Neutrophil‐Driven Inflammation in Pediatric Chronic Recurrent Multifocal Osteomyelitis
Authors' conclusion
These findings identify neutrophil activation and inflammation-sensitive PSTPIP2 deficiency as central features of human CRMO, suggest chemokines as potential biomarkers, and mechanistically explain why TNF blockade provides clinical benefit.
Study context
- Population
- Children with chronic recurrent multifocal osteomyelitis (CRMO) and controls
- Participants
- 34 vs 20
- Comparison
- Patients with CRMO vs controls
- CRMOn = 34
- Controlsn = 20reference
- Outcome
- Neutrophil activation and PSTPIP2 in CRMO vs controls
Methodological detailscase-control, flow cytometry, transcriptomic profiling of purified neutrophils
- Case-control
- Flow cytometry
- Transcriptomic profiling of purified neutrophils
Main finding
As reported in the abstract
- Neutrophil activation and PSTPIP2 down-regulation normalized in patients receiving anti-TNF therapy
- IL1B and CXCL8 expression not increased, unlike murine models
- CRMO vs Controls: P = 0.0016; Mann-Whitney test
- CRMO vs Controls: P = 0.0006
- CRMO vs Controls: P = 0.0005
Further findings
Transcriptomic profiling of neutrophils
- Enrichment of NF-κB signaling and inflammatory and chemotaxis pathways; up-regulation of CCL4, CCL4L2, ATL1, VNN1, H2BC7 and LINC02207; down-regulation of ISL2
- Several transcripts correlated with clinical measures of disease burden
- Four patients and three controls
Original publication
Neutrophil‐Driven Inflammation in Pediatric Chronic Recurrent Multifocal Osteomyelitis. Arthritis Rheumatol. Published 29 September 2026. doi:10.
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