Molecular regulation of odontoblast activity under dentin injury.
Pulp tissue responds to dentin damage by laying down a tertiary dentin matrix (reactionary or reparative) beneath the site of injury. Reactionary dentin is secreted by surviving odontoblasts in response to environmental stimuli, leading to an increase in metabolic activities of the cells. The inductive molecules that determine the success of the pulp healing may be released from the damaged dentin as well as from the pulp tissue subjacent to the injury. This paper will schematically consider two major growth factors probably implicated in the control of odontoblast activity: TGF beta-1 released from demineralized dentin and NGF from pulp. To analyze their role with an in vitro system that mimics the in vivo situation, we have used thick-sliced teeth cultured as described previously. The supply of factors was accomplished by means of a small tube glued onto the dentin. The tube was filled with TGF beta-1 (20 ng/mL) or NGF (50 ng/mL), and slices were cultured for 4 or 7 days. Results showed that TGF beta-1 binding sites are strongly detected on odontoblasts in the factor-rich zone. A strong expression of alpha 1(I) collagen transcripts was also detected. In the NGF-rich environment, p75NTR was re-expressed on odontoblasts and the transcription factor NF-kappa B activated. Modifications in the odontoblast morphology were observed with an atypical extension of the cell processes filled with actin filaments. These results suggest that odontoblasts respond to influences from both dentin and pulp tissue during pulp repair.
Magloire
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H
Laboratoire du Développement des Tissus Dentaires (EA 1892), Faculté d'Odontologie, Rue G, Paradin, 69372 Lyon, France. magloire@laennec.univ-lyonl.fr
Romeas
A
A
Melin
M
M
Couble
M L
ML
Bleicher
F
F
Farges
J C
JC
D008841:Actin Cytoskeleton / Q000648:ultrastructure; D000199:Actins / Q000032:analysis; D003094:Collagen / Q000032:analysis; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D046508:Culture Techniques; D003782:Dental Pulp / Q000378:metabolism / Q000503:physiopathology; D003804:Dentin / Q000293:injuries* / Q000503:physiopathology / Q000648:ultrastructure; D003809:Dentin, Secondary / Q000502:physiology* / Q000648:ultrastructure; D003810:Dentinogenesis / Q000502:physiology; D006801:Humans; D008967:Molecular Biology; D016328:NF-kappa B / Q000032:analysis; D020932:Nerve Growth Factor / Q000502:physiology; D009804:Odontoblasts / Q000502:physiology* / Q000648:ultrastructure; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000032:analysis; D018125:Receptors, Transforming Growth Factor beta / Q000032:analysis; D017001:Tooth Demineralization / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000502:physiology; D053773:Transforming Growth Factor beta1; D014945:Wound Healing / Q000502:physiology
D000199:Actins; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D016328:NF-kappa B; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D018125:Receptors, Transforming Growth Factor beta; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D003094:Collagen; D020932:Nerve Growth Factor