Teeth are mineralized organs composed of three unique hard tissues, enamel, dentin, and cementum, and supported by the surrounding alveolar bone. Although odontogenesis differs from osteogenesis in several respects, tooth mineralization is susceptible to similar developmental failures as bone. Here we discuss conditions fitting under the umbrella of rickets, which traditionally referred to skeletal disease associated with vitamin D deficiency but has been more recently expanded to include newly identified factors involved in endocrine regulation of vitamin D, phosphate, and calcium, including phosphate-regulating endopeptidase homolog, X-linked, fibroblast growth factor 23, and dentin matrix protein 1. Systemic mineral metabolism intersects with local regulation of mineralization, and factors including tissue nonspecific alkaline phosphatase are necessary for proper mineralization, where rickets can result from loss of activity of tissue nonspecific alkaline phosphatase. Individuals suffering from rickets often bear the additional burden of a defective dentition, and transgenic mouse models have aided in understanding the nature and mechanisms involved in tooth defects, which may or may not parallel rachitic bone defects. This report reviews dental effects of the range of rachitic disorders, including discussion of etiologies of hereditary forms of rickets, a survey of resulting bone and tooth mineralization disorders, and a discussion of mechanisms, known and hypothesized, involved in the observed dental pathologies. Descriptions of human pathology are augmented by analysis of transgenic mouse models, and new interpretations are brought to bear on questions of how teeth are affected under conditions of rickets. In short, the rachitic tooth will be revealed.

中文翻译：

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棘齿。

牙齿是由三种独特的硬组织（牙釉质、牙本质和牙骨质）组成的矿化器官，并由周围的牙槽骨支撑。尽管牙形成在几个方面与成骨不同，但牙齿矿化容易受到与骨骼类似的发育障碍的影响。在这里，我们讨论了符合佝偻病的条件，传统上指与维生素 D 缺乏相关的骨骼疾病，但最近已扩展到包括新发现的与维生素 D、磷酸盐和钙的内分泌调节有关的因素，包括磷酸盐调节内肽酶同源物、X 连锁、成纤维细胞生长因子 23 和牙本质基质蛋白 1。全身矿物质代谢与矿化的局部调节相交，包括组织非特异性碱性磷酸酶在内的因素是适当矿化所必需的，其中组织非特异性碱性磷酸酶的活性丧失会导致佝偻病。患有佝偻病的人通常承受着牙列缺陷的额外负担，转基因小鼠模型有助于理解牙齿缺陷的性质和机制，这些缺陷可能与轴状骨缺损平行，也可能不平行。本报告回顾了一系列佝偻病对牙齿的影响，包括对佝偻病遗传形式的病因的讨论，对由此产生的骨和牙齿矿化障碍的调查，以及对所观察到的牙齿病理所涉及的已知和假设机制的讨论。通过对转基因小鼠模型的分析，增强了人类病理学的描述，并对佝偻病情况下牙齿如何受到影响的问题提出了新的解释。简而言之，将显露轴齿。