Dental pain is a common complaint encountered in dental clinics. While most cases stem from obvious dental issues like caries, periodontitis, or trauma, a significant number of patients experience dental pain originating from non-dental sources. Diagnosing these atypical cases can be challenging for clinicians. This article aims to shed light on non-odontogenic dental pain, offering a comprehensive guide to diagnosis and management, utilizing a practical Dental Pain Diagnosis Chart. We will explore various categories of non-dental toothache through illustrative case reports, enhancing your understanding and diagnostic capabilities.
CASE REPORTS
Patient 1: Referred Pain from Muscle Trigger Points
A 28-year-old female presented with a peculiar complaint: “My lower front teeth hurt.” Clinical examination revealed no signs of caries, periodontitis, or occlusal issues. Radiographic examination further confirmed the absence of dental fractures or any other dental pathologies (Fig. 1). Notably, there was no pain upon percussion or palpation of the teeth.
Local anesthesia of the periapical gingivae of the mandibular central incisors through infiltration failed to alleviate her pain. Considering the possibility of non-dental origin, we employed a dental pain diagnosis chart (Fig. 2) to systematically evaluate potential causes, particularly referred pain and neuromodulation. The patient described the pain as a dull ache rather than throbbing, ruling out cluster headaches. She denied any history of depression but mentioned increased work-related stress recently. Palpation of the digastric muscle, both externally and intraorally, revealed a distinct trigger point. Upon pressing this specific point, the patient exclaimed, “I feel it in my tooth! That’s exactly where it hurts!”. This pinpointed the digastric muscle as the source of referred pain to her mandibular central incisors.
Treatment for muscle-referred pain involves physical therapy techniques such as neck stretches and rotations, combined with gentle massage of the trigger points. Non-steroidal anti-inflammatory drugs (NSAIDs) can be prescribed to manage inflammation associated with muscle fatigue. If pain persists despite NSAIDs, tricyclic antidepressants like amitriptyline can be considered. Amitriptyline enhances descending pain inhibition, effectively dampening pain transmission. It also exhibits analgesic properties through sodium channel blockade and opioid receptor modulation, proving particularly effective for muscle-referred pain. However, potential side effects like dizziness, dry mouth, and palpitations must be thoroughly discussed with the patient before prescription. A low starting dose of 10 mg/day is recommended, with gradual increments while monitoring both therapeutic and adverse effects.
Referred pain from muscles is a surprisingly frequent cause of non-odontogenic dental pain. Temporal muscle trigger points commonly refer pain to upper molars, while masseter muscle trigger points often manifest as lower molar pain. While local anesthetic or saline injections into trigger points of temporal or masseter muscles can be therapeutic, this approach is less feasible for the digastric muscle. Other treatment modalities include acupuncture, near-infrared therapy, centrally acting muscle relaxants, and occlusal splint therapy.
Patient 2: Neuromodulation and Persistent Post-Pulpectomy Pain
A 45-year-old woman presented with continuous, deep, throbbing dental pain in the left maxillary second premolar region. Despite undergoing pulpectomy of the affected tooth, the pain persisted. Subsequent root canal treatments also failed to provide relief, and the pain had been present for six months post-pulpectomy. Clinical examination showed no issues with the temporary filling, and there was no percussion pain or pain upon reamer insertion. Field-block anesthesia of the left first premolar and local anesthetic injection into the root canal offered insufficient pain relief. Utilizing the dental pain diagnosis chart (Fig. 3), we again considered referred pain and neuromodulation. The patient’s pain was not pulsating, and she lacked other cluster headache symptoms. She reported fatigue due to chronic pain, and psychological testing using the Hospital Anxiety and Depression Scale yielded a false-positive result for depression, likely due to her pain-related distress. No trigger points were found in the masticatory muscles. Based on these findings, a diagnosis of Category 2 neuromodulation-related pain was made (Fig. 3).
