索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]李鹏飞,杨永泽,马国榕,等.骨关节炎疼痛机制研究进展[J].国际骨科学杂志,2024,02:136-140.
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骨关节炎疼痛机制研究进展(PDF)

《国际骨科学杂志》[ISSN:1673-7083/CN:31-1952/R]

期数:
2024年02期
页码:
136-140
栏目:
综述
出版日期:
2024-03-25

文章信息/Info

Title:
-
作者:
李鹏飞; 杨永泽; 马国榕; 高玉婷; 张佳豪; 郭洪章; 金晓东
730000? 甘肃兰州，? 甘肃中医药大学第一临床医学院?（李鹏飞、杨永泽、马国榕）；730000? 甘肃兰州，? 甘肃省人民医院骨科（李鹏飞、杨永泽、马国榕、郭洪章）；730070? 甘肃兰州，? 中国科学院近代物理研究所（高玉婷、张佳豪、金晓东）；730000? 甘肃兰州，? 西北师范大学（高玉婷）；730000? 甘肃兰州，? 兰州大学（张佳豪）
Author(s):
-
关键词:
骨关节炎;  疼痛; 机制
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-7083.2024.02.013
文献标识码:
-
摘要:
骨关节炎（OA）是最常见的关节疾病，也是中老年人疼痛与残疾的主要原因。目前临床上有药物可以缓解OA的疼痛，但效果并不令人满意。疼痛是一种复杂的体验，整合炎症及外周和中枢伤害因素相关的感觉、情感和认知过程。目前关于OA相关疼痛的机制仍不清楚。该文就OA疼痛机制研究进展进行综述。
Abstract:
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参考文献/References

