内分泌激素在青少年特发性脊柱侧弯中的应用进展

王成龙; 武书丽

doi:10.16835/j.cnki.1000-9817.2023.08.035

内分泌激素在青少年特发性脊柱侧弯中的应用进展

doi: 10.16835/j.cnki.1000-9817.2023.08.035

王成龙^{1, 2},
武书丽^2, ,

1.
内蒙古医科大学研究生院，呼和浩特 010059
2.
内蒙古自治区人民医院儿科

基金项目:

2022年度自治区卫生健康科技计划项目 202201046

详细信息

作者简介:
王成龙(1998-)，男，内蒙古人，在读硕士，主要研究方向为儿童保健

通讯作者:
武书丽，E-mail：2389570362@qq.com

利益冲突声明 所有作者声明无利益冲突。
中图分类号: Q57 R726.8 R682.3
计量
- 文章访问数: 245
- HTML全文浏览量: 166
- PDF下载量: 38
- 被引次数: 0
出版历程
- 收稿日期: 2022-12-25
- 修回日期: 2023-03-07
- 网络出版日期: 2023-08-26
- 刊出日期: 2023-08-25

Application progress of endocrine hormones in adolescent idiopathic scoliosis

WANG Chenglong^{1, 2},
WU Shuli^{2
, ,}

1.
Graduate School, Inner Mongolia Medical University, Hohhot(010059), China

摘要

摘要: 青少年特发性脊柱侧弯(adolescent idiopathic scoliosis, AIS)是最常见的脊柱畸形，近几年发病率明显上升，已成为威胁青少年健康的重要公共卫生问题。青春期是人类生长发育加速的重要时期，该时期的内分泌激素会发生明显变化，研究显示褪黑素、雌激素、维生素D以及瘦素等与脊柱侧弯的产生和发展有密切关联。研究通过探讨内分泌激素在AIS发病机制中的作用，为AIS的防治提供参考。
- 内分泌激素 /
- 脊柱侧凸 /
- 青少年 /
- 维生素D
Abstract: Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity. With increasing incidence in recent years, it has become an important public health problem threatening the health of adolescents. Adolescence is an important period for accelerated human growth and development, and endocrine hormones will change significantly during this period. Studies have shown that melatonin, estrogen, vitamin D and leptin are closely related to the production and development of scoliosis. Exploring the role of endocrine hormones in the pathogenesis of AIS can provide a reference for the prevention and treatment of AIS.
- Endocrine hormone /
- Scoliosis /
- Adolescent /
- Vitamin D
注释:

1) 利益冲突声明 所有作者声明无利益冲突。

HTML全文

参考文献(74)

