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Objective: This article explores the multiple etiologies, diagnosis, and management of orofacial pain., Latest Developments: Published in 2019, the International Classification of Orofacial Pain has become the internationally accepted classification system for primary and secondary facial pain. New discoveries in temporomandibular disorders have demonstrated that they are far more complex than the traditional dental mechanistic point of view. A 2020 consensus report released by the National Academies of Sciences, Engineering, and Medicine entitled "Temporomandibular Disorders: Priorities for Research and Care" highlighted this paradigm shift and its importance for patient care, education, and research., Essential Points: Orofacial pain comprises many disorders with different etiologies and pathophysiologies. The subjectivity of the pain experience and the interrelated anatomy and physiology of the craniofacial area add to the complexity of diagnosis when the source and etiology of pain are not clear. As orofacial pain straddles the expertise of multiple disciplines, a multidisciplinary approach combining medication, physical therapy, and procedural and psychological strategies is essential in treating patients with orofacial pain., (Copyright © 2024 American Academy of Neurology.)

Temporomandibular disorders (TMDs) and headache disorders are highly prevalent in the population. TMDs can present headache symptoms as a secondary headache and, in addition, be comorbid with primary headache disorders. This overlap has significant clinical implications for which it is essential for the physician to be aware, and they should screen for the potential presence of TMDs in a headache patient. Bruxism is a parafunctional behavior also prevalent in the population which has a role in TMDs and may influence headache symptomatology, but it is still necessary to clarify this relationship., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background and Purpose: Temporomandibular disorders (TMD) and migraine can be co-morbid. This can be a significant factor in exacerbating and increasing the prevalence of migraine-like symptoms. However, the underlying mechanisms involved are unknown. Our objective was to investigate these neural mechanisms and the role of CGRP as a key modulator in this co-morbidity., Experimental Approach: We combined experimental approaches using CGRP, which triggers a migraine-like response in patients, with that of masseteric muscle injection of complete Freund's adjuvant (CFA), to model myofascial TMD-like inflammation. Using validated electrophysiological methods to assess each of the above approaches independently or in combination, we examined their effects on the response properties of migraine-like dural-trigeminocervical neurons., Key Results: Independently, in ~2/3 of animals (rats) each approach caused delayed migraine-like activation and sensitisation of dural-trigeminocervical neurons. The response to masseteric-CFA was attenuated by a selective CGRP receptor antagonist. The combination approach caused a migraine-like neuronal response in all animals tested, with somatosensory-evoked cranial hypersensitivity significantly exacerbated., Conclusion and Implications: The data demonstrate a neuronal phenotype that translates to the exacerbated clinical co-morbid phenotype, supporting this combination approach as a relevant model to study the mechanisms involved. It provides a pathophysiological rationale for this exacerbated phenotype, strongly implicating the involvement of CGRP. The results provide support for targeting the CGRP pathway as a novel monotherapy approach for treating this co-morbid condition. This has key implications into our understanding of this co-morbid condition, as well as potentially addressing the major unmet need for novel and effective therapeutic approaches., (© 2020 The British Pharmacological Society.)