Preview

Russian Journal of Spine Surgery (Khirurgiya Pozvonochnika)

Advanced search

POTENTIAL BIOCHEMICAL MARKERSOF IDIOPATHIC SCOLIOSIS PROGRESSION

https://doi.org/10.14531/ss2011.1.62-67

Abstract

Objective. To clarify specific signs of idiopathic scoliosis progression that may be associated with change in glycosaminoglycan turnover.

Material and Methods. Blood serum samples from 180 adolescents aged 11–14 years with grade I–IV idiopathic scoliosis were tested for sulphated glycosaminoglycan levels, and for activity of lysosomal glycosidases (hyaluronidase, N-acetyl- β-D-glucosaminidase, β-glucuronidase, and α-galactosidase) and cathepsine D.

Results. Reduction in serum sulfated glycosaminoglycan levels, as compared to the levels of healthy subjects, was revealed in 25 % of adolescents with early stages of spinal deformity development, and in more than 70 % of those with idiopathic scoliosis of grade III–IV. Activity of α-galactosidase in adolescents with high grade of deformity 3–10 times exceeded that of in normal subjects. Any correlation between a change in the activity of other blood lysosomal glycosidases and a degree of scoliosis was not revealed.

Conclusion. The obtained data demonstrate that levels of examined sulphated glycosaminoglycans and α-galactosidase activity are in certain correlation with a grade of scoliotic deformity of the spine. Thus, these characteristics may be considered as a kind of biochemical markers of idiopathic scoliosis progression, and further study of glycosaminoglycan and galactose metabolism may be one of the prospective directions in studies of idiopathic scoliosis pathogenesis.

About the Authors

Tatyana Vasilyevna Rusova
Novosibirsk Research Institute of Traumatology and Orthopaedics
Russian Federation


Natalya Valeryevna Shaidurova
Novosibirsk Research Institute of Traumatology and Orthopaedics
Russian Federation


Alla Mikhailovna Zaidman
Novosibirsk Research Institute of Traumatology and Orthopaedics
Russian Federation


References

1. Зайдман А.М., Аксенович Т.И., Садовой М.А. и др. Механизмы наследования идиопатического сколиоза // Хирургия позвоночника. 2005. № 1. С. 112–121.

2. Зимницкий А.Н. Гликозаминогликаны в биохимических механизмах адаптации организма к некоторым физиологическим и патофизиологическим состояниям. М., 2004.

3. Казьмин А.И., Герасимов А.М., Торопов А.Ю. и др. Связь результатов эпифезэктомии дисков у больных диспластическим сколиозом и биохимическим строением тел позвонков // Ортопед., травматол. и протезир. 1990. № 3. С. 42–45.

4. Казьмин А.И., Меркурьева Р.В. О роли нарушений метаболизма гликозаминогликанов в патогенезе сколиоза // Ортопед., травматол. и протезир. 1971. № 11. С. 87–91.

5. Кандауров В.В. Исследования гликозаминогликанов и ферментов их обмена у больных идиопатическим сколиозом // Повреждения и заболевания позвоночника. Л., 1986. С. 32–38.

6. Русова Т.В., Кулешова О.Н., Жуков Д.В. Гликозаминогликаны тканей межпозвоночных дисков у больных идиопатическим сколиозом // Хирургия позвоночника. 2006. № 3. С. 84–87.

7. Русова Т.В., Рыкова В.И., Зайдман А.М. и др.Гликозаминогликаны пластинки роста тела позвонков у больных идиопатическим сколиозом // Бюл. эксперим. биол. мед. 2005. Т. 139. С. 738–740.

8. Antoniou J., Arlet V., Goswami T., et al. Elevated synthetic activity in the convex side of scoliotic intervertebral discs and endplates compared with normal tissues // Spine. 2001. Vol. 26. P. E198–E206.

9. Burwell R.G., Cole A.A., Cook T.A., et al. Pathogenesis of idiopathic scoliosis. The Nottingham concept // Acta Orthop. Belg. 1992. Vol. 58. Suppl. 1. P. 33–58.

10. Burwell R.G., Freeman B.J., Dangerfield P.H., et al. Etiologic theories of idiopathic scoliosis: enantiomorph disorder concept of bilateral symmetry, physeally-created growth conflicts and possible prevention // Stud. Health Technol. Inform. 2006. Vol. 123. P. 391–397.

11. Byrd J.A. 3rd. Current theories on the etiology of idiopathic scoliosis // Clin. Orthop. Relat. Res. 1988. N 229. P. 114–119.

12. Grivas T.B., Vasiliadis E., Malakasis M., et al. Intervertebral disc biomechanics in the pathogenesis of idiopathic scoliosis // Stud. Health Technol. Inform. 2006. Vol. 123. P. 80–83.

13. Lien Y.H., Fu J., Rucker R.B., et al. Collagen, proteoglycan and hyaluronidase activity in cultures from normal and scoliotic chicken fibroblast // Biochim. Biophys. Acta. 1990. Vol. 1034. P. 318–325.

14. Lowe T.G., Edgar M., Margulies J.Y., et al. Etiology of idiopathic scoliosis: current trends in research // J. Bone Joint Surg. Am. 2000. Vol. 82. P. 1157–1168.

15. Marosy B., Justice C.M., Nzegwu N., et al. Lack association between the aggrecan gene and familial idiopathic scoliosis // Spine. 2006. Vol. 31. P. 1420–1425.

16. Purkiss S.B., Driscoll B., Cole W.G., et al. Idiopathic scoliosis in families of children with congenital scoliosis // Clin. Orthop. Relat. Res. 2002. N 401. P. 27–31.

17. Roberts S., Menage J., Eisenstein S.M. The cartilage end-plate and intervertebral disc in scoliosis: calcification and other sequelae // J. Orthop. Res. 1993. Vol. 11. P. 747–757.

18. Shangguan L., Fan X., Li M. Inheritance involved in the pathogenesis of idiopathic scoliosis // EXCLI J. 2008. Vol. 7. P. 104–114.

19. Thiele H., Sakano M., Kitagawa H., et al. Loss of chondroitin 6-O-sulfotransferase-1 function results in severe human chondrodysplasia with progressive spinal involvement // Proc. Natl. Acad. Sci. USA. 2004. Vol. 101. P. 10155–10160.

20. Willner S., Johnell O. Study of biochemical and hormonal data in idiopathic scoliosis in girls // Arch. Orthop. Trauma Surg. 1981. Vol. 98. P. 251–255.

21. Zaleske D.J., Ehrlich M.G., Hall J.E. Association of glycosaminoglycan depletion and degradative enzyme activity in scoliosis // Clin. Orthop. Relat. Res. 1980. Vol. 148. P. 177–181.


Review

For citations:


Rusova T.V., Shaidurova N.V., Zaidman A.M. POTENTIAL BIOCHEMICAL MARKERSOF IDIOPATHIC SCOLIOSIS PROGRESSION. Russian Journal of Spine Surgery (Khirurgiya Pozvonochnika). 2011;(1):062-067. (In Russ.) https://doi.org/10.14531/ss2011.1.62-67



Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


ISSN 1810-8997 (Print)
ISSN 2313-1497 (Online)