[1]	徐帅, 苏永佳, 王振波, 等. 中国大陆中小学生脊柱侧凸的患病特点: 关于72项研究的Meta分析[J]. 中国脊柱脊髓杂志, 2021, 31(10): 901-910. doi: 10.3969/j.issn.1004-406X.2021.10.05 XU S, SU Y J, WANG Z B, et al. Chinese mainland characteristics of scoliosis in primary and middle school students: Meta-analysis of 72 studies[J]. Chin J Spinal Cord, 2021, 31(10): 901-910. (in Chinese) doi: 10.3969/j.issn.1004-406X.2021.10.05
[2]	NORMAND E, FRANCO A, ALOS N, et al. Circulatory adipokines and incretins in adolescent idiopathic scoliosis: a pilot study[J]. Children (Basel), 2022, 9(11): 1619.
[3]	GARGANO G, OLIVA F, MIGLIORINI F, et al. Melatonin and adolescent idiopathic scoliosis: the present evidence[J]. Surgeon, 2022, 20(6): e315-e321. doi: 10.1016/j.surge.2021.07.008
[4]	MAN G C, WANG W W, YIM A P, et al. A review of pinealectomy-induced melatonin-deficient animal models for the study of etiopathogenesis of adolescent idiopathic scoliosis[J]. Int J Mol Sci, 2014, 15(9): 16484-16499. doi: 10.3390/ijms150916484
[5]	LATALSKI M, DANIELEWICZ-BROMBEREK A, FATYGA M, et al. Current insights into the aetiology of adolescent idiopathic scoliosis[J]. Arch Orthop Trauma Surg, 2017, 137(10): 1327-1333. doi: 10.1007/s00402-017-2756-1
[6]	LIANG Z T, GUO C F, LI J, et al. The role of endocrine hormones in the pathogenesis of adolescent idiopathic scoliosis[J]. Faseb J, 2021, 35(9): e21839. doi: 10.1096/fj.202100759R
[7]	CHU W C, LAM W M, NG B K, et al. Relative shortening and functional tethering of spinal cord in adolescent scoliosis-result of asynchronous neuro-osseous growth, summary of an electronic focus group debate of the IBSE[J]. Scoliosis, 2008, 3: 8. doi: 10.1186/1748-7161-3-8
[8]	TRESGUERRES I F, TAMIMI F, EIMAR H, et al. Melatonin dietary supplement as an anti-aging therapy for age-related bone loss[J]. Rejuven Res, 2014, 17(4): 341-346. doi: 10.1089/rej.2013.1542
[9]	WANG W W, MAN G C, WONG J H, et al. Abnormal response of the proliferation and differentiation of growth plate chondrocytes to melatonin in adolescent idiopathic scoliosis[J]. Int J Mol Sci, 2014, 15(9): 17100-17114. doi: 10.3390/ijms150917100
[10]	AZEDDINE B, LETELLIER K, WANG DA S, et al. Molecular determinants of melatonin signaling dysfunction in adolescent idiopathic scoliosis[J]. Clin Orthop Relat Res, 2007, 462: 45-52. doi: 10.1097/BLO.0b013e31811f39fa
[11]	LIU H, LIU Z, MAN C W, et al. The effect of exogenous melatonin on reducing scoliotic curvature and improving bone quality in melatonin-deficient C57BL/6J mice[J]. Sci Rep, 2019, 9(1): 6202. doi: 10.1038/s41598-019-42467-5
[12]	AKOUME M Y, ELBAKRY M, VEILLETTE M, et al. A differential hypofunctionality of Gαi proteins occurs in adolescent idiopathic scoliosis and correlates with the risk of disease progression[J]. Sci Rep, 2019, 9(1): 10074. doi: 10.1038/s41598-019-46325-2
[13]	GAO W, LIN M, LIANG A, et al. Melatonin enhances chondrogenic differentiation of human mesenchymal stem cells[J]. J Pineal Res, 2014, 56(1): 62-70. doi: 10.1111/jpi.12098
[14]	CHEN C, XU C, ZHOU T, et al. Abnormal osteogenic and chondrogenic differentiation of human mesenchymal stem cells from patients with adolescent idiopathic scoliosis in response to melatonin[J]. Mol Med Rep, 2016, 14(2): 1201-1209. doi: 10.3892/mmr.2016.5384
