切换至 "中华医学电子期刊资源库"

中华关节外科杂志(电子版) ›› 2022, Vol. 16 ›› Issue (06) : 745 -755. doi: 10.3877/cma.j.issn.1674-134X.2022.06.014

综述

骨关节炎危险因素与发病机制的研究进展
王旭东1, 张紫机1,()   
  1. 1. 510080 广州,中山大学附属第一医院关节外科
  • 收稿日期:2021-01-06 出版日期:2022-12-01
  • 通信作者: 张紫机

Research progress on risk factors and pathogenesis of osteoarthritis

Xudong Wang1, Ziji Zhang1,()   

  1. 1. Department of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2021-01-06 Published:2022-12-01
  • Corresponding author: Ziji Zhang
引用本文:

王旭东, 张紫机. 骨关节炎危险因素与发病机制的研究进展[J]. 中华关节外科杂志(电子版), 2022, 16(06): 745-755.

Xudong Wang, Ziji Zhang. Research progress on risk factors and pathogenesis of osteoarthritis[J]. Chinese Journal of Joint Surgery(Electronic Edition), 2022, 16(06): 745-755.

骨关节炎是一种由多因素作用造成关节软骨、软骨下骨或滑膜与半月板组织损伤以及代谢异常的全关节退变性疾病。随着人口的老龄化和肥胖人口的增多,骨关节炎发病率逐年增高,造成极大的社会影响与经济负担。目前其病因仍未明确,本文归纳探讨近年骨关节炎发病的危险因素及发病机制,为骨关节炎未来的防治提供新思路。

Osteoarthritis is a joint degenerative disease due to multiple reasons, featured with the damage and abnormal metabolism of articular cartilage, subchondral bone or synovium and meniscus tissue. With the aging of population and the increase of obese people, the incidence of osteoarthritis is increasing year by year, leading to great social impact and economic burden. At present, its etiology remains unclear. This article summarized the risk factors and possible pathogenesis of osteoarthritis in order to introduce new insight for the prevention and treatment of osteoarthritis in the future.

[1]
Prieto-Alhambra D, Judge A, Javaid MK, et al. Incidence and risk factors for clinically diagnosed knee, hip and hand osteoarthritis: influences of age, gender and osteoarthritis affecting other joints[J]. Ann Rheum Dis, 2014, 73(9): 1659-1664.
[2]
Hunter DJ, Schofield D, Callander E. The individual and socioeconomic impact of osteoarthritis[J]. Nat Rev Rheumatol, 2014, 10(7): 437-441.
[3]
Runciman WB, Hunt TD, Hannaford N, et al. CareTrack: assessing the appropriateness of health care delivery in Australia[J]. Med J Aust, 2012, 197(2): 100-105.
[4]
Brandt KD, Radin EL, Dieppe PA, et al. Yet more evidence that osteoarthritis is not a cartilage disease[J]. Ann Rheum Dis, 2006, 65(10): 1261-1264.
[5]
Zhang Y, Jordan JM. Epidemiology of osteoarthritis[J]. Rheum Dis Clin North Am, 2008, 34(3): 515-529.
[6]
Loeser RF, Collins JA, Diekman BO. Ageing and the pathogenesis of osteoarthritis[J]. Nat Rev Rheumatol, 2016, 12(7): 412-420.
[7]
Silverwood V, Blagojevic-Bucknall M, Jinks C, et al. Current evidence on risk factors for knee osteoarthritis in older adults: a systematic review and meta-analysis[J]. Osteoarthritis Cartilage, 2015, 23(4): 507-515.
[8]
Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States[J]. Arthritis Rheum, 1998, 41(5): 778-799.
[9]
Roman-Blas JA, Castaneda S, Largo RA. Osteoarthritis associated with estrogen deficiency[J/OL]. Arthritis Res Ther, 2009, 11(5): 241. DOI:10.1186/ar2791.
[10]
Reyes C, Leyland KM, Peat G, et al. Association between overweight and obesity and risk of clinically diagnosed knee, hip, and hand osteoarthritis: a population-based cohort study[J]. Arthritis Rheumatol, 2016, 68(8): 1869-1875.
[11]
Felson DT. Epidemiology of hip and knee osteoarthritis[J]. Epidemiol Rev, 1988, 10(1): 1-28.
[12]
Bortoluzzi A, Furini F, Scirè CA. Osteoarthritis and its management-epidemiology, nutritional aspects and environmental factors[J]. Autoimmun Rev, 2018, 17(11): 1097-1104.
[13]
Lohmander LS, Gerhardsson De Verdier M, Rollof J, et al. Incidence of severe knee and hip osteoarthritis in relation to different measures of body mass: a population-based prospective cohort study[J]. Ann Rheum Dis, 2009, 68(4): 490-496.
