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Abstract
Orofacial neuropathic pain is initiated by extraction of teeth or nerve injury from trauma in the trigeminal nerve that innervates the facial area. In the experiment, orofacial neuropathic pain usually occurred following injury of peripheral trigeminal nerve including infra-orbital nerve, inferior alveolar nerve, or mental nerve. In addition, pathology from trigeminal nerve root or ganglion is involved in orofacial neuropathic pain. This study introduced various animal models that help us study the underlying mechanisms of development or maintenance of orofacial neuropathic pain. One of the most typical symptoms of orofacial neuropathic pain is hypersensitivity to the innocuous mechanical stimuli. Our study presents a novel method to evaluate mechanical allodynia in rats with orofacial neuropathic pain. Recently, accumulate evidence support participation of central glial cells in the development or maintenance of orofacial neuropathic pain. Signaling molecules in glial cells also play an important role in neuropathic pain in the orofacial area.
Figures and Tables
Fig. 1
Illustration of various animal models for orofacial neuropathic pain. (A) Branches of the trigeminal nerve; infraorbital nerve, inferior alveolar nerve, mental nerve. (B) ION-CCI model. Infraorbital nerve was exposed and separated from adhering tissue and two ligatures were made around it. Arrow indicates infraorbital nerve.
Fig. 2
Time course in the ipsilateral and contralateral airpuff thresholds following ION-CCI in the rat. *p<0.05, shamvs. ION-CCI-treated group. Original date presented in Lim et al (2007).
Fig. 3
Images showing the animal model for malpositioned dental implant-induced neuropathic pain. The dental implant was placed in the alveolar socket after extraction of lower second molar tooth (A). The inferior alveolar canal was penetrated by incorrect placement of dental implant (B).
Fig. 4
Time course analysis of the changes in air-puff thresholds following incorrectly placed dental implants in rats. Treatment with mal-positioned dental implants produced significant mechanical allodynia in both ipsilateral (A) and contralateral sides (B). *p<0.05, malpositioned dental implant (MDI) vs. sham group. Original date presented in Han et al.(2010).
Fig. 5
Illustration of a trigeminal neuralgia animal model produced by compression of the trigeminal ganglion.
Fig. 6
Change in the a amount of pressure following application of air-puff (A) and von Frey filament (B). Both showed proportionate relationship between the amount of pressure and intensity of stimulation.
Fig. 7
Typical responses of a neuron to air-puff or Von Frey stimulation. The neuron (WDR) responded to brush (A), von Frey filament (B), air-puff (C), and pinch (D) stimulation. Neuronal firings increased by air puff and von Frey filament stimulation (E).
Fig. 8
The effects of an intracisternal injection of PD98059, a MEK inhibitor (A) and SB203580, a p38 MAPK inhibitor (B) on ION-CCI-induced mechanical allodynia in the orofacial area. P<0.05, the vehicle- vs. chemicalstreated group. #P<0.05, 1 µg of chemicals-treated group vs. 10 µg of chemicals-treated group. Original date presented in Lim et al.(2007).
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