Authors: Margaret R Byers Matthew M Rafie Ruth E Westenbroek
Publish Date: 2009/09/09
Volume: 338, Issue: 2, Pages: 217-226
Abstract
Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain Here we asked whether it also affected dental or periodontal cells or dental innervation by altering voltagegated sodium channel Nav16 immunoreactivity IR or neural synaptophysin Daily dexamethasone 02 mg/kg given for 1 week to rats caused 12fold increased intensity of Nav16IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment These cells also colocalized monocyte ED1 or dendritic cell CD11b/Ox42 markers and their location in molars expanded during dexamethasone treatment to include deeper pulp Furthermore dexamethasone caused a 10fold decrease in the number of Nav16immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets No changes occurred for neural Nav16 at axonal nodes of Ranvier even though IR for calcitonin generelated peptide was greatly decreased as expected and neural synaptophysinIR was decreased 59 by dexamethasone At 4 days after tooth injury pulpal vasodilation and increased Nav16immunoreactive pulp cells were similar for all groups Thus dexamethasone changes dental pulp cell and alveolar osteoclast Nav16IR in normal teeth but different mechanisms occur after tooth injury when tissue reactions were similar for dexamethasone and vehicletreated rats Steroidinduced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysinIR and with altered pulp cell Nav16IR and osteoclast number but not with any changes in Nav16IR for nodes of Ranvier in myelinated dental axonsThis work was supported by NIH grants DE055951 to MRB and DE13531 REW American Association of Endodondists Foundation to MRB Anesthesia Research Training U Washington to MRB and Washington Dental Service Foundation Research Fund MMR
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