[14]
Poulsen E, Goncalves GH, Bricca A, et al. Knee osteoarthritis risk is increased 4-6 fold after knee injury-a systematic review and meta-analysis[J]. Br J Sports Med, 2019, 53(23): 1454-1463.
[15]
Cinque ME, Gj D, Chahla J, et al. High rates of osteoarthritis develop after anterior cruciate ligament surgery: an analysis of 4108 patients[J]. Am J Sports Med, 2018, 46(8): 2011-2019.
[16]
Lieniversen T, Morgan D, Jensen C, et al. Does surgery reduce knee osteoarthritis, meniscal injury and subsequent complications compared with non-surgery after ACL rupture with at least 10 years follow-up? A systematic review and meta-analysis[J]. Brit J Sport Med, 2020, 54: 592-598.
[17]
Shelbourne KD, Benner RW, Gray T. Results of anterior cruciate ligament Reconstruction with patellar tendon autografts: objective factors associated with the development of osteoarthritis at 20 to 33 years after surgery[J]. Am J Sports Med, 2017, 45(12): 2730-2738.
[18]
Harris EC, Coggon D. HIP osteoarthritis and work[J]. Best Pract Res Clin Rheumatol, 2015, 29(3): 462-482.
[19]
Ezzat AM, Li LC. Occupational physical loading tasks and knee osteoarthritis: a review of the evidence[J]. Physiother Can, 2014, 66(1): 91-107.
[20]
Vigdorchik JM, Nepple JJ, Eftekhary N, et al. What is the association of elite sporting activities with the development of hip osteoarthritis?[J]. Am J Sports Med, 2017, 45(4): 961-964.
[21]
Driban JB, Hootman JM, Sitler MR, et al. Is participation in certain sports associated with knee osteoarthritis? A systematic review[J]. J Athl Train, 2017, 52(6): 497-506.
[22]
Fernandes GS, Parekh SM, Moses J, et al. Prevalence of knee pain, radiographic osteoarthritis and arthroplasty in retired professional footballers compared with men in the general population: a cross-sectional study[J]. Br J Sports Med, 2018, 52(10): 678-683.
[23]
Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis[J]. Nat Rev Rheumatol, 2013, 9(10): 630-634.
[24]
Berenbaum F, Wallace IJ, Lieberman D, et al. Modern-day environmental factors in the pathogenesis of osteoarthritis[J]. Nat Rev Rheumatol, 2018, 14(11): 674-681.
[25]
Mcculloch K, Litherland GJ, Rai TS. Cellular senescence in osteoarthritis pathology[J]. Aging Cell, 2017, 16(2): 210-218.
[26]
Rahmati M, Nalesso G, Mobasheri A, et al. Aging and osteoarthritis: central role of the extracellular matrix[J]. Ageing Res Rev, 2017, 40: 20-30.
[27]
Jeon OH, David N, Campisi J, et al. Senescent cells and osteoarthritis: a painful connection[J]. J Clin Invest, 2018, 128(4): 1229-1237.
[28]
Acosta JC, Banito A, Wuestefeld T, et al. A complex secretory program orchestrated by the inflammasome controls paracrine senescence[J]. Nat Cell Biol, 2013, 15(8): 978-990.
[29]
Philipot D, Guerit D, Platano D, et al. P16(INK4a) and its regulator miR-24 Link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis[J/OL]. Arthritis Res Ther, 2014, 16(1): R58. DOI:10.1186/ar4494.
[30]
Jeon OH, Kim C, Laberge RM, et al. Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment[J]. Nat Med, 2017, 23(6): 775-781.
[31]
Chen D, Shen J, Zhao W, et al. Osteoarthritis: toward a comprehensive understanding of pathological mechanism[J/OL]. Bone Res, 2017, 5(1): 16044. DOI:10.1038/boneres.2016.44.
[32]
Hosseinzadeh A, Kamrava SK, Joghataei MT, et al. Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin[J]. J Pineal Res, 2016, 61(4): 411-425.
[33]
Heinegard D. Proteoglycans and more--from molecules to biology[J]. Int J Exp Patho, 2009, 90(6): 575-586.
[34]
Cui N, Hu M, Khalil RA. Biochemical and biological attributes of matrix metalloproteinases[J]. Prog Mol Biol Transl Sci, 2017, 147: 1-73.
[35]
Liu J, Khalil RA. Matrix metalloproteinase inhibitors as investigational and therapeutic tools in unrestrained tissue remodeling and pathological disorders[J]. Prog Mol Biol Transl Sci, 2017, 148: 355-420.
[36]
Guilak F, Nims RJ, Dicks A, et al. Osteoarthritis as a disease of the cartilage pericellular matrix[J]. Matrix Biol, 2018, 71-72: 40-50.
[37]
许曼珊,姜婷,秦盈盈.骨关节炎发病机制研究进展[J].国际骨科学杂志202041(4):229-233.
