Category Archives: Orofacial Pain and Oral Medicine

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Clinical Features, Diagnosis, and Treatment of Erythema Multiforme

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Erythema multiforme (EM): First described in 1866 by Ferdinand von Hebra as an acute, self-limited cutaneous disease characterized by multiform skin lesions, now called EM minor [1]. In 1950, Bernard A. Thomas classified EM into erythema multiforme minor (von Hebra) and erythema multiforme major characterized by erosions or ulcerations involving the oral, genital, and/or ocular mucosae lesions accompanied by skin lesion seen in EM minor.

In addition to the mucosal involvement, a key difference between these two subtypes is systemic symptoms such as fever and arthralgia preceding and/or accompanying EM major.

The similarities in clinical and histopathologic findings between Erythema Multiforme Major and Stevens-Johnson Syndrome (SJS) have led to controversy over the distinction between these two mucocutaneous conditions. Historically, SJS and Toxic Epidermal Necrolysis (TEN) are considered a disease continuum of EM. In 1993 and 1995, Bastuji-Garin and colleagues proposed a new clinical classification for  EM, SJS, and TEN supporting that SJS and TEN are distinct conditions from EM [2, 3].

However, it is still firmly believed that SJS and TEN are a disease continuum. The term “erythema multiforme” should not be used to refer to SJS/TEN or vice versa. The validity of the Bastuji-Garin classification was later confirmed by a large epidemiological study [4]. Regardless of all these classifications efforts, in an analysis of 37 published cases of drug-induced EM, 24 case reports (65%) did not meet clinical criteria for EM. [5].

Bastuji-Garin, S., et al. classified EM, SJS, and TEN into five categories [3]:

  1. EM, detachment below 10% of the BSA plus localized typical targets or raised atypical targets.
  2. SJS, detachment below 10% of the BSA plus widespread macules or flat atypical targets.
  3. Overlap SJS-TEN, detachment between 10% and 30% of the BSA plus widespread macules or flat atypical targets.
  4. TEN with spots* with or without blisters, detachment above 30% of the BSA plus widespread macules or flat atypical targets.
  5. TEN without spots*, detachment above 10% of the BSA with large epidermal sheets and without any macule or target.

Spot*: EM-Likes skin lesions

Etiology:  EM etiology is divided into two main groups, infection and medication:

  1. Infections: There is strong evidence that EM is precipitated by infection (viral, bacterial, or fungal) in most cases. The most common inciting pathogen is Herpes Simplex Virus (HSV). This link between EM and HSV is evident by (i) developing EM a few weeks after an HSV infection, (ii) seropositivity for HSV antibody, and (iii) identify HSV antigen in EM patients. Mycoplasma pneumoniae infection is an important etiology to be considered for EM in children. Malignancy, autoimmune disease, sarcoidosis, menstruation, and radiation have also been reported in rare cases. With the current COVID pandemic, oral health providers need to recognize that EM-like lesions have also been observed in association with COVID-19 infection and after COVID-19 vaccination [6].
  1. Medications: It is important to understand that less than 10% of EM cases are triggered by medication such as NSAIDs, antibiotics, anticonvulsants such as Carbamazepine, and others. Medication-induced EM has contributed to the nosology controversy of EM and SJS/TEN, which is almost caused by medications. Looking carefully at the EM patient’s new medication and if there is a temporal relationship is key in identifying drug-induced EM. Identifying the offending drug is crucial in the treatment and improve the prognosis of EM. Exposure to the offending drug commonly precedes the onset of symptoms by one to four weeks, but re-exposure may result in the onset of symptoms in as little as 48 hours.


The suggested pathogenesis for HSV induces EM CD34+ cells to carry fragments of HSV DNA to the skin and mucosa where it incites a T cell‐type hypersensitivity reaction that generates interferon-γ, with the amplified immune system recruiting more T cells initiate acute inflammation causing the eruption of the EM lesions [7].

EM Clinical Findings:

The clinical course of EM varies depending on the cause. EM caused by infection is usually self-limited, resolving within a few weeks. In a minority of cases, the disease recurs over the years. Studies show that recurrent EM is mainly associated with recurrent HSV infections, which might happen two to three weeks before the EM clinical symptoms appear. As mentioned above, although less common, recurrence might happen when reexposed to an offending medication.

