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:
After this session, attendees will be able to:
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.
