Cytoskeleton, intercellular junctions, planar cell polarity, and cell movement in amelogenesis

Tooth enamel is composed of highly mineralized rods surrounded by interrod crystals that are formed by ameloblasts derived from dental epithelium. Secretory ameloblasts migrate during hard tissue formation, both away from the dentin and in groups that slide past each other, resulting in rod decussation. Enamel rod decussation is commonly observed in many animal teeth including humans. Cytoskeleton fibers, such as microtubules, intermediate filaments, and actin filaments, are associated with ameloblast movement. Rat incisor enamel is composed of initial, inner, outer, and final layers. Secretory ameloblasts forming the inner enamel layer move laterally and have proximal and distal junctional complexes attached to actomyosin filaments. Conversely, secretory ameloblasts forming the outer enamel layer cease lateral movement. Secretory ameloblasts forming the inner layer are characterized by anisotropic distribution of adherens junctions, desmosomes, and actomyosin filaments in transverse distal junctional complexes. Isotropic distribution is observed in distal junctional complexes in secretory ameloblasts forming the outer layer. Actin cytoskeleton and junctions may act as a motor apparatus to control the sideways movement of ameloblasts. However, the mechanism that determines whether secretory ameloblasts forming the inner layer move medially or laterally is unclear. One potential group of proteins that may be involved in this process is the core planar cell polarity (PCP) proteins. One core PCP protein, VANGL2, is proposed to be a key molecule determining the direction of ameloblast movement.