Endodontic Resident US Army Dental Activity, Ft Gordon Evans, Georgia, United States
Managing pain of endodontic origin is most often achieved via pulpotomy, pulpectomy, or nonsurgical root canal therapy in conjunction with postoperative analgesics. In the event endodontic treatment cannot be initiated promptly, an effective pain management protocol targeting reduction of inflammatory mediators is invaluable. Endodontic pain results from upregulation of host inflammatory mediators. Although the actions of inflammatory mediators vary, the cumulative effect leads to reduced threshold for nociceptor activation. In contrast to the selective nature of NSAIDs, glucocorticoid steroids like dexamethasone have multiple sites of action and anti-inflammatory effects. Glucocorticoids affect the acute inflammatory response by suppressing vasodilation, preventing the migration and phagocytosis of polymorphonuclear leukocytes, as well as inhibiting production of both prostaglandins and leukotrienes. For these reasons, dexamethasone may provide an optimal approach to managing symptomatic irreversible pulpitis when endodontic treatment cannot readily be provided. Reasons for delayed treatment include, but is not limited to, scheduling conflicts, lack of staffing support, inability to achieve profound anesthesia, difficult anatomy, or canal obstructions impeding adequate debridement. The purpose of this table clinic is to review inflammatory pathways, as well as dexamethasone’s mechanism of action to help facilitate discussion on its use for managing endodontic pain. Multiple routes for administering dexamethasone are available. However, providing patients with three 4 mg oral doses taken over 24 hours helps simplify and provide predictable systemic absorption. This case series documents dexamethasone’s ability to adequately manage pain associated with symptomatic irreversible pulpitis during delay of endodontics.
