ENDODONTICS
Selected Recent Publications
  • Ferraz CCR, Diogenes A, Henry MA, Hargreaves KM. LPS from Porphyromonas gingivalis Sensitizes Capsaicin-Sensitive Nociceptors. J Endod (In press).
  • Khan A, Diogenes A, Jeske N, Henry M, Akopian A, Hargreaves KM. Tumor necrosis Factor alpha enhances the sensitivity of trigeminal ganglion neurons to capsaicin. Neuroscience 155:503-9, 2008.
  • Diogenes A, Akopian AN, Hargreaves KM. NGF Upregulates TRPA1: Implications for Orofacial Pain. J Dent Res 86:550-5, 2007.
  • Diogenes A, Hargreaves KM. Endodontic Infections and Pain. In: Fouad A. (ed.) Endodontic Microbiology, Blackwell Munksgaard, 2008.
  • Jeske N, Diogenes A, Ruparel NB, Fehrenbacher JC, Henry M, Akopian AN, Hargreaves KM. A-kinase anchoring protine mediates TRPV1 thermal hyeralgesia through PKA phosphorlation of TRPV1. Pain 138:604-16, 2008.
  • Diogenes A, Akopian AN, Hargreaves KM. NGF Upregulates TRPA1: Implications for Orofacial Pain. J Dent Res 86:550-5, 2007.
  • Gibbs JL, Diogenes A, Hargreagves KM. Neuropeptide Y modulates effects of bradykinin and prostaglandin E2 on trigeminal nociceptors via activation of the Y1 and Y2 receptors. Br J Pharmacol 2007;150:72-9.
  • Diogenes A, Patwardhan A, Ruparel N, Goffin A, Akopian A, Hargreaves KM. Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons. J Neurosci 26:8126-36 2006.
  • Patwardhan A, Diogenes A, Berg K, Fehrenbacher J, Clarke W, Akopian A, Hargreaves KM. PAR-2 agonists activate trigeminal nociceptors and induce functional competence in the delta opioid receptor. Pain 2006;125:114-24.
  • Ferraz CCR, Diogenes A, Henry MA, Hargreaves KM. LPS from Porphyromonas gingivalis Sensitizes Capsaicin-Sensitive Nociceptors. J Endod (In press).
  • Diogenes A, Patwardhan A, Ruparel N, Goffin A, Akopian A, Hargreaves KM. Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons. J Neurosci (in press) 2006.
  • Patwardhan A, Diogenes A, Berg K, BS; Fehrenbacher J, Clarke W, Akopian A, Hargreaves K. PAR-2 agonists activate trigeminal nociceptors and induce functional competence in the Delta opioid receptor. Pain 125:114-24, 2006.
  • Price TJ, Louria MD, Candelario-Soto D, Dussor GO, Jeske NA, Patwardhan AM, Diogenes A, Trott AA, Hargreaves KM, Flores CM. Treatment of trigeminal ganglion neurons in vitro with NGF, GDNF and BDNF: effects on neuronal survival, neurochemical properties and TRPV1-mediated neuropeptide secretion. BMC Neurosci. 2005 Jan 24;6(1):4
  • Patel TB, Tonioli MB, Patwardhan A, Diogenes A, Naftel J, Keiser K, Hargreaves KM. Characterization of Bradykinin receptor-expressing neurons in rat trigeminal ganglia. J Endodon 2004;30:263.
  • Tonioli MB, Patel TB, Diogenes A, Patwardhan A, Keiser K, Hargreaves KM. Effect of Neurotrophic factors on Bradykinin receptor expression in rat trigeminal sensory neurons determined by real-time polymerase chain reaction. J Endodon 2004;30:263.

Research Group Faculty

 
Dr. Anibal Diogenes, D.D.S., Ph.D.

Anibal Diogenes, DDS, PhD

Assistant Professor of Endodontics
D.D.S., Federal Univ. of Pernambuco Recife, Brazil
Ph.D., UT Health Science Center San Antonio

Office: 210-567-6668
Email: Diogenes@uthscsa.edu

 

Keywords

Pain, Nociceptors, TRPV1, TRPA1, LPS , Electrophysiology, Calcium Imaging, CGRP, Stem Cells, SCAP cells, Regenerative Endodontics, Pulp-dentin complex

 

Research Summary

Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Pain management is a global health problem. It is responsible for approximately 20% of medical visits and 10% of all prescribed medication in the U.S. alone. We recognize the complexity of the sensation of pain. Therefore, our laboratory focuses mainly on studying peripheral pain mechanisms with the goal to block pain signaling where it is initiated, in the periphery. Moreover, we aim to understand how inflammatory mediators and microorganism modulate peripheral nociception. This approach could lead to the development of peripherally restricted analgesics, avoiding the well-documented side-effects of centrally acting analgesics.

 

We employ single cell molecular techniques to animal models of pain to understand mechanistically how nociceptors detect different modalities, become sensitized and how their function could pharmacologically controlled. We use the dental pulp as a model of isolated nociceptors to test experimental drugs that could potentially become successful analgesics. In this technique, dental pulp isolated from extracted teeth is superfused, and released neuropeptides are measured as a dependent measure of neuronal activation. This ex-vivo is a unique and crucial bridging technique between basic science and clinical research.

 

Additionally, we are investigating ways of using autologous stem cells present in the apical dental papilla (SCAP cells) to regenerate the pulp-dentin complex. We use undifferentiated mesenchymal stem cells isolated from human dental pulp to test different interventions with the goal to control the fate of their differentiation and function in vitro. We also conduct clinical trials to evaluate different techniques aiming to regenerate the pulp-dentin complex in teeth that would have an otherwise very compromised prognosis.

 
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