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What a Pain! by Dr. Seena Patel

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Categories: Oral Pathology, Pharmacology, and Cariology;
What a Pain! 

Quiz: Can you correctly diagnose the nondental causes of these patients’ tooth pains?

by Dr. Seena Patel

Cases of pain affecting the dentition and periodontium usually involve straightforward diagnoses because they often present with a clear source of pathology and positive findings on diagnostic tests. However, how do you approach the patient who presents with pain in the tooth with no signs of dental, pulpal or periodontal pathology? Nondental sources of tooth pain can lead to misdiagnoses, inappropriate and unnecessary dental procedures and a potential for pain exacerbation. Therefore, you as the dentist must be aware of such diagnoses to provide patients with the right treatment. Let’s see if you can correctly identify what kind of non-odontogenic pains each of these cases present with.

Case 1
A 35-year-old female presented to the dental clinic with a chief complaint of pain on #10. The pain had been present for many years, and previous treatments included two root canal therapies and an extraction followed by implant placement. The pain persisted and was described as a “severe pressure” type of pain that became constant and daily, rated at 9/10 on a pain severity scale. Bruxism increased the pain, and the patient reported both day and night parafunction.

The #10 implant site did not show any periimplant abnormalities or pathology in the gingival or alveolar bone regions. A musculoskeletal exam was performed, which showed severe pain on palpation of the temporomandibular joints (TMJs), superficial masseters, anterior temporalis, sternocleidomastoid and upper trapezius muscles. Interestingly, when the patient’s left anterior temporalis was palpated, the pain referred down her head and toward her anterior teeth, on the left side.

A diagnostic trigger-point injection was performed on the left anterior temporalis muscle using 0.5 cc of 1% xylocaine plain, followed by spray and stretch. Her reported pain level went from 9/10 to 3/10 at the #10 region.

Diagnosis: Myofascial pain-induced toothache
Myofascial pain is a type of regional pain disorder characterized by the presence of trigger points in the affected muscles. These trigger points are taut bands that refer pain to a distant site. The pain referral occurs shortly after palpating the trigger point.

Clinical symptoms of myofascial pain include dull, aching pain; stiffness; reduced range of motion; and muscle fatigue on sustained function. When the masticatory muscles are involved, the pain can refer into the teeth, mimicking odontogenic pains.

Treatments for myofascial pain include a combination of counseling to reduce overloading the jaw muscles and TMJs, stretching exercises, use of moist heat and/or ice, physical therapy, occlusal orthotics, trigger point injections and a short-term muscle relaxant. For simpler, more acute pains, fewer treatments are needed, while a multidisciplinary approach may be needed for chronic pain, particularly when multiple sites are involved (e.g., headaches, neck pain and jaw pain).

Clinical pearl: Pain quality is an important factor in detecting myofascial pain-induced toothache. Understanding the referral patterns of the masticatory and cervical muscles is helpful in the diagnostic process. Also, it’s important to look for other comorbidities such as a history of TMD, neck pain, tension-type headaches, migraines and unexplained otologic symptoms.

Case 2
A 57-year-old male presented to the orofacial pain clinic with a chief complaint of pain on Tooth #30 and the right jaw region. The patient had several, short-lived attacks throughout the day and the pain—described as “sharp,” “stabbing” and “electric-shock-like,” with a severity of 10/10—would last one or two seconds and radiate into the tongue, chin and sinus. Chewing, talking and brushing his teeth would worsen the symptoms. Odontogenic causes of pain had been ruled out by the patient’s dentist, and his musculoskeletal exam was unremarkable. A cone-beam CT scan of the TMJs was also unremarkable. His medical history was noncontributory.

Diagnosis: Trigeminal neuralgia (TN)
TN is an incredibly painful condition that can affect any of the branches of the trigeminal nerve. It usually affects V2 or V3, and rarely affects V1. Symptoms are typically unilateral. The pain is classically described as an episodic, sharp, stabbing or electric-shock-like pain and is short-lived, lasting a few seconds to a maximum of two minutes. In addition, the pain is triggered by nonpainful stimuli, such as washing the face, air touching the face, shaving, brushing the teeth or chewing. Many patients exhibit symptoms affecting the teeth and undergo dental procedures in attempts to resolve the pain.

TN is classified as classical, secondary or idiopathic. Classical TN involves vascular compression of the trigeminal nerve root, usually by the superior cerebellar artery. Secondary TN occurs because of a neurologic disease, such as an intracranial lesion or multiple sclerosis. When a cause cannot be identified, TN is classified as idiopathic.