[15]	PARK W W, SUH K T, KIM J I, et al. Decreased osteogenic differentiation of mesenchymal stem cells and reduced bone mineral density in patients with adolescent idiopathic scoliosis[J]. Eur Spine J, 2009, 18(12): 1920-1926. doi: 10.1007/s00586-009-1129-z
[16]	ZHUANG Q, LI J, WU Z, et al. Differential proteome analysis of bone marrow mesenchymal stem cells from adolescent idiopathic scoliosis patients[J]. PLoS One, 2011, 6(4): e18834. doi: 10.1371/journal.pone.0018834
[17]	ZHUANG Q, MAO W, XU P, et al. Identification of differential genes expression profiles and pathways of bone marrow mesenchymal stem cells of adolescent idiopathic scoliosis patients by microarray and integrated gene network analysis[J]. Spine, 2016, 41(10): 840-855. doi: 10.1097/BRS.0000000000001394
[18]	MAN G C, WANG W W, YEUNG B H, et al. Abnormal proliferation and differentiation of osteoblasts from girls with adolescent idiopathic scoliosis to melatonin[J]. J Pineal Res, 2010, 49(1): 69-77.
[19]	LI J, LI N, CHEN Y, et al. SPRY4 is responsible for pathogenesis of adolescent idiopathic scoliosis by contributing to osteogenic differentiation and melatonin response of bone marrow-derived mesenchymal stem cells[J]. Cell Death Dis, 2019, 10(11): 805. doi: 10.1038/s41419-019-1949-7
[20]	YIM A P, YEUNG H Y, SUN G, et al. Abnormal skeletal growth in adolescent idiopathic scoliosis is associated with abnormal quantitative expression of melatonin receptor, MT2[J]. Int J Mol Sci, 2013, 14(3): 6345-6358. doi: 10.3390/ijms14036345
[21]	MAN G C, WONG J H, WANG W W, et al. Abnormal melatonin receptor 1B expression in osteoblasts from girls with adolescent idiopathic scoliosis[J]. J Pineal Res, 2011, 50(4): 395-402. doi: 10.1111/j.1600-079X.2011.00857.x
[22]	QIU Y, WU L, WANG B, et al. Asymmetric expression of melatonin receptor mRNA in bilateral paravertebral muscles in adolescent idiopathic scoliosis[J]. Spine, 2007, 32(6): 667-672. doi: 10.1097/01.brs.0000257536.34431.96
[23]	QIU X S, TANG N L, YEUNG H Y, et al. Melatonin receptor 1B(MTNR1B) gene polymorphism is associated with the occurrence of adolescent idiopathic scoliosis[J]. Spine, 2007, 32(16): 1748-1753. doi: 10.1097/BRS.0b013e3180b9f0ff
[24]	YANG M, WEI X, YANG W, et al. The polymorphisms of melatonin receptor 1B gene(MTNR1B)(rs4753426 and rs10830963) and susceptibility to adolescent idiopathic scoliosis: a Meta-analysis[J]. J Orthop Sci, 2015, 20(4): 593-600. doi: 10.1007/s00776-015-0725-5
[25]	LETELLIER K, AZEDDINE B, PARENT S, et al. Estrogen cross-talk with the melatonin signaling pathway in human osteoblasts derived from adolescent idiopathic scoliosis patients[J]. J Pineal Res, 2008, 45(4): 383-393. doi: 10.1111/j.1600-079X.2008.00603.x
[26]	QIU S, TAO Z B, TAO L, et al. Melatonin induces mitochondrial apoptosis in osteoblasts by regulating the STIM1/cytosolic calcium elevation/ERK pathway[J]. Life Sci, 2020, 248: 117455. doi: 10.1016/j.lfs.2020.117455
[27]	SÁNCHEZ-BARCELÓ E J, MEDIAVILLA M D, TAN D X, et al. Scientific basis for the potential use of melatonin in bone diseases: osteoporosis and adolescent idiopathic scoliosis[J]. J Osteoporos, 2010, 2010: 830231.
[28]	HERDEA A, DRAGOMIRESCU M C, ULICI A, et al. Controlling the progression of curvature in children and adolescent idiopathic scoliosis following the administration of melatonin, calcium, and vitamin D[J]. Children, 2022, 9(5): 758. doi: 10.3390/children9050758
