DEXAMETHASONE TREATMENT REDUCES SENSORY NEUROPEPTIDES AND NERVE SPROUTING REACTIONS IN INJURED TEETH

Dental injuries have been shown to generate extensive structural and c ytochemical changes in sensory fibers that contain neuropeptides such as calcitonin gene-related peptide (CGRP) or substance P(SP). The pres ent study was designed to test whether the anti-inflammatory drug dexa methasone (DEX) can alter neural responses to dental injuries. DEX (20 mu g/100 g body weight) was given to adult rats (n = 10) prior to den tal surgery and daily thereafter for 4 days. Control animals received sterile saline vehicle (n = 6) or no injection (n = 1). Each rat was t hen anesthetized for dental surgery and a cavity was drilled partway t hrough dentin on the anterior side of the right maxillary first molar. Pulp exposure injuries were also made on two right mandibular molars in 14 of 17 rats. After 4 days of daily drug treatment, the rats were anesthetized and fixed by perfusion with formaldehyde-picric acid, and their jaws were prepared for immunocytochemistry. Neural CGRP immunor eactivity near the maxillary cavity injury site of DEX-treated rats wa s reduced more than 50% compared to controls, as determined both quali tatively and by digital analysis. The SP immunoreactive (IR) fibers in molar pulp also had extensive inhibition of neural reactions to cavit y injury. DEX also reduced the immunoreactivity for CGRP and SP in nor mal contralateral rat molars of all treated rats, and it caused a post operative loss of weight. Pretreatment for 1-5 days prior to the 4 day injury gave the same results as pretreatment for 1 h. The mandibular pulp exposure injuries induced a chronic abscess and advancing pulpal necrosis but did not show differences in nerve reactions between DEX-t reated rats and the controls. In conclusion, the synthetic steroid dex amethasone suppressed the CGRP and SP neuropeptide immunoreactivity in normal dental nerves and it reduced nerve-sprouting responses to dent in cavity injuries; however, sensory nerve reactions to pulpal exposur e injuries were not affected by DEX in these experiments.