[38]
Marks PH, Donaldson ML. Inflammatory cytokine profiles associated with chondral damage in the anterior cruciate ligament-deficient knee[J]. Arthroscopy, 2005, 21(11): 1342-1347.
[39]
Wang X, Li F, Fan C, et al. Effects and relationship of ERK1 and ERK2 in interleukin-1β-induced alterations in MMP3, MMP13, type II collagen and aggrecan expression in human chondrocytes[J]. Int J Mol Med, 2011, 27(4): 583-589.
[40]
Caramés B, López-Armada MJ, Cillero-Pastor B, et al. Differential effects of tumor necrosis factor-alpha and interleukin-1beta on cell death in human articular chondrocytes[J]. Osteoarthritis Cartilage, 2008, 16(6): 715-722.
[41]
García-Arnandis I, Guillén MI, Gomar F, et al. High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes[J/OL]. Arthritis Res Ther, 2010, 12(4): R165. DOI:10.1186/ar3124.
[42]
Kloppenburg M, Peterfy C, Haugen IK, et al. Phase IIa, placebo-controlled, randomised study of lutikizumab, an anti-interleukin-1α and anti-interleukin-1β dual variable domain immunoglobulin, in patients with erosive hand osteoarthritis[J]. Ann Rheum Dis, 2019, 78(3): 413-420.
[43]
Fleischmann RM, Bliddal H, Blanco FJ, et al. A phase II trial of lutikizumab, an Anti-Interleukin-1α/β dual variable domain immunoglobulin, in knee osteoarthritis patients with synovitis[J]. Arthritis Rheumatol, 2019, 71(7): 1056-1069.
[44]
Cheng C, Tian J, Zhang F. Can IL-1 be used as a target for osteoarthritis?[J/OL]. Ann Rheum Dis, 2020, 79(7): e88. DOI:10.1136/annrheumdis-2019-215513.
[45]
Wang T, He C. Pro-inflammatory cytokines: the Link between obesity and osteoarthritis[J]. Cytokine Growth Factor Rev, 2018, 44: 38-50.
[46]
Wang Y, Xu J, Zhang X, et al. TNF-α-induced LRG1 promotes angiogenesis and mesenchymal stem cell migration in the subchondral bone during osteoarthritis[J/OL]. Cell Death Dis, 2017, 8(3): e2715. DOI:10.1038/cddis.2017.129.
[47]
Hu G, Zhao X, Wang C, et al. MicroRNA-145 attenuates TNF-α-driven cartilage matrix degradation in osteoarthritis via direct suppression of MKK4[J/OL]. Cell Death Dis, 2017, 8(10): e3140. DOI:10.1038/cddis.2017.522.
[48]
Zhao Y, Li Y, Qu R, et al. Cortistatin binds to TNF-α receptors and protects against osteoarthritis[J]. EBio Medicine, 2019, 41: 556-570.
[49]
Loef M, Kroon F, Bergstra SA, et al. TNF inhibitor treatment is associated with a lower risk of hand osteoarthritis progression in rheumatoid arthritis patients after 10 years[J]. Rheumatology (Oxford), 2018, 57(11): 1917-1924.
[50]
Kloppenburg M, Ramonda R, Bobacz K, et al. Etanercept in patients with inflammatory hand osteoarthritis (EHOA): a multicentre, randomised, double-blind, placebo-controlled trial[J]. Ann Rheum Dis, 2018, 77(12): 1757-1764.
[51]
Ferrara N, Gerber HP, Lecouter J. The biology of VEGF and its receptors[J]. Nat Med, 2003, 9(6): 669-676.
[52]
Olsson AK, Dimberg A, Kreuger J, et al. VEGF receptor signalling- in control of vascular function[J]. Nat Rev Mol Cell Biol, 2006, 7(5): 359-371.
[53]
Maharaj AS, D′amore PA. Roles for VEGF in the adult[J]. Microvasc Res, 2007, 74(2/3): 100-113.
[54]
Hamilton JL, Nagao M, Levine BR, et al. Targeting VEGF and its receptors for the treatment of osteoarthritis and associated pain[J]. J Bone Miner Res, 2016, 31(5): 911-924.
[55]
Ludin A, Sela JJ, Schroeder A, et al. Injection of vascular endothelial growth factor into knee joints induces osteoarthritis in mice[J]. Osteoarthritis Cartilage, 2013, 21(3): 491-497.
[56]
Lu J, Zhang H, Cai D, et al. Positive-Feedback regulation of subchondral H-Type vessel formation by chondrocyte promotes osteoarthritis development in mice[J]. J Bone Miner Res, 2018, 33(5): 909-920.
[57]
Zhang X, Crawford R, Xiao Y. Inhibition of vascular endothelial growth factor with shRNA in chondrocytes ameliorates osteoarthritis[J]. J Mol Med (Berl), 2016, 94(7): 787-798.
