Oncostatin M-driven macrophage-fibroblast circuits as a drug target in autoimmune arthritis.

Background: Recent single-cell RNA sequencing (scRNA-seq) analysis revealed the functional heterogeneity and pathogenic cell subsets in immune cells, synovial fibroblasts and bone cells in rheumatoid arthritis (RA). JAK inhibitors which ameliorate joint inflammation and bone destruction in RA, suppress the activation of various types of cells in vitro. However, the key cellular and molecular mechanisms underlying the potent clinical effects of JAK inhibitors on RA remain to be determined.

Periosteal stem cells control growth plate stem cells during postnatal skeletal growth.

The ontogeny and fate of stem cells have been extensively investigated by lineage-tracing approaches. At distinct anatomical sites, bone tissue harbors multiple types of skeletal stem cells, which may independently supply osteogenic cells in a site-specific manner. Periosteal stem cells (PSCs) and growth plate resting zone stem cells (RZSCs) critically contribute to intramembranous and endochondral bone formation, respectively.

Plasma cells promote osteoclastogenesis and periarticular bone loss in autoimmune arthritis.

In rheumatoid arthritis (RA), osteoclastic bone resorption causes structural joint damage as well as periarticular and systemic bone loss. Periarticular bone loss is one of the earliest indices of RA, often preceding the onset of clinical symptoms via largely unknown mechanisms. Excessive osteoclastogenesis induced by receptor activator of NF-κB ligand (RANKL) expressed by synovial fibroblasts causes joint erosion, whereas the role of RANKL expressed by lymphocytes in various types of bone damage has yet to be elucidated.

Stepwise cell fate decision pathways during osteoclastogenesis at single-cell resolution.

Osteoclasts are the exclusive bone-resorbing cells, playing a central role in bone metabolism, as well as the bone damage that occurs under pathological conditions. In postnatal life, haematopoietic stem-cell-derived precursors give rise to osteoclasts in response to stimulation with macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand, both of which are produced by osteoclastogenesis-supporting cells such as osteoblasts and osteocytes. However, the precise mechanisms underlying cell fate specification during osteoclast differentiation remain unclear.

Host defense against oral microbiota by bone-damaging T cells.

The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic T17 cells induce bone destruction and autoimmune inflammation. However, whether a beneficial function of T-cell-induced bone damage exists is unclear.

Effect of buccal gap distance on alveolar ridge alteration after immediate implant placement: a microcomputed tomographic and morphometric analysis in dogs.

Introduction: The buccal bone resorption and the deformation of soft tissue contour are major problems of immediate implant treatment. This study aims to examine the changes of alveolar bone and soft tissue after immediate implant placement in different buccal gap distances.

Materials And Methods: Eight implants were placed randomly in the mandibular premolar sockets of 6 hybrid dogs with 1, 2, and 3 mm buccal gap distances.