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.