[58]
Li L, Liu F, Huang W, et al. Ricolinostat (ACY-1215) inhibits VEGF expression via PI3K/AKT pathway and promotes apoptosis in osteoarthritic osteoblasts[J/OL]. Biomed Pharmacother, 2019, 118: 109357. DOI:10.1016/j.biopha.2019.109357.
[59]
Saito T, Kawaguchi H. HIF-2α as a possible therapeutic target of osteoarthritis[J]. Osteoarthritis Cartilage, 2010, 18(12): 1552-1556.
[60]
Javelaud D, Mauviel A. Mammalian transforming growth factor-betas: Smad signaling and physio-pathological roles[J]. Int J Biochem Cell Biol, 2004, 36(7): 1161-1165.
[61]
Cuellar A, Reddi AH. Stimulation of superficial Zone protein/lubricin/PRG4 by transforming growth factor-β in superficial Zone articular chondrocytes and modulation by glycosaminoglycans[J]. Tissue Eng Part A, 2015, 21(13/14): 1973-1981.
[62]
Wang YJ, Shen M, Wang S, et al. RETRACTED: inhibition of the TGF-β1/Smad signaling pathway protects against cartilage injury and osteoarthritis in a rat model[J]. Life Sci, 2017, 189: 106-113.
[63]
Reyrico A, Venkatesan JK, Schmitt G, et al. rAAV-mediated overexpression of TGF-β via vector delivery in polymeric micelles stimulates the biological and reparative activities of human articular chondrocytes in vitro and in a human osteochondral defect model[J]. Int J Nanomed, 2017, 12: 6985-6996.
[64]
Reem T, Witte F, Willbold E, et al. Simultaneous regeneration of articular cartilage and subchondral bone induced by spatially presented TGF-beta and BMP-4 in a bilayer affinity binding system[J]. Acta Biomater, 2012, 8(9): 3283-3293.
[65]
Zheng L, Pi C, Zhang J, et al. Aberrant activation of latent transforming growth factor-β initiates the onset of temporomandibular joint osteoarthritis[J/OL]. Bone Res, 2018, 6(1): 26. DOI:10.1038/s41413-018-0027-6.
[66]
Xu X, Zheng L, Yuan Q, et al. Transforming growth factor-β in stem cells and tissue homeostasis[J/OL]. Bone Res, 2018, 6(1): 2. DOI:10.1038/s41413-017-0005-4.
[67]
Scharstuhl A, Vitters EL, Van Der Kraan PM, et al. Reduction of osteophyte formation and synovial thickening by adenoviral overexpression of transforming growth factor beta/bone morphogenetic protein inhibitors during experimental osteoarthritis[J]. Arthritis Rheum, 2003, 48(12): 3442-3451.
[68]
Loeser RF. Growth factor regulation of chondrocyte integrins. Differential effects of insulin-like growth factor 1 and transforming growth factor beta on alpha 1 beta 1 integrin expression and chondrocyte adhesion to type VI collagen[J]. Arthritis Rheum, 1997, 40(2): 270-276.
[69]
Wei FY, Lee JK, Wei L, et al. Correlation of insulin-like growth factor 1 and osteoarthritic cartilage degradation: a spontaneous osteoarthritis in guinea-pig[J]. Eur Rev Med Pharmacol Sci, 2017, 21(20): 4493-4500.
[70]
Yu Q, Zhao B, He Q, et al. microRNA-206 is required for osteoarthritis development through its effect on apoptosis and autophagy of articular chondrocytes via modulating the phosphoinositide 3-kinase/protein kinase B-mTOR pathway by targeting insulin-like growth factor-1[J]. J Cell Biochem, 2019, 120(4): 5287-5303.
[71]
Ekenstedt KJ, Sonntag WE, Loeser RF, et al. Effects of chronic growth hormone and insulin-like growth factor 1 deficiency on osteoarthritis severity in rat knee joints[J]. Arthritis Rheum, 2006, 54(12): 3850-3858.
[72]
Geiger BC, Wang S, Padera RJ, et al. Cartilage-penetrating nanocarriers improve delivery and efficacy of growth factor treatment of osteoarthritis[J/OL]. Sci Transl Med, 2018, 10(469): eaat8800. DOI:10.1126/scitranslmed.aat8800.
[73]
Uchimura T, Foote AT, Smith EL, et al. Insulin-like growth factor II (IGF-II) inhibits IL-1β-Induced cartilage matrix loss and promotes cartilage integrity in experimental osteoarthritis[J]. J Cell Biochem, 2015, 116(12): 2858-2869.
[74]
Yang Y, Wang Y, Kong Y, et al. Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF-κB signaling pathway[J]. J Cell Physiol, 2019, 234(6): 9156-9167.
