中国组织工程研究 ›› 2023, Vol. 27 ›› Issue (34): 5561-5569.doi: 10.12307/2023.717
• 生物材料综述 biomaterial review • 上一篇 下一篇
顾赢楚1,顾 叶1,吴泽睿1,方 涛1,王秋霏1,陈兵乾1,彭育沁1,耿德春2,徐耀增2
收稿日期:
2022-10-12
接受日期:
2022-11-25
出版日期:
2023-12-08
发布日期:
2023-04-23
通讯作者:
顾叶,博士,副主任医师,苏州大学附属常熟医院常熟市第一人民医院骨科,江苏省常熟市 215500
作者简介:
顾赢楚,男,硕士,医师,主要从事关节外科的基础与临床研究。
基金资助:
Gu Yingchu1, Gu Ye1, Wu Zerui1, Fang Tao1, Wang Qiufei1, Chen Bingqian1, Peng Yuqin1, Geng Dechun2, Xu Yaozeng2
Received:
2022-10-12
Accepted:
2022-11-25
Online:
2023-12-08
Published:
2023-04-23
Contact:
Gu Ye, MD, Associate chief physician, Department of Orthopedics, Changshu First People’s Hospital, Affiliated Changshu Hospital of Soochow University, Changshu 215500, Jiangsu Province, China
About author:
Gu Yingchu, Master, Physician, Department of Orthopedics, Changshu First People’s Hospital, Affiliated Changshu Hospital of Soochow University, Changshu 215500, Jiangsu Province, China
Supported by:
摘要:
文题释义:
假体周围骨溶解:人工关节置换后由于假体与骨组织之间的微动以及假体各部件之间的长期磨损会产生的磨损颗粒,磨损颗粒会诱导并趋化炎症因子、破坏成骨-破骨平衡,导致假体周围的骨质溶解,假体因此发生松动,最终造成人工关节置换的失败或其使用寿命减短。结果与结论:①在假体周围骨溶解中,磨损颗粒诱导的成骨细胞自噬能力的改变对于疾病的发展及转归有着关键性的作用。②多种信号通路共同介导成骨细胞自噬的过程,其中关键通路包括AMPK/ULK1/mTOR、核转录因子κB及Pink1/Parkin等,AMPK,mTOR及ULK1三者能够相互调节,共同维持自噬水平的稳定,核转录因子κB通路与自噬之间存在复杂的串扰,PINK1及Parkin在受损线粒体膜表面聚积,诱导线粒体自噬。③多条信号通路之间存在串扰,相互影响下构成了复杂的自噬网络,且在不同细胞中,相同自噬通路的激活可能会带来截然不同的影响。④磨损颗粒诱导的适度的自噬会减少成骨细胞的凋亡,同时增强其分化及矿化能力,改善假体周围骨溶解的预后;反之,自噬激活的不足或过度都会对成骨细胞带来损害,推动骨溶解的进展;因此,通过药物或者基因靶向调控磨损颗粒诱导的成骨细胞自噬水平可能是假体周围骨溶解治疗的方向之一。
https://orcid.org/0000-0002-6267-1614 (顾赢楚);https://orcid.org/0000-0003-0652-2996 (顾叶)
中国组织工程研究杂志出版内容重点:生物材料;骨生物材料;口腔生物材料;纳米材料;缓释材料;材料相容性;组织工程
中图分类号:
顾赢楚, 顾 叶, 吴泽睿, 方 涛, 王秋霏, 陈兵乾, 彭育沁, 耿德春, 徐耀增. 假体周围骨溶解中成骨细胞自噬的信号通路[J]. 中国组织工程研究, 2023, 27(34): 5561-5569.
Gu Yingchu, Gu Ye, Wu Zerui, Fang Tao, Wang Qiufei, Chen Bingqian, Peng Yuqin, Geng Dechun, Xu Yaozeng. Signaling pathway of osteoblast autophagy in periprosthetic osteolysis[J]. Chinese Journal of Tissue Engineering Research, 2023, 27(34): 5561-5569.
