Dataset Information

Continuous dental replacement in a hyper-chisel tooth digging rodent.

ABSTRACT: Contrary to their reptilian ancestors, which had numerous dental generations, mammals are known to usually develop only two generations of teeth. However, a few mammal species have acquired the ability to continuously replace their dentition by the constant addition of supernumerary teeth moving secondarily toward the front of the jaw. The resulting treadmill-like replacement is thus horizontal, and differs completely from the vertical dental succession of other mammals and their extinct relatives. Despite the developmental implications and prospects regarding the origin of supernumerary teeth, this striking innovation remains poorly documented. Here we report another case of continuous dental replacement in an African rodent, Heliophobius argenteocinereus, which combines this dental system with the progressive eruption of high-crowned teeth. The escalator-like mechanism of Heliophobius constitutes an original adaptation to hyper-chisel tooth digging involving high dental wear. Comparisons between Heliophobius and the few mammals that convergently acquired continuous dental replacement reveal that shared inherited traits, including dental mesial drift, delayed eruption, and supernumerary molars, comprise essential prerequisites to setting up this dental mechanism. Interestingly, these dental traits are present to a lesser extent in humans but are absent in mouse, the usual biological model. Consequently, Heliophobius represents a suitable model to investigate the molecular processes leading to the development of supernumerary teeth in mammals, and the accurate description of these processes could be a significant advance for further applications in humans, such as the regeneration of dental tissues.

SUBMITTER: Rodrigues HG

PROVIDER: S-EPMC3198356 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature

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Continuous dental replacement in a hyper-chisel tooth digging rodent.

Rodrigues Helder Gomes HG Marangoni Pauline P Šumbera Radim R Tafforeau Paul P Wendelen Wim W Viriot Laurent L

Proceedings of the National Academy of Sciences of the United States of America 20111010 42

Contrary to their reptilian ancestors, which had numerous dental generations, mammals are known to usually develop only two generations of teeth. However, a few mammal species have acquired the ability to continuously replace their dentition by the constant addition of supernumerary teeth moving secondarily toward the front of the jaw. The resulting treadmill-like replacement is thus horizontal, and differs completely from the vertical dental succession of other mammals and their extinct relativ ...[more]

PMID: 21987823

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Project description:Tooth morphogenesis involves dynamic changes in shape and size as it proceeds through the bud, cap, and bell stages. This process requires exact regulation of cell proliferation and differentiation. Smad7, a general antagonist against transforming growth factor-? (TGF-?) signaling, is necessary for maintaining homeostasis and proper functionality in many organs. While TGF-? signaling is widely involved in tooth morphogenesis, the precise role of Smad7 in tooth development remains unknown. In this study, we showed that Smad7 is expressed in the developing mouse molars with a high level in the dental epithelium but a moderate to weak level in the dental mesenchyme. Smad7 deficiency led to a profound decrease in tooth size primarily due to a severely compromised cell proliferation capability in the dental epithelium. Consistent with the tooth shrinkage phenotype, RNA sequencing (RNA-seq) analysis revealed that Smad7 ablation downregulated genes referred to epithelial cell proliferation and cell cycle G1/S phase transition, whereas the upregulated genes were involved in responding to TGF-? signaling and cell cycle arrest. Among these genes, the expression of Cdkn1a (encoding p21), a negative cell proliferation regulator, was remarkably elevated in parallel with the diminution of Ccnd1 encoding the crucial cell cycle regulator cyclin D1 in the dental epithelium. Meanwhile, the expression level of p-Smad2/3 was ectopically elevated in the developing tooth germ of Smad7 null mice, indicating the hyperactivation of the canonical TGF-? signaling. These effects were reversed by addition of TGF-? signaling inhibitor in cell cultures of Smad7-/- molar tooth germs, with rescued expression of cyclin D1 and cell proliferation rate. In sum, our studies demonstrate that Smad7 functions primarily as a positive regulator of cell proliferation via inhibition of the canonical TGF-? signaling during dental epithelium development and highlight a crucial role for Smad7 in regulating tooth size.

Project description:ObjectiveAssess the ability of an antimicrobial drug-releasing resin adhesive, containing octenidine dihydrochloride (OCT)-silica co-assembled particles (DSPs), to enhance the biostability and preserve the interfacial fracture toughness (FT) of composite restorations bonded to dentin. Enzyme-catalyzed degradation compromises the dental restoration-tooth interface, increasing cariogenic bacterial infiltration. In addition to bacterial ingress inhibition, antimicrobial-releasing adhesives may exhibit direct interfacial biodegradation inhibition as an additional benefit.MethodsMini short-rod restoration bonding specimens with total-etch adhesive with/without 10% wt. DSPs were made. Interfacial fracture toughness (FT) was measured as-manufactured or post-incubation in simulated human salivary esterase (SHSE) for up to 6-months. Effect of OCT on SHSE and whole saliva/bacterial enzyme activity was assessed. Release of OCT outside the restoration interface was assessed.ResultsNo deleterious effect of DSPs on initial bonding capacity was observed. Aging specimens in SHSE reduced FT of control but not DSP-adhesive-bonded specimens. OCT inhibited SHSE degradation of adhesive monomer and may inhibit endogenous proteases. OCT inhibited bacterial esterase and collagenase. No endogenous collagen breakdown was detected in the present study. OCT increased human saliva degradative esterase activity below its minimum inhibitory concentration towards S. mutans (MIC), but inhibited degradation above MIC. OCT release outside restoration margins was below detection.SignificanceDSP-adhesive preserves the restoration bond through a secondary enzyme-inhibitory effect of released OCT, which is virtually confined to the restoration interface microgap. Enzyme activity modulation may produce a positive-to-negative feedback switch, by increasing OCT concentration via biodegradation-triggered release to an effective dose, then subsequently slowing degradation and degradation-triggered release.

Dataset Information

Continuous dental replacement in a hyper-chisel tooth digging rodent.

Publications

Continuous dental replacement in a hyper-chisel tooth digging rodent.

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