Study design: Systematic review and meta-analysis.
Objective: To review and assess the current evidence from the literature on the potential association between disc infection with the development of symptomatic degenerative disc disease.
Summary of background data: The potential relationship between disc infection- and disc degeneration-related symptoms remains controversial, with contradictory evidence available in the literature. Several studies have demonstrated the presence of infected extruded nucleus tissue from first-time disc herniations, implicating the role of disc microbial infection as a pathway for disc degeneration. In contrast, other studies reported very low prevalence of bacterial infection in samples from patients with sciatica, quoting contamination as the predominant source. To summarize the available evidence to date, a systematic review and meta-analysis was conducted.
Methods: A comprehensive search from 6 electronic databases was performed for studies investigating the potential relationship between disc infection as a cause for degenerative disc disease and symptomatic neck/back pain or radiculopathy. Random-effects meta-analysis of proportions and odds ratio with 95% confidence intervals was used to pool the available evidence.
Results: Nine relevant studies involving 602 patients with degenerative disc disease or pain were identified. From 6 studies supporting the role of infection in the pathophysiology of disc degeneration, the pooled infection prevalence was 45.2% (34.5%-56.0%). Overall pooled prevalence in all studies was 36.2% (24.7%-47.7%). Proportion of disc infections was higher in patients with symptomatic disc disease than in patients without (37.4% vs. 5.9%; odds ratio, 6.1; 95% confidence intervals, 1.426-25.901). The majority of infections were due to Propionibacterium acnes in 59.6% (43.2%-76.1%).
Conclusion: From the limited evidence available, the possibility that disc infection may be linked with disc degeneration should not be ruled out. There is a need to investigate this further through larger, adequately powered multi-institutional studies with contaminant arm to control for specimen contamination.
Level of evidence: 2.