[1] TALMO CT, ROBBINS CE, BONO JV. Total joint replacement in the elderly patient. Clin Geriatr Med. 2010;26(3):517-529. [2] SLOAN M, PREMKUMAR A, SHETH NP. Projected volume of primary total joint arthroplasty in the U.S., 2014 to 2030. J Bone Joint Surg Am. 2018;100(17):1455-1460. [3] TALMO CT, AGHAZADEH M, BONO JV. Perioperative complications following total joint replacement. Clin Geriatr Med. 2012;28(3):471-487. [4] PURDUE PE, KOULOUVARIS P, POTTER HG, et al. The cellular and molecular biology of periprosthetic osteolysis. Clin Orthop Relat Res. 2007;454:251-261. [5] BLOM AW, HUNT LP, MATHARU GS, et al. The effect of surgical approach in total knee replacement on outcomes. An analysis of 875, 166 elective operations from the National Joint Registry for England, Wales, Northern Ireland and the Isle of Man. Knee. 2021;31:144-157. [6] OLLIVERE B, WIMHURST JA, CLARK IM, et al. Current concepts in osteolysis. J Bone Joint Surg Br. 2012;94(1):10-15. [7] NOORDIN S, MASRI B. Periprosthetic osteolysis: genetics, mechanisms and potential therapeutic interventions. Can J Surg. 2012;55(6):408-417. [8] KIM JM, LIN C, STAVRE Z, et al. Osteoblast-osteoclast communication and bone homeostasis. Cells. 2020;9(9):2073. [9] VERMES C, GLANT TT, HALLAB NJ, et al. The potential role of the osteoblast in the development of periprosthetic osteolysis: review of in vitro osteoblast responses to wear debris, corrosion products, and cytokines and growth factors. J Arthroplasty. 2001;16(8 Suppl 1):95-100. [10] O’NEILL SC, QUEALLY JM, DEVITT BM, et al. The role of osteoblasts in peri-prosthetic osteolysis. Bone Joint J. 2013;95-B(8):1022-1026. [11] DIKIC I, ELAZAR Z. Mechanism and medical implications of mammalian autophagy. Nat Rev Mol Cell Biol. 2018;19(6):349-364. [12] KIM KH, LEE MS. Autophagy--a key player in cellular and body metabolism. Nat Rev Endocrinol. 2014;10(6):322-337. [13] MAIURI MC, ZALCKVAR E, KIMCHI A, et al. Self-eating and self-killing: crosstalk between autophagy and apoptosis. Nat Rev Mol Cell Biol. 2007; 8(9):741-752. [14] MIZUSHIMA N, LEVINE B, CUERVO AM, et al. Autophagy fights disease through cellular self-digestion. Nature. 2008;451(7182):1069-1075. [15] DI GIACOMO V, CATALDI A, SANCILIO S. Biological factors, metals, and biomaterials regulating osteogenesis through autophagy. Int J Mol Sci. 2020; 21(8):2789. [16] MA B, GUAN G, LV Q, et al. Curcumin ameliorates palmitic acid-induced saos-2 cell apoptosis via inhibiting oxidative stress and autophagy. Evid Based Complement Alternat Med. 2021;2021:5563660. [17] 蔡燕,施勤,赵环,等.聚甲基丙烯酸甲酯颗粒诱导骨溶解实验研究[J].重庆医学,2013,42(34):4160-4161,4165. [18] WANG Z, LIU N, LIU K, et al. Autophagy mediated CoCrMo particle-induced peri-implant osteolysis by promoting osteoblast apoptosis. Autophagy. 2015;11(12):2358-2369. [19] LIU N, MENG J, WANG Z, et al. Autophagy mediated TiAl₆V₄ particle-induced peri-implant osteolysis by promoting expression of TNF-α. Biochem Biophys Res Commun. 2016;473(1):133-139. [20] WANG Z, DENG Z, GAN J, et al. TiAl6V4 particles promote osteoclast formation via autophagy-mediated downregulation of interferon-beta in osteocytes. Acta Biomater. 2017;48:489-498. [21] YAN JQ, ZHANG Y, LIU FS, et al. TCP wear particles causes injury of periprosthetic osteocytes in the mouse calvaria. