Muscle study in experimental scoliosis in rabbits with costotransversectomy: evidence of ischemic process

Abstract

Scoliosis involves the central nervous system diseases, ligaments, articulations and skeletal muscles, but there is no consensus on its pathogeny and progression of muscle abnormalities. In this study, we investigate the morphologic changes in the muscle of rabbit submitted to experimental scoliosis, with special emphasis on abnormalities related to blood supply. We studied 26 rabbits subjected to costotransversectomy by pulling out six transverse processes at thoracic level and six rabbits were used as controls. All the animals operated upon developed scoliosis showing an average angle of 29.1 degrees on the 60th day, with its apices located at T4 and T12 when they were subjected to paraspinal muscle biopsy on both sides. The muscle biopsies were subjected to histological stains and histochemical reactions, as well as to a morphometric study. On the concave side, the changes were not statistically significant regarding the control group. On the convex side conjunctive tissue proliferation, infiltration by adipose tissue, central nucleus excess, inflammatory reaction, segmental fibrosis, type 1 fiber hypertrophy, type 2 fiber hypertrophy and atrophic angular dark fibers in the unspecific esterase were statistically significant. The segmental fibrosis reached a circumscribed muscle segment, compatible with an ischemic phenomenon. The histological diagnoses on the concave side of the animals had unspecific alterations (atrophy and hypertrophy) in 13, myopathy in 3, denervation in 3 and normal in 7. The convex side diagnoses were myopathy in 14, denervation in 8, mixed in 3 and normal in 1. The procedure determined morphologic changes on the convex side indicating possible denervation or myopathy of ischemic origin.

Fig. 1

Progressive spine angulations in rabbits with unilateral costotransversectomy. a Control, b after 60 days 35°

Fig. 2

Muscle from control group. a Slight variation in fiber size (Hematoxylin-Eosin). b Type 2 muscle fiber atrophy (ATPase 9.4, dark fibers are type 2). Bar 100 μm

Fig. 3

a Fibers with necrosis and phagocytosis (arrow); b area of inflammatory infiltration in necrotic fiber (arrow) and atrophic fibers in the convex side (scoliotic group). Haematoxylin-eosin. Bar 50 μm

Fig. 4

Connective tissue proliferation, segmental fibrosis in the perifascicular area (arrows), inflammatory reaction, excess of central nuclei, atrophic fibers in the perifascicular region (star) and hypertrophic fibers. Scoliotic group, convex side. Haematoxylin-eosin. Bar 100 μm

Fig. 5

Vessel with the lumen occluded by thrombi. Scoliotic group, convex side. Haematoxylin-eosin, Bar 50 μm

Fig. 6

Large area of muscle infarct (arrows). Scoliotic group, convex side. Haematoxylin-eosin. Bar 100 μm

Fig. 7

Type 2 fiber atrophy (arrows) and type grouping (star). Scoliotic group, concave side. Type 2 fibers with strong reaction. ATPase 9.4, Bar 100 μm

Fig. 8

Dark small angulated fibers (arrows). Scoliotic group, convex side. Non-specific esterase, Bar 100 μm