MiR-106b inhibition suppresses inflammatory bone destruction of wear debris-induced periprosthetic osteolysis in rats.

Aseptic loosening caused by periprosthetic osteolysis (PPO) is the main reason for the primary artificial joint replacement. Inhibition of inflammatory osteolysis has become the main target of drug therapy for prosthesis loosening. MiR-106b is a newly discovered miRNA that plays an important role in tumour biology, inflammation and the regulation of bone mass.

Aspirin-Mediated Attenuation of Intervertebral Disc Degeneration by Ameliorating Reactive Oxygen Species and .

Intervertebral disc (IVD) degeneration (IDD) is a major cause of low back pain. The pathogenesis of IDD is associated with the disturbance of reactive oxygen species (ROS) equilibrium, inflammation, and matrix loss. Aspirin is a nonsteroidal anti-inflammatory drug that effectively inhibits inflammation and oxidative stress and has been widely used for the treatment of back pain.

Aspirin inhibits osteoclast formation and wear-debris-induced bone destruction by suppressing mitogen-activated protein kinases.

Excessive osteoclast recruitment and activation is the chief cause of periprosthetic osteolysis and subsequent aseptic loosening, so blocking osteolysis may be useful for protecting against osteoclastic bone resorption. We studied the effect of aspirin on titanium (Ti)-particle-induced osteolysis in vivo and in vitro using male C57BL/6J mice randomized to sham (sham surgery), Ti (Ti particles), low-dose aspirin (Ti/5 mg·kg ·d aspirin), and high-dose aspirin (Ti/30 mg·kg ·d aspirin). After 2 weeks, a three-dimensional reconstruction evaluation using micro-computed tomography and histomorphology assessment were performed on murine calvariae.

Melatonin Increases Bone Mass around the Prostheses of OVX Rats by Ameliorating Mitochondrial Oxidative Stress via the SIRT3/SOD2 Signaling Pathway.

Bone mass loss around prostheses is a major cause of implant failure, especially in postmenopausal osteoporosis patients. In osteoporosis, excess oxidative stress largely contributed abnormal bone remodeling. Melatonin, which is synthesized from the pineal gland, promotes osteoblast differentiation and bone formation and has effectively been used to combat oxidative stress.

Exenatide ameliorates inflammatory response in human rheumatoid arthritis fibroblast-like synoviocytes.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease of unknown etiology characterized by degradation of cartilage and bone, accompanied by unimpeded proliferation of synoviocytes of altered phenotype. In the present study, we investigated the involvement of the glucagon-like peptide 1 (GLP-1) receptor on human fibroblast-like synoviocytes (FLS) in the pathogenesis of RA using the selective GLP-1 agonist exenatide, a licensed drug used for the treatment of type 2 diabetes. Our results indicate that exenatide may play a role in regulating tumor necrosis factor-α-induced mitochondrial dysfunction by increasing mitochondrial membrane potential, oxidative stress by reducing the production of reactive oxygen species, the expression of NADPH oxidase 4, expression of matrix metalloproteinase (MMP)-3 and MMP-13, release of proinflammatory cytokines including interleukin-1β (IL-1β), IL-6, monocyte chemoattractant protein-1, and high-mobility group protein 1, as well as activation of the p38/nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor, α/nuclear factor κB signaling pathway in primary human RA FLS.

Efficient Inhibition of Wear-Debris-Induced Osteolysis by Surface Biomimetic Engineering of Titanium Implant with a Mussel-Derived Integrin-Targeting Peptide.

Wear-debris-induced osteolysis and subsequent aseptic loosening of the prosthesis are the main reasons for failed arthroplasty. Inhibition of wear-debris-induced osteoclastogenesis is thus a promising method to prolong the lifetime of prostheses. In this work, a mussel-derived peptide, capped with an integrin-targeting RGD tripeptide and a titanium (Ti)-affinity tetrapeptide with catechol groups at each end is biomimetically designed.

Tenocyte-derived exosomes induce the tenogenic differentiation of mesenchymal stem cells through TGF-β.

Mesenchymal stem cells (MSCs) hold great potential to treat tissue damage based on their multipotent property, and are also considered as suitable cell resources to create tissue-engineered grafts for tendon repair. However, the clinical application of MSCs is still limited by the lack of efficient methods to induce tenogenic differentiation. In this study, by performing the experiments in transwell system, we found that paracrine factors from tenocytes could induce MSCs to undergo the tenogenic differentiation.

KLF2 regulates osteoblast differentiation by targeting of Runx2.

Osteoblast differentiation plays a critical role in bone formation and maintaining balance in bone remodeling. Runt-related transcription factor 2 (Runx2) is a central transcription factor regulating osteoblast differentiation and promoting bone mineralization. Until now, the molecular regulatory basis and especially the gene regulatory network of osteogenic differentiation have been unclear.

Shikimic acid prevents cartilage matrix destruction in human chondrocytes.

Abnormal reduction of extracellular matrix (ECM), including type II collagen and aggrecan, caused by tumor necrosis factor-α (TNF-α) is an important pathological feature of osteoarthritis (OA). Shikimic acid (SA), derived from natural plants, has displayed effective pharmacological properties in diverse diseases. The biological roles of SA in OA have not been reported before.