Fig. 1.

Schematic of tooth pattern in the adult and embryonic mouse and a model of apoptosis regulation in tooth buds. (A) Each quadrant of the adult mouse dentition has one incisor and three molars separated by a toothless diastema. (B) Schematic of tooth pattern in one jaw quadrant in adult and embryonic mouse. In the anterior part of the embryonic diastema, either rudimentary small placodes/buds (D¹–D⁵) or an epithelial thickening (dashed line) develops in the maxilla or mandible, respectively, until ED 13.0, at which point they start to disappear (Peterkova et al., '95; Lesot et al., '99). In the posterior part of the diastema, two large rudimentary buds consecutively appear and become the most prominent tooth primordia in the cheek region at ED 12.5 and 13.5, respectively (R¹ and R² in the maxilla; MS and R₂ in the mandible), before their development ceases. After ED 13.0, R¹, R² and MS regress, whereas the R₂ bud is incorporated (large arrow) into the anterior part of the first molar cap (Peterkova et al., '96; Viriot et al., 2000). The remnants of R¹, R² and MS are thought to contribute during later morphogenesis to expansion of the first molar (Lesot et al., '96; Peterkova et al., 2005). Black spots indicate the primordia affected by programmed cell death (apoptosis), which occurs during elimination of D¹–D⁵, regression of R¹, R² and MS and growth retardation of R₂ (Tureckova et al., '96; Peterkova et al., '96; Viriot et al., 2000). The upper mouse incisor originates from five to six tooth placodes, whereas three placodes might occur in the lower incisor region at initial stages (Peterkova et al., 2002a) (not shown). I, incisor; M1, M2, M3, first, second and third molars, respectively. (C) A model for the regulation of apoptosis at the tip of a tooth bud by interaction between growth activators (e.g. FGFs) and inhibitors (e.g. BMPs). A local excess of inhibitors leads to the epithelial cells' failure to receive adequate growth-activating (apoptosis-suppressing) signals (e.g. FGF). This signaling imbalance (relative predominance of inhibitors) can stimulate apoptosis (modified from Peterkova et al., 2003). ED, embryonic day; FGF, fibroblast growth factor; BMP, bone morphogenetic protein.