[75]
Zheng W, Li X, Liu D, et al. Mechanical loading mitigates osteoarthritis symptoms by regulating endoplasmic reticulum stress and autophagy[J]. FASEB J, 2019, 33(3): 4077-4088.
[76]
Sumi C, Hirose N, Yanoshita M, et al. Semaphorin 3a inhibits inflammation in chondrocytes under excessive mechanical stress[J/OL]. Mediators Inflamm, 2018, 2018: 5703651. DOI:10.1155/2018/5703651.
[77]
Schroeder A, Nazet U, Muschter D, et al. Impact of mechanical load on the expression profile of synovial fibroblasts from patients with and without osteoarthritis[J/OL]. Int J Mol Sci, 2019, 20(3): 585. DOI: 10.3390/ijms20030585.
[78]
Liu Q, Hu XQ, Zhang X, et al. Effects of mechanical stress on chondrocyte phenotype and chondrocyte extracellular matrix expression[J/OL]. Sci Rep, 2016, 6(1): 37268. DOI:10.1038/srep37268.
[79]
Xu B, Xing R, Huang Z, et al. Excessive mechanical stress induces chondrocyte apoptosis through TRPV4 in an anterior cruciate ligament-transected rat osteoarthritis model[J]. Life Sci, 2019, 228: 158-166.
[80]
Zhang RK, Li GW, Zeng C, et al. Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1)[J]. Bone Joint Res, 2018, 7(11): 587-594.
[81]
Chang SH, Mori D, Kobayashi H, et al. Excessive mechanical loading promotes osteoarthritis through the gremlin-1-NF-κB pathway[J/OL]. Nat Commun, 2019, 10(1): 1442. DOI:10.1038/s41467-019-09491-5.
[82]
Lepetsos P, Papavassiliou KA, Papavassiliou AG. Redox and NF-κB signaling in osteoarthritis[J]. Free Radic Biol Med, 2019, 132: 90-100.
[83]
Jones DP. Redox theory of aging [J]. Redox Biol 2015, 5: 71-79.
[84]
Finkel T. Signal transduction by reactive oxygen species[J]. J Cell Biol, 2011, 194(1): 7-15.
[85]
Hui W, Young DA, Rowan AD, et al. Oxidative changes and signalling pathways are pivotal in initiating age-related changes in articular cartilage[J]. Ann Rheum Dis, 2016, 75(2): 449-458.
[86]
D′adamo S, Cetrullo S, Guidotti S, et al. Spermidine rescues the deregulated autophagic response to oxidative stress of osteoarthritic chondrocytes[J]. Free Radic Biol Med, 2020, 153: 159-172.
[87]
Chen QX, Shao XT, Ling PX, et al. Low molecular weight xanthan gum suppresses oxidative stress-induced apoptosis in rabbit chondrocytes[J]. Carbohydr Polym, 2017, 169: 255-263.
[88]
Feng K, Chen Z, Pengcheng L, et al. Quercetin attenuates oxidative stress-induced apoptosis via SIRT1/AMPK-mediated inhibition of ER stress in rat chondrocytes and prevents the progression of osteoarthritis in a rat model[J]. J Cell Physiol, 2019, 234(10): 18192-18205.
[89]
Leonidou A, Lepetsos P, Mintzas M, et al. Inducible nitric oxide synthase as a target for osteoarthritis treatment[J]. Expert Opin Ther Targets, 2018, 22(4): 299-318.
[90]
Millerand M, Berenbaum F, Jacques C. Danger signals and inflammaging in osteoarthritis[J]. Clin Exp Rheumatol, 2019, 37 Suppl 120(5): 48-56.
[91]
Wood MJ, Leckenby A, Reynolds G, et al. Macrophage proliferation distinguishes 2 subgroups of knee osteoarthritis patients[J/OL]. JCI Insight, 2019, 4(2): 125325. DOI:10.1172/jci.insight.125325.
[92]
谢锦伟,黄泽宇,裴福兴.固有免疫系统在骨关节炎发病机制中的作用及研究进展[J].中国修复重建外科杂志201933(3):370-376.
[93]
Zhang H, Lin C, Zeng C, et al. Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2[J]. Ann Rheum Dis, 2018, 77(10): 1524-1534.
[94]
Dai M, Sui B, Xue Y, et al. Cartilage repair in degenerative osteoarthritis mediated by squid type II collagen via immunomodulating activation of M2 macrophages, inhibiting apoptosis and hypertrophy of chondrocytes[J]. Biomaterials, 2018, 180: 91-103.
[95]
Geurts J, Patel A, Hirschmann MT, et al. Elevated marrow inflammatory cells and osteoclasts in subchondral osteosclerosis in human knee osteoarthritis[J]. J Orthop Res, 2016, 34(2): 262-269.
