Differences between normal and demineralized dentine pretreated with silver fluoride and potassium iodide after an in vitro challenge by Streptococcus mutans

The document attached has been archived with permission from the Australian Dental Association (8 March 2008). An external link to the publisher’s copy is included.Background: The application of diamine silver fluoride (Ag(NH3)2F) and potassium iodide (KI) to demineralized dentine has been shown to inhibit the growth of Streptococcus mutans. The purpose of this study was to observe the differences between demineralized and non-demineralized dentine treated with AgF/KI. Methods: Thirty-five dentine discs were bonded to the bases of 5mL polycarbonate screw top vials which were filled with nutrient medium, sterilized and placed into the overflow from a continuous culture of S. mutans. Samples were divided as follows: 10 samples of demineralized dentine; 10 samples of demineralized dentine treated with AgF/KI; 5 samples of non-demineralized dentine; and 10 samples of non-demineralized dentine treated with AgF/KI. Following two weeks connected to the Chemostat, an electron probe microanalysis (EPMA) of percentage weights and penetration depths of calcium, phosphorous silver and fluoride was conducted. Bacterial growth was monitored by taking optical density readings of the growth medium in each vial and outer surfaces of the specimens were examined by scanning electron microscopy (SEM). Results: AgF/KI treatment of demineralized and non-demineralized dentine prevented biofilm formation and reduced further demineralization by S. mutans. AgF/KI treatment of demineralized dentine was more effective in reducing dentine breakdown and the growth of S. mutans. Significantly higher levels of silver and fluoride were deposited within demineralized dentine. Conclusions: A topical treatment with AgF/KI on dentine reduced in vitro caries development and inhibited surface biofilm formation. Reduction of in vitro caries development and viability of S. mutans was more pronounced on the dentine samples that had been demineralized prior to the application of AgF/KI.GM Knight, JM McIntyre, GG Craig, Mulyani, PS Zilm and NJ Gull

Review of Matrix Metalloproteinases’ Effect on the Hybrid Dentin Bond Layer Stability and Chlorhexidine Clinical Use to Prevent Bond Failure

This review describes the relationship between dentin collagen hybrid bond layer degradation and the Matrix Metalloproteinases (MMPs) after their release by acid etch and rinse adhesives and self etching bonding adhesives that can reduce the bond stability over time. MMP-2, MMP-8 and MMP-9 are indicated as the active proteases that breakdown the collagen fibrils in the hybrid bond layer. Phosphoric acid in the acid etch and rinse bonding process and acid primers in the self etch process are implicated in the release of these proteases and their activation by several non-collagen proteins also released from dentin by the etching. MMPs are released in saliva by salivary glands, by cells in the gingival crevices to crevicular fluid and by pulpal odontoblasts cells to the dentinal fluids. These sources may affect the hybrid layer also. Evidence of the bond strength deterioration over time and the ability of Chlorhexidine to prevent bond deterioration by inhibiting MMP action are discussed. Dentin Bonding procedure utilizing Chlorhexidine for different application times and concentrations are being developed. The application of 2% Chlorhexidine to the phosphoric acid etch surface after rinsing off the acid is the only procedure that has been clinically tested for a longer period of time and shown to prevent bond strength degradation so far. The adoption of this procedure is recommended as means of improving bond stability at this time

Variability of systemic and oro-dental phenotype in two families with non-lethal Raine syndrome with FAM20C mutations

Background: Raine syndrome (RS) is a rare autosomal recessive bone dysplasia typified by osteosclerosis and dysmorphic facies due to FAM20C mutations. Initially reported as lethal in infancy, survival is possible into adulthood. We describe the molecular analysis and clinical phenotypes of five individuals from two consanguineous Brazilian families with attenuated Raine Syndrome with previously unreported features. Methods: The medical and dental clinical records were reviewed. Extracted deciduous and permanent teeth as well as oral soft tissues were analysed. Whole exome sequencing was undertaken and FAM20C cDNA sequenced in family 1. Results: Family 1 included 3 siblings with hypoplastic Amelogenesis Imperfecta (AI) (inherited abnormal dental enamel formation). Mild facial dysmorphism was noted in the absence of other obvious skeletal or growth abnormalities. A mild hypophosphataemia and soft tissue ectopic mineralization were present. A homozygous FAM20C donor splice site mutation (c.784 + 5 g > c) was identified which led to abnormal cDNA sequence. Family 2 included 2 siblings with hypoplastic AI and tooth dentine abnormalities as part of a more obvious syndrome with facial dysmorphism. There was hypophosphataemia, soft tissue ectopic mineralization, but no osteosclerosis. A homozygous missense mutation in FAM20C (c.1487C > T; p.P496L) was identified. Conclusions: The clinical phenotype of non-lethal Raine Syndrome is more variable, including between affected siblings, than previously described and an adverse impact on bone growth and health may not be a prominent feature. By contrast, a profound failure of dental enamel formation leading to a distinctive hypoplastic AI in all teeth should alert clinicians to the possibility of FAM20C mutations

