Upregulation of basal TGFβ1 levels by EMF coincident with chondrogenesis – implications for skeletal repair and tissue engineering

Abstract

Members of the TGFβ/BMP gene family regulate cartilage and bone development. These genes are re‐expressed in bone repair and are thought to mediate chondro‐ and osteoprogenitor cell differentiation. These observations have led to a therapeutic strategy of introducing these growth factors into experimental cartilage and bone defects. Therapeutic efficacy, however, has been limited by diffusion or inactivation of these growth factors from the desired site and by the inability to deliver sustained concentrations of growth factors. This study demonstrates an increase in basal TGFβ mRNA and protein levels in association with chondrogenic differentiation in endochondral ossification. mRNA is increased by 158%; protein by 23%, and cells immunopositive for TGFβ by 343% at maximal TGFβ expression. Importantly, the pattern of TGFβ expression is preserved throughout the developmental sequence. Our data suggest that the exposure to a specific electromagnetic field (EMF) enhances, but does not disorganize, chondrogenesis and endochondral calcification as well as the normal physiologic expression of TGFβ. The ability to increase TGFβ at a moderately low dose for sustained periods of time without disorganizing its physiology suggests the ability to establish temporal concentration gradients of growth factors for the purpose of stimulating skeletal repair. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.