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青少年特发性脊柱侧弯骨免疫微环境的研究进展

李 凯, 温剑 涛*, 黄 晋, 张 辰, 冷 寒, 侯 栋

摘要

脊柱侧弯是指冠状位 X 线片上 Cobb 角> 10°的脊柱畸形。脊柱侧弯类型很多,包括特发性、先天性、神经肌肉型、
综合征型以及其他原因导致的脊柱畸形,其中特发性脊柱侧弯(idiopathic scoliosis,IS)最为常见,尤其是 10 ~ 18 岁的青少年。
青少年特发性脊柱侧凸(Adolescent spinal side,AIS)是IS中常见的脊柱畸形之一,是青春期常见的脊柱畸形。AIS发病机理复杂,
发生发展的分子机制尚未确定,目前对 AIS 的发病机制研究主要包括遗传因素,神经系统异常,骨骼生长异常,激素和代
谢功能障碍,生物力学因素以及环境和生活方式因素等。AIS 患者存在全身性的 BMD 降低,并贯穿于 AIS 发生到进展的全
过程,是一种长期的表现。许多研究也认为 AIS 的低骨量可能是该疾病的原发病因。低骨密度是由于体内破骨细胞(OC)
生成增加,OC 与成骨细胞(OB)维持的“骨稳态”偏移,骨微环境失衡。基于“骨免疫学概念”观点,免疫系统和免疫
因子在骨微环境失衡的发生发展过程中起到了至关重要的作用。本综述将总结 AIS 相关的骨免疫微环境研究进展,探讨其
在疾病发生中的潜在机制及未来研究方向。

关键词

青少年特发性脊柱侧弯;骨免疫;骨细胞;免疫细胞;细胞因子

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参考

[1]Kim J M , Lin C , Stavre Z ,et al.Osteoblast-Osteoclast

Communication and Bone Homeostasis[J].Cells, 2020, 9(9).

DOI:10.3390/cells9092073.

[2]Lin X , Patil S , Gao Y G ,et al.The Bone Extracellular

Matrix in Bone Formation and Regeneration[J].Frontiers in

Pharmacology, 2020, 11.DOI:10.3389/fphar.2020.00757.

[3]Sachini A D , Hyeongseok Y , Sumi K ,et al.Regulation of

Osteoclast Differentiation by Cytokine Networks[J].Immune Netw,

2018, 18(1):e8-.DOI:10.4110/in.2018.18.e8.

[4]Boyce B F , Xing L .Functions of RANKL/RANK/

OPG in bone modeling and remodeling[J].Archives of

Biochemistry & Biophysics, 2008, 473(2):139-146.DOI:10.1016/

j.abb.2008.03.018.

[5]Schaffler M B , Cheung W Y , Majeska R ,et al.Osteocytes:

Master Orchestrators of Bone[J].Calcified Tissue International,

2013, 94(1):5-24.DOI:10.1007/s00223-013-9790-y.

[6]Huang Z , Pei X , Graves D T .The Interrelationship

Between Diabetes, IL-17 and Bone Loss[J].Current Osteoporosis

Reports, 2020, 18(10).DOI:10.1007/s11914-020-00559-6.

[7]Sch?N M P , Luise E .The Interleukin-23/Interleukin-17

Axis Links Adaptive and Innate Immunity in Psoriasis[J].Frontiers

in Immunology, 2018, 9:1323-.DOI:10.3389/fimmu.2018.01323.

[8]Takayanagi H .Osteoimmunology - Bidirectional dialogue

and inevitable union of the fields of bone and immunity.[J].Japan

Academy, 2020(4).DOI:10.2183/PJAB.96.013.

[9] Tang M , Lu L , Yu X .Interleukin-17A Interweaves the

Skeletal and Immune Systems[J].Frontiers in Immunology, 2021,

11:625034.DOI:10.3389/fimmu.2020.625034.

[10]Srivastava R K .Osteoimmunology: The Nexus between

bone and immune system[J].Frontiers in Bioscience, 2018,

23(2):464.DOI:10.2741/4600.

