Observations on continuously growing roots of the sloth and the K14‐Eda transgenic mice indicate that epithelial stem cells can give rise to both the ameloblast and root epithelium cell lineage creating distinct tooth patterns

Abstract

Root development is traditionally associated with the formation of Hertwig's epithelial root sheath (HERS), whose fragments give rise to the epithelial cell rests of Malassez (ERM). The HERS is formed by depletion of the core of stellate reticulum cells, the putative stem cells, in the cervical loop, leaving only a double layer of the basal epithelium with limited growth capacity. The continuously growing incisor of the rodent is subdivided into a crown analog half on the labial side, with a cervical loop containing a large core of stellate reticulum, and its progeny gives rise to enamel producing. The lingual side is known as the root analog and gives rise to ERM. We show that the lingual cervical loop contains a small core of stellate reticulum cells and suggest that it acts as a functional stem cell niche. Similarly we show that continuously growing roots represented by the sloth molar and K14-Eda transgenic incisor maintain a cervical loop with a small core of stellate reticulum cells around the entire circumference of the tooth and do not form a HERS, and still give rise to ERM. We propose that HERS is not a necessary structure to initiate root formation. Moreover, we conclude that crown vs. root formation, i.e. the production of enamel vs. cementum, and the differentiation of the epithelial cells into ameloblasts vs. ERM, can be regulated independently from the regulation of stem cell maintenance. This developmental flexibility may underlie the developmental and evolutionary diversity in tooth patterning.

Apc inhibition of Wnt signaling regulates supernumerary tooth formation during embryogenesis and throughout adulthood

“…Ablation of Apc or activation of Wnt/β-catenin signaling may reprogram or reactivate the oral and dental epithelia, which then interact with adjacent mesenchyme to form new teeth. Even mesenchymal cells along the lingual aspect of the mouse incisor, which represents the root analog of the molar tooth and contains periodontal ligaments (Tummers and Thesleff, 2008), retain responsiveness to initiation signals from the dental epithelium and are able to participate in new tooth formation. Notably, the supernumerary teeth form in the vicinity of the incisor and molar teeth.…”

The Pitx2:miR-200c/141:noggin pathway regulates Bmp signaling and ameloblast differentiation

“…The labial CL consists of the IEE and OEE, as well as SR cells, which although epithelialderived exhibit a mesenchyme-like morphology and are housed between the IEE and OEE (Fig. 8A) (Harada et al, 1999;Tummers and Thesleff, 2003;Tummers and Thesleff, 2008). Notably, LS-8 cells were isolated from the oral/enamel epithelium of embryonic mouse teeth (Chen et al, 1992;Xu et al, 2006), and their lack of a dental epithelial phenotype in culture, along with the low expression of Amel and the absence of expression of many ameloblast-specific genes such as ameloblastin, enamelin and tuftelin (data not shown), suggests a predominantly SR-like cell population.…”

“…The epithelial stem cells that control growth of the mouse incisor are located in niches called the labial and lingual cervical loop (CL) at the proximal end of the incisor (Harada et al, 1999); however, only the labial CL produces ameloblasts that generate enamel. Although it is well accepted that dental epithelial stem cells are housed in the labial CL, their precise location is still a matter of debate (Harada et al, 1999;Seidel et al, 2010;Tummers and Thesleff, 2003;Tummers and Thesleff, 2008).…”

Natural odontogenesis: cellular and molecular basis

“…Центр петли за-полнен клетками звездчатого ретикулума. Церви-кальные петли сохраняются в постоянно растущих резцах грызунов и образуют ниши взрослых ство-ловых клеток [19][20][21], которые обеспечивают рост зубов.…”

“…рис. 7) [21,26,88,91,93]. Так, увеличение размера ниши ство-ловых клеток у Spry4-/-; Spry2+/-мышей способ-ствует чрезмерному росту резцов, а снижение разме-ра ниш у FGF-3-/-и FGF10+/-мышей -умень-шению размера резцов.…”