FGF9 has complex and important roles in skeletal development and repair. We have previously observed that Fgf9 expression in osteoblasts (OBs) is regulated by G protein signaling and therefore the present study was done to determine whether OB-derived FGF9 was important in skeletal homeostasis. To directly test this idea, we deleted functional expression of Fgf9 gene in OBs using a 2.3 kb collagen type I promoter-driven Cre transgenic mouse line (Fgf9OB−/−). Both Fgf9 knockout (Fgf9OB−/−) and the Fgf9 floxed littermates (Fgf9fl/fl) mice were fully backcrossed and maintained in an FBV/N background.
Parathyroid Hormone Directs Bone Marrow Mesenchymal Cell Fate
Intermittent PTH administration builds bone mass and prevents fractures, but its mechanism of action is unclear. We genetically deleted the PTH/PTHrP receptor (PTH1R) in mesenchymal stem cells using Prx1Cre and found low bone formation, increased bone resorption, and high bone marrow adipose tissue (BMAT). Bone marrow adipocytes traced to Prx1 and expressed classic adipogenic markers and high receptor activator of nuclear factor kappa B ligand (Rankl) expression.
Effects of NSAIDs and hydroxyapatite coating on osseointegration Biomechanical and histological study on rabbits
Effect of Cast Modification on Denture Base Adaptation Following Maxillary Complete Denture Processing
A total of 60 edentulous maxillary casts (n = 10) were distributed among six groups. Group 1 was the control group with no modification, groups 2 through 6 included a butterfly postdam preparation, groups 3 and 4 also included a 10-mm wide/4-mm deep box with addition of four round holes in group 4, and groups 5 and 6 also included a 20-mm wide/4-mm deep box with addition of four round holes in group 6.
Interleukin-32 Gamma Stimulates Bone Formation by Increasing miR-29a in Osteoblastic Cells and Prevents the Development of Osteoporosis
Defective signaling, osteoblastogenesis and bone remodeling in a mouse model of connexin 43 C-terminal truncation
In skeletal tissue, loss or mutation of the gap junction protein connexin 43 (Cx43, also known as GJA1) in cells of the osteoblast lineage leads to a profound cortical bone phenotype and defective tissue remodeling. There is mounting evidence in bone cells that the C-terminus (CT) of Cx43 is a docking platform for signaling effectors and is required for efficient downstream signaling.