Background: PerioGlas® (PG) is an alloplastic material used for grafting periodontal osseous defects since 1995. In animal models, it has been proven that PG achieves histologically good repair of sur-gically created defects. In clinical trials, PG was effective as an adjunct to conventional surgery in the treatment of intrabony defects. Because the molecular events due to PG that are able to alter osteob-last activity to promote bone formation are poorly understood, we investigated the expression of os-teoblastic related genes in mesenchymal stem cells exposed to PG.
Methods: The expression levels of bone related genes like RUNX2, SP7, SPP1, COL1A1, COL3A1, BGLAP, ALPL, and FOSL1 and mesenchymal stem cells marker (CD105) were analyzed, using real time reverse transcription-polymerase chain reaction. Pearson's chi-square (χ(2)) test was used to detect markers with significant differences in gene expression.
Results: PG caused induction of osteoblast transcriptional factor (like RUNX2), bone related genes osteopontin (SPP1), osteocalcin (BGLAP) and alkaline phosphatase (ALPL). All had statistical sig-nificant P values (< 0.05).
Conclusion: PG has a differentiation effect on mesenchymal stem cells derived from peripheral blood. The obtained results can be relevant to better understanding of the molecular mechanism of bone regeneration and as a model for comparing other materials with similar clinical effects.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065339 | PMC |
Publication Analysis
Top Keywords
Similar Publications
Bone Marrow Mononuclear Cell Transplantation Promotes Bone Healing via Gap Junction-Mediated Cell-Cell Interaction.
Stem Cells
January 2025
Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe city, Hyogo 650-0017, Japan.
Aims: Bone marrow mononuclear cells (BM-MNCs) are a rich source of hematopoietic stem cells that have been widely used in experimental therapies for patients with various diseases, including fractures.Activation of angiogenesis is believed to be one of the major modes of action of BM-MNCs; however, the essential mechanism by which BM-MNCs activate angiogenesis remains elusive. This study aimed to demonstrate that BM-MNCs promote bone healing by enhancing angiogenesis through direct cell-to-cell interactions via gap junctions, in addition to a previously reported method.
View Article and Find Full Text PDFHuman Oncostatin M deficiency underlies an inherited severe bone marrow failure syndrome.
J Clin Invest
January 2025
Laboratory of Genome Dynamics in the Immune, INSERM UMR 116, Équipe Labellisée LIGUE 2023, Paris, France.
Oncostatin M (OSM) is a cytokine with the unique ability to interact with both the OSM receptor (OSMR) and the leukemia inhibitory factor receptor (LIFR). On the other hand, OSMR interacts with IL31RA to form the interleukin-31 receptor. This intricate network of cytokines and receptors makes it difficult to understand the specific function of OSM.
View Article and Find Full Text PDFCorneal Stromal Stem Cell-Derived Extracellular Vesicles Attenuate ANGPTL7 Expression in the Human Trabecular Meshwork.
Transl Vis Sci Technol
January 2025
Department of Ophthalmology, Stein Eye Institute, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Purpose: Regulating intraocular pressure (IOP), mainly via the trabecular meshwork (TM), is critical in developing glaucoma. Whereas current treatments aim to lower IOP, directly targeting the dysfunctional TM tissue for therapeutic intervention has proven challenging. In our study, we utilized Dexamethasone (Dex)-treated TM cells as a model to investigate how extracellular vesicles (EVs) from immortalized corneal stromal stem cells (imCSSCs) could influence ANGPTL7 and MYOC genes expression within TM cells.
View Article and Find Full Text PDFMicrofluidic vessel-on-chip platform for investigation of cellular defects in venous malformations and responses to various shear stress and flow conditions.
Lab Chip
January 2025
Oulu Center for Cell-Matrix Research, Biocenter Oulu and Faculty of Biochemistry and Molecular Medicine, University of Oulu, P.O. Box 5000, FI-90014 Oulu, Finland.
A novel microfluidic platform was designed to study the cellular architecture of endothelial cells (ECs) in an environment replicating the 3D organization and flow of blood vessels. In particular, the platform was constructed to investigate EC defects in slow-flow venous malformations (VMs) under varying shear stress and flow conditions. The platform featured a standard microtiter plate footprint containing 32 microfluidic units capable of replicating wall shear stress (WSS) in normal veins and enabling precise control of shear stress and flow directionality without the need for complex pumping systems.
View Article and Find Full Text PDFMesenchymal Traits as an Intrinsic Feature of Undifferentiated Cells.
J Dev Biol
December 2024
Department of Neuroscience, Biomedicine and Movement-Sec. Anatomy and Histology, University of Verona, Via Le Grazie 8, 37134 Verona, Italy.
Since its first conceptualization over a century ago, the mesenchymal phenotype has traditionally been viewed as either a transient phase between successive epithelial stages or as a feature of cell types primarily devoted to structural support. However, recent findings in cancer research challenge this limited view, demonstrating that mesenchymal traits and hybrid mesenchymal/epithelial states can mark cancer cells with stem cell properties. By analyzing publicly available single-cell transcriptome datasets from early embryonic stages and adult tissues, this study aims to extend this concept beyond pathological contexts, suggesting that a partial or fully mesenchymal phenotype may represent the morphological expression of undifferentiated and multipotent states in both the developing embryo and adult organs.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!