[96]
Saejung T, Sengprasert P, Apinun J, et al. Functional and T cell receptor repertoire analyses of peripheral blood and infrapatellar fat pad T cells in knee osteoarthritis[J]. J Rheumatol, 2019, 46(3): 309-317.
[97]
Hsieh JL, Shiau AL, Lee CH, et al. CD8+ T cell-induced expression of tissue inhibitor of metalloproteinses-1 exacerbated osteoarthritis[J]. Int J Mol Sci, 2013, 14(10): 19951-19970.
[98]
Shen PC, Wu CL, Jou IM, et al. T helper cells promote disease progression of osteoarthritis by inducing macrophage inflammatory protein-1γ[J]. Osteoarthritis Cartilage, 2011, 19(6): 728-736.
[99]
Yang S, Wang J, Chen F, et al. Elevated galectin-9 suppresses Th1 effector function and induces apoptosis of activated CD4(+) T cells in osteoarthritis[J]. Inflammation, 2017, 40(3): 1062-1071.
[100]
Struglics A, Okroj M, Swärd P, et al. The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis[J/OL]. Arthritis Res Ther, 2016, 18(1): 223. DOI: 10.1186/s13075-016-1123-x.
[101]
Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis[J]. Nat Med, 2011, 17(12): 1674-1679.
[102]
Biver E, Berenbaum F, Valdes AM, et al. Gut microbiota and osteoarthritis management: An expert consensus of the European society for clinical and economic aspects of osteoporosis, osteoarthritis and musculoskeletal diseases (ESCEO)[J/OL]. Ageing Res Rev, 2019, 55:100946. DOI:10.1016/j.arr.2019.100946.
[103]
Liu Y, Ding W, Wang HL, et al. Gut microbiota and obesity-associated osteoarthritis[J]. Osteoarthritis Cartilage, 2019, 27(9): 1257-1265.
[104]
Lorenzo D, Gianvincenzo Z, Carlo LR, et al. Oral-gut microbiota and arthritis: is there an evidence-based axis?[J/OL]. J Clin Med, 2019, 8(10): 0. DOI: 10.3390/jcm8101753.
[105]
Li Y, Luo W, Deng Z, et al. Diet-Intestinal microbiota axis in osteoarthritis: a possible role[J/OL]. Mediators Inflamm, 2016, 2016: 3495173. DOI:10.1155/2016/3495173.
[106]
Lee JY, Mannaa M, Kim Y, et al. Comparative analysis of fecal microbiota composition between rheumatoid arthritis and osteoarthritis patients[J/OL]. Genes, 2019, 10: 748. DOI: 10.3390/genes10100748.
[107]
Huang Z, Chen J, Li B, et al. Faecal microbiota transplantation from metabolically compromised human donors accelerates osteoarthritis in mice[J]. Ann Rheum Dis, 2020, 79(5): 646-656.
[108]
Boer CG, Radjabzadeh D, Medina-Gomez C, et al. Intestinal microbiome composition and its relation to joint pain and inflammation[J/OL]. Nat Commun, 2019, 10(1): 4881. DOI: 10.1038/s41467-019-12873-4.
[109]
Guss JD, Ziemian SN, Luna M, et al. The effects of metabolic syndrome, obesity, and the gut microbiome on load-induced osteoarthritis[J]. Osteoarthritis Cartilage, 2019, 27(1): 129-139.
[110]
Shang Q, Yin Y, Zhu L, et al. Degradation of chondroitin sulfate by the gut microbiota of Chinese individuals[J]. Int J Biol Macromol, 2016, 86: 112-118.
[111]
Schott EM, Farnsworth CW, Grier A, et al. Targeting the gut microbiome to treat the osteoarthritis of obesity[J/OL]. JCI Insight, 2018, 3(8): 95997. DOI:10.1172/jci.insight.95997.
[112]
Pedersini P, Turroni S, Villafañe JH. Gut microbiota and physical activity: Is there an evidence-based Link?[J/OL]. Sci Total Environ, 2020, 727: 138648. DOI:10.1016/j.scitotenv.2020.138648.
[113]
De SA, De SR, Petito V, et al. Gut-joint axis: the role of physical exercise on gut microbiota modulation in older people with osteoarthritis[J/OL]. Nutrients, 2020, 12(2): 574. DOI: 10.3390/nu12020574.
[114]
Zhuo Q, Yang W, Chen JY, et al. Metabolic syndrome meets osteoarthritis[J]. Nat Rev Rheumatol, 2012, 8(12): 729-737.
[115]
Mobasheri A, Rayman MP, Gualillo O, et al. The role of metabolism in the pathogenesis of osteoarthritis[J]. Nat Rev Rheumatol, 2017, 13(5): 302-311.
[116]
Puenpatom RA, Victor TW. Increased prevalence of metabolic syndrome in individuals with osteoarthritis: an analysis of NHANES III data[J]. Postgrad Med, 2009, 121(6): 9-20.
