Senescent-cell clearance impairs fracture repair

This proposed mechanism asks whether clearing senescent cells, cells that stop dividing but affect tissue, can impair bone fracture repair while bone-turnover markers improve. It proposes that early stromal cells, tissue support cells, provide net activity that activates plasminogen into plasmin, an enzyme that dissolves fibrin. Fibrin is a temporary mesh at a healing fracture. Clearing these cells could leave fibrin across the gap and prevent bone bridging. A decisive experiment would continue cell depletion while restoring fibrin removal. If verified clearance restored union, it would support this hypothesis. If union still failed, structural tension, molecular-signal placement or cell-to-cell communication would remain plausible. Study design is still required.