TGF-Beta 1 and CSF-1 as markers of fracture healing

Within the last ten years the fracture healing processes have been intensively investigated. More than 50 cytokines, angiogenesis factors, proteases and morphogens were described, which play a role in the fracture healing. Many animal studies have served the basic research to clear up the complex regulation mechanisms. However, despite the intensive research most of these remodelling processes are still unknown. Only little information about the systemic regulation of bone regeneration by growth factors exists. TGF-ß1 and CSF-1 have been shown to be important regulatory substances in fracture healing. The existence of TGF-ß 1 in callus has been reported in human and animal fracture models. The activating influence of TGF-ß 1 on osteoblasts, chondrocytes and chondroclasts is well known. Also CSF-1 plays an important roll in the bone remodelling. This cytokine enhances the osteogenesis by supporting the angiogenesis and by proliferation of osteoclast/ osteoblast population. TGF-ß1 and CSF-1 have been shown to be important regulatory substances in fracture healing but there is no detailed data on the presence of TGF-ß1 and CSF-1 in human serum, neither in patients with normal fracture healing nor in patients with pathologic fracture healing. To our knowledge only one single report on the serum concentration of TGF-ß1 exist. Zimmermann et al. could observe TGF-ß1 level variation in serum of patients with fracture of the long bone. A significant difference in the TGF-ß1 serum concentration between patients with normal fracture healing and patients with delayed-/ non union could be seen. Further, to our knowledge the systemic release of CSF-1 during the fracture healing is completely unexplored. In this prospective designed clinical study the TGF-ß1 and CSF-1 serum level of patients with fractures of long bone will be measured to document the course of systemic release and to evaluate the possible differences in the systemic release between patients with and without normal fracture healing.

Within the last ten years the fracture healing processes have been intensively investigated. More than 50 cytokines, angiogenesis factors, proteases and morphogens were described, which play a role in the fracture healing. Many animal studies have served the basic research to clear up the complex regulation mechanisms. However, despite the intensive research most of these remodelling processes are still unknown. Only little information about the systemic regulation of bone regeneration by growth factors exists. TGF-ß1 and CSF-1 have been shown to be important regulatory substances in fracture healing. The existence of TGF-ß1 in callus has been reported in human and animal fracture models. The activating influence of TGF-ß1 on osteoblasts, chondrocytes and chondroclasts is well known. Also CSF-1 plays an important roll in the bone remodelling. This cytokine enhances the osteogenesis by supporting the angiogenesis and by proliferation of osteoclast/ osteoblast population. TGF-ß1 and CSF-1 have been shown to be important regulatory substances in fracture healing but there is no detailed data on the presence of TGF-ß1 and CSF-1 in human serum, neither in patients with normal fracture healing nor in patients with pathologic fracture healing. To our knowledge only one single report on the serum concentration of TGF-ß1 exist. Zimmermann et al. could observe TGF-ß1 level variation in serum of patients with fracture of the long bone. A significant difference in the TGF-ß1 serum concentration between patients with normal fracture healing and patients with delayed-/ non union could be seen. Further, to our knowledge the systemic release of CSF-1 during the fracture healing is completely unexplored. In this prospective designed clinical study the TGF-ß1 and CSF-1 serum level of patients with fractures of long bone will be measured to document the course of systemic release and to evaluate the possible differences in the systemic release between patients with and without normal fracture healing.