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Elevated Production of Nociceptive CC-chemokines and sE-selectin in Patients with Low Back Pain and the Effects of Spinal Manipulation: A Non-randomized Clinical Trial

Elevated Production of Nociceptive CC-chemokines and sE-selectin in Patients with Low Back Pain and the Effects of Spinal Manipulation: A Non-randomized Clinical Trial

The Chiro.Org Blog


SOURCE:   Clin J Pain. 2017 (Apr 19) [Epub]

Julita A. Teodorczyk-Injeyan, PhD,
Marion McGregor, PhD, DC,
John J. Triano, DC, PhD,
H. Stephen Injeyan, PhD, DC

Graduate Education and Research Programs,
Canadian Memorial Chiropractic College,
Toronto, Ontario, Canada


BACKGROUND:   The involvement of inflammatory components in the pathophysiology of low back pain is poorly understood. It has been suggested that spinal manipulative therapy (SMT) may exert anti-inflammatory effects.

PURPOSE:   To determine the involvement of inflammation-associated chemokines (CC series) in the pathogenesis of non-specific low back pain and to evaluate the effect of SMT on that process.

METHODS:   Patients presenting with non-radicular, non-specific low back pain (minimum pain score 3 on 10 point visual analogue scale, VAS) were recruited according to stringent inclusion criteria. They were evaluated for appropriateness to treat using a high velocity low amplitude manipulative thrust (HVLT) in the lumbar-lumbosacral region. Blood samples were obtained at baseline and following the administration of a series of 6 HVLTs on alternate days over the period of two weeks. The in vitro levels of CC chemokines (CCL2, CCL3 and CCL4) production and plasma levels of an inflammatory biomarker, soluble E-selectin, were determined at baseline and at the termination of treatments two weeks later.

RESULTS:   Compared with asymptomatic controls baseline production of all chemokines was significantly elevated in acute (P=0.004 – <0.0001), and that of CCL2 and CCL4 in chronic LBP patients (P<0.0001). Furthermore, CCL4 production was significantly higher (P<0.0001) in the acute versus chronic LBP group. sE-selectin levels were significantly higher (P=0.003) in chronic but not in acute LBP patients. Following SMT, patient reported outcomes showed significant (P<0.0001) improvements in VAS and ODI scores. This was accompanied by a significant decline in CCL 3 production (P<0.0001) in both groups of patients. Change scores for CCL4 production differed significantly (P<0.0001) only for the acute LBP cohort, and no effect on the production of CCL2 or plasma sE-selectin levels was noted in either group.

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CONCLUSION:   The production of chemotactic cytokines is significantly and protractedly elevated in LBP patients. Changes in chemokine production levels, which might be related to SMT, differ in the acute and chronic LBP patient cohorts. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.


From the FULL TEXT Article:

INTRODUCTION

The etiology of non-specific (mechanical) low back pain (LBP) is multifaceted. [1, 2] Acute low back pain is generally considered to be associated with enhanced pain sensitivity of the spinal/paraspinal structures. [3] The persistence of spinal pain over 12 weeks, normally sufficient for completion of connective tissue healing, suggests that acute spinal pain has become chronic. [4]

Among nonpharmacological treatments for LBP, the use of spinal manipulative therapy (SMT) has been widely practiced and its relative effectiveness both for chronic and acute LBP has been reviewed. [5, 6] While correcting segmental restrictions and biomechanical aberrations may provide a feasible justification for efficacy of spinal manipulation, biological mechanisms associated with this form of therapy remain unclear. [7] Recent investigations, suggest that SMT may exert anti-inflammatory effect(s) [8] and thereby may impact the integrated network of inflammatory and immunoregulatory mediators inherent in spinal pain. [9]


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