Regardless of the cause, EM lesions erupt within a few weeks from the infection or taking the offending medication. Skin and oral lesions appear rapidly over a few days and begin as red macules that become papular in the skin, starting primarily in the hands and moving centripetally toward the trunk in a symmetrical distribution. This acute onset of the mucocutaneous lesions is one of the hallmarks of considering EM in the differential diagnosis.

In EM Major, it is not uncommon to have a prodrome of fever, arthralgias, malaise, headache proceeding or accompany the mucocutaneous lesions. In M. pneumoniae infection-associated EM, sore throat, rhinorrhea, and cough might be seen. Although not very common, skin lesions in EM Major might present with an epidermal detachment; if the skin detachment is more than 10% of body surface area (BSA), SJS/TEN should be considered. Hence the name multiforme, skin lesions have multiple forms. The morphology of EM lesions may vary between patients and may also evolve throughout the disease stage (Early Vs. Late) in a single patient [3]:

  1. Target lesion: The stander skin lesions for EM are defined as individual lesions less than 3 cm in diameter with a regular round shape, well-defined border, and at least three different zones.
  2. Raised atypical targets: Defined as round, edematous, palpable lesions, with only two zones and/or a poorly defined border.

Interestingly, skin lesions are mostly asymptomatic; however, some patients will complain of itching or burning sensation.


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The intraoral lesion is mainly seen in EM major, not minor. The lesions range from mild erythema and erosion to large painful ulcerations covered by a yellow-white fibrinous exudate Figure 1. Lip inflammation, ulceration, and crusting are very common in patients with EM major Figure 2. It is important to understand that these lesions are not exclusive to EM and can be seen in SJS/TEN, and other conditions include Paraneoplastic Pemphigoid.

EM Minor always presents with skin lesions similar to the major subtype described above but without epidermal detachment and without or only mild mucosal disease. Also, no associated systemic symptoms accompany EM minor.

Although not included in the Bastuji-Garin classification, oral health providers must realize that sometimes EM cases present with oral mucous membrane involvement only [8].

Laboratory findings: Clinical findings and course of the disease are usually enough to diagnose patients with EM. Laboratory tests such as CBC, CMP, and CRP are not specific. Histopathologically, basal layer liquefaction and inflammatory infiltrate (includes lymphocytes, histiocytes), spongiosis, and intracellular edema. Although these histopathological features are not specific, an oral biopsy could be performed with persistent EM to assist with the exclusion of other disorders or when the diagnosis of EM is questionable. Investigational tests can be done by infectious disease specialists when the infection is considered as a possible etiology.

Diagnosis of EM Major: Diagnosis of EM Major would be appropriate in a patient with the following clinical features [3, 4]:

  • A history of recent infection strongly suggests EM. Although medications are associated with 10% of EM, medications are the leading cause of  SJS/TEN.
  • A prodrome of febrile illness and malaise can be seen in EM but not specific and can be seen more often in SJS/TEN.
  • EM mostly does not have skin detachment and, if present, is it below 10% of the BSA. On the other hand, SJS/TEN is commonly associated with skin detachment. SJS is the less severe condition comparing to TEN, in which skin detachment is <10 percent of the BSA. TEN involves detachment of >30 percent of the BSA. When skin detachment is between 10 and 30 percent of BSA, it considers overlap SJS/TEN.
  • EM is characterized by typical target-like or raised atypical targets lesions (described above). SJS/TEN lesions are commonly flat atypical targets defined as round lesions with only two zones and/or a poorly defined border, nonpalpable with the exception of a potential central blister. Also, SJS/TEN lesions might present as purpuric macules with or without blisters. In general,  blisters often occur on all or part of the SJS/TEN lesions and are rare to be seen in EM. In rare instances, TEN occurred without any discrete atypical target lesions. These cases are classified as TEN without spots.
  • While EM skin lesions are symmetrical, localized, start from the extremities, and could move centripetally, SJS and TEN are widespread, start from the neck, face, and upper torso, and can extend centrifugally.
  • Finally, comparing to SJS/TEN, recurrences are more common with EM.


  1. Review the medical history to identify the cause is crucial. If a drug is suspected, contact the prescriber physician after approval, discontinue the medication. If an infection is suspected, consider a consultation with the patient’s primary physician or infectious disease specialist for appropriate treatment of the infection.
  2. When skin is involved, always consider a dermatology consultation.
  3. The pharmacological management will depend on the severity and recurrence of the condition:
    1. Limited oral mucosal involvement: For alleviating the pain, a mouthwash containing equal parts of viscous lidocaine 2%, diphenhydramine (12.5 mg/5 mL), and aluminum hydroxide and magnesium hydroxide mixture (e.g., Maalox) as a swish-and-spit, can be used as needed, up to four times per day. Dexamethasone (0.5 mg/5 mL) oral elixir 4 times/day swish-and-spit can be used for diffused ulcers. If the ulcers are limited to a small area, fluocinonide 0.05% gel is applied two to three times per day.
    2. Extensive oral mucosal involvement: Severe oral mucous membrane involvement that prevents sufficient oral intake consider hospitalization. If hospitalization is not needed, In the first-line treatment is systemic glucocorticoids. Dosage and tapering will depend on the severity of the case and response to the treatment.  Azathioprine and dapsone have been reported helpful in several cases.
    3. An antiviral suppersion therapy, such as Acyclovir 400mg twice a day, should be considered in recurrent EM associated with HSV.

All the above medications have contraindications which the clinician has to be aware of before prescription.

figure 1








Figure 1: Intraoral erythema multiforme: Diffused ulcers covered by a yellow-white exudate/fibrinous surface. Image courtesy of Orofacial Pain and Oral Medicine Center, Herman Ostrow School of Dentistry of USC.






Figure 2:
Erythema multiforme with ulcerative, hemorrhagic crusts of the lips. Image courtesy of Orofacial Pain and Oral Medicine Center, Herman Ostrow School of Dentistry of USC.

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1. F., v.H., Atlas der Hautkrankheiten. Vienna, Austria: Kaiserliche Akademie der Wissenschaften.

2. Assier, H., et al., Erythema multiforme with mucous membrane involvement and Stevens-Johnson syndrome are clinically different disorders with distinct causes. Arch Dermatol, 1995. 131(5): p. 539-43.

3. Bastuji-Garin, S., et al., Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermatol, 1993. 129(1): p. 92-6.

4. Auquier-Dunant, A., et al., Correlations between clinical patterns and causes of erythema multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis: results of an international prospective study. Arch Dermatol, 2002. 138(8): p. 1019-24.

5. Roujeau, J.C., Re-evaluation of ‘drug-induced’ erythema multiforme in the medical literature. Br J Dermatol, 2016. 175(3): p. 650-1.

6. McMahon, D.E., et al., Cutaneous reactions reported after Moderna and Pfizer COVID-19 vaccination: A registry-based study of 414 cases. J Am Acad Dermatol, 2021. 85(1): p. 46-55.

7. Ono, F., et al., CD34+ cells in the peripheral blood transport herpes simplex virus DNA fragments to the skin of patients with erythema multiforme (HAEM). J Invest Dermatol, 2005. 124(6): p. 1215-24.

8. Bean, S.F. and R.K. Quezada, Recurrent oral erythema multiforme. Clinical experience with 11 patients. Jama, 1983. 249(20): p. 2810-2.

Man holding his head in pain

CGRP: 4 Letters That Became a New Frontier in Pain Management

Man holding his head in pain

What Does CGRP Stand For?

Calcitonin gene-related peptide (CGRP) is a neuropeptide (neurotransmitter of the nervous system) discovered over 30 years ago. It has specific receptors located both centrally and in the periphery. CGRP is present in trigeminal neurons and is released into the cranial venous outflow in acute migraine and cluster headache attacks (1).

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CGRP has several functions (2), such as:

  • Appetite-suppressant
  • Contributes to gastric acid secretion
  • Temperature homeostasis
  • Increases heart rate
  • Plays a role in the release of the pituitary hormones 
  • Highly potent vasodilator with protective mechanisms 
  • Wound healing

CGRP is primarily released from sensory nerves and thus is implicated in pain. Increased levels of CGRP have been reported in migraines, cluster headaches, and might as well be present in temporomandibular disorders (3).

Within the brain, CGRP increases with ischemia, injury, hyperthermia, and seizures, activating neuroprotective processes (4).

The role of CGRP in pain management is likely mediated by modulating nociception and sustaining neurogenic inflammation that leads to peripheral and central pain sensitization (for example in migraine) (5).


CGRP as a Target For Pain Management

The use of monoclonal antibodies against CGRP is a novel therapeutic strategy for the management of some painful conditions, such as migraine and cluster headache (6).

