TGF-beta1 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-beta1 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-beta1 gene has been disrupted. The major phenotype of TGF-beta1(-/-) offspring is one of diffuse immune system activation with progressive inflammation, wasting and death. Our studies of adult TGF-beta1(-/-) 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-beta1(-/-) dentition are directly linked to the loss of TGF-beta1 rather than the inflammatory process itself, we studied adult dentition in TGF-beta1(-/-) mice backcrossed into immunodeficient backgrounds. Results of our histopathologic and radiographic analyses show that teeth of TGF-beta1(-/-) immunodeficient mice retain vitality in pulpal and periapical regions but show excessive wear of occlusal surfaces.[1]References
- TGF-beta1 is essential for the homeostasis of the dentin-pulp complex. D'Souza, R.N., Cavender, A., Dickinson, D., Roberts, A., Letterio, J. Eur. J. Oral Sci. (1998) [Pubmed]
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