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100+ Free ABOP Orofacial Pain Practice Questions

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Which primary afferent fibers mediate sharp, well-localized 'first' pain?

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to track
2026 Statistics

Key Facts: ABOP Orofacial Pain Exam

2020

ADA Specialty Recognition

Orofacial pain — 12th ADA-recognized dental specialty (March 2020)

2 yr

CODA Residency

CODA-accredited postdoctoral orofacial pain residency

~17%

Headache Disorders Weight

Largest single domain on 2026 ABOP content outline

~$2,000-$2,500

2026 Combined Fees

ABOP Written + Case Review (verify current schedule)

155 U

PREEMPT Botox Dose

Chronic migraine — 31 sites, 7 muscle groups, q12 weeks

DC/TMD 2014

TMD Diagnostic Standard

Axis I/II dual-axis diagnostic criteria for TMD

The ABOP Orofacial Pain Certification is administered by the American Board of Orofacial Pain — the certifying body for the 12th ADA-recognized dental specialty (2020). It comprises a computer-based Written examination at Pearson VUE (~4 hours, single-best-answer MCQs) plus a Case Review portfolio. Content spans headache disorders (~17%), TMD diagnosis (~15%), TMD management (~10%), neuropathic orofacial pain (~10%), pain neuroscience (~10%), pharmacology (~7%), pain assessment (~8%), sleep and bruxism (~8%), diagnostic blocks (~5%), persistent idiopathic facial pain (~5%), research (~2%), cervicogenic pain (~2%), and psychosocial/behavioral (~2%). Combined fees are approximately $2,000-$2,500; eligibility requires a CODA-accredited 2-year orofacial pain residency or a qualifying experience pathway.