Patients with TN must have an MRI of the brain to identify any secondary causes for pain, because up to 15% of patients can exhibit a structural abnormality. TN typically presents in older individuals (ages >50–60), so if TN symptoms are noted in younger individuals, they must be referred to a neurologist for a comprehensive evaluation. In addition, patients should be referred to the neurologist if the symptoms are bilateral. In younger patients with bilateral symptoms, there is a suspicion for multiple sclerosis.

The pathophysiology of classical TN is hypothesized to involve demyelination of the affected nerve, which is caused by vascular compression. Because of this compression injury, spontaneous action potentials and cross-talk of the nearby nerves occur.

First-line management involves medications. Carbamazepine is FDA-approved for the management of trigeminal neuralgia. Carbamazepine and oxcarbazepine are sodium channel blockers that can reduce the pain from TN. Second-line medications include baclofen, lamotrigine, phenytoin, gabapentin, pregabalin, topiramate, zonisamide and levetiracetam. It is important to be aware of side effects of these medications before prescribing. In addition, blood lab monitoring is necessary for patients taking carbamazepine or oxcarbazepine. Patients who cannot tolerate the medications or whose pain becomes refractory can be referred to a neurosurgeon for microvascular decompression. Gammaknife radiation is another treatment for TN.

Clinical pearl: The pain description is key in the diagnosis of TN and easily distinguishes it from typical dental pains. In addition, unlike dental pains, TN does not usually wake a patient up from their sleep.

Case 3
A 25-year-old male presented to the orofacial pain clinic with a history of an intermittent, severe, sharp pain that began in the mouth on the left side, then affected the left side of the face, head and TMJ. During the initial consultation visit, he described the pain as “sharp” and “achy” and pointed to the left masseter as the site of pain. Because the pain had begun in the mouth, he first visited his dentist and had some restorations placed, but the pain persisted, so he then consulted with an endodontist. No odontogenic causes to the pain were found. Over time, the pain worsened, occuring one or two times per week and lasting all day.

The patient reported the pain severity to be 9/10 and that he needed to sleep when the pain is so severe. His jaw pain was associated with headaches on the left jaw, temporal and sinus regions, and with photoand phonophobia, nausea and vomiting. Occasionally, he also experienced sharp, shooting pains lasting one minute on the upper left jaw, which would then radiate upward.

The patient’s musculoskeletal exam was unremarkable and showed a normal range of motion and no joint noises in the TMJs. The only remarkable findings on palpation of the head, neck and jaw structures were moderate tenderness on the left dorsal TMJ capsule, with mild pain on the left lateral TMJ capsule, the left superficial masseter, the left occipital nerve region and the left posterior temporalis. His CBCT was unremarkable for joint abnormalities, and his mother reported having migraines.

Diagnosis: Episodic migraine
This patient’s symptoms were related to migraine that also involved the facial region. As a diagnostic test, he was prescribed a trial of sumatriptan, a migraine-specific abortive medication. His pain was completely resolved after two hours.

Migraine is a primary headache disorder that is classified as a type of neurovascular pain. It affects 18% of women and 6.5% of men. The diagnostic criteria for migraine include:
  • The patient has at least five pain attacks.
  • The headache, when untreated, lasts between four and 72 hours.
  • The headache exhibits at least two of the following conditions: unilateral, pulsating, moderate or severe pain, and aggravated by or causing avoidance of physical activity.
  • During the headache, the patient experiences one of the following: nausea and/or vomiting, and photophobia and phonophobia.
While uncommon, patients can experience migraine in the V2 and V3 distributions, and this is known as orofacial migraine. Pain can involve the teeth, jaws, sinuses and the ears. Autonomic symptoms may also accompany the migraine.

In some, migraine begins with a prodrome phase, during which a patient can experience fatigue, depression, difficulty concentrating, neck stiffness, blurry vision, nausea, light and sound sensitivity and osmophobia. The prodrome starts a few hours to two days before the headache.

In 30% of patients with migraine, an aura occurs, which immediately precedes the headache and can last five to 60 minutes. The classic aura is a visual disturbance but can also include sensory and speech dysfunction. It’s important to remember that the aura is completely reversible. Then, the headache occurs, after which there is the postdrome phase, when the patient feels very tired and may also experience a lower-intensity headache.

The pathophysiology of migraine is not completely understood, but current understanding explains that in migraine, the dural trigeminovascular system is activated. Both peripheral and central mechanisms are at play. When migraine is triggered, trigeminal afferents in the dura are stimulated and secrete specific neurotransmitters that act on the dural vasculature, ultimately leading to vasodilation and inflammation. This causes pain and leads to central activation in the trigeminal nucleus, where painful neurotransmitters are released, leading to sterile neurogenic inflammation.

