ABOP Orofacial Pain cheat sheet

Trigeminal nerve: V1 ophthalmic, V2 maxillary, V3 mandibular; V3 is the only division carrying motor fibers (muscles of mastication, mylohyoid, anterior digastric, tensor tympani, tensor veli palatini).

TMJ is a synovial, ginglymoarthrodial joint with a fibrocartilaginous (not hyaline) disc; rotation occurs in the lower compartment, translation in the upper compartment.

Lateral pterygoid is the primary jaw opener via its inferior head; the superior head attaches to the disc and is active during clenching.

Normal maximum interincisal opening is approximately 40-50 mm; lateral and protrusive excursions are each about 8-12 mm.

Temporomandibular ligament limits excessive translation; sphenomandibular and stylomandibular ligaments are accessory restraints.

Pulp and periodontal ligament are densely innervated by A-delta and C fibers; pulpal A-delta fibers are activated by rapid fluid shifts (hydrodynamic theory).

Cranial nerve VII supplies facial expression and taste to the anterior two-thirds of the tongue via chorda tympani; CN IX supplies posterior third taste and gag reflex.

Orofacial pain afferents project to the spinal trigeminal nucleus (pars oralis, interpolaris, caudalis); pars caudalis is the principal relay homologous to the dorsal horn.

Nociceptors: A-delta fibers are thinly myelinated, fast, sharp/first pain; C fibers are unmyelinated, slow, dull/second pain.

Peripheral sensitization: inflammatory mediators (bradykinin, prostaglandins, substance P, CGRP, NGF) lower nociceptor threshold and increase firing.

Central sensitization: NMDA receptor-dependent wind-up, increased dorsal horn excitability, and expansion of receptive fields produce hyperalgesia and allodynia.

Descending modulation: periaqueductal gray to rostral ventromedial medulla (serotonergic/noradrenergic) can inhibit or facilitate nociception.

Gate control theory: large-fiber (A-beta) input and descending inhibition can suppress small-fiber nociceptive transmission in the dorsal horn.

Referred pain occurs when visceral or deep afferents converge on the same second-order neurons as cutaneous afferents (convergence-projection).

Neuropathic pain arises from a lesion or disease of the somatosensory system; nociceptive pain arises from actual or threatened tissue damage.

Ectopic impulse generation after nerve injury results from altered sodium channel expression (e.g., Nav1.7, Nav1.8) at neuromas and injured axons.

DC/TMD axis I groups: pain disorders (myalgia, arthralgia, headache attributed to TMD), intra-articular disorders (disc displacement with/without reduction), and degenerative joint disease.

Disc displacement with reduction: reciprocal click, normal opening; with reduction and intermittent locking adds episodic limited opening.

Disc displacement without reduction: limited opening (<40 mm), deviation to the affected side, history of click that ceased.

Myofascial pain is diagnosed by palpation reproducing familiar pain in masticatory muscles; referred pain patterns distinguish it from local myalgia.

Arthralgia requires pain in the joint region plus pain on palpation or function; crepitus suggests degenerative joint disease (osteoarthritis).

Axis II of the DC/TMD assesses pain-related disability (GCPS) and psychological status (PHQ-4, JFLS) to guide management.

First-line conservative care: education, self-management, jaw exercises, and short-term NSAIDs; irreversible occlusal or surgical treatment is reserved for refractory cases.

Imaging: panoramic or CBCT for osseous changes; MRI is the reference standard for disc position and effusion.

ICHD-3 migraine: 4-72 h, unilateral, pulsating, moderate-severe, aggravated by activity, with nausea and/or photo/phonophobia.

Tension-type headache: bilateral, pressing/tightening, mild-moderate, not aggravated by routine activity, no vomiting.

Cluster headache: severe unilateral orbital/temporal pain with ipsilateral autonomic signs (lacrimation, rhinorrhea, ptosis, miosis), 15-180 min.

Trigeminal autonomic cephalalgias include cluster, paroxysmal hemicrania (indomethacin-responsive), and SUNCT/SUNA.

Headache attributed to TMD is reproduced by palpation of the temporalis or masseter and confirmed by resolution after TMD treatment.

Giant cell arteritis: age >50, new headache, jaw claudication, elevated ESR/CRP; urgent corticosteroids to prevent vision loss.

Red flags (SNOOP): systemic symptoms, neurologic signs, sudden onset, older age, pattern change - prompt imaging or referral.

Post-traumatic headache is classified by temporal relationship to head/neck injury; persistence beyond 3 months defines the chronic form.

