P-2 - Cellular and Molecular Biology of AP and Its Clinical Translation

Thursday, April 28, 2022

10:00 AM – 11:30 AM PST

Location: 226

CE: 1.5

Speaker(s)

Anibal Diogenes, D.D.S., PhD

Professor
University of Texas at San Antonio
San Antonio, Texas

Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.
Gustavo P. Garlet, D.D.S., PhD

Professor - Dept of Biological Sciences
University of São Paulo
Bauru, Sao Paulo, Brazil

Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.

Session Host(s)

Amber Ather, D.D.S., B.D.S., M.D.S., M.S.

Assistant Professor
Virginia Commonwealth University
Richmond, Virginia

Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.

Apical periodontitis is characterized by pain and osteolytic lesions, two hallmarks of apical periodontics, that can co-exist or be present separately during different stages of the disease. As a general rule, host inflammatory mediators have been associated with tissue destruction while anti-inflammatory mediators counteract and attenuate disease progression. With the discovery of several T cell subsets bearing distinct immunoregulatory properties this pro- versus anti-inflammatory scenario become more complex, and a series of studies has been hypothesizing protective or destructive roles for Th1, Th2, Th17 and Tregs subpopulations of polarized lymphocytes. In addition, there is an increasing body of evidence that implicates nociceptors as active participants in the overall inflammatory process. Thus, pain-sensing fibers are not only serving a sensorial role but help orchestrate the shift between osteolytic and osteogenic responses in AP. These new findings have direct translational significance for our understanding of the progression and resolution of the disease that is the primary focus of Endodontics as a specialty.

Learning Objectives:

Upon completion, participants will be able to identify the elements of host inflammatory immune respose involved in AP pathogenesis
Understand how the modulation of host inflammatory immune respose elements can modify AP lesions outcome
Understand the molecular and cellular basis of the clinical presentation regarding pain and osteolytic lesions