CGRP-related therapies were designed specifically to act on the trigeminal pain system, with little or no adverse effects. Two groups of medications are available.

  1. Small molecule CGRP receptor antagonists (gepants) for acute relief of migraine headache
  2. Monoclonal antibodies against CGRP (Eptinezumab, Fremanezumab, and Galcanezumab) or the CGRP receptor (Erenumab) to prevent migraine attacks (7).

Considering the comorbidity between migraine and TMD and the role of CGRP in the trigeminal pain system, CGRP receptor antagonists may have therapeutic efficacy in the treatment of other facial pain conditions. Understanding the pain mechanisms offers opportunities to develop therapeutic strategies with better chances to improve patient’s wellbeing (8).


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  1.  Edvinsson L. The Trigeminovascular Pathway: Role of CGRP and CGRP Receptors in Migraine. Headache. 2017 May; 57 Suppl 2:47-55. doi: 10.1111/head.13081. PMID: 28485848.
  2. Russell, F. A., King, R., Smillie, S. J., Kodji, X., & Brain, S. D. (2014). Calcitonin gene-related peptide: physiology and pathophysiology. Physiological reviews, 94(4), 1099–1142.
  3.  Yuan H, Spare NM, Silberstein SD. Targeting CGRP for the Prevention of Migraine and Cluster Headache: A Narrative Review. Headache. 2019 Jul; 59 Suppl 2:20-32. doi: 10.1111/head.13583. PMID: 31291020.
  4.  Borkum, JM. CGRP and Brain Functioning: Cautions for Migraine Treatment. Headache. 2019 Sep; 59(8): 1339-1357. doi: 10.1111/head.13591. Epub 2019 Jul 21. PMID: 31328279.
  5.  Yuan H, Lauritsen CG, Kaiser EA, Silberstein SD. CGRP Monoclonal Antibodies for Migraine: Rationale and Progress. BioDrugs. 2017 Dec;31(6):487-501. doi: 10.1007/s40259-017-0250-5. PMID: 29116598.
  6.  Carmine Belin A, Ran C, Edvinsson L. Calcitonin Gene-Related Peptide (CGRP) and Cluster Headache. Brain Sci. 2020 Jan 6;10(1): 30. doi: 10.3390/brainsci10010030. PMID: 31935868; PMCID: PMC7016902. 
  7. Akerman S, Romero-Reyes M. Preclinical studies investigating the neural mechanisms involved in the co-morbidity of migraine and temporomandibular disorders: the role of CGRP. Br J Pharmacol. 2020 Dec; 177(24): 5555-5568. doi: 10.1111/bph. 15263. Epub 2020 Oct 21. PMID: 32929719; PMCID: PMC7707098.
  8. Edvinsson L. Role of CGRP in Migraine. Handb Exp Pharmacol. 2019; 255: 121-130. doi: 10.1007/164_2018_201. PMID: 30725283.
Woman grabbing her neck in pain

3 Elements of General Neck Examination

Woman grabbing her neck in pain

The evaluation of the neck provides useful information for the dental practitioner by identifying conditions that might contribute with the oral health of the patient and the appropriate function of the masticatory system. At the same time, it constitutes a triage, which allows for a timely referral. There are three elements to consider in the general neck examination: history, clinical examination, and imaging.

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During the interview, the patient should be specifically asked about neck pain, mobility, sounds, and if there is history of any trauma in the head. An example is a whiplash injury produced during a motor vehicle accident. Positive responses might alert the clinician of the possibility of having a patient with cervical arthritis or muscle contractions, with limitations to position the head for dental treatment.

It is also useful to ask about persistent contraction or pain in the shoulders, to identify a patient with stress, who will require some modifications during the regular dental care, such as shorter appointments and behavioral techniques to reduce the anxiety.

Another good question during the examination is the size of the neck. Usually the patients will know that number for clothing purposes. This will allow the clinician to consider the possibility of sleep apnea (17 inches or more might be related with Obstructive Sleep Apnea).


Clinical Examination

A way to perform the evaluation is to start with neck movements and then address the neck by sections (anterior, lateral and posterior).

