Pulsed electromagnetic fields reduce acute inflammation in the injured rat‐tail intervertebral disc

Abstract

Pro‐inflammatory cytokines are recognized contributors to intervertebral disc (IVD) degeneration and discogenic pain. We have recently reported the anti‐inflammatory effect of pulsed electromagnetic fields (PEMF) on IVD cells in vitro. Whether these potentially therapeutic effects are sufficiently potent to influence disc health in vivo has not been demonstrated. We report here the effect of PEMF on acute inflammation arising from a rat‐tail IVD injury model. Disc degeneration was induced by percutaneously stabbing the Co6‐7, Co7‐8, and Co8‐9 levels using a 20‐gauge needle. Seventy‐two (72) rats were divided into three groups: sham control, needle stab, needle stab+PEMF. Treated rats were exposed to PEMF immediately following surgery and for either 4 or 7 days (4 hr/d). Stab and PEMF effects were evaluated by measuring inflammatory cytokine gene expression (RT‐PCR) and protein levels (ELISA assay), anabolic and catabolic gene expression (RT‐PCR), and histologic changes. We observed in untreated animals that at day 7 after injury, inflammatory cytokines (interleukin [IL]‐6, tumor necrosis factor α, and IL‐1β) were significantly increased at both gene and protein levels (P < .05). Similarly, catabolic factors (MMP [metalloproteinases]‐2, MMP‐13 and the transcriptional factor NF‐kβ gene expression) were significantly increased (P < .05). At day 7, PEMF treatment significantly inhibited inflammatory cytokine gene and protein expression induced by needle stab injury (P < .05). At day 4, PEMF downregulated FGF‐1 and upregulated MMP‐2 compared to the stab‐only group. These data demonstrate that previously reported anti‐inflammatory effects of PEMF on disc cells carry over to the in vivo situation, suggesting potential therapeutic benefits. Though we observed an inhibitory effect of PEMF on acute inflammatory cytokine expression, a consistent effect was not observed for acute changes in disc histology and anabolic and catabolic factor expression. Therefore, these findings should be further investigated in studies of longer duration following needle‐stab injury.

Development of a standardized histopathology scoring system for intervertebral disc degeneration in rat models: An initiative of the ORS spine section

“…Both rat lumbar and coccygeal IVDs are structurally, morphologically and biochemically comparable with human IVDs, and are commonly used for studying IVD degeneration 2‐5 . Similar to human IVDs, the rat degenerated IVDs exhibited decreased NP volume, reduced NP cellularity, ruptured and disorganized AF, and a shift towards catabolism with reduced extracellular matrix production and increased matrix degrading enzymes and pro‐inflammatory cytokines 5,7,12‐23 . However, it should be noted that large vacuolated notochordal cells occupy the NP of skeletally mature rat IVDs, 37 while this phenotypic differentiation in humans occurs before skeletal maturity in human IVDs.…”

“…[2][3][4][5] Similar to human IVDs, the rat degenerated IVDs exhibited decreased NP volume, reduced NP cellularity, ruptured and disorganized AF, and a shift towards catabolism with reduced extracellular matrix production and increased matrix degrading enzymes and proinflammatory cytokines. 5,7,[12][13][14][15][16][17][18][19][20][21][22][23] However, it should be noted that large vacuolated notochordal cells occupy the NP of skeletally mature rat IVDs, 37 while this phenotypic differentiation in humans occurs before skeletal maturity in human IVDs. The notochordal cell phenotype is known to enhance proteoglycan synthesis, [51][52][53][54][55] and the presence of notochordal cells in rat IVDs therefore may result in different biochemical and histological changes when compared with human IVDs.…”

“…A reliable method to generate IVD defects is essential in order to investigate pathophysiology and therapeutic interventions for IVD degeneration. Different strategies have been used to induce degenerative changes in rats, including the naturally occurring disc degeneration in aged animals, [18][19][20][21] surgery injury, 4,5,7,12,13,[22][23][24][25][26][27] and mechanical loading. [28][29][30][31][32][33][34][35][36][37][38][39][40] The process of naturally induced IVD degeneration is slow and the severity of tissue damage can vary between animals.…”

Functional neurorehabilitation in a dog with acute non‐compressive nucleus pulposus extrusion

“…In veterinary medicine, there are few studies that show that the use of pulsed electromagnetic fields can be an adjunctive treatment modality on pain, 64,65 bone and wound healing, 60 inflammation 65–68 and oedema 60 cases, along with the fact that it can play a potential positive influence on neural regeneration 69 …”

Causes of and Molecular Targets for the Treatment of Intervertebral Disc Degeneration: A Review

“…In a rabbit model of IVDD generated by needle puncture, Fas expression was evident only in the punctured discs, and Fas-L expression was augmented in the punctured discs than in the control discs [71], indicating that injury can cause Fas-L-Fas binding to initiate apoptosis. An increase in the expression of inflammatory cytokines, such as IL-6, TNFα, and IL-1β, has been observed in a rat tail disc puncture model [72]. Considering the existence of TNFR1 and TNFR2 in NP [73], TNFα-TNFR binding can also lead to apoptosis in cells of the NP.…”