RANKL

Progesterone signaling is very complex.

It works through multiple mechanisms to promote cellular proliferation and cell survival, with downstream signaling effects on cyclin D1 and RANKL, MAPK, and AKT, WNT1, and EGFR.

The estrogen receptor can be activated directly by estrogen binding, which is the classic ligand-dependent pathway, but the estrogen receptor is also a downstream target of growth factor pathways.

The PI3K/AKT/mTOR axis, as well as the RAS/RAF/MEK and MAP kinase axis, both feed into the estrogen receptor activity.

But how exactly does periodontitis disrupt this communication at a cellular level?

If we connect this to the bigger picture, it really comes down to a molecular signaling pathway known as RANK, RANKL, and OPG.

Okay, the alphabet soup.

Break that down for us.

So in healthy bone remodeling, pre-osceoblasts express a protein called RANKL.

Pre-osteoclasts have a receptor called RANK.

When RANKL binds to the RANK receptor, it basically commands that cell to mature into an active bone-eating osteoclast.

Oh, I see.