Are persistently symptomatic vertebral compression fractures associated with abnormal inflammatory profiles? A prospective study.

STUDY DESIGN A case-control study with prospectively collected samples for laboratory analysis in a series of patients with spinal fragility fractures and a series of patients without fracture who underwent fusion for LBP. OBJECTIVE Was an exploratory data analysis for candidate cytokine biomarkers present in the fracture milieu of patients with persistent back pain associated with vertebral compression fracture. SUMMARY OF BACKGROUND DATA Lumbar and thoracic compression fractures are common. Little is known about the presence of inflammatory mediators within fractured vertebra in the clinical setting. METHODS Thirty patients diagnosed with a single thoracic or lumbar compression fracture were treated with single level vertebroplasty. At the time of intervention, needle aspiration was carried out at the fractured level. A multiplexed bead assay was used to assess the presence of 27 different cytokines and inflammatory mediators. A control group consisted of needle aspiration samples of 30 lumbar vertebra from 13 patients with chronic pain but no fracture undergoing open instrumented fusion. RESULTS Thirty patients with 30 fractures consisted of 23 female and 7 male with a mean age of 77.5 years (SD 13.6; range 42 to 97) and a mean of 3.9 weeks of pain (SD 3.1; range 1 to 12). The highest levels of inflammatory mediators were (in order): IL-1 receptor antagonist, PDGF, RANTES, IP-10, IL-8, and eotaxin. These mediators were present at concentrations>200 pg/mL. Compared with controls with chronic pain, significant differences were present for 4 mediators: TNF, MIP-1b, IL-9, and IL-12. The panel of these 4 markers was 93.3% specific and 66.7% sensitive for fracture compared with the control group. CONCLUSIONS Inflammatory mediators are present in needle aspirates of symptomatic vertebral compression fractures. Some of these mediators show different levels than in patients with chronic pain but no fracture. LEVEL OF EVIDENCE Diagnostic level of evidence II.