A rat model has been developed to characterize the responses of brainstem trigeminal neurons to orofacial deep and cutaneous tissue
inflammation and
hyperalgesia. Complete
Freund's adjuvant (CFA) was injected unilaterally into the rat temporomandibular joint (TMJ) or perioral (PO) skin to produce
inflammation in deep or cutaneous tissues, respectively. The TMJ and PO
inflammation resulted in orofacial behavioral
hyperalgesia and
allodynia that peaked within 4-24 h and persisted for at least 2 weeks. Compared to cutaneous CFA injection, the injection of CFA into the TMJ produced a significantly stronger
inflammation associated with a selective upregulation of
preprodynorphin mRNA in the trigeminal spinal complex, an enhanced medullary dorsal horn hyperexcitability, and a greater trigeminal Fos
protein expression, a marker of neuronal activation. The Fos-LI induced by TMJ
inflammation persisted longer, was more intense, particularly in the superficial laminae, and more widespread rostrocaudally. Thus, the inflammatory
irritant produces a stronger effect in deep than in cutaneous orofacial tissue. As there is heavy innervation of the TMJ by unmyelinated nerve endings, a strong nociceptive primary afferent barrage is expected following
inflammation. An increase in TMJ C-fiber input after
inflammation and strong central neuronal activation may initiate central hyperexcitability and contribute to persistent
pain associated with
temporomandibular disorders. Since deep inputs may be more effective in inducing central neuronal excitation than cutaneous inputs, greater sensory disturbances may occur in
pain conditions involving deep tissues than in those involving cutaneous tissues.