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2018;34(1):83-87. [22] LI D, WANG C, LI Z, et al. Nano-sized AlO particle-induced autophagy reduces osteolysis in aseptic loosening of total hip arthroplasty by negative feedback regulation of RANKL expression in fibroblasts. Cell Death Dis. 2018;9(8):840. [23] 陈洋,宁乐,杜嘉莉,等.c-Jun氨基末端激酶介导的细胞凋亡和自噬参与调控磷酸三钙磨损颗粒诱导的小鼠颅骨假体周围骨细胞死亡[J].解剖学报,2018,49(5):605-610. [24] 林琨,陈佳濠,方泽浩,等.原花青素对磷酸三钙磨损颗粒所致小鼠颅骨溶解的干预作用及其机制[J].中国应用生理学杂志,2019,35(3):250-255. [25] CARLING D. AMPK signalling in health and disease. Curr Opin Cell Biol. 2017; 45:31-37. [26] FRIIS RMN, GLAVES JP, HUAN T, et al. Rewiring AMPK and mitochondrial retrograde signaling for metabolic control of aging and histone acetylation in respiratory-defective cells. Cell Rep. 2014;7(2):565-574. [27] ALERS S, LÖFFLER AS, WESSELBORG S, et al. Role of AMPK-mTOR-Ulk1/2 in the regulation of autophagy: cross talk, shortcuts, and feedbacks. Mol Cell Biol. 2012;32(1):2-11. [28] LI Y, CHEN Y. AMPK and Autophagy. Adv Exp Med Biol. 2019;1206:85-108. [29] KIM J, KUNDU M, VIOLLET B, et al. AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1. Nat Cell Biol. 2011;13(2):132-141. [30] WONG PM, PUENTE C, GANLEY IG, et al. The ULK1 complex: sensing nutrient signals for autophagy activation. Autophagy. 2013;9(2):124-137. [31] ZHANG S, XIE Y, YAN F, et al. Negative pressure wound therapy improves bone regeneration by promoting osteogenic differentiation via the AMPK-ULK1-autophagy axis. Autophagy. 2022;18(9):2229-2245. [32] PANTOVIC A, KRSTIC A, JANJETOVIC K, et al. Coordinated time-dependent modulation of AMPK/Akt/mTOR signaling and autophagy controls osteogenic differentiation of human mesenchymal stem cells. Bone. 2013; 52(1):524-531. [33] VIDONI C, FERRARESI A, SECOMANDI E, et al. Autophagy drives osteogenic differentiation of human gingival mesenchymal stem cells. Cell Commun Signal. 2019;17(1):98. [34] XI G, ROSEN CJ, CLEMMONS DR. IGF-I and IGFBP-2 stimulate AMPK activation and autophagy, which are required for osteoblast differentiation. Endocrinology. 2016;157(1):268-281. [35] WANG Y, MEI R, HAO S, et al. Up-regulation of SIRT1 induced by 17beta-estradiol promotes autophagy and inhibits apoptosis in osteoblasts. Aging (Albany NY). 2021;13(20):23652-23671. [36] LU DG, LU MJ, YAO SH, et al. Long non-coding RNA TUG1 promotes the osteogenic differentiation of bone marrow mesenchymal stem cells by regulating the AMPK/mTOR/autophagy pathway. Biomed Res. 2021;42(6): 239-246. [37] YUE C, JIN H, ZHANG X, et al. Aucubin prevents steroid-induced osteoblast apoptosis by enhancing autophagy via AMPK activation. J Cell Mol Med. 2021;25(21):10175-10184. [38] SUN SC. The non-canonical NF-κB pathway in immunity and inflammation. Nat Rev Immunol. 2017;17(9):545-558. [39] HAYDEN MS, GHOSH S. Shared principles in NF-kappaB signaling. Cell. 2008;132(3):344-362. [40] SUN SC. Non-canonical NF-κB signaling pathway. Cell Res. 2011;21(1):71-85. [41] LAWRENCE T. The nuclear factor NF-kappaB pathway in inflammation. Cold Spring Harb Perspect Biol. 2009;1(6):a001651. [42] HOESEL B, SCHMID JA. The complexity of NF-κB signaling in inflammation and cancer. Mol Cancer. 2013;12:86. [43] VERZELLA D, PESCATORE A, CAPECE D, et al. Life, death, and autophagy in cancer: NF-κB turns up everywhere. Cell Death Dis. 2020;11(3):210. [44] DJAVAHERI-MERGNY M, AMELOTTI M, MATHIEU J, et al. Regulation of autophagy by NFkappaB transcription factor and reactives oxygen species. Autophagy. 2007;3(4):390-392. [45] MARTINEZ-OUTSCHOORN UE, WHITAKER-MENEZES D, PAVLIDES S, et al. The autophagic tumor stroma model of cancer or “battery-operated tumor growth”: a simple solution to the autophagy paradox. Cell Cycle. 2010;9(21):4297-4306. [46] NIVON M, RICHET E, CODOGNO P, et al. Autophagy activation by NFkappaB is essential for cell survival after heat shock. Autophagy. 2009;5(6):766-783. [47] TROCOLI A, DJAVAHERI-MERGNY M. The complex interplay between autophagy and NF-κB signaling pathways in cancer cells. Am J Cancer Res. 2011;1(5):629-649. [48] SHAW J, YURKOVA N, ZHANG T, et al. Antagonism of E2F-1 regulated Bnip3 transcription by NF-kappaB is essential for basal cell survival. Proc Natl Acad Sci U S A. 2008;105(52):20734-20739. [49] ZHANG L, SUN Y, XU W, et al. Baicalin inhibits Salmonella typhimurium-induced inflammation and mediates autophagy through TLR4/MAPK/NF-κB signalling pathway. Basic Clin Pharmacol Toxicol. 2021;128(2):241-255. [50] QIN H, XU HZ, GONG YQ. Mechanism of NF-κB signaling pathway and autophagy in the regulation of osteoblast differentiation. Mol Membr Biol. 2016;33(6-8):138-144. [51] ZHENG LW, WANG WC, MAO XZ, et al. TNF-α regulates the early development of avascular necrosis of the femoral head by mediating osteoblast autophagy and apoptosis via the p38 MAPK/NF-κB signaling pathway. Cell Biol Int. 2020;44(9):1881-1889. [52] XU MX, SUN XX, LI W, et al. LPS at low concentration promotes the fracture healing through regulating the autophagy of osteoblasts via NF-κB signal pathway. Eur Rev Med Pharmacol Sci. 2018;22(6):1569-1579. [53] ZHU C, BAO N, CHEN S, et al. Dioscin enhances osteoblastic cell differentiation and proliferation by inhibiting cell autophagy via the ASPP2/NF-κβ pathway. Mol Med Rep. 2017;16(4):4922-4926. [54] LINK W. Introduction to FOXO Biology. Methods Mol Biol. 2019;1890:1-9. [55] BHARDWAJ G, PENNIMAN CM, JENA J, et al. Insulin and IGF-1 receptors regulate complex I-dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle. J Clin Invest. 2021;131(18):e146415. [56] MORRIS BJ, WILLCOX DC, DONLON TA, et al. FOXO3: a major gene for human longevity--a mini-review. Gerontology. 2015;61(6):515-525. [57] LEE JW, NAM H, KIM LE, et al. TLR4 (toll-like receptor 4) activation suppresses autophagy through inhibition of FOXO3 and impairs phagocytic capacity of microglia. Autophagy. 2019;15(5):753-770. [58] FITZWALTER BE, THORBURN A. FOXO3 links autophagy to apoptosis. Autophagy. 2018;14(8):1467-1468. [59] GÓMEZ-PUERTO MC, VERHAGEN LP, BRAAT AK, et al. Activation of autophagy by FOXO3 regulates redox homeostasis during osteogenic differentiation. Autophagy. 2016;12(10):1804-1816. [60] KOMATSU M, WAGURI S, KOIKE M, et al. Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. Cell. 2007;131(6):1149-1163. [61] LIN X, LI S, ZHAO Y, et al. Interaction domains of p62: a bridge between p62 and selective autophagy. DNA Cell Biol. 2013;32(5):220-227. [62] MYEKU N, FIGUEIREDO-PEREIRA ME. Dynamics of the degradation of ubiquitinated proteins by proteasomes and autophagy: association with sequestosome 1/p62. J Biol Chem. 2011;286(25):22426-22440. [63] KATSURAGI Y, ICHIMURA Y, KOMATSU M. p62/SQSTM1 functions as a signaling hub and an autophagy adaptor. FEBS J. 2015;282(24):4672-4678. [64] PUISSANT A, FENOUILLE N, AUBERGER P. When autophagy meets cancer through p62/SQSTM1. Am J Cancer Res. 2012;2(4):397-413. [65] XU A, YANG Y, SHAO Y, et al. Activation of cannabinoid receptor type 2-induced osteogenic differentiation involves autophagy induction and p62-mediated Nrf2 deactivation. Cell Commun Signal. 2020;18(1):9. [66] CHEN X, YANG K, JIN X, et al. Bone autophagy: a potential way of exercise-mediated Meg3/P62/Runx2 pathway to regulate bone formation in T2DM mice. Diabetes Metab Syndr Obes. 2021;14:2753-2764. [67] LIU WJ, YE L, HUANG WF, et al. p62 links the autophagy pathway and the ubiqutin-proteasome system upon ubiquitinated protein degradation. Cell Mol Biol Lett. 2016;21:29. [68] HURLEY JH, YOUNG LN. Mechanisms of autophagy initiation. Annu Rev Biochem. 2017;86:225-244. [69] XU HD, QIN ZH. Beclin 1, Bcl-2 and Autophagy. Adv Exp Med Biol. 2019; 1206:109-126. [70] KANG R, ZEH HJ, LOTZE MT, et al. The Beclin 1 network regulates autophagy and apoptosis. Cell Death Differ. 2011;18(4):571-580. [71] WEI Y, PATTINGRE S, SINHA S, et al. JNK1-mediated phosphorylation of Bcl-2 regulates starvation-induced autophagy. Mol Cell. 2008;30(6):678-688. [72] LEVIN-SALOMON V, BIALIK S, KIMCHI A. DAP-kinase and autophagy. Apoptosis. 2014;19(2):346-356. [73] GURKAR AU, CHU K, RAJ L, et al. Identification of ROCK1 kinase as a critical regulator of Beclin1-mediated autophagy during metabolic stress. Nat Commun. 2013;4:2189. [74] MAEJIMA Y, KYOI S, ZHAI P, et al. Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2. Nat Med. 2013;19(11):1478-1488. [75] WU H, XUE Y, ZHANG Y, et al. PTH1-34 promotes osteoblast formation through Beclin1-dependent autophagic activation. J Bone Miner Metab. 2021;39(4):572-582. [76] YANG X, JIANG T, WANG Y, et al. The role and mechanism of sirt1 in resveratrol-regulated osteoblast autophagy in osteoporosis rats. Sci Rep. 2019;9(1):18424. [77] BRACHMANN CB, SHERMAN JM, DEVINE SE, et al. The SIR2 gene family, conserved from bacteria to humans, functions in silencing, cell cycle progression, and chromosome stability. Genes Dev. 1995;9(23):2888-2902. [78] TANG BL. Sirt1 and the mitochondria. Mol Cells. 2016;39(2):87-95. [79] WANG L, XU C, JOHANSEN T, et al. SIRT1 - a new mammalian substrate of nuclear autophagy. Autophagy. 2021;17(2):593-595. [80] NG F, TANG BL. Sirtuins’ modulation of autophagy. J Cell Physiol. 2013; 228(12):2262-2270. [81] LOUVET L, LETERME D, DELPLACE S, et al. Sirtuin 1 deficiency decreases bone mass and increases bone marrow adiposity in a mouse model of chronic energy deficiency. Bone. 2020;136:115361. [82] SHAO Z, DOU S, ZHU J, et al. Apelin-36 protects HT22 cells against oxygen-glucose deprivation/reperfusion-induced oxidative stress and mitochondrial dysfunction by promoting SIRT1-mediated PINK1/Parkin-dependent mitophagy. Neurotox Res. 2021;39(3):740-753. [83] DZULKO M, PONS M, HENKE A, et al. The PP2A subunit PR130 is a key regulator of cell development and oncogenic transformation. Biochim Biophys Acta Rev Cancer. 