Demonstration of TGF-beta 1 mRNA by in situ hybridization in normal human fracture healing.

Abstract

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-beta 1 gene expression in specimens of callus from normally healing human fractures, using in situ hybridization to a cDNA TGF-beta 1 probe and an autoradiographic disclosure system. TGF-beta 1 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-beta 1 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-beta 1, animal models accurately reflect human bone repair.