Because of the trigeminocervical inputs to the trigeminal nucleus caudalis, symptoms of neck pain and jaw pain can accompany the migraine. In addition, pain modulatory pathways in the central nervous system can be dysfunctional in those with migraine.

Migraine management depends on attack frequency and disability. Abortive medications can be used as needed for migraine attacks. These include over-the-counter analgesics, the triptan class of medications, and calcitonin gene-related peptide (CGRP) antagonists. For frequent migraines, preventive therapy is recommended. These include medications, supplements and injections. Preventive medications include anticonvulsants, beta-blockers, tricyclic antidepressants, CGRP antagonists and onabotulinum toxin injections. In addition, trigeminal and occipital nerve blocks can be helpful.

Clinical pearl: Migraine presents with specific clinical features that are easily differentiated from odontogenic pains. It is also important to recognize that sinusitis-like symptoms often accompany migraine and can lead to a misdiagnosis of sinusitis in these patients.

Case 4
A 74-year-old man presented to the dental clinic with severe, episodic, sharp, pulsating and short-lived pains in the left V2 and V3 distributions (jumping from upper left and lower left gingiva). This began three days before the consult, triggered by innocuous things like cold air. The patient also reported pain on the left temporal region and that the upper left lip felt swollen. During the consultation, the patient experienced these episodic, severe pains and visibly expressed his distress.

The oral exam showed multiple clusters of ulcerations on the left buccal mucosa and left hard palate. Over time, the patient developed vesicles on the skin of the left V2 distribution and an erosion on the upper left lip vermilion. The patient was unaware of the oral lesions at his initial consult. His dentist pointed them out, and his only reported symptom was pain.

Light touch and pinprick sensation to cranial nerve #5 were normal when tested extraorally. Cranial nerve 7 functions were also normal.
Patel Dental Pain Diagnosis
Fig. 1
Patel Dental Pain Diagnosis
Fig. 2
Patel Dental Pain Diagnosis
Fig. 3


Diagnosis: Herpes zoster virus (HZV, “shingles”)
HZV infection occurs as a result of the reactivation of varicella-zoster virus. Symptoms occur along the distribution of the involved sensory nerve. The most common sites of involvement are the thoracic dermatomes. When it affects the trigeminal nerve distribution, #6 is the most commonly involved.

The clinical presentation of HZV infection occurs through three phases: the prodrome, the acute phase and the chronic phase. In the prodrome, symptoms involve neuralgic pain and may include constitutional symptoms. During the acute phase, patients experience the rash, which presents as clusters of vesicles with an underlying erythematous base. This rash will involve the distribution of the nerve involved and stops at the midline. After about one week, the vesicles form into crusted lesions. It is important to note that the patient is contagious until these crusts develop. It can take two to three weeks for lesion resolution in immunocompetent patients. The rash can leave a scar and hypo- or hyperpigmentation of the affected skin. In some patients, chronic pain can develop, which is postherpetic neuralgia.

When there is intraoral involvement, there is usually skin involvement as well. Intraoral lesions can present on either or both keratinized or nonkeratinized tissue. Intraorally, small vesicles develop and break into ulcerations. In some cases, the teeth in that distribution can develop pulpal disease, pulpal calcification or root resorption. In addition, osteonecrosis and tooth loss may occur.

The treatment of HZV is to prescribe antivirals promptly, along with palliative treatment for pain relief. The optimal time for antiviral administration is within the first three days after the first vesicle forms.

The following are the regimens for antiviral treatment:
  • Acyclovir: 800 mg five times per day for seven days.
  • Valacyclovir: 1 g three times per day for seven days.
  • Famciclovir: 500 mg three times for seven days
Analgesics such as NSAIDs, acetaminophen, tricyclic antidepressants, antiepileptics or systemic corticosteroids are also recommended. In this case, the patient was successfully treated with acyclovir. Gabapentin was added for pain relief, and the patient noticed significant improvement in pain. Gabapentin was continued after completion of the acyclovir because the patient continued to have pain. He was then monitored by his physician for pain relief assessment and the decision for when he could taper off gabapentin.

Clinical pearl: Prompt recognition is critical. HZV in the trigeminal distribution is uncommon, but the symptoms are severe, so early intervention is impactful.

Case 5
A 72-year-old woman presents to the orofacial pain clinic with a chief complaint of persistent pain by #10 and #11. The pain began in #11, for which she reported have three root canal treatments. The pain persisted, and the patient admitted to insisting that her oral surgeon extract #11, which she says helped the pain. Subsequently, the pain began on #10, for which she had root canal therapy. The pain quality then changed and felt “aching and nagging.” The pain is daily and constant, and the patient reports relief with ibuprofen. She has also reported tension-type headache and ear pain on the left side.

Her medical history is remarkable for chronic back and neck pain, and her exam showed comorbid TMD. There were no odontogenic causes identified.

Diagnosis: Post-traumatic trigeminal neuropathic pain (PTTN)
PTTN occurs in the distribution of the trigeminal nerve that has sustained some type of injury, which can be from mechanical, thermal, radiation or chemical causes. Usually, the pain occurs after an invasive dental procedure, such as endodontic therapy or extraction. It is estimated that PTTN can occur in 3%–5% of patients treated with root canal therapy. The injury can cause deafferentation, which can lead to peripheral nerve damage.

The pain quality is different from the initial odontogenic-related pain that the tooth presented with, and can be described as dull, aching or burning. The pain is also continuous.

Patients can also present with allodynia or hyperalgesia. Clinical exam findings are unremarkable for any local pathologies. Mechanosensory testing and diagnostic anesthesia are helpful techniques in the diagnosis of PTTN.

If the pain can be blocked with topical anesthetic, the patient may be a candidate for management with topical medications; if not, systemic management with neuropathic pain medications is necessary. Management can be challenging, and the prognosis is guarded.

Risk factors for PTTN include:
  • Higher pain intensity and longer pain duration before the endodontic or surgical procedure.
  • The presence of percussion sensitivity on the tooth before treatment.
  • A more invasive and lengthier procedure.
  • Higher pain levels during the procedure.
  • A medical history remarkable for chronic pain problems.
  • The presence of psychological comorbidities, such as anxiety, depression, somatization and catastrophic attitude.
  • Female gender.
  • Older age.
  • A haplotype for catecholamine-O-methyltransferase.
Clinical pearls: Perform a risk assessment before the procedure and obtain a thorough informed consent. If the dentist cannot find odontogenic pathologies to confirm the pain, consult with an orofacial pain specialist before performing any additional dental procedures.

Conclusion
Non-odontogenic pains can be complex and challenging, but understanding the various sources of such pains will help clinicians make more accurate diagnoses and, most importantly, avoid unnecessary invasive and irreversible dental procedures. It is important to communicate these causes with the patient and work with an orofacial pain specialist to help manage these cases.

References
Baad-Hansen L, Benoliel R. Neuropathic orofacial pain: Facts and fiction. Cephalalgia. 2017 Jun; 37(7):670–679.

Kim ST. Myofascial pain and toothaches. Aust Endod J 2005; 31(3):106–110.

Simons DG, Travell JG, Simons LS. Travell & Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual: Upper Half of Body (Vol. 1). Philadelphia: Lippincott Williams & Wilkins, 1999.

International Classification of Orofacial Pain, 1st edition (ICOP). Cephalalgia. 2020; 40(2):129–221.

Klasser GD, Reyes MR, American Academy of Orofacial Pain. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management 7th Edition. Quintessence Publishing. 2023.

Clark GT, Padilla M, Dionne R. Medication treatment efficacy and chronic orofacial pain. Oral Maxillofac Surg: Clin North Am. 2016; 28(3):409–21.

Sharav Y, Katsarava Z, Charles A. Facial presentations of primary headache disorders. Cephalalgia. 2017; 37(7):714–19.

Clark GT. Persistent orodental pain, atypical odontalgia, and phantom tooth pain: When are they neuropathic disorders? J Calif Dent Assoc; 2006; 34(8):599–609.

Gronseth G, et al. Practice parameter: the diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review): Report of the quality standards subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies. Neurology. 2008; 71(15):1183–1190.

Author Bio
Seena Patel Seena Patel, DMD, MPH, is the director of oral medicine and an associate professor at A.T. Still University’s Arizona School of Dentistry & Oral Health (ATSU-ASDOH). Patel is also an associate at Southwest Orofacial Group in Phoenix, practicing orofacial pain, oral medicine and dental sleep medicine since 2012. A diplomate of the American Board of Orofacial Pain and the American Board of Oral Medicine, she earned her DMD and MPH degrees from ATSU-ASDOH and completed her residency in orofacial pain and oral medicine at the Herman Ostrow School of Dentistry at the University of Southern California.
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