[1] Safiri S, Kolahi AA, Smith E, et al. Global, regional and national burden of osteoarthritis 1990-2017: a systematic analysis of the Global Burden of Disease Study 2017[J]. Ann Rheum Dis, 2020, 79(6): 819-828.
[2] Chen D, Shen J, Zhao W, et al. Osteoarthritis: toward a comprehensive understanding of pathological mechanism[J]. Bone Res, 2017, 5: 16044.
[3] Katz JN, Arant KR, Loeser RF. Diagnosis and treatment of hip and knee osteoarthritis: a review[J]. JAMA, 2021, 325(6): 568-578.
[4] Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises[J]. Pain, 2020, 161(9): 1976-1982.
[5.] Cohen SP, Vase L, Hooten WM. Chronic pain: an update on burden, best practices, and new advances[J]. Lancet, 2021, 397(10289): 2082-2097.
[6] Song J, Chang AH, Chang RW, et al. Relationship of knee pain to time in moderate and light physical activities: data from osteoarthritis initiative[J]. Semin Arthritis Rheum, 2018, 47(5): 683-688.
[7] Motta F, Barone E, Sica A, et al. Inflammaging and osteoarthritis[J]. Clin Rev Allergy Immunol, 2023, 64(2): 222-238.
[8] Mezey GA, Máté Z, Paulik E. Factors influencing pain management of patients with osteoarthritis: a cross-sectional study[J]. J Clin Med, 2022, 11(5): 1352.
[9] Salaffi F, Ciapetti A, Carotti M. The sources of pain in osteoarthritis:a pathophysiological review[J]. Reumatismo, 2014, 66(1): 57-71.
[10] Zhang Y, Nevitt M, Niu J, et al. Fluctuation of knee pain and changes in bone marrow lesions, effusions, and synovitis on magnetic resonance imaging[J]. Arthritis Rheum, 2011, 63(3): 691-699.
[11] Hill CL, Gake DG, Chaisson CE, et al. Knee effusions, popliteal cysts, and synovial thickening: association with knee pain in osteoarthritis[J]. J Rheumatol, 2001, 28(6): 1330-1337.
[12] Emmi A, Stocco E, Boscolo-Berto R, et al. Infrapatellar fat pad-synovial membrane anatomo-fuctional unit: microscopic basis for Piezo1/2 mechanosensors involvement in osteoarthritis pain[J]. Front Cell Dev Biol, 2022, 10: 886604.
[13] Zhang H, Wang L, Cui J, et al. Maintaining hypoxia environment of subchondral bone alleviates osteoarthritis progression[J]. Sci Adv, 2023, 9(14): eabo7868.
[14] Bamps D, Vriens J, de Hoon J, et al. TRP channel cooperation for nociception: therapeutic opportunities[J]. Annu Rev Pharmacol Toxicol, 2021, 61: 655-677.
[15] Vincent TL. Peripheral pain mechanisms in osteoarthritis[J]. Pain, 2020, 161 Suppl 1(1): S138-S146.
[16] St?ckl S, Eitner A, Bauer RJ, et al. Substance P and alpha-calcitonin gene-related peptide differentially affect human osteoarthritic and healthy chondrocytes[J]. Front Immunol, 2021, 12: 722884.
[17] Soni A, Wanigasekera V, Mezue M, et al. Central sensitization in knee osteoarthritis: relating presurgical brainstem neuroimaging and painDETECT-based patient stratification to arthroplasty outcome[J]. Arthritis Rheumatol, 2019, 71(4): 550-560.
[18] Fu K, Robbins SR, McDougall JJ. Osteoarthritis: the genesis of pain[J]. Rheumatology (Oxford), 2018, 57(suppl_4): iv43-iv50.
[19] Hochman JR, French MR, Bermingham SL, et al. The nerve of osteoarthritis pain[J]. Arthritis Care Res (Hoboken), 2010, 62(7):1019-1023.
[20] O'Neill TW, Felson DT. Mechanisms of osteoarthritis (OA) pain[J]. Curr Osteoporos Rep, 2018, 16(5): 611-616.
[21] Eitner A, Hofmann GO, Schaible HG. Mechanisms of osteoarthritic pain. Studies in humans and experimental models[J]. Front Mol Neurosci, 2017, 10: 349.
[22] Dainese P, Wyngaert KV, de Mits S, et al. Association between knee inflammation and knee pain in patients with knee osteoarthritis: a systematic review[J]. Osteoarthritis Cartilage, 2022, 30(4): 516-534.
[23] Jrad AIS, Trad M, Bzeih W, et al. Role of pro-inflammatory interleukins in osteoarthritis: a narrative review[J]. Connect Tissue Res, 2023, 64(3): 238-247.
