 6-month period. (1) Yet this type of pain can be difficult to diagnose due to the many structures of the face and mouth, pain referral patterns, and insufficient diagnostic tools.

Specifically, extraoral facial pain can be the result of temporomandibular disorders, neuropathic disorders, vascular disorders, or atypical causes, whereas facial pain stemming from inside the mouth can have a dental or nondental cause (figure). Overlapping characteristics can make it difficult to distinguish these disorders. To help you to better diagnose and manage facial pain, we describe the most common causes and underlying pathological processes.

Extraoral facial pain

Extraoral pain refers to the pain that occurs on the face outside of the oral cavity. The TABLE215 summarizes the site, timing and severity, aggravating factors, history and exam findings, and management of several common causes of extraoral facial pain.

Musculoskeletal pain

Temporomandibular disorders (TMD) are a broad group of problems that affect the temporomandibular joint (TMJ), muscles of mastication, and/or associated bony and soft tissue structures. (6) They may occur secondary to malocclusion, traumatic injuries, oral parafunctional habits (eg, bruxism), hormonal influences, or psychogenic factors. (6) TMD is more prevalent in women, with a peak occurrence between ages 20 and 40 years. (6,8)

TMD can be articular (intracapsular) or nonarticular (extracapsular). Nonarticular disorders (>50% of TMD) usually affect the muscles of mastication and include chronic conditions such as fibromyalgia, muscle strain, and myopathies. (8) Muscle-related pain and dysfunction are believed to arise from parafunctional habits such as bruxism or clenching. Articular disorders include synovitis/capsulitis, joint effusion, trauma/fracture, internal derangement (disturbance in the normal anatomic relationship between the disc and condyle), arthritis, and neoplasm. (16)

* What you'll see. Orofacial pain (usually dull and located in the preauricular region), joint noise, and restricted jaw function are key signs and symptoms of TMD. Exacerbation of pain with mandibular functions (eg, chewing, yawning, or swallowing) is a pathognomonic sign. Joint sounds such as clicking or crepitus are common. In most cases, crepitus correlates with osteoarthritis. (6) Nonspecific TMD symptoms include headache, earache, insomnia, tinnitus, and neck and shoulder pain. (6)

The gold standard of diagnosis of TMD consists of taking a detailed history, evaluating the patient's head and neck, and conducting a general physical examination and behavioral/ psychological assessment. (17) Imaging of the TMJ and associated structures is essential. (17)

* Treatment. Nonsteroidal anti-inflammatory drugs, opioids, muscle relaxants, antidepressants, anticonvulsants, anxiolytics, and corticosteroids are options for treating TMD. (6,8) Isometric jaw exercises, maxillomandibular appliances, and physical therapy are valuable adjuncts for pain relief. Advise patients to establish a self-care routine to reduce TMJ pain that might include changing their head posture or sleeping position, and limiting activities that require using their jaw, such as clenching, bruxism, and excessive gum chewing. Some patients may need to adopt a non-chewing diet that consists of liquid or pureed food. Massage and moist heat can help relax muscles of mastication and improve range of motion.

Approximately 5% of patients with TMD undergo surgery, typically simple arthrocentesis, arthroscopy, arthrotomy, or modified condylotomy. (6) Total joint replacement is indicated only for patients with severely damaged joints with end-stage disease when all other conservative treatments have failed. Joint replacement primarily restores form and function; pain relief is a secondary benefit. (8)

Neuropathic pain

Trigeminal neuralgia (TN) is sudden, usually unilateral, severe, brief, stabbing, recurrent episodes of pain in the distribution of one or more branches of the trigeminal nerve. (9) It most commonly presents in the lower 2 branches of the trigeminal nerve and usually is caused by compression of the trigeminal nerve root by vascular or nonvascular causes. (4) The pain is severe and can profoundly impact a patient's quality of life.

