Are glia targets for neuropathic orofacial pain therapy

Post traumatic trigeminal neuropathy, presenting frequently as a complication of dental procedures, is often detrimental to the patient, with psychological and socioeconomic ramifications. Following a neuronal injury, numerous changes occur in both the peripheral (PNS) and central nervous systems (CNS) contributing to neuronal plasticity. Over the years, many studies have documented neuronal mechanisms involved in neuropathic pain, whereas non neuronal mechanisms, such as those based on glia have gained increased focus only recently. While the question of whether chronic neuropathic pain is a gliopathy remains enigmatic, activation and proliferation of glial cells and their interaction with neurons are believed to be key mechanisms underlying chronic neuropathic pain following a traumatic trigeminal nerve injury. Glial cells such as microglia, astrocytes and satellite glial cells have been extensively studied based on spinal neuropathic pain models, but the available literature on trigeminal pain models is very limited. In this review we aim to discuss i) available evidence on the role of central and peripheral glial cells in trigeminal neuropathic pain (TNP); and ii) gaps in knowledge between spinal and trigeminal pain models with regards to glial plasticity