[11]Walsh M C , Choi Y .Biology of the RANKL–RANK–

OPG System in Immunity, Bone, and Beyond[J].Frontiers in

Immunology, 2014, 5.DOI:10.3389/fimmu.2014.00511.

[12]Zhang Z , Yuan W , Deng J ,et al.Granulocyte colony

stimulating factor (G-CSF) regulates neutrophils infiltration and

periodontal tissue destruction in an experimental periodontitis[J].

Molecular immunology, 2020, 117:110-121.DOI:10.1016/

j.molimm.2019.11.003.

[13]Weitzmann M N. The role of inflammatory cytokines,

the RANKL/OPG axis, and the immunoskeletal interface in

physiological bone turnover and osteoporosis[J]. Scientifica, 2013,

2013(1): 125705.

[14]Sun W , Meednu N , Rosenberg A ,et al.B cells inhibit

bone formation in rheumatoid arthritis by suppressing osteoblast

differentiation[J].Nature Communications,2018,9(1).

[15] Zhang Y , B?Se T , Unger R E ,et al.Macrophage type

modulates osteogenic differentiation of adipose tissue MSCs[J].Cell

and Tissue Research,2017,369(7).

[16] Schlundt C , Khassawna T E , Serra A ,et al.Macrophages

in bone fracture healing: Their essential role in endochondral

ossification[J].Bone,2018,106:78-89.

[17] Yuan Y, Chen X, Zhang L, et al. The roles of

exercise in bone remodeling and in prevention and treatment

of osteoporosis[J]. Progress in Biophysics and Molecular

Biology,2016,122(2):122-130.

[ 1 8 ] T u r k N , C u k o v i c - C a v k a S , K o r s i c M , e t

al.Proinflammatory cytokines and receptor activator of nuclear

factor kappaB-ligand/osteoprotegerin associated with bone

deterioration in patients with Crohn’s disease.[J].European

journal of gastroenterology & hepatology,2009,21(2):159-166.

[19] Samelson E J , Broe K E , Serkalem D ,et al.Increased

Plasma Osteoprotegerin Concentrations Are Associated with

Indices of Bone Strength of the Hip[J].Journal of Clinical

Endocrinology & Metabolism(5):1789[2024-08-13].

[20] Gottesman G S , Madson K L , Mcalister W H

,et al.Auricular ossification: A newly recognized feature of

osteoprotegerin‐deficiency juvenile Paget disease[J].American

Journal of Medical Genetics Part A, 2016, 170(4):978-985.

[21] Ruscitti P , Cipriani P , Carubbi F ,et al.the role of il-1

in the bone loss during rheumatic diseases[J]. 2019.

[22] Kim J H , Jin H M , Kim K ,et al.The Mechanism

of Osteoclast Differentiation Induced by IL-1[J].Journal of

Immunology, 2009, 183(3):1862-1870.

[23] Guo C , Yang X G , Wang F ,et al.IL-1α induces

apoptosis and inhibits the osteoblast differentiation of MC3T3-E1

cells through the JNK and p38 MAPK pathways[J].International

Journal of Molecular Medicine, 2016.

[24] Rossi M , Buonuomo P S , Battafarano G ,et al.Dissecting

the mechanisms of bone loss in Gorham-Stout disease[J].Bone,

2019:115068.

[25] Faruqi T , Dhawan N , Bahl J ,et al.Molecular,

Phenotypic Aspects and Therapeutic Horizons of Rare

Genetic Bone Disorders[J].Biomed Research Internation

al,2014,2014:670842-670842.

[26] Ahmetgjekaj, Ilir, et al. “Gorham-Stout disease, a

diagnosis of exclusion.” Radiology Case Reports 17.9 (2022):

3243-3246.

[27] Li Y , Bckesj C M ,Lars-Arne Haldosén,et al.IL-6

receptor expression and IL-6 effects change during osteoblast

differentiation.[J].Cytokine, 2008, 43(2):165-173.

[28] Weitzmann M N , Cenci S , Rifas L ,et al.Interleukin-7

stimulates osteoclast formation by up-regulating the

T-cell production of soluble osteoclastogenic cytokines.[J].

