DEMONSTRATION OF TGF-BETA-1 MESSENGER-RNA BY INSITU HYBRIDIZATION IN NORMAL HUMAN FRACTURE-HEALING

The role of transforming growth factor beta (TGF-beta) in fracture healing has previously been investigated in a rodent model, but not in human material. We investigated TGF-beta1 gene expression in specimens of callus from normally healing human fractures, using in situ hybridization to a cDNA TGF-beta1 probe and an autoradiographic disclosure system. TGF-beta1 mRNA was present in areas of proliferation of mesenchymal tissue, bone, and cartilage. Levels of expression were lower in cells in the fracture hematoma and in differentiated (hypertrophic) chondrocytes. These results are compatible with those found in various animal models using immunohistochemistry and support the view that locally produced TGF-beta1 is a regulator of fracture repair in humans from the early (mesenchymal proliferation) stage to the stage of remodeling of woven bone. They also indicate that, for TGF-beta1, animal models accurately reflect human bone repair.