We demonstrate that CD39/CD73 expression and extracellular adenosine levels in the bone marrow are substantially decreased in animals with osteoporotic bone loss.
Loss of <i>Slc7a5</i> impaired activation of the mechanistic target of rapamycin complex 1 (mTORC1) pathway in osteoclasts, whereas genetic activation of mTORC1 corrected the enhanced osteoclastogenesis and bone loss in <i>Slc7a5</i>-deficient mice.
Compared with Ti + PBS and Ti + Lip group, macrophage density (1.64 ± 0.86%) infiltrated into peri-implant tissue and bone loss (0.17 ± 0.03 mm) around implant decreased significantly in the Ti + LipClod group.
These findings demonstrate that PYY acts as a negative regulator of osteoblastic bone formation, implicating increased PYY levels in the pathogenesis of bone loss during anorexia or following bariatric surgery.
In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-α, IL-6, and IL-1β), chemokines (MCP-1 and SDF-1), and MIF's cognate receptors CXCR4 and CD74.
Our findings show for the first time that TREM-1 regulates the IL-17A-RANKL/OPG axis and bone loss in experimental periodontitis, and its therapeutic blockade may pave the way to a novel treatment for human periodontitis.
To determine whether circulating levels of two matrix metalloproteinases, MMP-2 and MMP-9, are associated with loss of alveolar bone density (ABD) or height (ABH), or with progression of periodontitis (relative clinical attachment level [RCAL]), among postmenopausal women with local and systemic bone loss.
In addition, degeneration of cartilage was found from 8 weeks, accompanied by decreased expression of mechanically sensitive TRPV4 and collagen II, and increased expression of MMP-13.<b>Conclusions</b>: This study proved that trochlear dysplasia can be caused by patellar dislocation in growing rabbits, accompanied by significant subchondral bone loss.
<b>Conclusion</b>: PSMAb mediated TRIM24 siRNA delivery platform could significantly inhibit cell proliferation, colony-formation, and invasion in PSMA+ CRPC <i>in vitro</i> and suppressed tumor growth and bone loss in PSMA+ CRPC xenograft and bone metastasis model.
Modern modular implants and the use of bone graft enriched by tissue engineering techniques such as a concentration of autologous mesenchymal cells or PRP may be helpful to compensate all bone loss and anatomic alterations due to failures of orthopaedic implants.
Compared with Ti + PBS and Ti + Lip group, macrophage density (1.64 ± 0.86%) infiltrated into peri-implant tissue and bone loss (0.17 ± 0.03 mm) around implant decreased significantly in the Ti + LipClod group.
Understanding the molecular pathways through which CCR3 acts to regulate osteoclast and osteoblast functions could lead to new therapeutic approaches to prevent inflammation-induced bone loss.