[24] Miller RE, Miller RJ, Malfait AM. Osteoarthritis joint pain: the cytokine connection[J]. Cytokine, 2014, 70(2): 185-193.
[25] Hattori T, Shimo K, Niwa Y, et al. Association of chronic pain with radiologic severity and central sensitization in hip osteoarthritis patients[J]. J Pain Res, 2021, 14: 1153-1160.
[26] Bjurstr?m MF, Blennow K, Zetterberg H, et al. Central nervous system monoaminergic activity in hip osteoarthritis patients with disabling pain: associations with pain severity and central sensitization[J]. Pain Rep, 2022, 7(1): e988.
[27] Ohashi Y, Fukushima K, Uchida K, et al. Adverse effects of higher preoperative pain at rest, a central sensitization-related symptom, on outcomes after total hip arthroplasty in patients with osteoarthritis[J]. J Pain Res, 2021, 14: 3345-3352.
[28] Iyengar S, Ossipov MH, Johnson KW. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine[J]. Pain, 2017, 158(4): 543-559.
[29] Russo AF. Calcitonin gene-related peptide (CGRP): a new target for migraine[J]. Annu Rev Pharmacol Toxicol, 2015, 55: 533-552.
[30] Walsh DA, Mapp PI, Kelly S. Calcitonin gene-related peptide in the joint: contributions to pain and inflammation[J]. Br J Clin Pharmacol, 2015, 80(5): 965-978.
[31] Bullock CM, Wookey P, Bennett A, et al. Peripheral calcitonin gene-related peptide receptor activation and mechanical sensitization of the joint in rat models of osteoarthritis pain[J]. Arthritis Rheumatol, 2014, 66(8): 2188-2200.
[32] Zhang Y, Xu J, Ruan YC, et al. Implant-derived magnesium induces local neuronal production of CGRP to improve bone-fracture healing in rats[J]. Nat Med, 2016, 22(10): 1160-1169.
[33] Dong T, Chang H, Zhang F, et al. Calcitonin gene-related peptide can be selected as a predictive biomarker on progression and prognosis of knee osteoarthritis[J]. Int Orthop, 2015, 39(6): 1237-1243.
[34] Benschop RJ, Collins EC, Darlling RJ, et al. Development of a novel antibody to calcitonin gene-related peptide for the treatment of osteoarthritis-related pain[J]. Osteoarthritis Cartilage, 2014, 22(4):578-585.
[35] Powell R, Young VA, Pryce KD, et al. Inhibiting endocytosis in CGRP(+) nociceptors attenuates inflammatory pain-like behavior[J]. Nat Commun, 2021, 12(1): 5812.
[36] De Logu F, Nassini R, Hegron A, et al. Schwann cell endosome CGRP signals elicit periorbital mechanical allodynia in mice[J]. Nat Commun, 2022, 13(1): 646.
[37] Uchida K, Takano S, Takata K, et al. Differential synovial CGRP/RAMP1 expression in men and women with knee osteoarthritis[J]. Cureus, 2021, 13(6): e15483.
[38] Yoshimura T, Robinson EA, Tanaka S, et al. Purification and amino acid analysis of two human glioma-derived monocyte chemoattractants[J]. J Exp Med, 1989, 169(4): 1449-1459.
[39] White GE, Iqbal AJ, Greaves DR. CC chemokine receptors and chronic inflammation: therapeutic opportunities and pharmacological challenges[J]. Pharmacol Rev, 2013, 65(1): 47-89.
[40] Zhu S, Liu M, Bennett S, et al. The molecular structure and role of CCL2 (MCP-1) and C-C chemokine receptor CCR2 in skeletal biology and diseases[J]. J Cell Physiol, 2021, 236(10): 7211-7222.
[41] Miller RE, Tran PB, Das R, et al. CCR2 chemokine receptor signaling mediates pain in experimental osteoarthritis[J]. Proc Natl Acad Sci U S A, 2012, 109(50): 20602-20607.
[42] Raghu H, Lepus CM, Wang Q, et al. CCL2/CCR2, but not CCL5/CCR5, mediates monocyte recruitment, inflammation and cartilage destruction in osteoarthritis[J]. Ann Rheum Dis, 2017, 76(5): 914-922.
[43] Ishihara S, Obeidat AM, Wokosin DL, et al. The role of intra-articular neuronal CCR2 receptors in knee joint pain associated with experimental osteoarthritis in mice[J]. Arthritis Res Ther, 2021, 23(1):103.
[44] Auw Yang KG, Raijmakers NJ, van Arkel ER, et al. Autologous interleukin-1 receptor antagonist improves function and symptoms in osteoarthritis when compared to placebo in a prospective randomized controlled trial[J]. Osteoarthritis Cartilage, 2008, 16(4): 498-505.
