CHRONIC DEXAMETHASONE TREATMENT AND ITS EFFECTS ON SENSORY NEUROPEPTIDES, PULPAL INJURY REACTIONS AND REPARATIVE DENTIN

Initial sensory nerve reactions to dental injuries include terminal sp routing and intensified immunoreactivity for calcitonin gene-related p eptide (CGRP) and substance P (SP); those reactions are reduced at 4 d ays after injury when rats are treated daily with dexamethasone (DEX) [17]. Here we have analyzed long-term effects of DEX (daily, 0.2 mg/kg ) on wound healing, sensory nerve sprouting, and CGRP/SP intensity at 7-14 days after cavity preparation. All DEX treated rats had loss of a ppetite and stopped growing during the postoperative periods while con trols had normal postoperative growth. After 7-14 days, CGRP immunorea ctivity (IR) was decreased to one-third of normal (P < 0.05) compared to vehicle in both the intact and injured molar pulp, and SP also decr eased, but the neuropeptide intensity in adjacent periodontal innervat ion was not changed. Pulpal injury and inflammation were reduced by DE X treatment, but reparative dentin was formed just as well in the DEX rats as in the vehicle group. When the injured teeth formed fibrous de ntin, there was sprouting of nerves towards that matrix, and DEX did n ot inhibit that reaction. The sprouts could contain intense neuropepti de immunoreactivity in DEX rats even though the CGRP/SP intensity in u ninjured pulp was reduced. We conclude that (1) chronic DEX treatment causes a generalized decrease in CGRP and SP neuropeptides in pulpal n erves but not in periodontal ligament; (2) it reduces abscess formatio n in injured teeth; (3) it does not block reparative dentin formation; and (4) it does not block sprouting of pulpal nerves towards fibrous dentin. The selective loss of pulpal neuropeptides CGRP and SP during dexamethasone treatment may be caused by reduced dental function since there was substantial loss of appetite and chronic weight loss during the 1-2 week treatment periods.