Osteoimmunology

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Osteoimmunology (όστέον, osteon from Greek, "bone"; immunitas from Latin, "immunity"; and λόγος, logos, from Greek "study") is a field that emerged about 40 years ago that studies the interface between the

periodontitis. Studies in osteoimmunology reveal relationships between molecular communication among blood cells and structural pathologies in the body.[5]

System similarities

The

myeloid progenitor cells. Surface RANKL on osteoblasts as well as secreted RANKL provide necessary signals for osteoclast precursors to differentiate into osteoclasts. RANKL expression on activated T cells leads to DC activation through binding to RANK expressed on DCs. OPG, produced by DCs, is a soluble decoy receptor for RANKL that competitively inhibits RANKL binding to RANK.[7]

Crosstalk

The

TNFa, ILs, and IFNs, affect the differentiation and activity of osteoclasts and bone resorption.[8][9] Such inflammatory osteoclastogenesis and osteoclast activation can be seen in ex vivo primary cultures of cells from the inflamed synovial fluid of patients with disease flare of the autoimmune disease rheumatoid arthritis.[9][10]

Clinical osteoimmunology

Clinical osteoimmunology is a field that studies a treatment or prevention of the bone related diseases caused by disorders of the immune system. Aberrant and/or prolonged activation of immune system leads to derangement of bone modeling and remodeling. Common diseases caused by disorder of osteoimmune system is osteoporosis and bone destruction accompanied by RA characterized by high infiltration of CD4+ T cells in rheumatoid joints, in which two mechanisms are involved: One is an indirect effect on osteoclastogenesis from rheumatoid synovial cells in joints since synovial cells have osteoclast precursors and osteoclast supporting cells, synovial macrophages are highly differentiated into osteoclasts with help of RANKL released from osteoclast supporting cells.[11][12] The second is an indirect effect on osteoclast differentiation and activity by the secretion of inflammatory cytokines such as

TNFa, in synovium of RA, which increase RANKL signaling and finally bone destruction. A clinical approach to prevent bone related diseases caused by RA is OPG and RANKL treatment in arthritis. There is some evidence that infections (e.g. respiratory virus infection) can reduce the numbers of osteoblasts in bone, the key cells involved in bone formation.[13]

See also

References

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  8. S2CID 28125222
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  9. ^
    PMID 36410109
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  11. PMID 9388467
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  12. S2CID 25695543
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  13. PMID 29212906
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