Amitriptyline was chosen for treatment. Starting at 10 mg/day, the dosage was gradually increased to 60 mg/day over 40 days. Remarkably, the pain was completely controlled at this dosage. Fifty-three days after the initial examination, the root canal was successfully filled without complications (Fig. 4). Amitriptyline was continued at 60mg/day for ten months, followed by a gradual taper. After one year and two months, the medication was discontinued, and the patient remained pain-free. This case exemplifies “atypical odontalgia,” now understood as pain arising from neuromodulation, for which tricyclic antidepressants are highly effective.
Patient 3: Neuropathic Phantom Tooth Pain
A 39-year-old woman complained of persistent dental pain following pulpectomy of the left mandibular second molar. Root canal treatments exacerbated the pain, which had persisted for five months, causing significant sleep disturbance. Examination revealed no issues with the temporary filling, no percussion pain, but occasional pain with reamer insertion. Local anesthesia via field block of the left mandibular second molar and local anesthetic injection into the root canal provided only temporary relief. Cone beam CT and microscopic examination revealed no dental anomalies. However, allodynia and dysesthesia were observed on the mucosa surrounding the tooth. These findings pointed towards Category 3 neuropathic pain, as indicated in the dental pain diagnosis chart (Fig. 3).
This case was diagnosed as phantom tooth pain. Treatment with carbamazepine (600 mg/day) and amitriptyline (90 mg/day) provided slow and insufficient pain relief. Other tricyclic antidepressants, the antiepileptic drug clonazepam, and mexiletine hydrochloride also proved ineffective. Intravenous ketamine, magnesium (Mg2+), and/or lidocaine offered dramatic, albeit temporary, pain relief. Continuous drip infusion of adenosine triphosphate (ATP) sustained pain relief for approximately two weeks. Therefore, the patient was placed on a regimen of bi-weekly continuous ATP drip infusions and intravenous lidocaine. ATP is rapidly metabolized to adenosine in the blood, and its analgesic effect is mediated by A1 receptors. Continuous infusion of ATP at 5-6 mg/kg/h for two hours or longer can provide significant temporary relief from phantom tooth pain [1]. The onset of effect is slow, but the duration can range from days to weeks. Notably, phantom tooth pain is not relieved by tooth extraction. In this case, the tooth was extracted ten years later due to fracture, but the pain symptoms remained unchanged. Allodynia persisted on the mucosal surfaces post-extraction (Fig. 5). The patient continues to manage her pain with bi-weekly continuous ATP or intravenous Mg2+ and lidocaine infusions, along with oral stent therapy with capsaicin cream.
DISCUSSION
Diagnosing non-odontogenic dental pain requires a thorough understanding of pain mechanisms and potential extra-dental sources. Pain serves as a crucial sensory function, alerting us to tissue damage, infection, or fatigue. Dysfunction in pain pathways can have severe consequences, as illustrated by patients with congenital insensitivity to pain (Fig. 6), who are prone to extensive injuries due to the absence of pain as a warning signal.
Pain transmission is a complex process involving peripheral sensory nerve receptors, numerous neurons, and the somatosensory cortex. Along this pathway, pain signals are modulated by various neural networks, including the descending pain inhibitory system (acting as a “brake”), the excitatory system (acting as an “accelerator”), and the emotional and sympathetic nervous systems (Fig. 7). Dysregulation of these systems, such as inhibitory system failure or excitatory system overactivity, can lead to pain perception in the absence of a direct dental pathology. This “abnormal dental pain” poses diagnostic challenges.
Based on etiology, non-odontogenic dental pain can be categorized into: (1) referred pain, (2) neuromodulation-related pain, and (3) neuropathic pain. When confronted with diagnostically challenging dental pain, clinicians should consider these alternative categories, utilizing a dental pain diagnosis chart to guide their assessment.
