Authors :
Rejina C.; Dr. A. Pandiselvi; HarishKumar E.; SaranKarthikeyan S.
Volume/Issue :
Volume 10 - 2025, Issue 8 - August
Google Scholar :
https://tinyurl.com/4ce82ysu
Scribd :
https://tinyurl.com/6cb24css
DOI :
https://doi.org/10.38124/ijisrt/25aug1101
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
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Abstract :
Inflammation serves as both a stimulus for bone regeneration and a driver of deterioration. Although the process
of bone remodelling is strictly regulated by osteoblasts, osteoclasts, osteocytes, and bone-lining cells, immunological
signalling significantly affects how it is balanced. Acute inflammation is crucial for initiating bone repair because cytokines
such as IL-1, IL-6, and TNF-α draw neutrophils and macrophages to the fracture site, clear debris, and encourage
mesenchymal stem cell differentiation into osteoblasts. However, prolonged or dysregulated inflammation promotes bone
loss by tilting the RANKL/OPG axis in favour of osteoclastogenesis, a characteristic of diseases such as inflammatory bowel
disease, periodontitis, and rheumatoid arthritis. The new field of osteoimmunology shows how immune cells have two
different effects: Th17 cells, hyperactivated neutrophils, and pro-inflammatory macrophages speed up bone resorption,
while Tregs, osteomacs, and B cell-derived OPG encourage regeneration. This review emphasises how inflammation's
temporal, cellular, and molecular context determines skeletal outcomes, highlighting the thin line separating repair from
ruin. Comprehending this osteoimmune paradox offers therapeutic options, such as immune cell reprogramming, cytokine
modulation, and RANKL inhibition, to promote bone regeneration while reducing inflammation-induced bone loss.
Keywords :
Inflammation, Bone Remodelling, Osteoimmunology, Osteoclastogenesis, RANKL/OPG Axis, Cytokines, T Regulatory Cells, Th17 Cells, Osteomacs, Bone Regeneration.
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Inflammation serves as both a stimulus for bone regeneration and a driver of deterioration. Although the process
of bone remodelling is strictly regulated by osteoblasts, osteoclasts, osteocytes, and bone-lining cells, immunological
signalling significantly affects how it is balanced. Acute inflammation is crucial for initiating bone repair because cytokines
such as IL-1, IL-6, and TNF-α draw neutrophils and macrophages to the fracture site, clear debris, and encourage
mesenchymal stem cell differentiation into osteoblasts. However, prolonged or dysregulated inflammation promotes bone
loss by tilting the RANKL/OPG axis in favour of osteoclastogenesis, a characteristic of diseases such as inflammatory bowel
disease, periodontitis, and rheumatoid arthritis. The new field of osteoimmunology shows how immune cells have two
different effects: Th17 cells, hyperactivated neutrophils, and pro-inflammatory macrophages speed up bone resorption,
while Tregs, osteomacs, and B cell-derived OPG encourage regeneration. This review emphasises how inflammation's
temporal, cellular, and molecular context determines skeletal outcomes, highlighting the thin line separating repair from
ruin. Comprehending this osteoimmune paradox offers therapeutic options, such as immune cell reprogramming, cytokine
modulation, and RANKL inhibition, to promote bone regeneration while reducing inflammation-induced bone loss.
Keywords :
Inflammation, Bone Remodelling, Osteoimmunology, Osteoclastogenesis, RANKL/OPG Axis, Cytokines, T Regulatory Cells, Th17 Cells, Osteomacs, Bone Regeneration.