Skip to main content
Article thumbnail
Location of Repository

The role of melatonin in the pathogenesis of adolescent idiopathic scoliosis (AIS)

By M. Girardo, N. Bettini, E. Dema and S. Cervellati

Abstract

The cause of adolescent idiopathic scoliosis (AIS) in humans remains obscure and probably multifactorial. At present, there is no proven method or test available to identify children or adolescent at risk of developing AIS or identify which of the affected individuals are at risk of progression. Reported associations are linked in pathogenesis rather than etiologic factors. Melatonin may play a role in the pathogenesis of scoliosis (neuroendocrine hypothesis), but at present, the data available cannot clearly show the role of melatonin in producing scoliosis in humans. The data regarding human melatonin levels are mixed at best, and the melatonin deficiency as a causative factor in the etiology of scoliosis cannot be supported. It will be an important issue of future research to investigate the role of melatonin in human biology, the clinical efficacy, and safety of melatonin under different pathological situations. Research is needed to better define the role of all factors in AIS development

Topics: Original Article
Publisher: Springer-Verlag
OAI identifier: oai:pubmedcentral.nih.gov:3087042
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles

    Citations

    1. (2003). Allelic variants of human melatonin 1A receptor in patients with familial adolescent idiopathic scoliosis.
    2. (1993). An experimental study in chickens for the pathogenesis of idiopathic scoliosis.
    3. (2008). Association study of tryptophan hydroxylase 1 and arylalkylamine N-acetyltransferase polymorphisms with adolescent idiopathic scoliosis in Han Chinese.
    4. (2007). Asymmetric expression of melatonin receptor mRNA in bilateral paravertebral muscles in adolescent idiopathic scoliosis.
    5. (2006). Bipedal ambulation induces experimental scoliosis in C57BL/6J mice with reduced plasma and pineal melatonin levels.
    6. (1972). Can experimental dorsal rhizotomy produce scoliosis? J Bone Joint Surg [Am]
    7. (1999). Causes of idiopathic scoliosis.
    8. (1998). Cellular mechanisms of melatonin action.
    9. (2002). Cukiert A
    10. (1975). Daily rhythm in human urinary melatonin.
    11. (1999). Differential signaling of human Mel1a and Mel1b melatonin receptors through the cyclic guanosine 30-50-monophosphate pathway.
    12. (1999). Dual signaling of human
    13. (1992). Effect of constant light, pinealectomy and guanosine triphosphate gamma-S on the density of melatonin receptors in the rat suprachiasmatic nucleus: a possible implication on melatonin action.
    14. (2003). Effect of melatonin suppression on scoliosis development in chickens by either constant light or surgical pinealectomy.
    15. (2000). Etiology of idiopathic scoliosis: current trends in research.
    16. (1984). Etiology of idiopathic scoliosis.
    17. (1983). Experimental scoliosis induced by pineal and diencephalic lesions in young chickens: its relation with clinical findings.
    18. (1984). Fall in nocturnal serum melatonin during prepuberty and pubescence.
    19. (1997). Fiber transformation in multifidus muscle of young patients with idiopathic scoliosis.
    20. (1981). Histochemistry and ultrastructure of the paraspinal muscles in idiopathic scoliosis and in control subjects.
    21. (1981). Human chorionic gonadotropin-secreting pineal tumor: relation to pathogenesis and sex limitation of sexual precocity.
    22. (2007). Idiopathic scoliosis and pineal lesions in Australian children.
    23. (1985). Idiopathic scoliosis and the central nervous system: a motor control problem: the Hamngton Lecture,
    24. (2009). Idiopathic-type scoliosis is not exclusive to bipedalism.
    25. (2008). Lack of association between the promoter polymorphism of the MTNR1A gene and adolescent idiopathic scoliosis.
    26. (2002). Mammalian melatonin receptors: molecular biology and signal transduction.
