The site of tendon insertion into bone, known as enthesis, is susceptible to injury and disease. Yet, due to the complexity of this transitional tissue, the ability to repair it surgically is very limited. Previously, we discovered that the embryonic enthesis develops modularly from a unique population of progenitor cells, which are distinct from the lineages that give rise to tendon and bone. We also identified the molecular signaling pathways that control these progenitors. Based on these findings, we set out to demonstrate that delivering the embryonic progenitors to an injured adult enthesis stimulates a regenerative process. If successful, this approach would revolutionize the treatment of enthesis injuries. However, while trying to establish the technical feasibility of our idea, we made a remarkable discovery. We saw that during postnatal development, the descendants of the embryonic enthesis progenitors are replaced by another cell population. This exceptional developmental strategy implies that the embryonic progenitors enthesis are inutile for adult enthesis regeneration. Since making this discovery, we have tried to find and characterize the cell populations that inhabit the mature enthesis. Thus far, we have identified two highly likely candidate populations. Once their role in enthesis maturation is validated, we will be able to resume our proof-of-concept project.
