The influence of extracellular matrix on human periodontal ligament stem cell properties

Abstract

The periodontal ligament (PDL) is a crucial tissue connecting teeth to surrounding alveolar bone, withstanding the mechanical forces of mastication, speech, and deglutition. The extracellular matrix (ECM) of the PDL plays a critical role in maintaining PDL cell stability and function in response to external forces. Mechanotransduction, the process by which cells convert mechanical signals into biochemical signals, is essential for PDL cells to sense and respond to mechanical stimuli. The ECM is a critical mediator of mechanotransduction, as it is responsible for transmitting mechanical forces to cells and regulating cellular responses to mechanical stress. Matricellular proteins, such as periostin (PN) and osteopontin (OPN), are two important components of the PDL ECM that play significant roles in regulating PDL function and bone remodeling under mechanical stress. PN is primarily located in areas exposed to mechanical loading, such as teeth and bone, and functions as a matrix-cell attachment protein that regulates cell adhesion and motility. OPN is involved in cell adhesion, migration, and biomineralization in the PDL and bone, and can regulate cellular responses to external stimulation through multiple pathways.

This dissertation focuses on the role of matricellular proteins in outside-in signaling from the surrounding ECM, specifically in maintaining the homeostasis of PDL tissue. Firstly, we investigated the importance of the OPN protein on the osteogenic capacity of human periodontal ligament stem cells (hPDLSCs). Additionally, we demonstrated the role of PN as a mediator of hPDLSCs mechanotransduction. Finally, we extended our understanding of the profile of PDL-ECM components under the influence of mechanical force using a rat occlusal hypofunction model.

Understanding the role of the ECM in PDL mechanotransduction is critical for developing new insights into the prevention and treatment of tooth loss. Further studies are needed to fully elucidate the mechanisms underlying ECM mechanotransduction and the roles of ECM protein in regulating osteogenic differentiation, bone formation, and remodeling.