Biomedical subjects

A Romeas

Publications and source records attributed to A Romeas.

4 recordsLinked to original sources

PubMed2004

Alpha v beta 3 integrin expression in human odontoblasts and co-localization with osteoadherin.

Integrins are heterodimeric transmembrane receptors which promote cell adhesion, thus contributing to the maintenance of tissue organization in both normal and pathological conditions. To characterize the way odontoblasts may interact with other cells and the extracellular matrix in human teeth, we studied expression of alpha v beta 3 integrin, a putative receptor for osteoadherin. We showed that alpha v beta 3 integrin expression was restricted to odontoblasts, blood vessels, and small rounded cells in sound and carious pulp. Odontoblast staining intensity increased from the apical to the cusp region. Osteoadherin staining was strong in the whole odontoblast layer (with a slight decrease in the cusp region) and in predentin. Odontoblasts differentiating in vitro were stained with the anti-alpha v beta 3 integrin antibody, first at the level of intercellular contacts, then throughout the cell membrane. These results suggest that the alpha v beta 3 integrin could play a role in interodontoblast adhesion and odontoblast binding to the surrounding predentin/dentin/pulp matrix, possibly through osteoadherin.

Adolescent↗

PubMed2003

In vitro evaluation of apical microleakage following canal filling with a coated carrier system compared with lateral and thermomechanical Gutta-Percha condensation techniques.

AIM: The apical sealing ability of a coated carrier system was evaluated in extracted human teeth and compared with lateral and thermomechanical condensation techniques using dye penetration. METHODOLOGY: Sixty-four extracted single-rooted teeth were instrumented to an apical size 30 using 4% taper Hero 642 trade mark instruments (Micromega, Besançon, France). The sample was divided into three experimental groups. Twenty teeth were randomly obturated with lateral condensation, 20 with thermomechanical compaction and 20 teeth with the Herofill trade mark Soft-Core system. Four teeth were used as positive and negative controls. The teeth were covered with nail varnish up to 2 mm from the apical foramen and immersed in a 2% aqueous methylene blue dye solution for 1 week and then washed, dehydrated and embedded in resin. The apical 1 mm of each tooth was removed to reveal the apical limit of the preparation. Transverse sections of the teeth were taken at 500, 1000 and 1500 micro m from this point and evaluated for apical leakage. Significant differences between the preparations were analysed with a semiautomatic analyser and the ratio of the dye-penetrated surface to the total dentinal surface was calculated. RESULTS: Statistical analysis of the results demonstrated significantly less leakage for the Herofill trade mark Soft-Core system compared to lateral condensation in terms of total mean dentinal surface and at the 500 micro m level. No other differences were noted between Herofill trade mark Soft-Core and thermomechanical or lateral condensation, either for the total mean value or at each level. CONCLUSIONS: The Herofill trade mark Soft-Core system was a reliable obturation system in the apical portion and compared favourably with other gutta-percha filling techniques.

Coloring Agents↗

PubMed2003

TGF-beta1 induces accumulation of dendritic cells in the odontoblast layer.

TGF-beta1 released from dentin degraded by bacterial or iatrogenic agents is suspected to influence dental pulp response, including the modulation of cell migration. To determine the consequences of TGF-beta1 action on pulp immune cells, we analyzed, by immunohistochemistry, the effect of transdentinally diffusing TGF-beta1 on their localization in a human tooth slice culture model. TGF-beta1 induced an accumulation of HLA-DR-positive cells in both odontoblast and subodontoblast layers of the stimulated zone. Together with HLA-DR, these cells co-expressed Factor XIIIa and CD68, two features of immature antigen-presenting dendritic cells (DC), as well as the TGF-beta1 specific receptor TbetaRII. In contrast, no effect could be detected on the localization of either mature DC-LAMP-positive DC or of T- and B-lymphocytes. Analysis of these data suggests that TGF-beta1 released from dentin degraded by bacterial or iatrogenic agents could be involved in the immune response of the dental pulp resulting from tooth injury.

Adolescent↗

PubMed2001

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.

Actin Cytoskeleton↗