Role of Glia in Orofacial Pain

Abstract

Several acute and chronic pain conditions in the face or mouth are very common, and some are unique to the orofacial region. However, the etiology and pathogenesis of most orofacial chronic pain conditions are unresolved, and they are difficult to diagnose and manage. This article provides a brief overview of the neural mechanisms underlying orofacial pain and then highlights recent findings indicating that nonneural cells, specifically satellite cells in the sensory ganglia and astroglia and microglia cells in the central nervous system, are important players in both acute and chronic inflammatory and neuropathic orofacial pain conditions and may offer new targets for management of these conditions.

Neuron-glia interaction is a key mechanism underlying persistent orofacial pain

“…Activated SGCs also generate molecules involved in modulating TG neuronal excitability, and TG neurons also release various molecules (7). These findings suggest that neuron-satellite glial cell communication is a primary mechanism underlying the modulation of TG neuronal excitability associated with orofacial inflammation and trigeminal nerve injury (6). In addition, microglial cells and astrocytes in the Vc and C1-C2 are activated after orofacial inflammation and trigeminal nerve injury (2).…”

“…The soma of TG neurons is tightly encircled by SGCs, which help modulate TG neuronal excitability and have roles in nutrition and structure formation (6). SGCs are activated and change their morphological features, which may become glial fibrillary acidic protein (GFAP)-immunoreactive after orofacial inflammation or trigeminal nerve injury.…”

New Targets in Pain, Non-Neuronal Cells, and the Role of Palmitoylethanolamide

“…[13][14][15] In this regard, non-neuronal cells and nuclear receptors such as peroxisome proliferator-activated receptors (PPARs) have emerged as important targets in a variety of pain states. [4,5,[16][17][18] In this short review we will address some aspects in this emerging field related to non-neuronal targets in chronic and neuropathic pain.…”

“…[1][2][3][4][5][6] Mast cells, for example, have been the recognized to play a causative role in the development of hyperalgesia following nerve injury, [19] and their pathogenic involvement has also been demonstrated in chronic low back pain, [20] visceral or pelvic pain, [21][22][23][24][25] and migraine. [26][27][28].…”

“…[29] Together with glia, and especially microglia that are known to functionally interact with mast cells, [30] these immune cell types are now considered to be key to the phenomena of central and peripheral sensitization. [1][2][3][4][5][6].…”