[29]	WEINSTEIN S L, DOLAN L A, CHENG J C, et al. Adolescent idiopathic scoliosis[J]. Lancet, 2008, 371(9623): 1527-1537. doi: 10.1016/S0140-6736(08)60658-3
[30]	ZENG K, ZHANG H Q, CHEN Y, et al. Estradiol via estrogen receptor beta inhibits chondrogenesis of mouse vertebral growth plate in vitro[J]. Childs Nerv Syst, 2016, 32(3): 461-465. doi: 10.1007/s00381-015-2973-2
[31]	LEBOEUF D, LETELLIER K, ALOS N, et al. Do estrogens impact adolescent idiopathic scoliosis?[J]. Trends Endocrinol Metab, 2009, 20(4): 147-152. doi: 10.1016/j.tem.2008.12.004
[32]	KRUM S A. Direct transcriptional targets of sex steroid hormones in bone[J]. J Cell Biochem, 2011, 112(2): 401-408. doi: 10.1002/jcb.22970
[33]	KULIS A, GOZDZIALSKA A, DRąG J, et al. Participation of sex hormones in multifactorial pathogenesis of adolescent idiopathic scoliosis[J]. Int Orthop, 2015, 9(6): 1227-1236.
[34]	WARREN M P, BROOKS-GUNN J, HAMILTON L H, et al. Scoliosis and fractures in young ballet dancers, relation to delayed menarche and secondary amenorrhea[J]. N Engl J Med, 1986, 314(21): 1348-1353. doi: 10.1056/NEJM198605223142104
[35]	LETELLIER K, AZEDDINE B, PARENT S, et al. Estrogen cross-talk with the melatonin signaling pathway in human osteoblasts derived from adolescent idiopathic scoliosis patients[J]. J Pineal Res, 2008, 45(4): 383-393. doi: 10.1111/j.1600-079X.2008.00603.x
[36]	CHEN S, ZHAO L, ROFFEY D M, et al. Association between the ESR1-351A>G single nucleotide polymorphism (rs9340799) and adolescent idiopathic scoliosis: a systematic review and Meta-analysis[J]. Eur Spine J, 2014, 23(12): 2586-2593. doi: 10.1007/s00586-014-3481-x
[37]	PENG Y, LIANG G, PEI Y, et al. Genomic polymorphisms of G-protein estrogen receptor 1 are associated with severity of adolescent idiopathic scoliosis[J]. Int Orthop, 2012, 36(3): 671-677. doi: 10.1007/s00264-011-1374-8
[38]	ZHAO D, QIU G X, WANG Y P, et al. Association between adolescent idiopathic scoliosis with double curve and polymorphisms of calmodulin1 gene/estrogen receptor-α gene[J]. Orthop Surg, 2009, 1(3): 222-230. doi: 10.1111/j.1757-7861.2009.00038.x
[39]	HASSAN A, BAGU E T, LEVESQUE M, et al. The 17β-estradiol induced upregulation of the adhesion G-protein coupled receptor (ADGRG7) is modulated by ESRα and SP1 complex[J]. Biol Open, 2019, 8(1): bio037390.
[40]	ZHAO L, ROFFEY D M, CHEN S. Association between the estrogen receptor beta (esr2) rs1256120 single nucleotide polymorphism and adolescent idiopathic scoliosis: a systematic review and Meta-analysis[J]. Spine, 2017, 42(11): 871-878. doi: 10.1097/BRS.0000000000001932
[41]	JANUSZ P, KOTWICKI T, ANDRUSIEWICZ M, et al. XbaI and PvuII polymorphisms of estrogen receptor 1 gene in females with idiopathic scoliosis: no association with occurrence or clinical form[J]. PLoS One, 2013, 8(10): e76806. doi: 10.1371/journal.pone.0076806
[42]	TANG N L, YEUNG H Y, LEE K M, et al. A relook into the association of the estrogen receptor [alpha] gene (PvuII, XbaI) and adolescent idiopathic scoliosis: a study of 540 Chinese cases[J]. Spine, 2006, 31(21): 2463-2468. doi: 10.1097/01.brs.0000239179.81596.2b
[43]	CHIRU M. Adolescent idiopathic scoliosis and osteopenia[J]. Maedica, 2011, 6(1): 17-22.