1. Category 1: Referred Pain – Pain Perceived Away from the Source
Referred pain manifests as pain perceived in a location distant from its origin. Dental pain of non-dental origin often falls into this category, misleading clinicians. What mechanisms underlie referred pain? Convergence of sensory information is a key factor. Afferent signals from teeth, muscles, blood vessels, and other tissues converge at synapses of trigeminal nerve neurons and the spinal trigeminal nucleus (Fig. 8). For instance, pain from masseter muscles travels through the masseteric nerve, converging at these central points. Similarly, the inferior alveolar nerve transmits signals from the mandibular molar region to the same convergence points. Persistent pain, such as chronic masseter muscle pain, can induce central sensitization, a state of neuronal hyperexcitability, effectively “pressing down the accelerator” of pain transmission. Consequently, even minor stimuli can trigger pain signals that are perceived as originating from the inferior alveolar nerve distribution, i.e., mandibular molar pain, even though the actual source is the masseter muscle (Fig. 9).
Trigger points play a crucial role in diagnosing muscle-referred dental pain. A trigger point within the masseter muscle (Fig. 10) can refer pain to the mandibular molar region. Similarly, temporal muscle trigger points (Fig. 11) can refer pain to the maxillary molar region, and digastric muscle trigger points (Fig. 12) can refer pain to the mandibular central incisors. These are termed “muscular toothaches.” Dental treatments are ineffective in these cases. Identifying trigger points by palpation and noting pain referral to the dental region is key to accurate diagnosis.
Referred pain is not limited to muscular origins. Neurovascular headaches like migraines and cluster headaches can also refer pain to teeth, termed “neurovascular toothaches.” In neurovascular headaches, neuropeptides released from trigeminal nerve endings in intracranial blood vessels induce vasodilation and inflammation, thought to be the source of pain. This mechanism can also manifest as dental pain. Migraine-related dental pain is often episodic, pulsating, and vascular, commonly affecting upper and lower premolars and upper canines. If accompanied by headache, diagnosis is relatively straightforward. However, isolated toothache presentation can be challenging, mimicking pulpitis and potentially leading to inappropriate pulpectomy.
Visceral toothache represents another form of referred pain, originating from internal organs like the heart or stomach. Cardiac toothache, for example, can occur due to angina pectoris pain referred to the teeth and may even precede the onset of overt heart disease.
2. Category 2: Neuromodulation – Pain Modulated by Psychological and Emotional Factors
Pain transmission can be significantly modulated by psychological stress and emotional fluctuations. The cerebrum, the final destination of pain signals, integrates diverse inputs, including psychological states, profoundly influencing pain perception. Chronic pain and psychological distress are thought to have a major impact on pain modulation at this central level. The sympathetic nervous system also plays a role in modulating pain transmission, and its dysregulation can contribute to severe, debilitating pain. This is often observed in patients with orofacial pain or toothache of unknown etiology referred from emergency departments. Intravenous anxiolytics or stellate ganglion blocks can provide dramatic pain relief in such cases, highlighting the role of neuromodulation.
3. Category 3: Neuropathic Pain – Pain from Nerve Pathway Dysfunction
The intricate nature of pain transmission pathways makes them vulnerable to dysfunction. Injury to a nerve pathway can disrupt normal signal transmission, leading to abnormal sensations or pain. For example, inferior alveolar nerve injury rarely results in complete recovery due to its diverse sensory fiber composition (pressure, touch, temperature, pain). Nerve regeneration post-injury can lead to “jumbled” pathways [3]. While most fine pulp nerves are primarily nociceptive, historically, procedures like pulpectomy and tooth extraction were performed with the assumption that neuropathic pain was unlikely even with nerve severance. However, post-pulpectomy or extraction neuropathic pain can indeed develop. “Phantom tooth pain” describes neuropathic pain syndromes analogous to phantom limb pain after amputation [4]. This condition can present with diagnostically perplexing pain symptoms following dental procedures.
In conclusion, this article presented three distinct cases of non-odontogenic dental pain: referred pain, neuromodulation-related pain, and neuropathic pain. The dental pain diagnosis chart proved instrumental in systematically evaluating and diagnosing each case. All patients experienced satisfactory pain relief following targeted treatment. Alleviating pain is paramount in patient care, and accurate diagnosis, guided by tools like a dental pain diagnosis chart, is crucial for effectively managing facial and dental pain complaints.
References
[1] (Original reference 1 from the article)
[2] (Original reference 2 from the article)
[3] (Original reference 3 from the article)
[4] (Original reference 4 from the article)
