Melatonin and adolescent idiopathic scoliosis: The present evidence

被引：17
作者：
Gargano, Giuseppe [1 ,2 ]
Oliva, Francesco [1 ,2 ]
Migliorini, Filippo [3 ]
Maffulli, Nicola [1 ,2 ,4 ,5 ]
机构：
[1] AOU San Giovanni Dio & Ruggi Aragona, Dept Trauma & Orthopaed Surg, Via San Leonardo 1, I-84131 Salerno, Italy
[2] Univ Salerno, Dept Med Surg & Dent, Via S Allende, I-84081 Baronissi 7, SA, Italy
[3] RWTH Univ Hosp, Dept Orthopaed Trauma Reconstruct Surg, D-52074 Aachen, Germany
[4] Queen Mary Univ London, Mile End Hosp, Ctr Sports & Exercise Med, Barts & London Sch Med & Dent, 275 Bancroft Rd, London 10, England
[5] Keele Univ, Sch Pharm & Bioengn, Sch Med, Thornburrow Dr, Stoke On Trent, England
来源：
SURGEON-JOURNAL OF THE ROYAL COLLEGES OF SURGEONS OF EDINBURGH AND IRELAND | 2022年 / 20卷 / 06期
关键词：
Adolescent idiopathic scoliosis; Spine deformity; Hormonal imbalance; Melatonin; BONE-MARROW; RECEPTOR; DIFFERENTIATION; PATHOGENESIS; EXPRESSION; GROWTH; RHYTHM;
D O I：
10.1016/j.surge.2021.07.008
中图分类号：
R61 [外科手术学];
学科分类号：
摘要：
Introduction: Adolescent idiopathic scoliosis (AIS) is a multifactorial condition with genetic predisposing factors, and several causes have been put forward for its aetiopathogenesis, including possible hormonal dysfunction. Melatonin seems to play significant role in AIS.Methods: A systematic search in different database, to July 2021, was performed to define the role of melatonin in the pathophysiology of adolescent idiopathic scoliosis. Eight suitable studies were identified. Results: The concentration and rhythm of melatonin secretion can play an important role by influencing the pathogenesis of adolescent idiopathic scoliosis.Conclusions: Although there are many alterations of melatonin in subjects with adolescent idiopathic scoliosis, the many variables present do not allow to establish a direct cause-effect relationship.Level of evidence: Level IV.(c) 2021 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码：E315 / E321
页数：7
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