|1663 Periradicular inflammatory effects on iSP release in human PDL neurons|
V. BINGHAM, J. ADCOCK, S.K.A. LEUNE, C. TURNER, X. SUN, K. KEISER, and K. HARGREAVES, University of Texas San Antonio / Health Science Ctr, USA|
Objective: The elegant studies of Byers, Rudd and others have demonstrated that pulpal necrosis leads to inflammation and sprouting of peptidergic neurons terminating in inflamed periradicular tissue. However, few studies have characterized the functional consequences of increased sprouting of human periradicular nociceptors. In this study, we tested the hypothesis that clinical inflammation leads to enhanced exocytotic activity of peripheral human PDL neurons, as measured by evoked release of immunoreactive substance P (iSP) from superfusates of isolated human apical root PDL neurons. Method: Following informed consent and local anesthesia, healthy teeth with fully formed apices, or teeth with necrotic pulp tissue and chronic apical periodontitis (CAP), were extracted; the apical 6mm of root was resected and placed in Hanks buffer. Baseline superfusates were collected over a 20 min period and at the end of the experiment, tissue was lysed to provide a measure of total cellular iSP. Both the spontaneously released iSP and total iSP (ie, sum of released iSP and cellular content of iSP) were measured by RIA and data analyzed by t-test. A total of 297 patients were placed on this study, with N=190 control teeth and N=97 teeth with necrotic pulps and chronic apical periodontitis. Results: As compared to iSP levels measured in root apices from control teeth, there was a 21% increase in spontaneous release of iSP (p<0.001) and a 61% in the total cellular content of iSP (p<0.001) collected from apices of teeth with pulpal necrosis and chronic apical periodontitis. Conclusions: These studies demonstrate that periradicular inflammation in teeth with necrotic pulp tissue and CAP evokes a significant change in content and exocytotic activity of peptidergic neurons, implicating neurogenic inflammation as an important component of this inflammatory response. Supported in part by P01 DA16719(KMH), R01 NS435186(KMH), AADR student research fellowships(SL,CT) and the CO*STAR training program(T32DE14318).
|Seq #194 - Pulpal Blood Flow and Innervation, Dentinal Fluid, Neuropeptides, and Pain|
10:15 AM-11:30 AM, Friday, 12 March 2004 Hawaii Convention Center Exhibit Hall 1-2