Abstract
BackgroundThe inflammatory profiles of patients with acute and chronic nonspecific low back pain (LBP) patients are distinct. Spinal manipulative therapy (SMT) has been shown to modulate the production of nociceptive chemokines differently in these patient cohorts. The present study further investigates the effect(s) of SMT on other inflammatory mediators in the same LBP patient cohorts.MethodsAcute (n = 22) and chronic (n = 25) LBP patients with minimum pain scores of 3 on a 10-point numeric scale, and asymptomatic controls (n = 24) were recruited according to stringent exclusion criteria. Blood samples were obtained at baseline and after 2 weeks during which patients received 6 SMTs in the lumbar or lumbosacral region. The in vitro production of tumor necrosis factor (TNFα), interleukin-1 β (IL-1β), IL-6, IL-2, interferon ɣ (IFNɣ), IL-1 receptor antagonist (IL-1RA), TNF soluble receptor type 2 (sTNFR2) and IL-10 was determined by specific immunoassays. Parametric as well as non-parametric statistics (PAST 3.18 beta software) was used to determine significance of differences between and within study groups prior and post-SMT. Effect size (ES) estimates were obtained using Cohen’s d.ResultsCompared with asymptomatic controls, SMT-related change scores were significant (P = 0.03–0.01) in reducing the production levels of TNFα in both patient cohorts and those of IL-6, IFNɣ and sTNFR2 (P = 0.001–0.02) in patients with chronic LBP. Above-moderate to large ES (d > 0.6–1.4) was observed for these mediators. Compared with respective baselines, a significant post-SMT reduction (P = 0.01) of IL-6 production was detected only in patients with chronic LBP while a significant increase of IL-2 production (P = 0.001 vs. control, and P = 0.004 vs. chronic LBP group) and a large ES (d = 0.87) were observed in patients with acute LBP. Pain and disability scores declined significantly (P < 0.001) in all LBP patients, and were positively correlated (P = 0.03) with IFNɣ and IL-2 levels in the acute LBP cohort.ConclusionThe short course of SMT treatments of non-specific LBP patients resulted in significant albeit limited and diverse alterations in the production of several of the mediators investigated in this study. This exploratory study highlights the potential of SMT to modulate the production of inflammatory components in acute and chronic non-specific LBP patients and suggests a need for further, randomized controlled clinical trials in this area.Trial registrationThis study was prospectively registered April 2012 with Clinical Trials.gov (#NCT01766141).https://register.clinicaltrials.gov/prs/app/action/SelectProtocol?sid=S0003ZIL&selectaction=Edit&uid=U0001V74&ts=2&cx=-axvqtg
Highlights
The inflammatory profiles of patients with acute and chronic nonspecific low back pain (LBP) patients are distinct
The short course of Spinal manipulative therapy (SMT) treatments of non-specific LBP patients resulted in significant albeit limited and diverse alterations in the production of several of the mediators investigated in this study
This exploratory study highlights the potential of SMT to modulate the production of inflammatory components in acute and chronic non-specific LBP patients and suggests a need for further, randomized controlled clinical trials in this area
Summary
The inflammatory profiles of patients with acute and chronic nonspecific low back pain (LBP) patients are distinct. The present study further investigates the effect(s) of SMT on other inflammatory mediators in the same LBP patient cohorts. The use of spinal manipulative therapy (SMT) has been recognized as an effective form of non-pharmacological treatment of non-specific low back pain (LBP) [1,2,3]. Only one study has explored the relationship between SMT and the production of nociceptive/chemotactic cytokines in acute and chronic low back patients utilizing an in vitro model [18]. Pain scores in SMT-treated patients with acute and chronic LBP were associated with a significant reduction of the nociceptive chemokine, macrophage inflammatory protein 1α (CC chemokine ligand, CCL3) levels. It was of interest to investigate, in the same patient cohorts, whether SMT effects might differ with respect to the production of other nociceptive/inflammatory mediators
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