Search

Dental pain arises from exposed dentin following bacterial, chemical, or mechanical erosion of enamel and/or recession of gingiva. Thus, dentin tissue and more specifically patent dentinal tubules represent the first structure involved in dentin sensitivity. Interestingly, the architecture of dentin could allow for the transfer of information to the underlying dental pulp via odontoblasts (dentin-forming cells), via their apical extension bathed in the dentinal fluid running in the tubules, or via a dense network of trigeminal sensory axons intimately related to odontoblasts. Therefore, external stimuli causing dentinal fluid movements and odontoblasts and/or nerve complex responses may represent a unique mechanosensory system bringing a new role for odontoblasts as sensor cells. How cells sense signals and how the latter are transmitted to axons represent the main questions to be resolved. However, several lines of evidence have demonstrated that odontoblasts express mechano- and/or thermosensitive transient receptor potential ion channels (TRPV1, TRPV2, TRPV3, TRPV4, TRPM3, KCa, TREK-1) that are likely to sense heat and/or cold or movements of dentinal fluid within tubules. Added to this, voltage-gated sodium channels confer excitable properties of odontoblasts in vitro in response to injection of depolarizing currents. In vivo, sodium channels co-localize with nerve terminals at the apical pole of odontoblasts and correlate with the spatial distribution of stretch-activated KCa channels. This highlights the terminal web as the pivotal zone of the pulp/dentin complex for sensing external stimuli. Crosstalk between odontoblasts and axons may take place by the release of mediators in the gap space between odontoblasts and axons in view of evidence for nociception-transducing receptors on trigeminal afferent fibers and expression of putative effectors by odontoblasts. Finally, how axons are guided to the target cells and which kind of signaling molecules are involved is extensively discussed in this review. [ABSTRACT FROM AUTHOR]

The article presents a study which examined the function of odontoblast. Odontoblasts are specialized cells arranged as a single layer and responsible for the formation of dentine and for playing a role in tooth pain transmission. Every cell has an extension which runs into a dentinal tubule and bathing in the dentinal fluid. It concludes that odontoblast could be considered a unique cell and is both a highly specialized cell for the synthesis and secretion of dentine under the control of external stimuli through cilia sensing. It adds that these cells should be given an important role in the dynamic of the pulp/dentine complex.

The author talks about the contribution of Jean-Victor Ruch to the study of odontogenesis. The author offers a brief overview of research made by Ruch which focused on the epigenetic control of the symmetrization of amphibians and avian eggs and embryos. The author also explores the collaborations and exchanges with other researchers.

Transforming growth factor beta 1 (TGF beta 1) is generally considered to be a potent inducer of dentin formation. In order to further assess this role, we studied the influence of this factor in human dental pulp cells on the expression of osteoadherin (OSAD), a newly described proteoglycan found in bone and dentin and suspected to play a role in mineralization events. We performed TGF beta 1 stimulation both in cultures of human tooth thick slices including mature odontoblasts and in pulp explant cultures giving rise to early secretory odontoblasts or pulpal fibroblasts. We first showed by immunohistochemistry that molecules involved in TGF beta 1 signal transduction, that is, membrane receptors T beta RI and T beta RII and intracellular proteins SMAD-2, SMAD-3, and SMAD-4, were present in human dental cells in vivo and were all maintained after culture of thick-sliced teeth in cells undergoing TGF beta 1 stimulation. In this culture system, OSAD synthesis was increased in mature odontoblasts close to the TGF beta 1 delivery system. In explant cultures, semiquantitative reverse-transcription polymerase chain reaction (RT-PCR) analysis indicated that the growth factor stimulated OSAD gene expression in early secretory odontoblasts and in pulpal fibroblasts. Taken together, these results indicate that OSAD expression is stimulated by TGF beta 1 in pulpal fibroblasts and in early secretory and mature odontoblasts. We suggest that TGF beta 1 in this way could control the organization and the mineralization of the extracellular matrix deposited by these cells during dentin formation.