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TGF‐β1 is essential for the homeostasis of the dentin‐pulp complex
Author(s) -
D'Souza Re.,
Cavender Adriana,
Dickinson Douglas,
Roberts Anita,
Letterio John
Publication year - 1998
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.1998.tb02174.x
Subject(s) - homeostasis , pulp (tooth) , dentin , dentistry , chemistry , medicine
Among the complex network of cytokines that influence odontoblast function during development and repair, TGF‐β1 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‐β1 gene has been disrupted. The major phenotype of TGF‐β1 (−/−) offspring is one of diffuse immune system activation with progressive inflammation, wasting and death. Our studies of adult TGF‐β1 (−/−) 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‐β1 (−/−) dentition are directly linked to the loss of TGF‐β1 rather than the inflammatory process itself, we studied adult dentition in TGF‐β1 (−/−) mice backcrossed into immunodeficient backgrounds. Results of our histopathologic and radiographic analyses show that teeth of TGF‐β1 (−/−) immunodeficient mice retain vitality in pulpal and periapical regions but show excessive wear of occlusal surfaces.