Dental Roots: Formation, Lengthening and Malformations of Roots

The Hertwig’s Epithelial Root Sheath (HERS) includes two layers: the Outer Enamel Epithelial Root Sheath and the Inner Enamel Epithelium Epithelium (IEE and OEE). They contribute both to the root formation. The inner columnar epithelial cells (IEE) of the dental papilla are formed by cells located near the dental papilla. They are at the origin of odontoblasts expressing FGF-4, -8 and -9 and at later stages BMP-2 and BMP7. The Outer Epithelial cells (OEE) express SHH, Msx2, enamel matrix proteins, paxillin, and Pax-6. When the cells of the HERS dissociate, intercellular spaces enlarge. Cells migrate from the epithelial sac, and underwent phenotypic inter conversion into cementoblasts and later cementocytes. The Hertwigs enamel epithelium contributes to cementum formation. Epithelial rest of Malassez is remnants of the Hertwig’s root sheath. They are implicated in cementogenesis. Root lengthening and dentin thickening are involved in root elongation and dentin thickening to the detriment of the pulp chamber that is gradually reduced in volume. Apexogenesis and apexification contribute to root formation. Defects and abnormal root formation implicate missing teeth(hypodontia), orteeth in excess (supernumary teeth or hyperdontia) or mis-shapped structures. Genetic defects (Nfic, Ptc, Dkk1, Osx, Smad4, and Wls) have been identified. Premature arrests of root formation are due to apical infection, radiation, chemotherapy, as well as genes alterations. Roots malformations include root dilacerations which are abnormal curvature of the root and sharp bend of the crown or root axis. Taurodontism and other misshaped root structures are also frequently seen in man. Two main forms have been recognized: 1) the CLCN7 encoding a chloride channel, and 2) the second related to a defective PLG gene (encoding plasminogen). Altogether, theses defects contribute to major endodontic difficulties.