Neck Range of Motion

Ask the patient to gently bend forward, rotate the head, and side-bend to each side. Observe if the movements are symmetrical and if the range of motion is near normal parameters. Bending forward or cervical flexion is usually 70-80 degrees; cervical rotation might reach 90 degrees; and side-bending is usually 40-50 degrees). A restriction in the range of motion might indicate pain, muscle contraction, cervical nerve root impingement, or even a neurological condition and the patient has to be referred for proper diagnostic work-up.

Evaluation of the Anterior Section of the Neck

Start in the midline by assessing the thyroid gland, and by palpation identifying position, asymmetry, or enlargement. The patient might have a scar from a surgical procedure. Patients with thyroid problems are more prone to some oral diseases. Interdisciplinary care with the endocrinologist will be required in many cases.

The auscultation of the carotid artery is not a common practice in dentistry, but if palpation of the bifurcation area produces pain, one possible diagnosis is carotidynia, it might be the cause of facial neuralgic pain. In the anterior region, submental and supraclavicular nodes examination would identify tender or enlarge lymph nodes, requiring to rule out infections or neoplasms.

Evaluation of the lateral section of the neck

There are several neck muscles that closely relate to mandibular function and posture, such as the sternocleidomastoid (SCM) and the upper trapezius. During the lateral exam of the neck, palpation of those two muscles might be evidence of referral pain to the face (myofascial pain), being the source of pain that could be confused with odontalgia.

In between the SCM and trapezius, the scalene muscles are in close proximity with the brachial plexus, and some patients might experience a compression of that nerve bundle, producing numbness in the arm and lower pulse rate (thoracic outlet syndrome or TOS).

In the lateral region, the identification of tender or enlarged lymph nodes (cervical or
submandibular) will indicate the possibility of infections or even neoplastic
conditions requiring further evaluation.

An anatomical structure that can be evaluated by palpation is the atlas or first cervical vertebrae. The transverse process is located inferior to the ear between the angle of the mandible and the styloid process of the temporal bone. By asking the patient to move the jaw forward, the clinician can locate the structure and assess if it is symmetric and non-painful. In case of local or referred pain, a physician should assess the patient and physical therapy might be suggested.

Evaluation of the Posterior Section of the Neck

Several muscles can be palpated, starting in the nuchal line and moving the fingers downward to the seventh vertebrae. This group of muscles are post occipital and paracervical muscles and could refer pain to the temporal region. In the nuchal area, the occipital nerves emerge from the skull, and if the patient has an occipital neuralgia, tapping on that area produces pain which travels to the frontal region.

It is important to consider that if the patient has any condition in the posterior neck, the dental chair might need to be adjusted to prevent activation of pain as the patient receives dental care. As with the other regions, the evaluation of tender or enlarged lymph nodes should be performed.



The prescription of any imaging for the neck is not in the scope of practice of dentistry; however, it is important to understand some of the options patients have.

For neck visualization, plain X-ray and ultrasound (US) are a good place to start. Plain images will provide information about general structure, presence of osteophytes, and the integrity of the intravertebral spaces. US will give information of soft tissues. It is the image of choice for salivary glands, thyroid gland, parathyroid, lymph nodes and cysts.

Advanced techniques include CT (usually with contrast) for cervical adenopathy, tumors, and any other condition where anatomic delineation is needed. An MRI will help to assess presence and extension of neurogenic tumors, vascular malformations, neck masses, and angiofibromas.

The dental professional has a great responsibility identifying alterations in the neck that might contribute with orofacial conditions or complicate dental provision.


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Man grabbing his head in pain

Physical Medicine and Primary Headache Pain Disorders

Man grabbing his head in pain

A headache can be a small effect of a bigger primary headache disorder. These disorders include migraines, tension type headaches, cluster headaches, or medication-overuse headaches.

There are treatments both with and without the use of physical medicine. Treatment methods without the use of physical medicine vary in levels of success and pain relief.

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Women grabbing her back from pain in the spine

Causes of Multiple Sclerosis

Women grabbing her back from pain in the spine

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system, specifically the brain and spinal cord. This disease affects women twice the amount as men. Onset commonly occurs between ages 20 and 50 years.

There are many negative consequences of multiple sclerosis. It is known to cause chronic neuroinflammation and demyelination. The cause of this disease remains unknown.

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Person grabbing wrist in pain from sympathetic pains

Three Types of Sympathetic Maintained Pain

Person grabbing wrist in pain from sympathetic pains

The idea that sympathetic pain exists is based on clinical findings seen in a small subset of patients suffering from neuropathic pain. Sympathetic pains occurs when the pain is clearly dependent on activity in the sympathetic nervous system. This is often referred to the ‘sympathetically maintained pains.’

