Exploring the Role of SPP1 in Macrophage-Osteogenic Cell Crosstalk and its involvement in Heterotopic Ossification in Fibrodysplasia Ossificans Progressiva

Fibrodysplasia Ossificans Progressiva (FOP) is a rare genetic disorder where soft tissues like muscles and ligaments turn into bone, leading to severe disability from a young age. This is caused by changes in a gene called ACVR1, which makes the body create bone where it shouldn't, a process known as heterotopic ossification (HO). Current treatments are limited and not very effective, so new approaches are needed.

Our research focuses on a protein called SPP1, which our preliminary studies show is involved in how immune cells and bone-forming cells interact, promoting unwanted bone growth. We aim to understand exactly how SPP1 influences these interactions and contributes to HO in FOP patients.

We will use specially bred mice that mimic the human condition of FOP to study the effects of SPP1. We will look at how blocking SPP1 affects the behavior of immune cells and bone-forming cells in both cells and living animals. Techniques like gene editing (using CRISPR-Cas9) will help us see what happens when SPP1 is removed from these cells.

By uncovering the role of SPP1 in FOP, we hope to find new targets for therapy that could prevent or reduce the abnormal bone growth in patients. This research could lead to the development of better treatments, improving the quality of life for those affected by this debilitating condition.

Our ultimate goal is to provide insights that will aid ongoing clinical trials and foster new strategies to combat FOP, offering hope for patients and advancing scientific knowledge