[44]	SUH K T, EUN I S, LEE J S. Polymorphism in vitamin D receptor is associated with bone mineral density in patients with adolescent idiopathic scoliosis[J]. Eur Spine J, 2010, 19(9): 1545-1550. doi: 10.1007/s00586-010-1385-y
[45]	KOTWICKI T, TOMASZEWSKI M, ANDRUSIEWICZ M, et al. Estrogen receptor type 1 and type 2 presence in paravertebral skeletal muscles: expression level and relation to phenotype in children with idiopathic scoliosis[J]. Genes, 2022, 13(5): 739. doi: 10.3390/genes13050739
[46]	SKIBINSKA I, TOMASZEWSKI M, ANDRUSIEWICZ M, et al. Expression of estrogen receptor coactivator proline-glutamic acid-and leucine-rich protein 1 within paraspinal muscles in adolescents with idiopathic scoliosis[J]. PLoS One, 2016, 11(4): e0152286. doi: 10.1371/journal.pone.0152286
[47]	HOLICK M F. Vitamin D: a millenium perspective[J]. J Cell Biochem, 2003, 88(2): 296-307. doi: 10.1002/jcb.10338
[48]	PATTON C M, POWELL A P, PATEL A A. Vitamin D in orthopaedics[J]. J Am Acad Orthop Surg, 2012, 20(3): 123-129. doi: 10.5435/JAAOS-20-03-123
[49]	PELLICANE A J, WYSOCKI N M, MALLINSON T R, et al. Prevalence of 25-hydroxy vitamin D deficiency in the acute inpatient rehabilitation population and its effect on function[J]. Arch Phys Med Rehabil, 2011, 92(5): 705-711. doi: 10.1016/j.apmr.2010.12.028
[50]	BALIOGLU M B, AYDIN C, KARGIN D, et al. Vitamin-D measurement in patients with adolescent idiopathic scoliosis[J]. J Pediatr Orthop B, 2017, 26(1): 48-52. doi: 10.1097/BPB.0000000000000320
[51]	HERDEA A, CHARKAOUI A, ULICI A. Prevalence of 25-OH-Vitamin D and calcium deficiency in adolescent idiopathic scoliosis[J]. J Med Life, 2020, 13(2): 260-264. doi: 10.25122/jml-2020-0101
[52]	KINUTA K, TANAKA H, MORIWAKE T, et al. Vitamin D is an important factor in estrogen biosynthesis of both female and male gonads[J]. Endocrinology, 2000, 141(4): 1317-1324. doi: 10.1210/endo.141.4.7403
[53]	GOZDZIALSKA A, JASKIEWICZ J, KNAPIK-CZAJKA M, et al. Association of calcium and phosphate balance, vitamin D, PTH, and calcitonin in patients with adolescent idiopathic scoliosis[J]. Spine, 2016, 41(8): 693-697. doi: 10.1097/BRS.0000000000001286
[54]	SILVA R T E, FERNANDES R J R, ONO A H A, et al. Role of different hormones in the pathogenesis and severity of adolescent idiopathic scoliosis[J]. Acta Ortop Bras, 2017, 25(1): 15-17. doi: 10.1590/1413-785220172501168600
[55]	KIM J H, CHOI J H. Pathophysiology and clinical characteristics of hypothalamic obesity in children and adolescents[J]. Ann Pediatr Endocrinol Metab, 2013, 18(4): 161-167. doi: 10.6065/apem.2013.18.4.161
[56]	NG S Y, BETTANY-SALTIKOV J, CHEUNG I Y K, et al. The role of Vitamin D in the pathogenesis of adolescent idiopathic scoliosis[J]. Asian Spine J, 2018, 12(6): 1127-1145. doi: 10.31616/asj.2018.12.6.1127
[57]	BEAULIEU M, TOULOTTE C, GATTO L, et al. Postural imbalance in non-treated adolescent idiopathic scoliosis at different periods of progression[J]. Eur Spine J, 2009, 18(1): 38-44. doi: 10.1007/s00586-008-0831-6
[58]	HAUMONT T, GAUCHARD G C, LASCOMBES P, et al. Postural instability in early-stage idiopathic scoliosis in adolescent girls[J]. Spine, 2011, 36(13): E847-E854. doi: 10.1097/BRS.0b013e3181ff5837