TN attacks typically last from a few seconds to up to 2 minutes. As many as 30 attacks can occur daily, with refractory periods between attacks. After the initial attack, individuals are left with a residual dull or burning pain. TN can be triggered by face washing, teeth brushing, speaking, eating, shaving, or cold wind. (4)

* Diagnosis can be tricky because more than half of patients with TN experience less severe pain after the main sharp attack; this presentation is called TN type II. (7) A detailed patient history and careful evaluation can help identify patients with TN type II. TN can be misdiagnosed as TMD, especially if it presents unilaterally. (15)

* Treatment. Anticonvulsants are the primary medications used to treat TN.

* Post-traumatic trigeminal pain is usually the result of an injury or dental procedure, such as facial trauma, tooth extraction, root canal, or dental implants. (12,18,19) Nerve injury is assumed to be the cause. This type of pain can start within 3 to 6 months of a trauma. It is located in the trigeminal area and patients describe it as burning, tingling and, at times, sharp. (15) Patients who have sustained injury to the lingual or inferior alveolar nerves have reported feeling "pins and needles." (12)

Common triggers include temperature changes or simple touch. Not all injuries result in pain; some patients may have only sensory impairment (15) or sensory deficits such as allodynia or hypoesthesia.

* Treatment. The first line of treatment for post-traumatic trigeminal pain is tricyclic antidepressants (TCAs) followed by pregabalin or gabapentin. (14)

* Glossopharyngeal neuralgia (GN) is similar in presentation to TN but is much rarer. (15) GN pain occurs deep in the throat, ear, or posterior tongue. (15) When the pain occurs in the inner ear, GN can be misdiagnosed as TMD. In most cases, no cause of GN can be determined.

Patients describe GN pain as shooting, sharp, and electrical shock-like, lasting from seconds to minutes, with recurrent attacks throughout the day. Like TN, GN can present as episodes of attacks that last weeks to months. Triggers include chewing, drinking, swallowing, and talking, as well as light touch. (13,15) Some patients with GN experience syncope due to the anatomical proximity of the vagus nerve. (14)

* Treatment. Anticonvulsants are the first-line treatment for GN. Local anesthetics or surgery can be considered for patients who don't improve after medical therapy. (15)

* Postherpetic neuralgia (PHN) can cause facial pain when the characteristic vesicular rash of the varicella zoster virus (shingles) occurs on the face. PHN usually affects the first division of trigeminal nerve, but the second and third divisions can be affected as well. (13)

* What you'll see. The acute phase of PHN begins a few days before the initial rash has resolved and can last up to a month after. A new pain may begin one to 6 months after the initial rash has healed. (20) This pain, which patients often describe as sharp, stabbing, or burning, can be constant or intermittent. Dysesthesia, hypoesthesia, and allodynia may also occur within the affected dermatome.

PHN is usually diagnosed based on the patient's history and clinical presentation. However, direct fluorescent antibody stain, viral culture, or polymerase chain reaction performed on vesicular fluid from a herpetic lesion during the initial rash are the laboratory tests of choice if confirmation is needed.

* Treatment. PHN is managed with anticonvulsants and TCAs.

* Numb chin syndrome (NCS) is characterized by hypoesthesia, paresthesia, thermalgesic anesthesia, or pain over the chin in the region supplied by the mental nerve, a terminal branch of the mandibular division of the trigeminal nerve. (5,21,22)

NCS can be caused by odontogenic conditions, such as dental abscess, dental anesthesia, dental trauma, or osteomyelitis; systemic conditions such as amyloidosis, sickle cell disease, sarcoidosis, multiple sclerosis, human immunodeficiency virus, or diabetes; or malignancies such as lymphoma, leukemia, breast cancer, lung cancer, prostate cancer, or head and neck cancers. (21) In one study of patients with NCS, cancer was the cause of the condition in 89% of patients. (22)

* What you'll see. NCS is characterized by numbness of the skin in the lower lip, chin and mucous membrane inside the lip that extends to the midline. (5) Depending upon the etiology, patients may present with percussion-induced pain, loosening of teeth, sequestra, and mobility of fractured segments. Patients with metastatic malignancy may develop constitutional symptoms.

