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Updated: Feb 18, 2026
Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
Published on: January 27, 2023
Oxidized low-density lipoprotein promotes osteoclast differentiation from CD68 positive mononuclear cells by
Chunfeng Hou1, Luan Luan1, Chunfeng Ren1
1Department of Rheumatology, Jining First People's Hospital, Jining, Shandong 272001, PR China.
Insights
Ankylosing spondylitis patients show elevated oxidized LDL/LDL ratio, promoting cardiovascular risk. These changes also favor osteoclastogenesis, potentially impacting bone health in AS.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Rheumatology
Background:
- Ankylosing spondylitis (AS) patients face higher cardiovascular mortality risk.
- Oxidized low-density lipoprotein (ox-LDL)/LDL ratio links to atherosclerosis in other inflammatory conditions.
Purpose of the Study:
- Investigate the role of ox-LDL/LDL ratio in AS.
- Explore the association between ox-LDL/LDL ratio and osteoclastogenesis markers in AS.
Main Methods:
- Measured ox-LDL/LDL ratio, serum RANKL, and HMGB1 in AS patients.
- Quantified CD68+/RANK+ cells in peripheral blood.
- Utilized in vitro models with ox-LDL to study HMGB1 and RANK expression.
Main Results:
- AS patients exhibited increased ox-LDL/LDL ratio, serum RANKL, and HMGB1.
- Elevated CD68+/RANK+ cells were observed in AS patients' peripheral blood.
- Ox-LDL exposure induced HMGB1 release and RANK expression, promoting osteoclast precursor formation.
Conclusions:
- Elevated ox-LDL/LDL ratio, increased CD68+/RANK+ cells, and higher RANKL/HMGB1 levels in AS patients favor osteoclastogenesis.
- These findings suggest a potential mechanism linking cardiovascular risk and bone metabolism in AS.
Abstract:
Patients with ankylosing spondylitis (AS) have an increased risk for cardiovascular mortality. The circulating ox-LDL/LDL ratio is associated with subclinical atherosclerosis in patients with systemic lupus erythematosus. In this study, we found that the ox-LDL/LDL ratio was increased in AS patients. The levels of serum RANKL and HMGB1 were also elevated in AS patients, and the number of CD68+/RANK+ cells was increased in peripheral blood from AS patients. 0.03% ox-LDL in LDL, similar to the ox-LDL/LDL ratio in peripheral blood from AS patients, promoted cytoplasmic translocation and release of HMGB1 as well as RANK expression. Further investigation evidenced that ox-LDL-induced EGR1 expression contributed to the cytoplasmic translocation of HMGB1 and CD68 assisted the secretion of HMGB1 from cytoplasm to extracellular matrix. Extracellular HMGB1 induced RANK expression in CD68+ mononuclear cells, forming osteoclast precursors that were differentiated to osteoclasts in response to RANKL. Taken together, these results suggested that the changes, including ox-LDL/LDL ratio, CD68+/RANK+ cells number, and the levels of RANKL and HMGB1 in AS patients, favored osteoclastogenesis.