Rôle de protéines non collagéniques dans la physiopathologie de la dentine humaine

Ce travail a pour objectif principal d'étudier la physiopathologie de la matrice dentinaire. Dans ce but, deux modèles de pathologie de la dentine ont servi de support: la carie dentinaire et la dentine hypophosphatémique. A travers ces modèles, nous avons cherché à mieux comprendre le rôle des protéines non collagéniques dans la minéralisation, la structure et la dégradation de la dentine humaine. Dans le premier modèle, le rôle des MMPs dentinaires dans la dégradation des protéines de la dentine cariée a été tout particulièrement développé. Ainsi, nous avons essayé de comprendre comment la MMP-3 (dont la présence dans la dentine humaine mature a été démontrée pour la première fois par ce travail) initiait la libération des molécules de la matrice extracellulaire dentinaire à partir de dentine humaine artificiellement déminéralisée. Ce premier travail ouvre des perspectives d'une part en ternie de réparation de la dent, la dégradation de matrice pouvant fournir des peptides bioactifs, et d'autre part et à plus court terme, en terme de thérapeutique adhésive. En effet, un traitement de la dentine par des MMPs pourrait améliorer le collage d'un composite à la dentine traitée. Le deuxième modèle concerne la dentine de dents de patients atteints de rachitisme hypophosphatémique lié à la mutation de PHEX. Chez ces patients, des défauts de minéralisation de la dentine sont observés. Nous avons étudié la structure, la composition et la distribution des molécules de la matrice extracellulaire dentinaire de dents temporaires provenant de patients hypophosphatémiques. Nous avons ainsi montré une accumulation des protéines de la matrice sous forme dégradée au niveau des plages de dentine non minéralisée. Dans ces conditions pathologiques, MEPE semble jouer un rôle critique et notre travail a ^contribué àjme meilleure compréhension de ses fonctions.The aim of this work was to study the physiopathology of dentin extracellular matrix. With this end, two models of pathological dentin were carried out: artificial caries-affected dentin and hypophosphatemic dentin. Through these models, we tried to better understand the role of non collagenous proteins in the mineralization, the structure and the degradation of human dentin. Therefore, in the first model, we investigated how recombinant MMP-3 initiates the release of ECM molecules from artificially demineralized human dentin. That way, we identified for the first time to the best of our knowledge, the presence of endogenous MMP-3 in mature dentin. In this first approach, the use of MMP-3 as a potential agent for dentin preparation may improve resin adhesion. The second model concerned dentin from hypophosphatemic patients. Familial hypophosphatemic rickets results from the mutation of the PHEX gene. Patients have reported to display important dentin defects, and therefore, we explored the dentin structure, composition, and distribution of ECM molecules in hypophosphatemic human deciduous teeth. The abnormal presence of low-molecular weight protein complexes in large interglobular spaces was shown. In these pathological conditions, MEPE seems to display important role and our work aimed to better understand this function.MONTROUGE-BUFR Odontol.PARIS5 (920492101) / SudocSudocFranceF

Rôle du fibroblaste dermique et gingival dans la cicatrisation (Modulation de l'organisation matricielle in vitro)

MONTROUGE-BUFR Odontol.PARIS5 (920492101) / SudocSudocFranceF

Le rôle du chirurgien-dentiste dans la nutrition

MONTROUGE-BUFR Odontol.PARIS5 (920492101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

L' évaluation du risque carieux

MONTROUGE-BUFR Odontol.PARIS5 (920492101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF