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OR11 - The Role of KDM3C in Oral Inflammation During Aging

Thursday, April 28, 2022

2:00 PM – 2:10 PM PST

Location: 225

Presenter(s)

AA

Abdullah Alshaikh, B.D.S., M.S.

Resident
University of California, Los Angeles
Los Angeles, California

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

Co-Author(s)

Mo Kang, D.D.S., M.S., Ph.D.

Professor and Chair
University of California, Los Angeles
Los Angeles, California

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

Wei Chen, M.S., Ph.D.

N/A
University of California, Los Angeles
Los Angeles, California

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

Jaeyoung Lee, Ph.D.

Post-doc
University of Alberta
Los Angeles, California

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

Abstract: Objectives: Aging is associated with a decline in immune function and their response to an infection, including oral infection. Our lab identified histone lys-specific demethylases (KDM3C) as a regulator to inflammatory signaling against Porphyromonos gingivalis (Pg). Specifically, we found that KDM3C regulates inflammatory cytokines through the suppression of NF-κB signaling. In the current study, we investigated the role of KDM3C during aging and the impact of KDM3C on the pathogenesis of apical periodontitis (AP) in mice after pulp exposure. Methods: Dental pulp of maxillary first molars of young KDM3C knockout (kdm3c-/-), KDM3C wildtype (kdm3c+/+) and aged mice were exposed to induce AP. Apical lesion development was assessed by µCT analysis, and histological analysis. Results: Pulp exposure led to AP formation in mice at 21 days, and the size of AP was notably increased in KDM3C-/- mice and aged mice compared with the KDM3C+/+ mice. H&E staining revealed strong infiltration of inflammatory cells to periapex in KDM3C-/- mice and aged mice. Expression of the inflammatory cytokines, for example, IL-1β, TNF-α and IL-6 were significantly increased in bone marrow derived macrophage (BMDM) from KDM3C-/- and aged mice compared to KDM3C+/+ mice. Conclusion: These findings highlight the role of KDM3C on immune responses to oral bacterial infection in the root canals during aging, and demonstrate a possibility of developing novel anti-inflammatory therapeutics for management and treatment of oral inflammatory conditions.