Odontoblast response under carious lesions.
The local regulation of odontoblast response to caries is viewed through initiation and elaboration of sclerotic as well as reparative dentin. Dentin tissue represents a multiple source of potent environment factors when teeth are affected by the demineralization phases of carious process. Some of them have already been identified in sound tissue (matrix glycoproteins, proteoglycans, growth factors, Bone Morphogenetic Protein) and may act on the cell through membrane receptors. Thus, the amplification in collagen synthesis and alkaline phosphatase activity previously observed during sclerotic dentin deposition can be related to the interaction between matrix signals and cell receptors such as the 165 kDa protein shown only by odontoblasts under the affected zone. Similarly, under established lesions generating cell death, the specific matrix made of odontoblasts debris and damage tissues, probably rich in active molecules, may trigger pulp cells to elaborate a cartilage-like layer (identified by type II and XI collagen) followed by odontoblast-like cells to give rise to abnormal tubular dentin. Here, odontoblast response is identical to bone-cells response to injury. What remains to be elucidated concern: The nature of signals found in carious dentin (matrix components, growth factors, bacterial products). The nature and regulation of expression of cell membrane receptors during tooth repair. How the odontoblast produces specific responses to each of these signaling molecules will be the focus of important new investigations.
Magloire
H
H
Laboratoire d'Histophysiologie et de Pathologie des Tissus Dentaires, CNRS UPR 412, Faculté d'Odontologie, Lyon, France.
Bouvier
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M
Joffre
A
A
D002454:Cell Differentiation; D003731:Dental Caries / Q000473:pathology*; D003804:Dentin / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003809:Dentin, Secondary / Q000378:metabolism / Q000502:physiology; D006801:Humans; D009804:Odontoblasts / Q000378:metabolism / Q000473:pathology / Q000502:physiology*