Dr. Chung Projects
Molecular Mechanisms of Tooth Pain
Dental pain is one of the most common and unpleasant types of pain and is described as intense, throbbing, miserable, or unbearable. About 39 million people report experiencing one of five types of orofacial pain more than once during the previous 6 months. Among this cohort, there were 22 million toothaches. Although dental pain provides an important warning signal preventing further damage of our body, extreme dental pain needs to be reduced by dental professionals. Moreover, pain during or after dental operative procedures is the biggest barrier against regular visits for dental care. Therefore, in order to enhance the overall quality of dental care, it is critical to understand the mechanism of pathological and postoperative dental pain, and to develop more efficient strategies of prevention and management of dental pain. In spite of its high incidence and importance, our knowledge of mechanisms underlying tooth pain is relatively limited. We investigate molecular mechanisms of tooth pain using various animal models.
The Roles of Thermosensitive Transient Receptor Potential (TRP) Channels in Nociception
Our lab is interested in the function and modulation of nociceptive molecules in primary afferents. We primarily focus on the roles of thermosensitive TRP channels, especially TRPV1 and TRPA1. TRPV1 and TRPA1 are colocalized in a subset of sensory neurons having neurochemical properties of polymodal nociceptors. The pungency and pain induced by capsaicin is solely mediated by TRPV1 in mammal. TRPV1 can also be activated by noxious heat and acid. Under inflammatory condition, signals from multiple inflammatory mediators converge to enhance the expression and function of this receptor resulting in the sensitization of nociceptors to thermal stimuli and therby thermal hyperalgesia. Therefore, TRPV1 acts not only as a polymodal nocisensor but also the integrator of inflammatory signals. TRPA1 play critical roles as a sensor of tissue damage. TRPA1 is activated by remarkably various agents directly evoking pain and tissue damages such as natural pungent compounds (mustard oil, cinnamon, allicin, nicotine), an environmental pollutant (acrolein) and a toxic chemical (formalin). TRPA1 can also be activated by various endogenous substances that are generated under inflammation or injury such as hydrogen peroxide, 4-hydroxynonenal, bradykinin, and prostaglandin. Also, a growing number of evidence shows the involvement of TRPA1 in mechanical and cold hyperalgesia under inflammatory or nerve injury conditions in experimental animals. We study how the function and expression of these receptors are regulated under pathological conditions and contribute to pathological pain using electrophysiological, biochemical, mutagenic and mouse genetics approaches.
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