Can proinflammatory cytokine gene expression explain multifidus muscle fiber changes after an intervertebral disc lesion?
METHODS
Longitudinal case-controlled animal study.


OBJECTIVE
To investigate the effect of an intervertebral disc (IVD) lesion on the proportion of slow, fast, and intermediate muscle fiber types in the multifidus muscle in sheep, and whether muscle fiber changes were paralleled by local gene expression of the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1-β.


BACKGROUND
Structure and behavior of the multifidus muscle change in acute and chronic back pain, but the mechanisms are surprisingly poorly understood and the link between structure and behavior is tenuous. Although changes in muscle fiber types have the potential to unify the observations, the effect of injury on muscle fiber distribution has not been adequately tested, and understanding of possible mechanisms is limited.


METHODS
The L1-L2, L3-L4, and L5-L6 IVDs of 11 castrated male sheep received anterolateral lesions. Six control sheep underwent no surgical procedures. Multifidus muscle tissue was harvested at L4 for muscle fiber analysis using immunohistochemistry and L2 for cytokine analysis with polymerase chain reaction for local gene expression of TNF-α and interleukin-1β.


RESULTS
The proportion of slow muscle fibers in multifidus was significantly less in the lesioned animals both ipsilateral and contralateral to the IVD lesion. The greatest reduction in slow fibers was in the deep medial muscle region. A greater prevalence of intermediate fibers on the uninjured side implies a delayed fiber-type transformation on that side. TNF-α gene expression in multifidus was greater on both sides in the lesion animals than in the muscle of control animals. Interleukin-1β was increased only on the injured side.


CONCLUSIONS
These data provide evidence of muscle fiber changes after induction of an IVD lesion and a parallel increase in TNF-α expression. Proinflammatory cytokine changes provide a novel mechanism to explain behavioral and structural changes in multifidus.


METHODS
N/A.
*The University of Queensland, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia; and †University of Sydney, Raymond Purves Bone and Joint Research Laboratories, Kolling Institute of Medical Research, Royal North Shore Hospital, St. Leonards, Australia.
Paul W
PW
Hodges
Gregory
G
James
Linda
L
Blomster
Leanne
L
Hall
Annina B
AB
Schmid
Cindy
C
Shu
Chris
C
Little
James
J
Melrose
D000818:Animals; D004195:Disease Models, Animal; D015870:Gene Expression / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics* / Q000276:immunology; D055959:Intervertebral Disc Degeneration / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D008159:Lumbar Vertebrae; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000276:immunology* / Q000473:pathology; D018657:Muscle Fibers, Slow-Twitch / Q000276:immunology / Q000473:pathology; D009919:Orchiectomy; D064170:Paraspinal Muscles / Q000276:immunology* / Q000473:pathology; D012756:Sheep; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000276:immunology
D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha