Among the complex network of cytokines that influence odontoblast func
tion during development and repair. TGF-beta 1 is unique in its dual a
bilities to function as a potent immunosuppressant and as an inducer o
f extracellular matrix production. These properties underscore the imp
ortance of this molecule in maintaining the homeostasis of the dentin-
pulp complex after injury. The purpose of this paper is to describe ne
w findings of our phenotypic analysis of dentition in mice in which th
e TGF-beta 1 gene has been disrupted. The major phenotype of TGF-beta
1(-/-) offspring is one of diffuse immune system activation with progr
essive inflammation; wasting and death. Our studies elf adult TGF-beta
1(-/-) dentition show widespread pulpal and periapical inflammation a
nd necroses. In addition, the coronal surfaces of occluding molars sho
w marked attrition. To determine whether the phenotypic changes in TGF
-beta 1(-/-) dentition are directly linked to the loss of TGF-beta 1 r
ather 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 te
eth of TGF-beta 1(-/-) immunodeficient mice retain vitality in pulpal
and periapical regions but show excessive wear of occlusal surfaces.