Dental Injury Models: Experimental Tools for Understanding Neuroinflammatory Interactions and Polymodal Nociceptor Functions

Abstract

Recent research has shown that peripheral mechanisms of pain are much more complex than previously thought, and they differ for acutely injured normal tissues compared with chronic inflammation or neuropathic (nerve injury) pain. The purpose of the present review is to describe uses of dental injury models as experimental tools for understanding the normal functions of polymodal nociceptive nerves in healthy tissues, their neuroinflammatory interactions, and their roles in healing. A brief review of normal dental innervation and its interactions with healthy pulp tissue will be presented first, as a framework for understanding the changes that occur after injury. Then, the different types of dental injury that allow gradation of the extent of tissue damage will be described, along with the degree and duration of inflammation, the types of reactions in the trigeminal ganglion and brainstem, and the type of healing. The dental injury models have some unique features compared with neuroinflammation paradigms that affect other peripheral tissues such as skin, viscera, and joints. Peripheral inflammation models can all be contrasted to nerve injury studies that produce a different kind of neuroplasticity and neuropathic pain. Each of these models provides different insights about the normal and pathologic functions of peripheral nerve fibers and their effects on tissue homeostasis, inflammation, and wound healing. The physical confinement of dental pulp and its innervation within the tooth, the high incidence of polymodal A-delta and C-fibers in pulp and dentin, and the somatotopic organization of the trigeminal ganglion provide some special advantages for experimental design when dental injury models are used for the study of neuroinflammatory interactions.

Integration of tooth morphogenesis and innervation by local tissue interactions, signaling networks, and semaphorin 3A

“…These sensory nerves mediate the sensation of pain. [10][11][12] The periodontal space between the root of the tooth and the adjacent alveolar bone, is the second major target area for sensory nerves, with these mediating pain, as well as pressure and touch. [10][11][12] Nerves emanating from the sympathetic superior cervical ganglion are found in association with dental blood vessels in both the dental pulp, and periodontal space, and are involved in vasoregulatory functions.…”

L’odontoblaste

“…, Henri Magloire 3,4 > La sensibilité dentinaire est une situation clinique à laquelle est quotidiennement confronté le praticien, et elle constitue la symptomatologie de l'hyperesthésie dentinaire. L'hyperesthésie dentinaire est une pathologie fréquente, affectant le confort et la fonction buccale.…”

“…L'ensemble forme un réseau de fibres nerveuses nociceptives hautement plastique, qui participe à la préservation de l'organe dentaire en prévenant et en limitant les dommages survenant au sein du tissu pulpaire. Impliquées dans le contrôle des processus inflammatoires et des réactions immunitaires, ces fibres facilitent les processus de réparation et de cicatrisation [3]. Ainsi, l'étroite proximité établie entre ce réseau dense de fibres nerveuses sensitives et les odontoblastes pose la question du rôle respectif joué par ces cellules dans la perception de la douleur dentinaire.…”

Anti-Inflammatory Effects of Matrix Metalloproteinase-3 on Irreversible Pulpitis of Mature Erupted Teeth

“…doi:10.1371/journal.pone.0052523.g001 erupted premolar model to determine the role of MMP-3 in the inflammation and damage of dental pulp tissues. In addition, the dental, periodontal, and neural reactions to chronic pulpitis and pulpal necrosis have previously been investigated in a model of infected pulpitis triggered by the exposure of pulp tissues [18]. However, there have been no studies that have determined or modeled the sequential stages of irreversible pulpitis.…”