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.
