Akshay Basireddy
Pronouns: He/Him
Research Mentor(s): Ann Decker
Research Mentor School/College/Department: Periodontics and Oral Medicine / Dentistry
Program:
Authors: Akshay Basireddy, Jim Sugai, Kelsey Martin, Ann Decker
Session: Session 4: 1:40 pm – 2:30 pm
Poster: 10
Abstract
Periodontitis is a chronic inflammatory disease in the oral cavity affecting over 40% of the population in the United States. The periodontium consists of four underlying structures: alveolar bone, gingiva, periodontal ligament and tooth cementum structures. Periodontitis causes the destruction of the periodontium through chronic inflammation and persistently activated pathways of osteoclastogenesis in the mouth. Understanding mechanisms that limit periodontal disease progression and preservation of periodontal structures in the context of these chronic inflammatory stimulants essential to improving the quality of life of patients living with periodontal disease. We have previously observed that inhibition of merTK, a receptor expressed on both mesenchymal and hematopoietic lineage cell types, affects bone homeostasis. However, the receptor dynamics are not characterized in the context of periodontal disease. Thus, the goal of our work is to understand the mechanism that relates merTK and periodontitis progression. Our hypothesis is that inhibition of merTK receptors alter immune cell infiltrate and phenotype into the local periodontal space. As such, periodontitis was induced by placement of a silk suture ligature around the second molar of wildtype (c57blk/6) and merTK-/- mice. After 21 days of ligature placement, maxillae were harvested and processed for uCT and histological analysis. To identify neutrophil quantity and phenotype, sections were labeled using DAPI, Lys6G, and Histone H3 antibodies and confocal images acquired. Bone destruction was observed to be limited in merTK-/- mice compared to wild type controls. Thus, it is possible inhibition of merTK may direct neutrophil infiltration and netosis capabilities at the local site of chronic inflammatory stimulus.
