Association of glycosaminoglycan depletion and degradative enzyme activity in scoliosis.
Although several theories have been advanced about etiology of idiopathic scoliosis, the pathogenesis still remains unknown. One study detected a decrease in the glycosaminoglycan content of the nucleus pulposus in idiopathic scoliosis, and it was theorized that this represented increased degradation. The present study was designed to investigate degradative enzyme activity in scoliotic intervertebral disks. Twenty-three disks from 5 patients with idiopathic scoliosis and 18 disks from 3 patients with scoliosis resulting from myelomeningocele were obtained at surgery (Dwyer procedure). Five disks were obtained during 2 postmortem examinations. Analyses of hydroxyproline, hexosamine and acid phosphatase were performed separately on the annulus and nucleus of each disk. Hexosamine was decreased in idiopathic scoliotic nuclei versus controls (p less than 0.001) by approximately 25%. Hydroxyproline was proportionately increased (p less than 0.05). Similar changes of a greater magnitude were seen when comparing myelomeningoceles to controls. In both types of scoliosis, acid phosphatase was elevated in nuclear and annular tissue. Acid phosphatase activity and hexosamine varied inversely in the nucleus. Finding similar biochemical patterns in idiopathic and neurovascular scoliosis raises the possibility that these changes may be secondary.
D000135:Acid Phosphatase / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D002648:Child; D006025:Glycosaminoglycans / Q000378:metabolism*; D006595:Hexosamines / Q000378:metabolism; D006801:Humans; D006909:Hydroxyproline / Q000378:metabolism; D007403:Intervertebral Disc / Q000201:enzymology; D008591:Meningomyelocele / Q000201:enzymology; D012600:Scoliosis / Q000201:enzymology*
D006025:Glycosaminoglycans; D006595:Hexosamines; D000135:Acid Phosphatase; D006909:Hydroxyproline