2020;1874(2):188453. [84] MAZHAR S, LEONARD D, SOSA A, et al. Challenges and reinterpretation of antibody-based research on phosphorylation of Tyr307 on PP2Ac. Cell Rep. 2020;30(9):3164-3170.e3. [85] XU Y, WEI L, TANG S, et al. Regulation PP2Ac methylation ameliorating autophagy dysfunction caused by Mn is associated with mTORC1/ULK1 pathway. Food Chem Toxicol. 2021;156:112441. [86] HUSSAIN T, ZHAO D, SHAH SZA, et al. PP2Ac modulates AMPK-mediated induction of autophagy in mycobacterium bovis-infected macrophages. Int J Mol Sci. 2019;20(23):6030. [87] MENG L, LU C, WU B, et al. Taurine antagonizes macrophages M1 polarization by mitophagy-glycolysis switch blockage via dragging SAM-PP2Ac transmethylation. Front Immunol. 2021;12:648913. [88] OKAMURA H, YOSHIDA K, MORIMOTO H, et al. Role of protein phosphatase 2A in osteoblast differentiation and function. J Clin Med. 2017;6(3):23. [89] ONISHI M, YAMANO K, SATO M, et al. Molecular mechanisms and physiological functions of mitophagy. EMBO J. 2021;40(3):e104705. [90] LOU G, PALIKARAS K, LAUTRUP S, et al. Mitophagy and neuroprotection. Trends Mol Med. 2020;26(1):8-20. [91] PICKRELL AM, YOULE RJ. The roles of PINK1, parkin, and mitochondrial fidelity in Parkinson’s disease. Neuron. 2015;85(2):257-273. [92] SINGLETON AB, FARRER MJ, BONIFATI V. The genetics of Parkinson’s disease: progress and therapeutic implications. Mov Disord. 2013;28(1):14-23. [93] NARDIN A, SCHREPFER E, ZIVIANI E. Counteracting PINK/Parkin deficiency in the activation of mitophagy: a potential therapeutic intervention for Parkinson’s disease. Curr Neuropharmacol. 2016;14(3):250-259. [94] NGUYEN TN, PADMAN BS, LAZAROU M. Deciphering the molecular signals of PINK1/Parkin mitophagy. Trends Cell Biol. 2016;26(10):733-744. [95] BINGOL B, SHENG M. Mechanisms of mitophagy: PINK1, Parkin, USP30 and beyond. Free Radic Biol Med. 2016;100:210-222. [96] WANG B, ABRAHAM N, GAO G, et al. Dysregulation of autophagy and mitochondrial function in Parkinson’s disease. Transl Neurodegener. 2016; 5:19. [97] ZHANG W, HOU W, CHEN M, et al. Upregulation of parkin accelerates osteoblastic differentiation of bone marrow-derived mesenchymal stem cells and bone regeneration by enhancing autophagy and β-catenin signaling. Front Cell Dev Biol. 2020;8:576104. [98] CHEN L, SHI X, WENG SJ, et al. Vitamin K2 can rescue the dexamethasone-induced downregulation of osteoblast autophagy and mitophagy thereby restoring osteoblast function in vitro and in vivo. Front Pharmacol. 2020; 11:1209. |
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[13] | 张 琪, 于 湄, 刘 磊, 田卫东. 工程化外泌体研究现状与临床转化的挑战[J]. 中国组织工程研究, 2023, 27(19): 3052-3060. |
[14] | 刘 闯, 谭龙旺, 周禾山, 张 弛. 脂肪间充质干细胞外泌体治疗创伤性中枢神经系统损伤[J]. 中国组织工程研究, 2023, 27(19): 3061-3069. |
[15] | 马 刚, 郑小红, 王敬博, 韩 英. 间充质干细胞移植不同的途径可影响肝纤维化治疗效果[J]. 中国组织工程研究, 2023, 27(19): 3099-3107. |
1.1.6 检索策略 以PubMed数据库检索策略为例,见图1。
1.1.7 文献检索量 初步检索到293篇文章。
1.3 文献质量评估及数据提取 对检索到的293篇文献阅读文题、摘要后,经所有作者共同商议后纳入98篇进入综述分析,见表2。
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文题释义:
假体周围骨溶解:人工关节置换后由于假体与骨组织之间的微动以及假体各部件之间的长期磨损会产生的磨损颗粒,磨损颗粒会诱导并趋化炎症因子、破坏成骨-破骨平衡,导致假体周围的骨质溶解,假体因此发生松动,最终造成人工关节置换的失败或其使用寿命减短。成骨细胞来源于存在于骨髓中的间充质干细胞,该细胞一般黏附于骨表面,其功能主要包括生成骨基质以及调控破骨细胞功能。它们通过I型胶原的合成和分泌功能来产生骨基质,并帮助骨基质矿化[8]。羟基磷灰石构成骨组织的大部分无机成分。在磨损颗粒导致的骨溶解微环境中,成骨细胞表型会发生改变,且相应基因也会发生转变,成骨细胞的骨形成能力因此受损[9]。有文献指出,磨损颗粒诱导的成骨细胞成骨能力的受损以及骨胶原合成的减少是假体周围骨溶解发生发展的直接原因,并且磨损颗粒所诱导的炎症和氧化应激等可以直接杀伤成骨细胞,导致其数量减少[10]。
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