Bioinspired Nanofeatured Substrates: Suitable Environment for Bone Regeneration.

Bone mimicking coatings provide a complex microenvironment in which material, through its inherent properties (such as nanostructure and composition), affects the commitment of stem cells into bone lineage and the production of bone tissue regulating factors required for bone healing and regeneration. Herein, a bioactive mineral/biopolymer composite made of calcium phosphate/chitosan and hyaluronic acid (CaP-CHI-HA) was elaborated using a versatile simultaneous spray coating of interacting species. The resulting CaP-CHI-HA coating was mainly constituted of bioactive, carbonated and crystalline hydroxyapatite with 277 ± 98 nm of roughness, 1 μm of thickness, and 2.3 ± 1 GPa of stiffness. After five days of culture, CaP-CHI-HA suggested a synergistic effect of intrinsic biophysical features and biopolymers on stem cell mechanobiology and nuclear organization, leading to the expression of an early osteoblast-like phenotype and the production of bone tissue regulating factors such as osteoprotegerin and vascular endothelial growth factor. More interestingly, amalgamation with biopolymers conferred to the mineral a bacterial antiadhesive property. These significant data shed light on the potential regenerative application of CaP-CHI-HA bioinspired coating in providing a suitable environment for stem cell bone regeneration and an ideal strategy to prevent implant-associated infections.journal article2017 Apr 122017 03 30importe

Serum albumin-alginate coated microsphere : role of the inner gel in binding and release of the KRFK peptide

International audienc

Importance of the surface area ratio on cytokines production by human monocytes in vitro induced by various hydroxyapatite particles.

A possible complication associated with the implantation of hydroxyapatite (HA)-based prosthesis is the release of particles. Those particles can be phagocyted by monocytes that are among the first cells to colonize the inflammatory site. The activated monocytes produce inflammatory mediators, such as cytokines, which cause osteoclasts activation. It has previously been demonstrated using a surface area ratio (ratio of the total surface of the given particles to the surface area of cells) of 1 to 1 that there was a correlation between the expression and production of cytokines induced by HA. The present work studies the effect of physical characteristics of HA particles on the production of various inflammatory cytokines (tumour necrosis factor-alpha, interleukin (IL)-6, and IL-8) and anti-inflammatory cytokine (IL-10). However, the experiments were performed using a surface area ratio of 10 to 1. Our data demonstrate that all the particles, whatever their characteristics, induced a high expression of cytokines but the production was different, meaning that there was a post-transcriptional regulation. The size and sintering temperature seemed to be a characteristics that were less important compared to the shape; the needle particles appeared to induce the most important production of all the cytokines studied

Influence de l'élastolyse dans la physiopathologie gingivale

Les peptides d'élastine (kE) augmentent l'expression des MMP3 et MMP1 dans les fibroblastes gingivaux humains cultivés en 2D sur plastique alors qu'ils n'ont aucune influence sur la production d'uPA, des MMPs2, 13, 14 et des TIMPs1 et 2. L'effet de kE sur la production de MMP3 dépend du récepteur membranaire S-Gal tandis qu'il est inhibé par le lactose et reproduit par des peptides contenant la séquence VGVAPG capable de se fixer sur S-Gal. Afin d'évaluer l'implication des peptides d'élastine dans la collagénolyse, des cultures cellulaires en 3D ou lattis de collagène attaché sont utilisés : kE ou le plasminogène (Plgn) seuls n'induisent pas de façon significative une collagénolyse des lattis de collagène. Toutefois, kE, en présence de Plgn, augmente de façon synergique la dégradation du collagène et l'activation des MMPs. Au sein des lattis en présence de peptides d'élastine, la collagénolyse serait dépendante d'une sur-expression de la cascade protéolytique MMP3/MMP1 par les fibroblastes gingivaux humains, associée à une sous-expression des TIMP1 et de TIMP2. (Med Buccale Chir Buccale 2009 ; 15 : 75-85)