Sample ABOP Orofacial Pain Practice Questions

Try these sample questions to test your ABOP Orofacial Pain exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Which primary afferent fibers mediate sharp, well-localized 'first' pain?
A.Unmyelinated C fibers
B.Thinly myelinated A-delta fibers
C.Large myelinated A-beta fibers
D.Autonomic B fibers
Explanation: A-delta fibers are thinly myelinated and conduct at 5-30 m/s, mediating rapid, sharp, well-localized 'first' pain. Unmyelinated C fibers (0.5-2 m/s) carry dull, burning 'second' pain. A-beta fibers transmit non-nociceptive touch and proprioception.
2The four classic steps of nociceptive processing are, in order:
A.Perception, modulation, transmission, transduction
B.Transmission, transduction, perception, modulation
C.Transduction, transmission, modulation, perception
D.Modulation, perception, transduction, transmission
Explanation: Nociception proceeds from transduction (noxious stimulus converted to electrical signal at peripheral terminal), to transmission (conduction along afferent to CNS), to modulation (amplification or inhibition at spinal/brainstem levels), and finally to perception (cortical interpretation).
3Which cranial nerve carries the majority of orofacial sensory input to the CNS?
A.Facial nerve (CN VII)
B.Glossopharyngeal nerve (CN IX)
C.Vagus nerve (CN X)
D.Trigeminal nerve (CN V)
Explanation: The trigeminal nerve (CN V) provides somatosensory innervation to the face, anterior scalp, oral cavity, TMJ, and dura. Its three divisions (V1 ophthalmic, V2 maxillary, V3 mandibular) converge on the trigeminal ganglion and project to the trigeminal brainstem sensory nuclear complex.
4According to Melzack and Wall's gate control theory, what modulates pain transmission at the dorsal horn?
A.Only descending cortical signals
B.Activity in large-diameter A-beta fibers inhibiting nociceptive transmission
C.Sympathetic outflow from the intermediolateral cell column
D.Peripheral prostaglandin release alone
Explanation: Gate control theory proposes that large A-beta afferent activity (touch, vibration, rubbing) excites inhibitory interneurons in the substantia gelatinosa, 'closing the gate' on nociceptive C-fiber input. This underlies the clinical rationale for TENS and counter-stimulation.
5Central sensitization in chronic orofacial pain is best characterized by:
A.Reduced peripheral nerve conduction velocity only
B.Increased responsiveness of CNS nociceptive neurons to normal or subthreshold input
C.Purely psychogenic amplification without neural substrate
D.Selective loss of A-delta fibers
Explanation: Central sensitization is an IASP-defined state of heightened CNS responsiveness, driven by NMDA receptor upregulation, loss of inhibitory tone, and synaptic plasticity. It manifests clinically as allodynia, hyperalgesia, spread of pain, and aftersensations.
6'Wind-up' refers to:
A.Habituation of second-order neurons over time
B.Progressive increase in dorsal horn neuron response to repetitive C-fiber input at constant intensity
C.Spontaneous peripheral nerve firing without stimulus
D.Sympathetically maintained pain
Explanation: Wind-up is a short-term activity-dependent facilitation of wide-dynamic-range neurons to repeated low-frequency C-fiber stimulation. It is NMDA-dependent and a precursor phenomenon to central sensitization.
7The periaqueductal gray (PAG) contributes to descending pain modulation primarily via:
A.Direct corticospinal projections to muscle
B.Projections through the rostral ventromedial medulla (RVM) to the dorsal horn
C.Cerebellar output to thalamic relay
D.Hypothalamic-pituitary axis only
Explanation: Opioid-rich PAG neurons activate the RVM, which sends serotonergic and noradrenergic fibers via the dorsolateral funiculus to the spinal and trigeminal dorsal horns, producing descending inhibition. This is a target of stimulation-produced analgesia and opioid action.
8Endogenous opioid peptides include all of the following EXCEPT:
A.Enkephalins
B.Endorphins
C.Substance P
D.Dynorphins
Explanation: Enkephalins, endorphins, and dynorphins are the three major endogenous opioid peptide families, acting at mu, delta, and kappa receptors respectively. Substance P is a pro-nociceptive neuropeptide co-released with glutamate from C fibers.
9Neuroplasticity contributing to chronic orofacial pain is supported by changes in:
A.Only peripheral receptor density
B.Cortical, thalamic, and brainstem structural and functional reorganization
C.Skeletal muscle fiber type distribution
D.Salivary gland secretion patterns
Explanation: Chronic pain is associated with gray-matter volume changes in insula, anterior cingulate, prefrontal cortex, thalamus, and brainstem, along with altered connectivity. These maladaptive plastic changes help explain pain persistence after peripheral input resolves.
10In the trigeminal brainstem sensory nuclear complex, nociceptive input from the face is processed predominantly in the:
A.Main sensory nucleus
B.Mesencephalic nucleus
C.Subnucleus caudalis of the spinal trigeminal nucleus (medullary dorsal horn)
D.Nucleus solitarius
Explanation: Subnucleus caudalis (Sp5C), also called the medullary dorsal horn, is the principal relay for nociceptive and thermal orofacial input. Its laminar organization parallels the spinal dorsal horn and contains wide-dynamic-range and nociceptive-specific neurons.

About the ABOP Orofacial Pain Exam

The ABOP Orofacial Pain Certification validates expertise in the diagnosis and management of temporomandibular disorders (TMD), headache disorders, neuropathic orofacial pain, sleep-related oromotor conditions, and associated comorbidities. Orofacial pain was recognized as the 12th ADA dental specialty in 2020. Content spans ICHD-3 headache classification (migraine, tension-type, cluster and other TACs, medication-overuse, secondary), DC/TMD 2014 Axis I/II dual-axis diagnosis, TMD management (conservative therapy, splints, arthrocentesis, TJR), neuropathic pain (trigeminal neuralgia — carbamazepine first-line, microvascular decompression, burning mouth syndrome, painful trigeminal neuropathy), pain neuroscience (central sensitization, OPPERA findings, biopsychosocial model), pharmacology (NSAIDs, TCAs, SNRIs, anticonvulsants, CGRP monoclonals — erenumab/fremanezumab/galcanezumab, gepants, PREEMPT Botox protocol, topicals, opioid stewardship), pain assessment (GCPS, PHQ-9, GAD-7, JFLS, CSI), sleep and bruxism (ICSD-3, OSA with MAD, sleep bruxism RMMA), diagnostic local anesthetic blocks, persistent idiopathic facial pain (PIFP/PIDAP), cervicogenic headache, and psychosocial/behavioral management. The examination has a Written component and a Case Review portfolio. Candidates qualify through a CODA-accredited 2-year orofacial pain residency or an experience pathway.

Questions

200 scored questions

Time Limit

Written CBT (~4 hours) + Case Review portfolio

Passing Score

Criterion-referenced scaled score set by ABOP (modified Angoff standard)

Exam Fee

~$2,000-$2,500 combined Written + Case Review fees (ABOP 2026 — verify current schedule) (American Board of Orofacial Pain (ABOP) / Pearson VUE)

ABOP Orofacial Pain Exam Content Outline

~17%

Headache Disorders

ICHD-3 classification — migraine (with/without aura, chronic migraine ≥15 days/month with ≥8 migraine days), tension-type (episodic vs chronic), trigeminal autonomic cephalalgias (cluster, paroxysmal hemicrania — indomethacin-responsive, SUNCT/SUNA, hemicrania continua — indomethacin-responsive), medication-overuse headache (≥15 days/month with overuse of acute medication), secondary headaches and red flags (SNOOP10). PREEMPT Botox protocol for chronic migraine (155 U across 31 sites, 7 muscle groups, every 12 weeks). CGRP monoclonal antibodies — erenumab (receptor), fremanezumab/galcanezumab/eptinezumab (ligand). Gepants (ubrogepant, rimegepant acute; atogepant, rimegepant prevention). Triptans and cardiovascular contraindications.

~15%

TMD Diagnosis (DC/TMD 2014)

DC/TMD 2014 Axis I/II dual-axis framework. Axis I pain: myalgia, myofascial pain with referral, arthralgia, headache attributed to TMD. Axis I intra-articular: disc displacement with reduction (± intermittent locking), disc displacement without reduction (with/without limited opening), degenerative joint disease, subluxation. Clinical exam — palpation, range of motion (normal pain-free opening ≥40 mm), joint sounds (click vs crepitus). Imaging — panoramic screening, CBCT for osseous, MRI gold standard for disc position. Axis II psychosocial — Graded Chronic Pain Scale (GCPS), PHQ-9, GAD-7, JFLS, OBC, PCS. Wilkes staging I-V of internal derangement.

~10%

TMD Management

Stepped-care, conservative/reversible first. Patient education, self-care, jaw rest, soft diet, moist heat/cold, physical therapy, postural training. Occlusal splints — stabilization (flat-plane, full-arch, nighttime) preferred; anterior repositioning selective and time-limited. Pharmacotherapy — NSAIDs, short-term muscle relaxants (cyclobenzaprine), low-dose tricyclics (amitriptyline/nortriptyline for chronic myofascial pain), gabapentinoids. Arthrocentesis and arthroscopy for persistent intra-articular pathology. Open TMJ surgery (discectomy, disc repositioning, TMJ total joint replacement — Stryker/TMJ Concepts) for end-stage disease. Intra-articular injections (corticosteroid, HA, PRP). Behavioral — CBT, biofeedback, relaxation, graded motor imagery.

~10%

Neuropathic Orofacial Pain

Classical trigeminal neuralgia — ICHD-3 criteria, paroxysmal electric-shock pain in V2/V3 most common, trigger zones, neurovascular compression (superior cerebellar artery most common). Secondary TN — MS, cerebellopontine angle tumor (imaging required in atypical features). Painful trigeminal neuropathy — post-traumatic (peripheral nerve injury, post-endodontic), post-herpetic (VZV V1 most common), idiopathic. Glossopharyngeal neuralgia. Burning mouth syndrome — primary (idiopathic) vs secondary (nutritional — B12/folate/iron/zinc, candidiasis, xerostomia, medications). Carbamazepine first-line for TN (monitor CBC, Na, hepatic; HLA-B*1502 Asian populations); oxcarbazepine second-line; baclofen and lamotrigine add-on. MVD (Jannetta procedure), gamma knife, percutaneous glycerol/balloon/RF rhizotomy.

~10%

Pain Neuroscience

Nociception (A-delta fast/sharp vs C-fiber slow/burning) vs pain experience. Peripheral sensitization (inflammatory soup — bradykinin, prostaglandins, substance P, CGRP). Central sensitization — NMDA receptor, wind-up, LTP. Descending modulation — PAG, RVM, locus coeruleus; serotonergic and noradrenergic pathways (rationale for TCAs/SNRIs in chronic pain). Gate control theory (Melzack & Wall). Trigeminal nucleus caudalis (subnucleus caudalis, medullary dorsal horn) — convergence with C2-C3 afferents explains trigeminocervical referral. OPPERA prospective cohort — identified pain amplification, psychological distress, and clinical orofacial factors as risk for first-onset TMD.

~8%

Sleep & Bruxism

ICSD-3 sleep disorders. Obstructive sleep apnea — STOP-BANG screen, Epworth Sleepiness Scale, polysomnography AHI thresholds (mild 5-14, moderate 15-29, severe ≥30). CPAP gold standard; mandibular advancement device (MAD) for mild-moderate OSA or CPAP-intolerant — titration, side effects (TMD discomfort, salivation, occlusal changes — posterior open bite over time). Sleep bruxism — rhythmic masticatory muscle activity (RMMA), PSG confirmation with audio; comorbidity with OSA, GERD, SSRIs. Awake bruxism — ecological momentary assessment (EMA). Insomnia, circadian rhythm disorders, periodic limb movement, restless legs.

~8%

Pain Assessment

Multidimensional pain assessment. VAS/NRS 0-10, Faces Pain Scale-Revised (FPS-R pediatric/cognitive). McGill Pain Questionnaire (sensory/affective/evaluative descriptors). Brief Pain Inventory (severity and interference). Graded Chronic Pain Scale (GCPS — severity grades 0-IV). PHQ-9 depression (cutoffs 5/10/15/20), GAD-7 anxiety. Pain Catastrophizing Scale (PCS). Jaw Functional Limitation Scale (JFLS-8/JFLS-20). Central Sensitization Inventory (CSI). Oral Behaviors Checklist (OBC). Quantitative sensory testing — thermal, mechanical, pressure pain thresholds.

~7%

Pharmacology

NSAIDs (non-selective vs COX-2 selective celecoxib; GI/renal/CV risk). Acetaminophen (hepatic ceiling 3-4 g/day). Opioid stewardship — tramadol, tapentadol; risks include dependence, hyperalgesia, respiratory depression; CDC MED guidance. Tricyclic antidepressants — amitriptyline, nortriptyline (low-dose 10-50 mg qhs for chronic orofacial pain). SNRIs — duloxetine, venlafaxine. Anticonvulsants — gabapentin, pregabalin (neuropathic), carbamazepine/oxcarbazepine (TN), lamotrigine, topiramate (migraine prevention, renal stones/paresthesia). Muscle relaxants — cyclobenzaprine, tizanidine, methocarbamol (short-term). Topicals — lidocaine, capsaicin, ketamine, clonazepam for BMS. Benzodiazepines short-term only.

~5%

Diagnostic Blocks

Local anesthetic pharmacology — lidocaine (amide, max 4.4 mg/kg plain, 7 mg/kg with epinephrine; 300 mg max plain adult), bupivacaine (longer duration, cardiotoxicity). Diagnostic/therapeutic blocks — infraorbital (V2 — cheek, upper lip), mental (V3 branch — lower lip, chin), inferior alveolar, auriculotemporal (TMJ and preauricular region), greater occipital (cervicogenic headache, occipital neuralgia), sphenopalatine ganglion (cluster headache adjunct), stellate ganglion (sympathetic-mediated pain). Trigger point injections. Intra-articular TMJ blocks. Interpretation — placebo response, false-positive, controlled comparative blocks.

~5%

Persistent Idiopathic Facial Pain

Persistent idiopathic facial pain (PIFP, formerly atypical facial pain) — ICHD-3 criteria: persistent facial or oral pain recurring daily >2 hours/day for >3 months, poorly localized, not following peripheral nerve distribution, normal examination and imaging. Persistent idiopathic dentoalveolar pain (PIDAP, atypical odontalgia) — dentoalveolar pain without identifiable pathology. Diagnosis of exclusion — thorough workup, imaging, rule out structural/neuropathic causes. Management — TCAs, SNRIs, topical lidocaine/capsaicin, CBT. Strongly avoid iatrogenic endodontics/extractions/surgery in absence of clear pathology.

~2%

Research & Evidence

Study designs — RCT (gold standard for interventions), cohort, case-control, cross-sectional, case series. Biostatistics — sensitivity, specificity, PPV, NPV, likelihood ratios, NNT/NNH, relative and absolute risk reduction. Evidence-based medicine hierarchy (systematic review/meta-analysis > RCT > cohort > case-control > case series > expert opinion). Critical appraisal tools (Cochrane RoB 2, GRADE). PRISMA reporting. IMMPACT recommendations for chronic pain trials. Placebo response in pain research.