Trigeminal neuralgia: paroxysmal, electric-shock-like, unilateral, triggered by light touch; classic type has neurovascular compression at the root entry zone.

First-line pharmacotherapy for trigeminal neuralgia is carbamazepine or oxcarbazepine; baclofen or lamotrigine are adjuncts.

Trigeminal neuropathic pain (painful post-traumatic trigeminal neuropathy) is constant, burning, and associated with sensory loss after injury.

Burning mouth syndrome: intraoral burning with normal mucosa and no identifiable cause; consider secondary causes (B12, iron, folate, diabetes, candidiasis, xerostomia).

Postherpetic neuralgia follows varicella-zoster reactivation in a dermatomal distribution; gabapentinoids or tricyclics are first-line.

Persistent idiopathic facial pain is continuous, poorly localized, and not explained by another disorder; it is a diagnosis of exclusion.

Atypical odontalgia is neuropathic dental pain in an intact tooth; repeated endodontic or surgical treatment typically worsens symptoms.

Neurovascular pains (migraine, cluster) involve trigeminovascular activation with CGRP release; triptans and gepants target this pathway.

Bruxism is classified as sleep (SB) or awake (AB); SB is diagnosed by EMG or by report plus clinical findings, not by tooth wear alone.

Sleep bruxism is associated with arousals and often coexists with obstructive sleep apnea; treating apnea may reduce bruxism.

Obstructive sleep apnea: recurrent upper airway collapse with apneas/hypopneas; STOP-BANG is a screening tool.

First-line therapy for OSA is CPAP; oral appliances (mandibular advancement devices) are alternatives for mild-moderate OSA.

Mandibular advancement devices advance the mandible to enlarge the airway; adverse effects include dental movement and TMJ discomfort.

Insomnia disorder and poor sleep quality amplify pain sensitivity and are risk factors for chronic TMD and headache.

Sleep-related headaches (e.g., hypnic headache) occur only during sleep; hypnic headache is typically in older adults.

Polysomnography is the reference standard for diagnosing sleep apnea and sleep-related movement disorders.

Comprehensive history: onset, location, quality, duration, triggers, associated symptoms, prior treatments, and psychosocial factors.

Clinical exam includes palpation of masticatory and cervical muscles, TMJ palpation, range-of-motion measurement, and joint sound auscultation.

Range of motion: maximum opening ~40-50 mm; measure lateral and protrusive excursions (~8-12 mm) and note deviation.

Diagnostic imaging: CBCT for osseous structures; MRI for disc position and joint effusion; panoramic radiograph for broad osseous survey.

DC/TMD provides validated axis I diagnostic criteria and axis II psychosocial screening instruments.

Differential diagnosis must exclude odontogenic, sinus, vascular, neurologic, and neoplastic causes before attributing pain to TMD.

Quantitative sensory testing and diagnostic blocks can help localize neuropathic pain sources.

Document psychosocial screeners (PHQ-4, GCPS) to guide multidisciplinary management.

NSAIDs (e.g., ibuprofen, naproxen) are first-line for acute TMD pain; limit duration and screen for GI/renal/cardiovascular risk.

Muscle relaxants and benzodiazepines have limited short-term roles; avoid long-term use due to dependence.

Tricyclic antidepressants (amitriptyline, nortriptyline) are used for chronic pain and sleep; monitor anticholinergic effects.

Gabapentinoids are used for neuropathic pain; titrate slowly and monitor sedation.

Carbamazepine is first-line for trigeminal neuralgia; monitor for hyponatremia and drug interactions.

Non-pharmacologic: education, self-management, jaw exercises, physical therapy, cognitive behavioral therapy, and occlusal appliances.

Occlusal splints may reduce pain in some patients; irreversible occlusal adjustment is not recommended as routine care.

Interventional options (trigger point injections, botulinum toxin) are considered when conservative care fails.

Biopsychosocial model: pain results from interacting biological, psychological, and social factors; assess all three domains.

Axis II of DC/TMD screens for pain-related disability (GCPS) and psychological distress (PHQ-4, JFLS).

Cognitive behavioral therapy reduces pain catastrophizing and improves coping in chronic TMD and orofacial pain.

Multidisciplinary teams (dentistry, medicine, psychology, physical therapy) improve outcomes in complex chronic pain.

Patient education and self-management are core components of first-line care for TMD.

Screen for depression, anxiety, and sleep disturbance as they amplify pain and affect treatment response.

Motivational interviewing supports adherence to self-management and behavioral change.

Referral to mental health or pain specialists is indicated when psychosocial factors dominate the clinical picture.