D'Souza R N, Cavender A, Dickinson D, Roberts A, Letterio J
Department of Basic Sciences, University of Texas Houston Health Science Center, Dental Branch, 77030, USA.
Eur J Oral Sci. 1998 Jan;106 Suppl 1:185-91. doi: 10.1111/j.1600-0722.1998.tb02174.x.
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.
在发育和修复过程中影响成牙本质细胞功能的复杂细胞因子网络中，转化生长因子β1（TGF-β1）具有独特的双重功能，既能作为一种强效免疫抑制剂，又能作为细胞外基质产生的诱导剂。这些特性突出了该分子在损伤后维持牙髓牙本质复合体稳态中的重要性。本文旨在描述我们对TGF-β1基因敲除小鼠牙列进行表型分析的新发现。TGF-β1（-/-）后代的主要表型是弥漫性免疫系统激活伴进行性炎症、消瘦和死亡。我们对成年TGF-β1（-/-）牙列的研究显示广泛的牙髓和根尖周炎症及坏死。此外，咬合磨牙的冠面显示出明显磨损。为了确定TGF-β1（-/-）牙列中的表型变化是否直接与TGF-β1的缺失相关，而非炎症过程本身，我们研究了回交到免疫缺陷背景的成年TGF-β1（-/-）小鼠的牙列。我们的组织病理学和影像学分析结果表明，TGF-β1（-/-）免疫缺陷小鼠的牙齿在牙髓和根尖周区域保持活力，但咬合面出现过度磨损。
