Cellular Senescence Of RANKL+ Osteoblasts And Th17 Cells In Severe Periodontitis With Occlusal Trauma

Aging Theory
Aging Pathway
Therapeutic
The study revealed that senescent RANKL+ osteoblasts and Th17 cells contribute to bone resorption in severe periodontitis exacerbated by occlusal trauma.
Author

Gemini

Published

December 3, 2025

Have you ever wondered why some gum diseases are so severe, especially when combined with issues like teeth grinding or an improper bite? Recent research sheds light on a crucial factor: “senescent cells.” These are essentially “aged” cells that have stopped dividing but remain active, often releasing harmful substances. This study focused on severe gum disease, also known as periodontitis, particularly when it’s made worse by excessive biting forces, like those from an ill-fitting dental prosthesis. Researchers discovered that in these severe cases, there’s an increase in these senescent cells, specifically certain bone-forming cells (osteoblasts) and immune cells (Th17 cells). What’s more, these aged cells were found to be actively involved in the process of bone destruction. Think of it this way: normally, your body has a balance between building and breaking down bone. But in severe periodontitis with excessive force, these senescent cells tip the scales towards bone breakdown, leading to the loss of the bone that supports your teeth. The good news is that when researchers used special drugs called “senolytics” – which are designed to clear out these senescent cells – they observed a reduction in both the aged cells and the bone-destroying cells, ultimately preventing further bone loss. This discovery is exciting because it points to a new way to tackle severe gum disease by targeting these problematic senescent cells, potentially offering a novel approach to treatment beyond traditional methods.


Source: link to paper