Osteoimmunology in Bone Health and Disease
Summary
Osteoimmunology examines the dynamic interplay between the skeletal and immune systems, recognising that bone remodelling is not solely governed by osteoblasts and osteoclasts but is profoundly influenced by immune cells and their mediators. Under normal conditions, osteoblasts synthesise new bone matrix while osteoclasts resorb aged bone, maintaining skeletal integrity. Immune cells—particularly T lymphocytes, B lymphocytes and monocytes—secrete cytokines such as receptor activator of nuclear factor-κB ligand (RANKL), tumour necrosis factor-α and interleukins that modulate this balance. Perturbations in immune regulation can lead to bone loss in conditions such as osteoporosis, rheumatoid arthritis and infection-associated bone erosion. Recent advances have elucidated molecular pathways—including JAK-STAT signalling, hypoxia-inducible factors and costimulatory receptors—that underpin immune-driven changes in osteoclastogenesis and osteoblastogenesis. This integrated perspective has opened novel therapeutic avenues, from cytokine blockade to targeted modulation of lymphocyte activity, with implications for global health as the burden of bone fragility and inflammatory bone disease rises with an ageing population.
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Osteoimmunology in Bone Health and Disease publication trend
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Technical terms
Osteoclast: A specialised multinucleated cell responsible for bone resorption.
Osteoblast: A cell that synthesises and mineralises new bone matrix.
RANKL (Receptor Activator of NF-κB Ligand): A cytokine critical for osteoclast differentiation and activation.
Osteoprotegerin (OPG): A decoy receptor for RANKL that inhibits osteoclastogenesis.
Cytokine: A signalling protein secreted by immune cells that regulates inflammation and cell communication in bone remodelling.
References
- Low‐Dose Staphylococcal Enterotoxin C2 Mutant Maintains Bone Homeostasis via Regulating Crosstalk between Bone Formation and Host T‐Cell Effector Immunity. Advanced Science (2023).
- Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis. International Journal of Molecular Sciences (2024).
- Estrogen-mediated downregulation of HIF-1α signaling in B lymphocytes influences postmenopausal bone loss. Bone Research (2022).
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