[45] Maksymowych WP, Russell AS, Chiu P, et al. Targeting tumour necrosis factor alleviates signs and symptoms of inflammatory osteoarthritis of the knee[J]. Arthritis Res Ther, 2012, 14(5): R206.
[46] Leung YY, Huebner JL, Haaland B, et al. Synovial fluid pro-inflammatory profile differs according to the characteristics of knee pain[J]. Osteoarthritis Cartilage, 2017, 25(9): 1420-1427.
[47] Li L, Li Z, Li Y, et al. Profiling of inflammatory mediators in the synovial fluid related to pain in knee osteoarthritis[J]. BMC Musculoskelet Disord, 2020, 21(1): 99.
[48] Orita S, Ishikawa T, Miyagi M, et al. Percutaneously absorbed NSAIDs attenuate local production of proinflammatory cytokines and suppress the expression of c-Fos in the spinal cord of a rodent model of knee osteoarthritis[J]. J Orthop Sci, 2012, 17(1): 77-86.
[49] Richter F, Natura G, Loser S, et al. Tumor necrosis factor causes persistent sensitization of joint nociceptors to mechanical stimuli in rats[J]. Arthritis Rheum, 2010, 62(12): 3806-3814.
[50] Hempstead BL, Martin-Zanca D, Kaplan DR, et al. High-affinity NGF binding requires coexpression of the trk proto-oncogene and the low-affinity NGF receptor[J]. Nature, 1991, 350(6320): 678-683.
[51] Malfait AM, Miller RE, Miller RJ. Basic mechanisms of pain in osteoarthritis: experimental observations and new perspectives[J]. Rheum Dis Clin North Am, 2021, 47(2): 165-180.
[52] Ohashi Y, Uchida K, Fukushima K, et al. NGF expression and elevation in hip osteoarthritis patients with pain and central sensitization[J]. Biomed Res Int, 2021, 2021: 9212585.
[53] Skaper SD. Nerve growth factor: a neuroimmune crosstalk mediator for all seasons[J]. Immunology, 2017, 151(1): 1-15.
[54] Ohashi Y, Uchida K, Fukushima K, et al. Correlation between CD163 expression and resting pain in patients with hip osteoarthritis:Possible contribution of CD163+ monocytes/macrophages to pain pathogenesis[J]. J Orthop Res, 2022, 40(6): 1365-1374.
[55] Kc R, Li X, Kroin JS, et al. PKCδ null mutations in a mouse model of osteoarthritis alter osteoarthritic pain independently of joint pathology by augmenting NGF/TrkA-induced axonal outgrowth[J]. Ann Rheum Dis, 2016, 75(12): 2133-2141.
[56] Zhao L, Huang J, Fan Y, et al. Exploration of CRISPR/Cas9-based gene editing as therapy for osteoarthritis[J]. Ann Rheum Dis, 2019, 78(5): 676-682.
[57] Lane NE, Schnitzer TJ, Birbara CA, et al. Tanezumab for the treatment of pain from osteoarthritis of the knee[J]. N Engl J Med, 2010, 363(16): 1521-1531.
[58] Swanson KV, Deng M, Ting JP. The NLRP3 inflammasome:molecular activation and regulation to therapeutics[J]. Nat Rev Immunol, 2019, 19(8): 477-489.
[59] Yu H, Yao S, Zhou C, et al. Morroniside attenuates apoptosis and pyroptosis of chondrocytes and ameliorates osteoarthritic development by inhibiting NF-κB signaling[J]. J Ethnopharmacol, 2021, 266:113447.
[60] Liu CC, Huang ZX, Li X, et al. Upregulation of NLRP3 via STAT3-dependent histone acetylation contributes to painful neuropathy induced by bortezomib[J]. Exp Neurol, 2018, 302: 104-111.
[61] Grace PM, Strand KA, Galer EL, et al. Morphine paradoxically prolongs neuropathic pain in rats by amplifying spinal NLRP3 inflammasome activation[J]. Proc Natl Acad Sci U S A, 2016, 113(24): E3441-E3450.
[62] Cheng F, Yan FF, Liu YP, et al. Dexmedetomidine inhibits the NF-κB pathway and NLRP3 inflammasome to attenuate papain-induced osteoarthritis in rats[J]. Pharm Biol, 2019, 57(1): 649-659.

备注/Memo

备注/Memo:
基金项目：甘肃省创新基金和人才计划（20JR10RA358）、甘肃省人民医院院内科研基金（23GSSYD-9)、兰州市科技计划项目（2023-2-101）
通信作者：郭洪章? E-mail: hongzhangguo2022@126.com
? ? ? ? ? 金晓东? E-mail: jinxd@impcas.ac.cn
更新日期/Last Update: 2024-03-25