[117]
Engstrom G, De Verdier MG, Rollof J, et al. C-reactive protein, metabolic syndrome and incidence of severe hip and knee osteoarthritis. A population-based cohort study[J]. Osteoarthritis Cartilage, 2009, 17(2): 168-173.
[118]
Courties A, Berenbaum F, Sellam J, et al. The phenotypic approach to osteoarthritis: a look at metabolic syndrome-associated osteoarthritis[J]. Joint Bone Spine, 2019, 86(6): 725-730.
[119]
Veronese N, Stubbs B, Solmi M, et al. Knee osteoarthritis and risk of hypertension: a longitudinal cohort study[J]. Rejuvenation Res, 2018, 21(1): 15-21.
[120]
Lo GH, Mcalindon TE, Katz JN, et al. Systolic and pulse pressure associate with incident knee osteoarthritis: data from the Osteoarthritis Initiative[J]. Clin Rheumatol, 2017, 36(9): 2121-2128.
[121]
Funck-Brentano T, Nethander M, Movérare-Skrtic S, et al. Causal factors for knee, hip, and hand osteoarthritis: a mendelian randomization study in the UK biobank[J]. Arthritis Rheumatol, 2019, 71(10): 1634-1641.
[122]
Wen C. High blood pressure and osteoarthritis: friends or Foes? comment on the article by funck-brentano et al[J]. Arthritis Rheumatol, 2019, 71(12): 2131-2132.
[123]
Gkretsi V, Simopoulou T, Tsezou A. Lipid metabolism and osteoarthritis: lessons from atherosclerosis[J]. Prog Lipid Res, 2011, 50(2): 133-140.
[124]
Alarfaj AS. Radiographic osteoarthritis and serum cholesterol[J]. Saudi Med J, 2003, 24(7): 745-747.
[125]
Choi WS, Lee G, Song WH, et al. The CH25H-CYP7B1-RORα axis of cholesterol metabolism regulates osteoarthritis[J]. Nature, 2019, 566(7743): 254-258.
[126]
Aspden RM, Scheven BA, Hutchison JD. Osteoarthritis as a systemic disorder including stromal cell differentiation and lipid metabolism[J]. Lancet, 2001, 357(9262): 1118-1120.
[127]
Ioan-Facsinay A, Kloppenburg M. Bioactive lipids in osteoarthritis: risk or benefit?[J]. Curr Opin Rheumatol, 2018, 30(1): 108-113.
[128]
Xie Y, Zhou W, Zhong Z, et al. Metabolic syndrome, hypertension, and hyperglycemia were positively associated with knee osteoarthritis, while dyslipidemia showed no association with knee osteoarthritis[J]. Clin Rheumatol, 2021, 40(2): 711-724.
[129]
Dubey NK, Ningrum D, Dubey R, et al. Correlation between diabetes mellitus and knee osteoarthritis: a dry-to-wet lab approach[J]. Int J Mol Sci, 2018, 19(10): 3021. DOI: 10.3390/ijms19103021.
[130]
Njoto I, Kalim H, Soeatmadji DW, et al. Effect of hyperglycemia to the mRNA level and protein expression of perlecan at rat model of osteoarthritis with diabetes mellitus type 1[J]. Med Arch, 2019, 73(3): 144-148.
[131]
Hiraiwa H, Sakai T, Mitsuyama H, et al. Inflammatory effect of advanced glycation end products on human meniscal cells from osteoarthritic knees[J]. Inflamm Res, 2011, 60(11): 1039-1048.
[132]
Veronese N, Cooper C, Jy R, et al. Type 2 diabetes mellitus and osteoarthritis[J]. Semin Arthritis Rheum, 2019, 49(1): 9-19.
[133]
El Karib AO, Al-Ani B, Al-Hashem F, et al. Insulin and Vanadium protect against osteoarthritis development secondary to diabetes mellitus in rats[J]. Arch Physiol Biochem, 2016, 122(3): 148-154.
[134]
Rice SJ, Beier F, Young DA, et al. Interplay between genetics and epigenetics in osteoarthritis[J]. Nat Rev Rheumatol, 2020, 16(5): 268-281.
[135]
Grandi FC, Bhutani N. Epigenetic therapies for osteoarthritis[J]. Trends Pharmacol Sci, 2020, 41(8): 557-569.
[136]
Fathollahi A, Aslani S, Jamshidi A, et al. Epigenetics in osteoarthritis: novel spotlight[J]. J Cell Physiol, 2019, 234(8): 12309-12324.
[137]
文星钊,张志奇.非编码RNA在骨关节炎中的研究进展[J/CD].中华关节外科杂志(电子版)202014(2):189-195.
