Biomedical subjects

L Vermelin

Publications and source records attributed to L Vermelin.

8 recordsLinked to original sources

PubMed2005

Effects of essential fatty acid deficiency on periodontal tissue adaptation to spontaneous tooth migration.

Essential fatty acids (EFAs) play a significant role in bone metabolism. Herein we studied the adaptation of alveolar bone to physiologic tooth drift in young rats deprived of essential fatty acids from birth. Reductions in femur size and trabecular bone volume reflected body growth impairment. Along the alveolar wall, osteoclastic resorption and bone formation were depressed, disrupting the adaptive deformation of the tooth socket to ongoing migration. As a result, the periodontal ligament narrowed considerably, and further adaptation was achieved through root resorption. Essential fatty acid deficiency (EFAD), did not affect precursor recruitment or differentiation in the periodontal ligament (PDL), but caused redistribution of nonspecific-esterase (NSE)-positive osteoclast precursors and tartrate-resistant acid phosphatase (TRAP)-positive pre-osteoclasts between the bone compartment (which was depleted) and the root compartment (which was enriched). EFAD had also a marked effect on the PDL vasculature; the number of vessels was reduced, whereas their size was markedly increased. As a whole, our results show that EFAD disturbs alveolar bone adaptation to drift, but that a reaction (detrimental to root integrity) prevents root collision with the bone surface, thereby preserving the PDL as a source of precursor cells for bone and cementum homeostasis. Moreover, our results confirm that although alveolar bone resorption is arachidonic acid-dependent, the factors activating root resorption are different.

Animals↗

PubMed2004

Is the lingual forming part of the incisor a structural entity? Evidences from the fragilitas ossium (fro/fro) mouse mutation and the TGFbeta1 overexpressing transgenic strain.

Our objective was to study the teeth of a mutant mice fro/fro that display severe forms of osteogenesis imperfecta. One day and 8 week-old fro/fro and +/fro heterozygote mice (wild type, WT) were processed for light and scanning electron microscopy. The genetic defect, shown to be located on chromosome 8, induced alveolar bone and teeth hypomineralisation. Due to defective cell proliferation in the fro/fro, the distal growth of the mandibular incisors was impaired. Immunolabelling revealed an increase of chondroitin/dermatan sulphate, whereas no difference was detected in dental tissues for decorin and biglycan. Amelogenin expression was decreased in the incisor and enhanced in the molar. Dentin sialoprotein was below the level of detection in the fro/fro, whereas osteonectin and osteopontin were unchanged. The main target of the mutation was seen in the lingual part of the incisor near the apex where dentine formation was delayed. In the molars, bulbous roots with obliteration of the pulp chamber were seen. In the TGFbeta1 overexpressing mice, the lingual root-analogue part of the incisor was missing. In the molar, short roots, circumpulpal dentine of the osteodentine type and pulp obliteration were seen. It may be noted that, although the mutant and transgenic strains mutations are two different genetic alterations not related to the same defective gene, in both cases the expression of the dentin sialoprotein is altered. Altogether, the present data suggest that the lingual forming part of the incisor seems to be an anatomical entity bearing its own biological specificities.

Amelogenin↗

PubMed1999

[3H]choline uptake and turnover into membrane and extracellular matrix phospholipids, visualized by radioautography in rat incisor dentin and enamel.

In order to study the uptake and fate of [3H]choline into cellular and extracellular phospholipids in the forming part of mandibular rat incisors, radioautography was carried out after treatment with the iodoplatinate reaction which retains phospholipids. Thirty minutes and 1 hour after the intravenous injection of the radiolabeled precursor, grain density in secretory odontoblasts and ameloblasts was not significantly above background labeling whereas dentin was actually labeled. Therefore, at this early period, odontoblasts cannot be responsible for the secretion of phospholipids incorporated into dentin, and intercellular diffusion of components originating from blood could explain this early dentin labeling. After 2 hours, odontoblasts and ameloblasts were labeled. In cells, grain density reached a maximum at 4 hours, reduced at 24 hours, and strongly decreased at 4 days. In predentin and enamel, grain density peaked at 24 hours and diminished at 4 days. However, in the forming enamel 4 days after the injection, labeling was twice as high as in any other compartment. Altogether, the results highlighted two distinct pathways for phospholipids in dental mineralized dental tissues: a first one shows evidence of early incorporation of [3H]choline into dentin resulting from intercellular diffusion independently from odontoblasts secretion, whereas inside the forming enamel, higher labeling and longer retention of choline-containing membrane components were detected between 4 hours and 4 days. This suggests an accumulation of membranes that are not subjected to rapid turnover in contrast with other dental compartments.