~2%

Cervicogenic Pain

Cervicogenic headache — Sjaastad criteria, ICHD-3 secondary headache attributed to disorder of cervical spine. Anatomy — trigeminocervical complex, convergence of C1-C3 afferents with trigeminal nucleus caudalis. Clinical features — unilateral, non-throbbing, triggered by neck movement/sustained posture, reduced cervical range of motion, tender upper cervical facets. Diagnostic blocks — C2-C3 zygapophyseal joint, third occipital nerve, greater occipital nerve. Treatment — manual therapy, physical therapy, trigger point injection, radiofrequency neurotomy.

~2%

Psychosocial & Behavioral

Biopsychosocial model of pain. Pain catastrophizing, fear-avoidance (Vlaeyen model), kinesiophobia (TSK). Depression and anxiety comorbidity with chronic orofacial pain. Somatic symptom disorder (DSM-5). Central sensitivity syndromes overlap — fibromyalgia (ACR 2016), IBS, chronic fatigue syndrome, vulvodynia. Cognitive behavioral therapy (CBT), acceptance and commitment therapy (ACT), mindfulness-based stress reduction (MBSR), motivational interviewing, pain self-management, sleep hygiene.

How to Pass the ABOP Orofacial Pain Exam

What You Need to Know

  • Passing score: Criterion-referenced scaled score set by ABOP (modified Angoff standard)
  • Exam length: 200 questions
  • Time limit: Written CBT (~4 hours) + Case Review portfolio
  • Exam fee: ~$2,000-$2,500 combined Written + Case Review fees (ABOP 2026 — verify current schedule)

Keys to Passing

  • Complete 500+ practice questions
  • Score 80%+ consistently before scheduling
  • Focus on highest-weighted sections
  • Use our AI tutor for tough concepts

ABOP Orofacial Pain Study Tips from Top Performers

1DC/TMD 2014 is the single highest-yield framework for TMD diagnosis. Axis I pain diagnoses: myalgia, myofascial pain with referral, arthralgia, headache attributed to TMD. Axis I intra-articular: disc displacement with reduction (± intermittent locking), disc displacement without reduction (with/without limited opening), degenerative joint disease, subluxation. Axis II is mandatory psychosocial assessment — GCPS, PHQ-9, GAD-7, JFLS, OBC, PCS. MRI is gold standard for disc position; CBCT best for osseous changes.
2ICHD-3 primary headache memorization — Migraine without aura requires ≥5 attacks, 4-72 hours, at least 2 of 4 characteristics (unilateral, pulsating, moderate/severe, aggravated by routine activity) plus nausea/vomiting or photophobia/phonophobia. Chronic migraine = ≥15 days/month for >3 months with ≥8 migraine days. Cluster headache is strictly unilateral V1 with cranial autonomic features, 15-180 minutes, high frequency (up to 8/day). Paroxysmal hemicrania and hemicrania continua are indomethacin-responsive — a defining diagnostic test.
3Trigeminal neuralgia — classical TN is paroxysmal electric-shock pain in V2/V3 with trigger zones; MRI shows neurovascular compression (superior cerebellar artery most common). Carbamazepine is first-line (check HLA-B*1502 in Asian ancestry to screen for Stevens-Johnson risk, monitor Na for hyponatremia, CBC, LFTs). Oxcarbazepine is second-line with better tolerability. Baclofen and lamotrigine are add-ons. Microvascular decompression (Jannetta) offers durable relief; gamma knife and percutaneous rhizotomy are alternatives for surgical candidates.
4Chronic migraine pharmacology — PREEMPT Botox protocol: 155 units across 31 fixed injection sites in 7 muscle groups (corrugator, procerus, frontalis, temporalis, occipitalis, cervical paraspinal, trapezius), repeated every 12 weeks. CGRP monoclonal antibodies: erenumab blocks the receptor; fremanezumab, galcanezumab, and eptinezumab bind the CGRP ligand. Gepants — ubrogepant and rimegepant for acute; atogepant and rimegepant for prevention. Triptans are contraindicated in CAD, uncontrolled HTN, and hemiplegic/basilar migraine.
5OSA management — STOP-BANG ≥3 suggests high risk; polysomnography AHI grades severity (mild 5-14, moderate 15-29, severe ≥30). CPAP is gold standard and preferred for moderate-severe OSA. Mandibular advancement device (MAD) is indicated for mild-moderate OSA or CPAP intolerance. Side effects of MAD include TMJ/muscle discomfort, salivation changes, and long-term posterior open bite from occlusal changes — document baseline occlusion and monitor. Sleep bruxism is confirmed on PSG by RMMA (rhythmic masticatory muscle activity) with audio; commonly comorbid with OSA, GERD, and SSRI use.