* Making the diagnosis. Panoramic radiography is a useful starting point. If possible, a computerized tomography scan of the head and neck should also be done. Nuclear bone scintigraphy (bone scanning) may help identify bone disease such as osteomyelitis. A biopsy may be needed if a mass lesion is present.

* Treatment. In NCS that is the result of a dental etiology, the prognosis usually is good. For example, NCS that is the result of an abscess usually resolves after the abscess is drained. However, if NCS is caused by metastasis, the prognosis is grim; the average length of survival after diagnosis is approximately 5 months if NCS is caused by mandibular metastasis and 12 months if leptomeningeal metastasis is present. Treatment does little to affect the outcome in these cases. (21,22)

Atypical pain

Persistent idiopathic facial pain (PIFP), previously known as atypical facial pain, is a persistent facial pain that does not have the classical characteristics of cranial neuralgias and for which there is no obvious cause. (2,10,23) PIFP is not triggered by any of the factors that typically precipitate neuralgias. (2) The onset may be spontaneous or associated with dental intervention or facial injury, but it usually does not have a demonstrable local cause. (24,25)

Neuropathic mechanisms that might be at work in PIFP include nociceptor sensitization, phenotypic changes and ectopic activity from the nociceptors, central sensitization possibly maintained by ongoing activity from initially damaged peripheral tissues, sympathetic abnormal activity, alteration of segmental inhibitory control, or hyperactivity or hypoactivity of descending controls. (2)

PIFP is most frequently reported in women in their 40s and 50s. (25) The history of a patient with PIFP often include mood disorders, chronic pain, or poor coping skills. (14) Patients complain of a steady, unilateral, poorly localized pain that is deep, constant, aching, pulling, or crushing. It is usually present all day, every day. The constancy of the pain is its distinguishing feature. In the beginning, this pain may be in a limited area on one side of the face, usually the nasolabial folds or the angle of the mandible. Later, it may affect both sides of the face and extend to the neck and upper limbs. (23,24) Most patients with PIFP report other symptoms, including headache, neck and backache, dermatitis, pruritus, irritable bowel, and dysfunctional uterine bleeding. (26)

* Making the diagnosis. A targeted history and accurate clinical examination are essential. (2,10) Although there are no formal diagnostic criteria, a patient can be assumed to have PIFP if: (2,10)

* There is pain in the face for most of the day or all day, every day.

* Initially, the pain may be confined to a portion of the face, but it is poorly localized and deep.

* The pain is not associated with other physical signs or loss of sensation.

* Imaging does not reveal an obvious anatomic or structural cause.

* Treatment. Treatment of PIFP can be difficult and unsatisfactory. (23) Counseling to educate patients about the chronic and nonmalignant nature of the illness is the mainstay of treatment, followed by pharmacotherapy. (23) TCAs have shown a moderate effect in several trials. Gabapentin, topiramate, carbamazepine, and pregabalin also have shown limited to modest benefit in some patients. Surgical therapies appear to be of little or no use. (23) Experimental treatments such as pulsed radiofrequency, low-energy level diode laser have shown success in small studies. (10,23)

Vascular pain

Giant cell arteritis (GCA) is a systemic, chronic vasculitis involving the large and medium-sized vessels, mainly the extracranial branches of the carotid artery. (6,11) It predominantly affects people older than age 50 and is more common among women and those of Scandinavian ethnicity. (27)

The cause of GCA is unclear. Genetic predisposition linked to humoral and cell-mediated immunity is believed to play a role. (28) Familial aggregation and predominance of the HLA-DR4 allele has been reported in patients with GCA. (6)

