TGF-β1 is essential for the homeostasis of the dentin-pulp complex

Among the complex network of cytokines that influence odontoblast function during development and repair. TGF-beta 1 is unique in its dual abilities to function as a potent immunosuppressant and as an inducer of extracellular matrix production. These properties underscore the importance of this molecule in maintaining the homeostasis of the dentin-pulp complex after injury. The purpose of this paper is to describe new findings of our phenotypic analysis of dentition in mice in which the TGF-beta 1 gene has been disrupted. The major phenotype of TGF-beta 1(-/-) offspring is one of diffuse immune system activation with progressive inflammation; wasting and death. Our studies elf adult TGF-beta 1(-/-) dentition show widespread pulpal and periapical inflammation and necroses. In addition, the coronal surfaces of occluding molars show marked attrition. To determine whether the phenotypic changes in TGF-beta 1(-/-) dentition are directly linked to the loss of TGF-beta 1 rather than the inflammatory process itself, we studied adult dentition in TGF-beta 1(-/-) mice backcrossed into immunodeficient backgrounds. Results of our histopathologic and radiographic analyses show that teeth of TGF-beta 1(-/-) immunodeficient mice retain vitality in pulpal and periapical regions but show excessive wear of occlusal surfaces.