[59]	CUI X, GOOCH H, PETTY A, et al. Vitamin D and the brain: genomic and non-genomic actions[J]. Mol Cell Endocrinol, 2017, 453: 131-143. doi: 10.1016/j.mce.2017.05.035
[60]	BALDOCK P A, THOMAS G P, HODGE J M, et al. Vitamin D action and regulation of bone remodeling: suppression of osteoclastogenesis by the mature osteoblast[J]. J Bone Miner Res, 2006, 21(10): 1618-1626. doi: 10.1359/jbmr.060714
[61]	DAI J, LYU Z T, HUANG J M, et al. Association between polymorphisms in vitamin D receptor gene and adolescent idiopathic scoliosis: a Meta-analysis[J]. Eur Spine J, 2018, 27(9): 2175-2183. doi: 10.1007/s00586-018-5614-0
[62]	YIN X, WANG H, GUO J, et al. Association of vitamin D receptor BsmI rs1544410 and ApaI rs7975232 polymorphisms with susceptibility to adolescent idiopathic scoliosis: a systematic review and Meta-analysis[J]. Medicine, 2018, 97(2): e9627. doi: 10.1097/MD.0000000000009627
[63]	QIU Y, SUN X, QIU X, et al. Decreased circulating leptin level and its association with body and bone mass in girls with adolescent idiopathic scoliosis[J]. Spine, 2007, 32(24): 2703-2710. doi: 10.1097/BRS.0b013e31815a59e5
[64]	STEPPAN C M, CRAWFORD D T, CHIDSEY-FRINK K L, et al. Leptin is a potent stimulator of bone growth in ob/ob mice[J]. Regul Pept, 2000, 92(1-3): 73-78. doi: 10.1016/S0167-0115(00)00152-X
[65]	GORDELADZE J O, DREVON C A, SYVERSEN U, et al. Leptin stimulates human osteoblastic cell proliferation, de novo collagen synthesis, and mineralization: impact on differentiation markers, apoptosis, and osteoclastic signaling[J]. J Cell Biochem, 2002, 85(4): 825-836. doi: 10.1002/jcb.10156
[66]	MAOR G, ROCHWERGER M, SEGEV Y, et al. Leptin acts as a growth factor on the chondrocytes of skeletal growth centers[J]. J Bone Miner Res, 2002, 17(6): 1034-1043. doi: 10.1359/jbmr.2002.17.6.1034
[67]	TURNER R T, KALRA S P, WONG C P, et al. Peripheral leptin regulates bone formation[J]. J Bone Miner Res, 2013, 28(1): 22-34. doi: 10.1002/jbmr.1734
[68]	GONG Y, SLEE R B, FUKAI N, et al. LDL receptor-related protein 5(LRP5) affects bone accrual and eye development[J]. Cell, 2001, 107(4): 513-523. doi: 10.1016/S0092-8674(01)00571-2
[69]	REID I R, BALDOCK P A, CORNISH J. Effects of leptin on the skeleton[J]. Endocrinol Rev, 2018, 39(6): 938-959. doi: 10.1210/er.2017-00226
[70]	MAN G C, TAM E M, WONG Y S, et al. Abnormal osteoblastic response to leptin in patients with adolescent idiopathic scoliosis[J]. Sci Rep, 2019, 9(1): 17128. doi: 10.1038/s41598-019-53757-3
[71]	TAM E M S, LIU Z, LAM T P, et al. Lower muscle mass and body fat in adolescent idiopathic scoliosis are associated with abnormal leptin bioavailability[J]. Spine, 2016, 41(11): 940-946. doi: 10.1097/BRS.0000000000001376
[72]	LIU Z, WANG F, XU L L, et al. Polymorphism of rs2767485 in leptin receptor gene is associated with the occurrence of adolescent idiopathic scoliosis[J]. Spine, 2015, 40(20): 1593-1598. doi: 10.1097/BRS.0000000000001095
[73]	ZOABLI G, MATHIEU P A, AUBIN C E. Back muscles biometry in adolescent idiopathic scoliosis[J]. Spine J, 2007, 7(3): 338-344. doi: 10.1016/j.spinee.2006.04.001
[74]	SÁINZ N, RODRÍGUEZ A, CATALÁN V, et al. Leptin administration favors muscle mass accretion by decreasing FoxO3a and increasing PGC-1alpha in ob/ob mice[J]. PLoS One, 2009, 4(9): e6808. doi: 10.1371/journal.pone.0006808