VR1- and VRL-1-like immunoreactivity in normal and injured trigeminal dental primary sensory neurons of the rat

Abstract

The vanilloid receptor VR1 and the vanilloid receptor-like protein VRL-1 are associated with polymodal nociceptors, and may be important for pain processing in normal and injured teeth. Using immunohistochemistry, we have studied the distribution of these receptors in rat pulpal or gingival trigeminal ganglion neurons that were identified through retrograde labeling with fluoro-gold. Twenty-one percent to 34% of tooth pulp-innervating neurons were VRl-positive, while 32%-51% were VRL-1-immunoreactive. However, double-labeling experiments revealed that VR1 and VRL-1 rarely co-existed in the same cells, but rather seemed to be confined to separate subpopulations. Among the gingival neurons, about 25% were VR1-positive and about 41% were VRL-1-immunoreactive. A lesion of the inferior alveolar nerve, which supplies mandibular teeth and gingiva, resulted in a marked down-regulation of VR1 in the affected trigeminal ganglion cells. A down-regulation of VRL-l was also indicated. The results suggest that both VR1 and VRL-1 could have significant roles in pulpal and gingival nociceptive transduction.

A Prospective, Randomized, Single-blind Comparative Evaluation of Anesthetic Efficacy of Posterior Superior Alveolar Nerve Blocks, Buccal Infiltrations, and Buccal Plus Palatal Infiltrations in Patients with Irreversible Pulpitis

“…This leads to ion trapping of local anesthetic molecules in ionized form, causing a decrease in the number of local anesthetic molecules crossing the nerve membrane (8). Secondly, and a more accepted reason, is the activation of nociceptors by inflammatory mediators (8)(9)(10). In an uninjured or uninflamed pulp, the nociceptors are normally not activated by mild temperature or pH changes.…”

“…There are various proposed reasons to explain this phenomenon including a decreased local pH (8), tachyphylaxis of anesthetic solutions (8), accessory innervations (8), and the activation of nociceptors (8)(9)(10). The most plausible explanation is the inflammatory activation of tetrodotoxin and capsaicin-sensitive transient receptor potential vanilloid types 1 and 4 (8)(9)(10).…”

Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

“…There are also lesswell-characterized nociceptive receptors for other inflammatory molecules, including peptides (bradykinin), lipids (prostaglandins), and neurotrophins (NGF). Little is known about the distribution of nociceptive receptors in the periodontal tissues; however, a recent study has identified the VR1 receptor on about 25% of gingival neurones (Stenholm et al, 2002). Analysis of data from other tissues suggests that VR1 expression is limited to polymodal nociceptors on unmyelinated C fibers but that, during inflammation, A␦ neurones begin to express VR1 (Amaya et al, 2003).…”

Comparison of Effect of Oral Premedication with Ibuprofen or Dexamethasone on Anesthetic Efficacy of Inferior Alveolar Nerve Block in Patients with Irreversible Pulpitis: A Prospective, Randomized, Controlled, Double-blind Study

“…The success rate of IANB drastically decreases, however, in patients with irreversible pulpitis 4,11,18,21,26) . Activation of nociceptors by inflammatory mediators such as prostaglandins (PGs) is considered a major cause of this phenomenon 3,6,20,24) . Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the chemical inflammatory mediators that activate or sensitize peripheral nociceptors 7) .…”