* What you'll see. The most common signs and symptoms of GCA are temporal headache (seen in two-thirds of patients), jaw claudication and tenderness, and swelling of the temporal artery. (6,11) The headache of GCA usually is unilateral, severe, boring or lancinating, and localized to the temporal or occipital regions of the scalp. (6) Other orofacial manifestations include trismus, throat pain that develops while chewing, changes in tongue sensation and tongue claudication, tooth pain, dysphagia, dysarthria, submandibular mass, lip and chin numbness, macroglossia, glossitis, lip and tongue necrosis, and facial swelling. (11)

Visual symptoms include diplopia, ptosis, and possibly blindness if treatment is not instituted at first suspicion. Ocular symptoms result from anterior ischemic optic neuropathy, posterior ischemic optic neuropathy, or central retinal or cilioretinal artery occlusion. (6,28) Patients have also reported low-grade fever, asthenia, anorexia, weight loss, and generalized aches. (11,28)

* Making the diagnosis. Arterial biopsy is the gold standard for diagnosis of GCA. It is usually performed on the temporal artery and is positive in 80% to 95% of people with the condition. (28) Other useful lab tests include erythrocyte sedimentation rate (ESR; elevated), white blood cell count (mildly elevated), and C-reactive protein (elevated).

* Treatment. Prednisone is used to treat GCA, in initial doses ranging from 30 to 80 mg. A maintenance dose may be required for up to 2 years, with close follow-up and periodic ESR measurements. (28)

* Malignancy is a rare cause of facial pain. The pain may be due to metastasis of extracranial bony or soft tissue as it compresses cervical and cranial nerves. (3) Lung cancer can cause referred pain in the periauricular region by compressing the vagus nerve, and this pain can be misdiagnosed as dental pain, atypical facial pain, TMD, or TN. (3,29) The facial pain of lung cancer is unilateral and on the same side as the lung neoplasm, and commonly is referred to the jaw, ear, or temporal region. While many patients have continuous pain, some report intermittent pain or pain that lasts for hours. (3) Facial pain caused by a malignancy is differentiated from other sources of facial pain by the presence of associated symptoms such as weight loss, cough, and hemoptysis.

* Treatment. Treatment can include radiation or chemotherapy. (29)

The mouth is often the source of lower facial pain

Pain in the oral cavity is the most common cause of pain in the lower face. (15) Intraoral pain usually is caused by disease in the following structures:

1. Dentition (eg, caries, dentin sensitivity, pulpal disease)

2. Periodontium (eg, gingivitis, acute or chronic periodontal disease, sensitivity related to gum recession, alveolar bone pathology)

3. Other soft and hard tissues, such as the palate, floor of mouth, buccal mucosa, non-tooth supporting bone, and tongue (eg, mucosal diseases, neoplasms, pain related to parafunction or trauma).

Rarely, intraoral pain may be referred. For- example, myofascial pain might cause diffuse tooth pain. (30)

See TABLE W1 (31,35) at the end of this article at for a summary of the etiology, signs/symptoms, diagnosis, and management of these and other dental causes of oral facial pain.

Nondental causes of oral facial pain can be associated with oral mucosal disorders, malignant disease and its therapy, salivary gland disorders, maxillary sinusitis, burning mouth syndrome, or atypical odontalgia. See table W2 (36-41) at for a more detailed description of these conditions.


* Advise patients who have a temporomandibular disorder that in addition to taking their medication as prescribed, they should limit activities that require moving their jaw, modify their diet, and minimize stress; they may require physical therapy and therapeutic exercises, (c)

* Consider prescribing a tricyclic antidepressant for patients with persistent idiopathic facial pain. (c)

Strength of recommendation (SOR)

(A) Good-quality patient-oriented evidence

(B) Inconsistent or limited-quality patient-oriented evidence

(C) Consensus, usual practice, opinion, disease-oriented evidence, case series

Feras Ghazal, DDS; Mohammed Ahmad, MD; Hussein Elrawy, DDS; Tamer Said, MD Department of Oral Health (Drs. Ghazal and Elrawy) and Department of Family Medicine/Geriatrics (Drs. Ahmad and Said), MetroHealth Medical Center, Cleveland, Ohio

The authors reported no potential conflict of interest relevant to this article.