[138]
Maruotti N, Corrado A, Cantatore FP. Osteoblast role in osteoarthritis pathogenesis[J]. J Cell Physiol, 2017, 232(11): 2957-2963.
[139]
Burr DB, Gallant MA. Bone remodelling in osteoarthritis[J]. Nat Rev Rheumatol, 2012, 8(11): 665-673.
[140]
杨明义,马尧,许珂,等.软骨下骨硬化在骨关节炎发病机制中的作用研究[J/CD].中华关节外科杂志(电子版)202014(5):602-607.
[141]
Jiang LS, Zhang ZM, Jiang SD, et al. Differential bone metabolism between postmenopausal women with osteoarthritis and osteoporosis[J]. J Bone Miner Res, 2008, 23(4): 475-483.
[1] 刘欢颜, 华扬, 贾凌云, 赵新宇, 刘蓓蓓. 颈内动脉闭塞病变管腔结构和血流动力学特征分析[J]. 中华医学超声杂志(电子版), 2023, 20(08): 809-815.
[2] 马艳波, 华扬, 刘桂梅, 孟秀峰, 崔立平. 中青年人颈动脉粥样硬化病变的相关危险因素分析[J]. 中华医学超声杂志(电子版), 2023, 20(08): 822-826.
[3] 陈旭渊, 罗仕云, 李文忠, 李毅. 腺源性肛瘘经手术治疗后创面愈合困难的危险因素分析[J]. 中华普外科手术学杂志(电子版), 2024, 18(01): 82-85.
[4] 唐旭, 韩冰, 刘威, 陈茹星. 结直肠癌根治术后隐匿性肝转移危险因素分析及预测模型构建[J]. 中华普外科手术学杂志(电子版), 2024, 18(01): 16-20.
[5] 吴方园, 孙霞, 林昌锋, 张震生. HBV相关肝硬化合并急性上消化道出血的危险因素分析[J]. 中华普外科手术学杂志(电子版), 2024, 18(01): 45-47.
[6] 倪文凯, 齐翀, 许小丹, 周燮程, 殷庆章, 蔡元坤. 结直肠癌患者术后发生延迟性肠麻痹的影响因素分析[J]. 中华结直肠疾病电子杂志, 2023, 12(06): 484-489.
[7] 王旭, 师绍敏, 毛燕, 季上, 刘亚玲. 肝酶代谢与骨关节炎相关性的研究进展[J]. 中华老年骨科与康复电子杂志, 2023, 09(06): 379-384.
[8] 侯超, 潘美辰, 吴文明, 黄兴广, 李翔, 程凌雪, 朱玉轩, 李文波. 早期食管癌及上皮内瘤变内镜黏膜下剥离术后食管狭窄的危险因素[J]. 中华消化病与影像杂志(电子版), 2023, 13(06): 383-387.
[9] 张雯, 宋牡丹, 邓雪婷, 张云. 强化营养支持辅助奥曲肽治疗肝硬化合并食管胃底静脉曲张破裂出血的疗效及再出血危险因素[J]. 中华消化病与影像杂志(电子版), 2023, 13(06): 456-460.
[10] 陆猛桂, 黄斌, 李秋林, 何媛梅. 蜂蛰伤患者发生多器官功能障碍综合征的危险因素分析[J]. 中华临床医师杂志(电子版), 2023, 17(9): 1010-1015.
[11] 李达, 张大涯, 陈润祥, 张晓冬, 黄士美, 陈晨, 曾凡, 陈世锔, 白飞虎. 海南省东方市幽门螺杆菌感染现状的调查与相关危险因素分析[J]. 中华临床医师杂志(电子版), 2023, 17(08): 858-864.
[12] 李琪, 黄钟莹, 袁平, 关振鹏. 基于某三级医院的ICU多重耐药菌医院感染影响因素的分析[J]. 中华临床医师杂志(电子版), 2023, 17(07): 777-782.
[13] 孟科, 李燕, 闫婧爽, 闫斌. 胶囊内镜胃通过时间的影响因素分析[J]. 中华临床医师杂志(电子版), 2023, 17(06): 671-675.
[14] 杨艳丽, 陈昱, 赵若辰, 杜伟, 马海娟, 许珂, 张莉芸. 系统性红斑狼疮合并血流感染的危险因素及细菌学分析[J]. 中华临床医师杂志(电子版), 2023, 17(06): 694-699.
[15] 孙培培, 张二明, 时延伟, 赵春燕, 宋萍萍, 张硕, 张克, 周玉娇, 赵璨, 闫维, 吴蓉菊, 宋丽萍, 郭伟安, 马石头, 安欣华, 包曹歆, 向平超. 北京市石景山区40岁及以上居民慢性阻塞性肺疾病患病情况及相关危险因素分析[J]. 中华临床医师杂志(电子版), 2023, 17(06): 711-719.
阅读次数
全文


摘要