    27. (2004). Melatonin A chronobiotic that only shifts rhythms. In: Pandi-Perumal SR, Cardinali D (eds) Melatonin: biological basis of its function in health and disease.
    28. (2000). Melatonin and adolescent idiopathic scoliosis.
    29. (1998). Melatonin and the pineal gland: influence on mammalian seasonal and circadian physiology. Rev Reprod 3:13–22
    30. (1997). Melatonin in humans.
    31. (1997). Melatonin levels in idiopathic scoliosis.
    32. (1996). Melatonin levels in idiopathic scoliosis. Diurnal and nocturnal serum melatonin levels in girls with adolescent idiopathic scoliosis.
    33. (2007). Melatonin receptor 1B (MTNR1B) gene polymorphism is associated with the occurrence of adolescent idiopathic scoliosis.
    34. (1998). Melatonin receptor genes.
    35. (2003). Melatonin receptors and their regulation: biochemical and structural mechanisms.
    36. (1994). Melatonin receptors: localization, molecular pharmacology and physiological significance.
    37. (2004). Melatonin signaling dysfunction in adolescent idiopathic scoliosis.
    38. (2007). Melatonin the ‘‘light of night’’ in human biology and adolescent idiopathic scoliosis.
    39. (1998). Melatonin the aetiology of idiopathic scoliosis.
    40. (2004). Melatonin, sleep, and circadian rhythms: rationale for development of specific melatonin agonists.
    41. (1996). Melatonin: a possible role in pathogenesis of adolescent idiopathic scoliosis.
    42. (1995). Molecular characterization of a second melatonin receptor expressed in human retina and brain: the Mel 1b melatonin receptor.
    43. (2007). Moreau A
    44. (1988). Muscle spindles in the paraspinal musculature of patients with adolescent idiopathic scoliosis.
    45. (1998). Paraspinal muscle fiber type alterations associated with scoliosis: an old problem revisited with new evidence.
    46. (1984). Paraspinal muscle imbalance in adolescent idiopathic scoliosis.
    47. (1994). Pathogenesis of idiopathic scoliosis: SEPs in chickens with experimentally induced scoliosis and in patients with idiopathic scoliosis.
    48. (1999). Pathogenesis of idiopathic scoliosis.
    49. (2005). Pathological mechanism of idiopathic scoliosis: experimental scoliosis in pinealectomized rats.
    50. (1954). Pineal lesions and precocious puberty: a review.
    51. (2001). Precocious puberty in children with tumours of the suprasellar and pineal areas: organic central precocious puberty.
    52. (2003). Primary thoracolumbar scoliosis in pinealectomized chickens.
    53. (1988). Putative melatonin receptors in human biological clock.
    54. (1995). Role of melatonin deficiency in the development of scoliosis in pinealectomised chickens.
    55. (1984). Scoliosis caused by section of dorsal spinal nerve roots.
    56. (1987). Scoliosis induced by medullary damage: an experimental study in rabbits.
    57. (1982). Tails LF
    58. (1994). The adult human cerebellum is a target of the neuro endocrine system involved in the circadian timing.
    59. (2005). The effect of pinealectomy on scoliosis development in young nonhuman primates.
    60. (1999). The effects of melatonin therapy on the development of scoliosis after pinealectomy in the chicken.
    61. (2003). The effects of pineal gland transplantation on the production of spinal deformity and serum melatonin level following pinealectomy in the chicken.
    62. (1999). The production of scoliosis following pinealectomy in young chickens, rats and hamsters.
    63. (1996). The role of melatonin in the pathogenesis of adolescent idiopathic scoliosis.
    64. (1999). Tight association of the human Mel(1a)-melatonin receptor and G(i): precoupling and constitutive activity.
    65. (1998). Total 24-hour melatonin secretion in adolescent idiopathic scoliosis: a case– control study.
    66. (1998). Twenty four hour rhythm of melatonin in patients with a history of pineal and/or hypothalamo-neurohypophyseal germinoma.

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.