Frequently Asked Questions

What is the ABOP Orofacial Pain Certification?

The ABOP Orofacial Pain Certification is administered by the American Board of Orofacial Pain — the certifying body for the 12th ADA-recognized dental specialty (recognized March 2020). It validates expertise in the diagnosis and management of temporomandibular disorders (TMD), headaches, neuropathic orofacial pain, sleep-related oromotor conditions, and related chronic pain disorders. Certification requires both a computer-based Written Examination and a Case Review portfolio.

Who is eligible to sit for the ABOP exam?

Candidates must hold a D.D.S./D.M.D. or equivalent dental degree with a valid unrestricted license. The primary pathway is completion of a CODA-accredited 2-year postdoctoral orofacial pain residency. An experience pathway is available for dentists with documented qualifying clinical hours, continuing education, mentorship, and case documentation per ABOP policy. Candidates must also be in good professional standing without pending board actions.

What is the format of the ABOP examination?

The examination has two components. The Written Examination is a computer-based test delivered at Pearson VUE (~4 hours) with single-best-answer multiple-choice questions blueprinted to the ABOP content outline — headache, TMD, neuropathic pain, pain neuroscience, pharmacology, sleep, diagnostic blocks, and assessment. The Case Review is a submitted portfolio of documented clinical cases demonstrating diagnostic reasoning and evidence-based management across the specialty scope.

How much does the 2026 ABOP exam cost?

Combined Written + Case Review fees are approximately $2,000-$2,500 for 2026 — always verify the current schedule on abop.net. Additional costs include application fees, Pearson VUE seat, and ongoing recertification/continuing certification fees after passing. Cancellation and refund policies follow the ABOP schedule with decreasing refunds as the exam date approaches. Retakes require re-registration and fee payment within the allowed eligibility window.

When is the 2026 exam administered?

The ABOP Written Examination is typically offered on scheduled testing windows annually; candidates schedule specific Pearson VUE appointments after application approval. The Case Review portfolio is submitted on a defined timeline relative to the Written exam cycle. Exact 2026 dates, application deadlines, and Case Review submission windows should be confirmed directly on the ABOP website (abop.net).

How is the ABOP exam scored?

ABOP uses criterion-referenced scaled scoring with a passing standard set by subject-matter experts using the modified Angoff method. Pass/fail depends on performance relative to a fixed cut-score, not on other candidates. Written score reports include domain-level feedback. The Case Review is evaluated separately against defined rubrics covering diagnosis, differential, evidence-based management, and follow-up. Both components must be passed to achieve certification.

What are the highest-yield topics?

Highest-yield topics include DC/TMD 2014 Axis I/II diagnostic criteria and decision tree, ICHD-3 primary headache classification (migraine, TTH, cluster and other TACs, MOH), PREEMPT Botox protocol and CGRP monoclonal antibodies for chronic migraine, trigeminal neuralgia workup and carbamazepine first-line, MAD indications and titration for OSA, sleep bruxism RMMA criteria, central sensitization and trigeminocervical convergence, pain assessment instruments (GCPS, PHQ-9, GAD-7, JFLS), and persistent idiopathic facial pain (PIFP) as a diagnosis of exclusion.

How should I study for the ABOP exam?

Use a structured 6-12 month plan mapped to the ABOP content outline. Begin with pain neuroscience and assessment, then drill DC/TMD 2014 and ICHD-3 headache criteria, followed by neuropathic pain, sleep/bruxism, and pharmacology. Integrate the AAOP textbook (de Leeuw/Klasser), Okeson, Sharav & Benoliel, and the DC/TMD training materials. Complete 2-3 timed full-length mock exams. Prepare the Case Review portfolio in parallel, documenting Axis I/II reasoning and evidence-based treatment plans across TMD, headache, and neuropathic pain cases.