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Thomas M. Graber Award of Special Merit; Molecular Rescue of a Mouse Model: Primary Failure of Eruption
Date
May 4, 2024
It has been well studied that primary failure of eruption (PFE) is resultant from haploinsufficiency in the receptor for parathyroid hormone (PTH)/PTH related protein (PTHrP), PPR. However, the exact pathway and its downstream effects responsible for the PFE phenotype are not well understood. This presentation discusses a pilot aimed to evaluate structural changes of a rescued PFE mouse by genetically removing CD200, a downstream protein of the PPR pathway, from a PFE mouse model to assess if CD200 may be a therapeutic target to rescue PFE, providing a promising avenue for orthodontists to treat PFE.
Learning Objectives
- Demonstrate the implications of CD200 glycoprotein in its role of the PFE phenotype.
- Discuss structural changes in root length and eruption height due to CD200 gene knockout in the rescued PFE mouse models.
- Illustrate histological changes in Periostin+ periodontal ligament cells in the rescued PFE mice.
Speaker
Brittany Trinh, DDS, MS