Tamer H. Said, MD, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, Ohio 44109; tsaid@


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Extraoral facial pain: Differential diagnosis (2-15)

Site                  Timing; severity     Aggravating factors

Temporomandibular disorders

TMJ, muscles of       Abrupt but often     Chewing that is
mastication, ear.     constant; moderate   prolonged,
May radiate to the    to severe            opening mouth

Trigeminal neuralgia

Along the             Sudden onset,        Eating, light
distribution of       lasts seconds to     touch, cold, some
the second and        minutes, up to 30    attacks could be
third division of     attacks daily;       spontaneous
the trigeminal        moderate to severe

Post-traumatic trigeminal pain

Trigeminal area       3-6 months after     Touch, cold or heat
                      traumatic event;
                      moderate to severe

Glossopharyngeal neuralgia

Deep in the ear,      Sudden attacks,      Chewing, talking,
throat, and           lasts seconds to     drinking,
posterior tongue      minutes, often       swallowing
                      multiple attacks
                      daily; moderate to

Postherpetic neuralgia

Site of zoster        Constant or          Light touch
rash                  intermittent;
                      moderate to severe

Numb chin syndrome

Over the chin in      Abrupt or gradual    Odontogenic
the region                                 causes (eg,
supplied by the                            dental abscess,
mental nerve                               dental trauma.
                                           Systemic causes
                                           (sarcoidosis, HIV,

Persistent idiopathic facial pain

Not well localized    Constant; moderate   Stress, fatigue
                      to severe

Giant cell arteritis

Temporal region       Sudden onset,        Mastication
                      moderate to severe

                      History and
Site                  physical exam        Management

Temporomandibular disorders

TMJ, muscles of       Clicking or          NSAIDs, muscle
mastication, ear.     locking of TMJ,      relaxants,
May radiate to the    headaches,           surgery
neck                  bruxism. Attrition
                      of teeth,
                      tenderness along
                      the TMJ, clicking,
                      reduced opening of

Trigeminal neuralgia

Along the             Depression, fear     Anticonvulsants
distribution of       of pain returning.
the second and        Attack can be
third division of     triggered with
the trigeminal        light touch;
nerve                 sensory changes
                      very rare

Post-traumatic trigeminal pain

Trigeminal area       History of trauma    TCAs,
                      or dental            pregabalin,
                      procedure. Sensory   gabapentin
                      changes, including

Glossopharyngeal neuralgia

Deep in the ear,      Syncope (rare).      Anticonvulsants,
throat, and           Provoked by light    TCAs, neuropath-
posterior tongue      touch                ic medications,
                                           local anesthetics,

Postherpetic neuralgia

Site of zoster        History of zoster.   Anticonvulsants,
rash                  Skin changes.        TCAs

Numb chin syndrome

Over the chin in      Hypoesthesia,        Varies based on
the region            paresthesia,         etiology
supplied by the       thermalgesic
mental nerve          anesthesia or pain
                      over the chin. If
                      related to dental
                      induced pain,
                      loosening of
                      teeth. If
                      malignancy is
                      symptoms may be

Persistent idiopathic facial pain

Not well localized    Other chronic        TCAs, CBT
                      pain, significant
                      life events. Exam
                      is usually normal

Giant cell arteritis

Temporal region       Vision changes,      Prednisone
                      often associated
                      with polymyalgia
                      Temporal area

CBT, cognitive behavioral therapy; HIV, human
immunodeficiency virus; NSAIDs, nonsteroidal
anti-inflammatory drugs; TCAs, tricyclic
antidepressants; TMJ, temporomandibular joint.
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Author:Ghazal, Feras; Ahmad, Mohammed; Elrawy, Hussein; Said, Tamer
Publication:Journal of Family Practice
Article Type:Report
Date:Sep 1, 2015
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