ENDODONTICS
Selected Publications
  • Henry M.A., Luo S., Foley B.D., Rzasa R.S., Johnson L.R. and Levinson S.R. Sodium channel expression and localization at demyelinated sites in painful human dental pulp. Journal of Pain, in press, 2009.
  • Fehrenbacher J.C., Sun X.X., Locke E.E., Henry M.A. and Hargreaves K.M.  Capsaicin-evoked iCGRP release from human dental pulp: a model system for the study of peripheral neuropeptide secretion in normal healthy tissue. Pain, in press, 2009.
  • Jeske N.A., Patwardhan A.M., Henry M.A. and Milam S.B. Fibronectin stimulates TRPV1 translocation in primary sensory neurons.  Journal of Neurochemistry, in press, 2008.
  • Hargreaves K.M., Geisler T., Wang Y. and Henry M.A.  Regeneration potential of the young permanent tooth: what does the future hold?  Journal of Endodontics, 34(7S): S51-56, 2008.
  • Jeske N,A., Diogenes A., Ruparel N.B., Fehrenbacher J.C., Henry M., Akopian A.N. and Hargreaves K.M. A-kinase anchoring protein mediates TRPV1 thermal hyperalgesia through PKA phosphorylation of TRPV1. Pain, 138:604-616, 2008.
     
    Luo S., Perry G.M., Levinson S.R. and Henry M.A.  Nav1.7 expression is increased in painful human dental pulp. Molecular Pain, 4:16, 2008.
  • Henry M.A., Freking, A.R., Johnson, L.R., and Levinson S.R.  Sodium channel Nav1.6 accumulates at the site of infraorbital nerve injury. BMC Neuroscience, 8:56, 2007.
  • Alvarado L.T., Perry G.M., Hargreaves K.M., and Henry M.A.  TRPM8 axonal expression is decreased in painful human teeth with irreversible pulpitis and cold hyperalgesia. Journal of Endodontics, 33(10):1167-1171, 2007.
  • Henry M.A., and Hargreaves K.M. Peripheral mechanisms of odontogenic pain. In: Dental Clinics of North America, Temporomandibular Disorders and Orofacial Pain, H. A. Gremillion (Ed.) Saunders, Philadelphia, 51:19-44, 2007.
  • Henry M.A., Freking A.R., Johnson L.R., and Levinson S.R.  Increased sodium channel immunofluorescence at myelinated and demyelinated sites following an inflammatory and partial axotomy lesion of the rat infraorbital nerve. Pain, 124:222-233, 2006.
  • Henry M.A., Sorensen H.J., Johnson L.R. and Levinson S.R.  Localization of the Nav1.8 sodium channel isoform at nodes of Ranvier in normal human radicular tooth pulp.  Neurosci. Lett., 380 (1-2):32-36, 2005.
  • Henry, M.A., Rzasa R.S., Beeler J.L., and Levinson S.R.  Caspr reveals an aggregation of nodes and flanking free zones at the rat trigeminal sensory root and dorsal root entry zones.  GLIA, 49:445-450, 2005.
  • Savage M.G. and Henry M.A.  Preoperative nonsteroidal anti-inflammatory agents: review of the literature.  Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod., 98(2):146-152, 2004.

Research Group Faculty

 
Michael A. Henry

Michael A. Henry, DDS, PhD

Professor
D.D.S., University of Washington School of Dentistry
Ph.D., University of Washington School of Medicine
Certificate, Facial Pain, University of Florida College of Dentistry

Office: 210-567-0877
Email: Henrym2@uthscsa.edu

 

Keywords

Neuroanatomy, Trigeminal, Electron Microscopy, Confocal Microscopy, Orofacial, Pain, Immunocytochemistry, Regenerative Endodontics

 

Research Summary

My primary research interests are related to the neuroanatomical basis for pain transmission and modulation within the trigeminal system. These interests are tied to my clinical background with training in Orofacial Pain and as an Orofacial Pain clinician. A major focus of these studies has involved changes in sodium channel expression in painful human dental pulp as a model for inflammatory pain and in the rat trigeminal system following nerve lesions as a model for neuropathic pain. More recent studies are evaluating contributions from glia, immune and vascular systems to these inflammatory and neuropathic pain conditions, and stem-cell based therapies to regenerate the human pulpodentin complex. These studies are mostly accomplished with the use of the confocal microscope and the application of quantitative analysis techniques that objectively evaluate differences in immunofluorescence intensity within structures located in painful tissues as compared to normal tissues.

 
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