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Träfflista för sökning "WFRF:(Reseland J.) "

Sökning: WFRF:(Reseland J.)

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1.
  • Yan, Hongji, et al. (författare)
  • Regenerative Endodontics by Cell Homing : A Review of Recent Clinical trials
  • 2023
  • Ingår i: Journal of Endodontics. - : Elsevier BV. - 0099-2399 .- 1878-3554. ; 49:1, s. 4-17
  • Forskningsöversikt (refereegranskat)abstract
    • Introduction: The conventional treatment for irreversibly inflamed or necrotic teeth is root canal treatment or apexification. Regenerative endodontics aims to regenerate the damaged “pulp-like” tissue, which can preserve the teeth' vitality and sensitivity while avoiding necrosis. The main clinical benefit is root maturation. The “pulp-like” tissue does not refer to regenerated pulp tissue with an odontoblastic layer or the formation of pulp-dentin complexes. The cell homing technique is built on endogenous stem cells and their capacity to regenerate tissue. Cell homing refers to endogenous cells’ migration or infiltration into the cite when stimulated by physiochemical or biological stimuli or by passive flow with a blood clot from the apical tissue. Its Regenerative Endodontic Procedures success criteria are defined by the American Association of Endodontists. The purpose of this article is to provide an overview of vital pulp tissue and various strategies to promote regeneration of damaged pulp tissue. The cell homing technique will be reviewed through clinical trials. Methods: We performed a comprehensive literature review on a total of nine clinical trials of regenerative endodontics using the cell-homing technique based on three databases and duplicate manuscripts were removed. Results: Regenerative endodontics using the cell-homing technique shows promising results that can be translated into clinical practice. However, a favorable result was observed in immature teeth, and the results are contradictory in mature teeth. Conclusion: Regeneration therapy is an attractive new alternative to conventional endodontic treatments. Preservation of vitality and continuation of root development in damaged teeth would be a clear advantage.
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2.
  • Giannobile, W. V., et al. (författare)
  • Biological factors involved in alveolar bone regeneration Consensus report of Working Group 1 of the 15(th) European Workshop on Periodontology on Bone Regeneration
  • 2019
  • Ingår i: Journal of Clinical Periodontology. - : Wiley. - 0303-6979 .- 1600-051X. ; 46, s. 6-11
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Aims To describe the biology of alveolar bone regeneration. Material and Methods Four comprehensive reviews were performed on (a) mesenchymal cells and differentiation factors leading to bone formation; (b) the critical interplay between bone resorbing and formative cells; (c) the role of osteoimmunology in the formation and maintenance of alveolar bone; and (d) the self-regenerative capacity following bone injury or tooth extraction were prepared prior to the workshop. Results and Conclusions This summary information adds to the fuller understanding of the alveolar bone regenerative response with implications to reconstructive procedures for patient oral rehabilitation. The group collectively formulated and addressed critical questions based on each of the reviews in this consensus report to advance the field. The report concludes with identified areas of future research.
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3.
  • Mosti, M P, et al. (författare)
  • Effects of the peroxisome proliferator-activated receptor (PPAR)-δ agonist GW501516 on bone and muscle in ovariectomized rats
  • 2014
  • Ingår i: Endocrinology. - : Endocrine Society. - 0013-7227 .- 1945-7170. ; 155:6, s. 2178-2189
  • Tidskriftsartikel (refereegranskat)abstract
    • Estrogen deficiency promotes bone loss and skeletal muscle dysfunction. Peroxisome proliferator-activated receptors (PPARs) have 3 subtypes (α, δ, and γ). PPARγ agonists induce bone loss, whereas PPARα agonists increase bone mass. Although PPARδ agonists are known to influence skeletal muscle metabolism, the skeletal effects are unsettled. This study investigated the musculoskeletal effects of the PPARδ agonist GW501516 in ovariectomized (OVX) rats. Female Sprague Dawley rats, 12 weeks of age, were allocated to a sham-operated group and 3 OVX groups; high-dose GW501516 (OVX-GW5), low-dose GW501516 (OVX-GW1), and a control group (OVX-CTR), respectively (n = 12 per group). Animals received GW501516 or vehicle (methylcellulose) daily for 4 months by gavage. Bone mineral density (BMD) was assessed by dual x-ray absorptiometry at the femur, spine, and whole body. Bone microarchitecture at the proximal tibia was assessed by microcomputed tomography, and dynamic histomorphometry was performed. Quadriceps muscle morphology and the relative expression of mitochondrial proteins were analyzed. Bone metabolism markers and metabolic markers were measured in plasma. After 4 months, the OVX-GW5 group displayed lower femoral BMD than OVX-CTR. Trabecular separation was higher in the GW-treated groups, compared with OVX-CTR. The OVX-GW5 group also exhibited lower cortical area fraction and a higher structure model index than OVX-CTR. These effects coincided with impaired bone formation in both GW groups. The OVX-GW5 group displayed elevated triglyceride levels and reduced adiponectin levels, whereas no effects on muscle morphology or mitochondrial gene expression appeared. In summary, the PPARδ agonist GW501516 negatively affected bone properties in OVX rats, whereas no effects were detected in skeletal muscle.
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4.
  • Obregon-Whittle, Maria V, et al. (författare)
  • Enamel matrix derivative stimulates expression and secretion of resistin in mesenchymal cells.
  • 2011
  • Ingår i: European journal of oral sciences. - : Wiley. - 1600-0722 .- 0909-8836. ; 119 Suppl 1, s. 366-72
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study we wanted to identify the effect of enamel matrix derivative (EMD) on adipocytokines, so-called adipokines. Primary human cells of mesenchymal origin (osteoblasts, periodontal ligament cells, mesenchymal stem cells, and pulp cells) and hematopoietic origin (monocytes) were incubated with EMD. The levels of adipokines in cell culture medium were quantified using the Lincoplex human adipocyte panel (Luminex) and by real-time PCR of mRNA isolated from cell lysates. Rats were injected with 2 mg of EMD or saline intramuscularly every third day for 14 d. Blood samples were taken before and after injections, and the level of resistin in rat plasma was measured by ELISA. We found a dramatic increase in the secretion of resistin from mesenchymal stem cells, and verified this result in all the cells of mesenchymal origin tested. However, we observed no significant changes in the amount of resistin secreted from monocytes exposed to EMD compared with the control. Injections of EMD significantly enhanced the circulating levels of resistin in rats, and EMD also significantly enhanced the activity of the resistin promoter in transfected mesenchymal stem cells, indicating a direct effect on resistin expression. Our results indicate that resistin may play a role in mediating the biological effect of EMD in mesenchymal tissues.
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