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Silas Weir Mitchell, who lived from 1830 to 1914, was the first to describe sympathetically maintained pains. During the Civil War, he studied nerve injuries. He described these pathological states and causalgia.


Sympathetic pains are classified into three groups:

  1. Various Autonomic Dysfunctions
  2. NPP with sympathetic activation
  3. Complex Regional Pain Syndrome


Autonomic Dysfunctions

Autonomic dysfunctions develop when certain Autonomic Nervous System (ANS) nerves are damaged. There are multiple types of the dysfunctions. Once common type is Raynaud’s Disease.

Raynaud’s Disease is characterized by constriction of the blood vessels. It can be caused or provoked by exposure to cold or extreme emotional stress.

Related Reading: Does Emotional Approach Coping Ease Chronic Pain?


Complex Neuropathic Pain

Complex Neuropathic Pain (NPP with sympathetic activation) occurs when the pain is clearly aggravated by the sympathetic nervous system. For example, stress makes the pain more severe, and there is an enhanced vasoconstriction reaction associated with the
pain. Complex NPP is sometimes described as sympathetic maintained pain and is distinguished from CRPS in that SMP is not as severe and does not meet all of the criteria for CRPS-I or CRPS-II.

Related Reading: RGS4 Protein May Help Play a Role in Chronic Pain Maintenance


Complex Regional Pain Syndrome

There are two types of Complex Regional Pain Syndrome. The first is called Reflex Sympathetic Dystrophy (CRPS – I), commonly caused by an innocuous injury. The symptoms vary in duration and can develop over weeks or months. Sometimes, no symptoms can be identified. In CRPS – I, genetic predisposition is likely.

The second type is Causalgia (CRPS – II). This is caused by a clearcut nerve trunk injury. The onset of symptoms is immediate and obvious after the injury. The symptoms in CRPS – II are more severe than the symptoms of CRPS – I. Genetic predisposition is likely.

Related Reading: Understanding Complex Regional Pain Syndrome (CRPS)


Clinical Features of Sympathetic Pains

  • Allodynia (vibrational or thermal)
  • Disproportionate pain to injury
  • Periphery pain that spreads centrally
  • Contralateral side involvement
  • Color changes in affected limbs
  • Sweating in affected limbs
  • Cold periphery with vasoconstriction in affected limbs
  • Piloerection

Related Reading: Does Self-Compassion Help with Chronic Pain Management?


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Woman sitting outside grabbing her jaw in pain

Alternative Medications to Uncommon TMJ Disorders

Woman sitting outside grabbing her jaw in pain

Motor Neurectomy

Motor neurectomy involves identifying the select branches of the motor nerve and perform radiofrequency lysis of the motor nerve itself. This will denervate a portion of the motor nerve and cause a resulting atrophy of the muscle. The area of the muscle that atrophies produce is irregular, and the resulting shape of the muscle is non-cosmetically acceptable.

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Man holding jaw in pain due to jaw disorder

Ankylosis and Facial Asymmetry Disorders

Man holding jaw in pain due to jaw disorder

High Condylectomy & Temporal Fascia Graft

In cases where the jaw opening ability is severely compromised due to ankylosis, it is necessary to perform surgical treatment of the TM joint. This involves a high condylectomy (removing approximately 4 mm on top of condyle) and grafting tissue between the bone components. In most cases, the oral surgeon will place an interposition autologous graft between the fossa and remaining portion of the condyle to prevent adhesion or re-ankylosis. One successful graft is a piece of temporal muscle fascia, although other autologous grafts have been used.

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Man grabs his face in pain from his jaw

7 Imaging-Based Diagnostic Tests for TMJ Disorders

1. Jaw Bone Scan with Radionucleotide

Bone scans are utilized to assess bone tissue growth. It is an older technology and less specific technology (2D) than SPECT (3D), but it still has a role in diagnosis of bone scan. After the injection of the nucleotide, a gamma camera is used to capture the radiation emitted by the radiotracer (nucleotide) and generates a representative two-dimensional image of the uptake. This method is used to determine if a TMJ lesion, such as osteochondroma, is still actively growing.

Continue reading 7 Imaging-Based Diagnostic Tests for TMJ Disorders