Margaret R Byers1. 1. Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, 98195-6540 USA. Electronic address: byersm@uw.edu.
Abstract
OBJECTIVE: This study tests the hypothesis that normal use of teeth (chewing) causes changes in immunoreactive-(IR) patterns for endings of large Aβ and CGRP axons in rat molar cusps. DESIGN: First, a new paradigm to test chewing in adult male rats was developed. Then IR patterns for large dental axons were analysed for a calcium-binding protein, parvalbumin (PV), heavy neurofilament protein-200 (NFP), and vesicle-release molecule synaptophysin (SYN) that all typify large dental axons and proprioceptors for comparison with endings of CGRP-IR neuropeptide axons. The behavior groups were: (1) daytime sleeping/fasting (Group:SF); (2) brief feeding after 8-11 h of daytime sleeping/fasting (Group:SF-C); (3) normal nocturnal feeding (Group:N); (4) nocturnal fasting (Group:NF); (5) brief feeding/chewing after nocturnal fasting (Group:NF-C). RESULTS: Nerve endings with NFP-, PV-, or SYN-IR were lost or altered in pulp and dentin in all chewing groups. Other endings with CGRP-IR were near those with PV-, NFP- and SYN-IR at the pulp-dentin border and in dentin, and they also lost immunoreactivity in all chewing groups. The special beaded regions along the crown pulp/dentin borders lost neural labeling in all chewing groups. Nerves of molar roots and periodontal ligament were not changed. CONCLUSIONS: Rapid neural reactions to chewing show extensive, reversible, non-nociceptive depletions of crown innervation. Those changes were rapid enough to occur during normal feeding followed by recovery during rest. The new dental paradigm related to chewing and fasting allows dissection of intradental proprioceptive-like mechanisms during normal tooth functions for comparison with nociceptive and mechanosensitive reactions after injury or inflammation.
OBJECTIVE: This study tests the hypothesis that normal use of teeth (chewing) causes changes in immunoreactive-(IR) patterns for endings of large Aβ and CGRP axons in rat molar cusps. DESIGN: First, a new paradigm to test chewing in adult male rats was developed. Then IR patterns for large dental axons were analysed for a calcium-binding protein, parvalbumin (PV), heavy neurofilament protein-200 (NFP), and vesicle-release molecule synaptophysin (SYN) that all typify large dental axons and proprioceptors for comparison with endings of CGRP-IR neuropeptide axons. The behavior groups were: (1) daytime sleeping/fasting (Group:SF); (2) brief feeding after 8-11 h of daytime sleeping/fasting (Group:SF-C); (3) normal nocturnal feeding (Group:N); (4) nocturnal fasting (Group:NF); (5) brief feeding/chewing after nocturnal fasting (Group:NF-C). RESULTS: Nerve endings with NFP-, PV-, or SYN-IR were lost or altered in pulp and dentin in all chewing groups. Other endings with CGRP-IR were near those with PV-, NFP- and SYN-IR at the pulp-dentin border and in dentin, and they also lost immunoreactivity in all chewing groups. The special beaded regions along the crown pulp/dentin borders lost neural labeling in all chewing groups. Nerves of molar roots and periodontal ligament were not changed. CONCLUSIONS: Rapid neural reactions to chewing show extensive, reversible, non-nociceptive depletions of crown innervation. Those changes were rapid enough to occur during normal feeding followed by recovery during rest. The new dental paradigm related to chewing and fasting allows dissection of intradental proprioceptive-like mechanisms during normal tooth functions for comparison with nociceptive and mechanosensitive reactions after injury or inflammation.