Blood,2000,96(5):1873-1878.

[29] Cong-Xiang,Jian,Quan-Shui,et al.IL-7 suppresses

osteogenic differentiation of periodontal ligament stem cells

through inactivation of mitogen-activated protein kinase

pathway[J].Organogenesis,2016,12(4):183-193.

[30] Erman,Chen,Guanyi,et al.Concentration-dependent,

dual roles of IL-10 in the osteogenesis of human BMSCs via

P38/MAPK and NF-κB signaling pathways.[J].FASEB journal

: official publication of the Federation of American Societies for

Experimental Biology,2018.

[31] Croes M , Ner F C , Neerven D V ,et al.Proinflammatory

T cells and IL-17 stimulate osteoblast differentiation[J].

Elsevier,2016.

[3 2 ] Y u f a W , Ji e u n K , A n d r e a C ,e t a l . A t w o

phase regulation of bone regeneration: IL-17F mediates

osteoblastogenesis via C/EBP-β in vitro[J].Bone,2018,116:47-

57.

[33] Jing-Ru Z , Dan-Dan P , Qiang T ,et al.Different

Modulatory Effects of IL-17, IL-22, and IL-23 on Osteoblast

Differentiation[J].Mediators of Inflammation, 2017, 2017:5950395.

[34]Kitaura Hideki,Kimura Keisuke,Ishida Masahiko,et

al.Immunological Reaction in TNF- α -Mediated Osteoclast

Formation and Bone Resorption In Vitro and In Vivo[J].Clinical &

Developmental Immunology,2013,2013:1-8.

[35]Constanze B, Popper B, Aggarwal B B, et al. Evidence

that TNF-β suppresses osteoblast differentiation of mesenchymal

stem cells and resveratrol reverses it through modulation of NF-

κB, Sirt1 and Runx2[J]. Cell and tissue research, 2020, 381: 83-

98.

[36] 郑丹枫 , 李君禹 , 李佳曦 ,et al. 青少年特发性脊柱

侧凸椎旁肌的病理特征 [J]. 北京大学学报 : 医学版 , 2023,

55(2):283-291.

[37]Pearson M J , Philp A M , Haq H ,et al.Evidence of

Intrinsic Impairment of Osteoblast Phenotype at the Curve Apex in

Girls With Adolescent Idiopathic Scoliosis.[J].Elsevier, 2019(4).

[38]Aulisa A G , Pola E , Papaleo P ,et al.The association

between IL-6 and MMP-3 gene polymorphisms and adolescent

idiopathic scoliosis: a case-control study[J].Scoliosis, 2009,

4(Suppl 1).

[39]Xiao, LigeZhang, HongqiWang, YunjiaLi, JiongYang,

GuantengWang, LongjieLiang, Zhuotao.Dysregulation of the

ghrelin/RANKL/OPG pathway in bone mass is related to AIS

osteopenia[J].Bone,2020,134(1).

[40]Zhang H Q , Wang L J , Liu S H ,et al.Adiponectin

regulates bone mass in AIS osteopenia via RANKL/OPG and IL6

pathway[J].Journal of Translational Medicine,2019,17(1).

[41]Zhao X , Liu J , Zhang L ,et al.Gut microbiota,

inflammatory factors, and scoliosis: A Mendelian randomization

study[J].Medicine,2024,103(24):38561-26.

[42]Chiru M .Adolescent idiopathic scoliosis and osteopenia).

[J].Mdica,2011,6(1).

[43]Ko D S , Kim Y H , Goh T S ,et al.Altered

physiology of mesenchymal stem cells in the pathogenesis of

adolescent idiopathic scoliosis[J].World Journal of Clinical

Cases,2020,8(11):9.

[44] Wang Y , Zhang H , Yang G ,et al.Dysregulated Bone

Metabolism Is Related to High Expression of miR-151a-3p

in Severe Adolescent Idiopathic Scoliosis[J].BioMed Research

International, 2020,2020:1-12.


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