Ameloblasts↗

PubMed1995

Effects of essential fatty acid deficiency on rat molar pulp cells.

In rats fed an essential fatty acid deficient (EFAD) diet, either during pregnancy (DN) or for 4 wk postnatally (ND), the cell density in the central part of the pulp increased about two- and threefold, respectively, of that in rats who had received a conventional diet containing sunflower oil. Cells were especially numerous around capillaries. The cell density was also increased twofold in the subodontoblastic layer in the outer part of the pulp, cells being smaller in ND compared with DN. In contrast, the odontoblasts were reduced in height, and the Höhl cells formed a thin layer in EFAD rats. This emphasizes some aspects of pulp specificity which reacted differently from odontoblasts. We suggest that the function of killer cells which normally destroy cells at the periphery of the pulp may be impaired by the diet, leading to cell accumulation.

Animals↗

PubMed1995

Lipids in predentine and dentine.

Using two histochemical methods, malachite green-aldehyde and iodoplatinate, phospholipids were visualized in the predentine of rat incisors in the spaces located between collagen fibers and in dentine as needle-like structures located along individual or groups of mineralizing collagen fibers. The same staining pattern was seen with phospholipase A2-gold. Autoradiographic investigation using 3H choline as labelled precursor, visualized the incorporation of membrane-associated and extracellular choline-containing phosphatidyl choline and sphingomyelin. The cell and membrane-associated labelling decreased gradually between 24 and 4 days, whereas incorporation of the labelled precursor as stable extracellular matrix component was seen in dentine. In addition to these investigations, pharmacologically induced (suramine) and genetically (Krabbe's disease) lysosomal storage pathology was investigated. Defects due to lipid metabolism alterations were seen in predentine and/or in dentine. The major differences visualized here between the non-mineralized and mineralized compartments and interactions between phospholipids and proteoglycans, support the view that phospholipids as matrix components play an important role in the mechanisms of dentine formation and mineralization.

Animals↗

PubMed1995

Dental mineralization.

Extracellular matrix components and cell-derived microstructures are implicated in mineralization processes which occur in dental tissues. The respective role(s) of collagenic and non-collagenic matrix components are reviewed: phosphorylated and non-phosphorylated proteins, proteoglycans and phosphpholipids. Space-filling amphiphilic molecules seem to play an important role in the preorganization and oriented deposition of calcium phosphate on structures serving more or less as passive support in dentine as well as in enamel.

Amelogenesis↗

PubMed1994

Iodoplatinate visualization of phospholipids in rat incisor predentine and dentine, compared with malachite green aldehyde.

The iodoplatinate (IP) reaction, a selective method for visualization of phospholipids, was applied to the predentine and dentine of rat incisors and compared with malachite green aldehyde (MG) fixation/staining. Spot tests indicated (1) that IP specifically stains phospholipids, but not amino acids, displaying as do phospholipids, quaternary ammonium groups; and (2) phosphatidylserine and sphingomyelin were also stained by MGA. Although this reagent is known to interact with phosphorus, phosphoproteins remained unstained. In the rat incisor, an IP-positive network including granules and thin filaments was seen in predentine in the inter-collagen spaces, in many cases closely associated with collagen fibres and their periodic striations. In dentine, positively stained needle-like structures were located along individual collagen fibres, or at the surface of groups of collagen fibres. This staining pattern was unchanged on sections of material pretreated with acetone, whereas the staining was abolished or markedly reduced when the samples were treated either with chloroform/methanol or phospholipase C prior to the IP reaction. Pretreatment of the samples with hyaluronidase promoted subsequent diffusion of the staining. A very similar staining pattern was observed with MGA, in accordance with earlier reports. The present findings validate the histochemical results reported previously on the distribution and potential role(s) of phospholipids in dentine biomineralization.

Animals↗

PubMedDate not supplied

Apoptosis in human and rat dental pulp.

Apoptotic cells were visualized in human premolar and rat molar pulps using either the TUNEL method, which stains DNA strand breaks by in situ nick end labeling, or labeling sections with an anti-transglutaminase antibody. Apoptotic cells were evident at the periphery of the pulp, mostly in a sub-odontoblastic location, and were more numerous in the crown than in the root region of the pulp. Most odontoblasts were unlabeled. A few apoptotic nuclei in the pulp of rat molars displayed the characteristics of chromatin condensation, as observed by electron microscopy. Many cell debris resembling apoptotic bodies were also observed. The 3 methods support the occurrence of apoptosis in the dental pulp. As this phenomenon was observed in healthy teeth apoptosis is probably involved in the regulation of the pulp cell population.

Animals↗