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關節退行性變-德國重要研究發現

来源:www.uuuwell.com  2020-11-21 12:48

   

  老人面對關節退行性變引起的疼痛很普遍,輕則行動不便,重者撐拐杖坐輪椅,生活素質大受影響;近年來,隨著手機的刷屏習慣,大量的年輕男女都成了低頭族,頸椎退行性變問題(包括富貴包)越來越普及,甚至手指的關節也出現不同程度的勞損退行性變。

  關節退行性變導致

  一、關節軟骨進行性勞損和破壞;二、軟骨下骨增厚;三、骨刺形成滑膜炎;四、膝關節韌帶半月板變性;五、關節囊肥大(7,8,9,10,11,12)

  主要臨床癥狀

  一、慢性疼痛;二、關節不穩;三、關節僵硬;四、關節間隙狹窄(18,19)

  

  成因:

  炎症炎症介質通過MMPs和ADAMTS活性的增加導致軟骨ECM降解(13,14,15,16,17)

  老化:老化細胞表現出氧化應激增加,從而促進細胞衰老並改變線粒體功能(20,21,22,23)

  肥胖:除了增加膝關節的生物力學負荷外,肥胖還被認為通過分泌脂肪組織來源的細胞因子(稱為脂肪因子)而導致低級別的全身炎症。(24,25,26)

  運動勞動損傷、機械性磨損

  創傷相關的運動損傷可引起骨、軟骨、韌帶和半月板損傷,所有這些都會對關穩定產生負面影響(26,27,28);軟骨組織撕裂、關節脫位韌帶拉傷和撕裂是臨床上最常見的可能導致關節炎的損傷(29,30)。

  遺傳傾向性:

  主要通過誘導軟骨細胞分解反應來促進關節炎的發展和進展(6);成纖維細胞生長因子(FGF)通路的改變主要通過誘導軟骨細胞分解反應來促進關節炎的發展和進展(31,32,33,34,35,36)

  當我們面對關節退行性變導致的疼痛,目前在藥物上面的治療,廣泛使用的是氨基葡萄糖,但治療效果差強人意。關於氨基葡萄糖的問題,國際上也有了更新的研究,這個研究成果我們以後再專門介紹。我們現在有更安全更理想的修補方案可選擇。

  今天就跟大家探討一下德國最新的一些與關節退行性變有關的新臨床研究。先探討關節退行性變導致的疼痛或者行動不便,甚至坐輪椅撐拐杖;以後還會與大家探討別的關節問題,包括痛的要命的痛風、還有類風濕XX節炎、強直性脊椎炎等等。希望大家多加留意或者關注我們。

  早於2000年時,克利夫蘭大學醫院的Moskowitz RW博士等人已進行了膠原水解物在骨關節疾病中的作用(2,37);2016和2017 M Schunck 及S Oesser兩位學者在德國的研究發現,用新鮮牛皮提煉的可以修復關節軟組織,促進軟骨的再生。水解骨膠原蛋白是膠原蛋白的水解產物,與關節軟骨中主要成分2型的膠原蛋白相似(3)。與大分子的膠原相比,水解產物更容易被人體吸收,用來修補因關節退行性變而導致的關節軟骨的流失,同時減少關節的疼痛(1,5)。

  

  此外,德國弗賴堡大學施瓦茲沃德斯特爾分校的Daniel KönigSteffen Oesser, Stephan Scharla, Denise Zdzieblik及 Albert Gollhofer 等學者在2018年的另一項研究,發現每天口服5克的水解骨膠原蛋白,可以增加停經后婦女腰椎股骨頸密度,大大緩解礦物元素流失而引起的骨質疏鬆症的風險(4)。

  水解骨膠原蛋白也可以刺激韌帶細胞外基質的生物合成,在2013年的研究發現,水解骨膠原蛋白可以增加50%彈性蛋白生物的合成,同時增加了2.4倍的膠原蛋白的合成,在預防韌帶和肌腱病理性的病變起到了積極的作用(3)。

  

  除了針對軟組織的修補外,醫學界同時還要面對其它關節退行性變的挑戰;怎樣解決關節內粘連(Intraarticular adhesion)(38)、纖維化(fibrosis)()、軟骨鈣化(cartilage calcification) (40)(骨刺-骨質增生)問題。因要解決骨關節整體退行性變問題,修補軟組織只完成小部份任務;發炎、粘連、纖維化、軟骨鈣化也需要別的研究突破來處理的,所以我們必須從生物醫學營養醫學等各方面,全面去研究。 希望國內相關大學、醫學院、科研機構也能投入更多資源、精力在相關領域的臨床研究,能夠超越歐美成就,帶領醫學XX新階段! 下次再跟大家分享更多國際上的新研究;如痛風、強直性脊椎炎、類風濕XX節炎等等。有興趣了解更多關節研究話題的,歡迎關注我們。

  身邊如果有任何人正在面對關節疼痛的問題,歡迎大家把這一篇內容轉發給他們。希望這些學術研究成果能為他們帶來新的希望,為他們帶來更理想的治療方案。

  本文章屬於拜塞復康中心團隊原創,如要轉載請聯同作者機構一併轉發,否則需取得作者書面同意方能節錄引用。

  醫學文章需要專業、認真、嚴謹的態度,您的轉發和點贊會成為我們的重大動力,謝謝。

  原創:拜塞復康中心

  張陽生(顧醫生)、高建偉(顧問醫生)

  歐陽宏基(香港脊骨神經科醫生)、

  馬圓(英國註冊營養師)、施丹虹(香港營養學家)

  鄭志雄(加拿大放XX影像物理學家)

  了解更多

  參考文獻:

  1.Bakilan F, et al. (2016) "Effects of Native Type II Collagen Treatment on Knee Osteoarthritis: A Randomized Controlled Trial." The Eurasian Journal of Medicine. 48(2): 95-101

  2.Moskowitz RW et al. Role of collagen hydrolysate in bone and joint disease. Seminars in arthritis and rheumatism Vol 30, No 2 (Oct) 2000 pp87-99.

  3.Schunk M, et al. (2013) "Specific collagen peptides benefit the biosynthesis of matrix molecules of tendons and ligament." Journal of the international Society of Sports Nutrition. 10(1):23

  4.Oesser S, et al. (2018) "Specific Collagen Peptides Improve Bone Mineral Density and Bone Markers in Postmenopausal Women—A Randomized Controlled Study." Nutrients. 10(1):97.

  5.Oesser S, et al. (2017) "Improvement of activity-related knee joint discomfort following supplementation of specific collagen peptides." Applied Physiology, Nutrition, and Metabolism. 42: 588–595

  6.Modulating hedgehog signaling can attenuate the severity of osteoarthritis.Lin AC, Seeto BL, Bartoszko JM, Khoury MA, Whetstone H, Ho L, Hsu C, Ali SA, Alman BA Nat Med. 2009 Dec; 15(12):1421-5.

  7.Osteoarthritis: a disease of the joint as an organ.Loeser RF, Goldring SR, Scanzello CR, Goldring MB Arthritis Rheum. 2012 Jun; 64(6):1697-707.

  8.Loeser RF, Goldring SR, Scanzello CR et al. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum 2012; 64: 1697–1707.

  9.Felson DT. Clinical practice. Osteoarthritis of the knee. N Engl J Med 2006; 354: 841–848.

  10.Goldring MB, Goldring SR. Osteoarthritis. J Cell Physiol 2007; 213: 626–634.

  11.Krasnokutsky S, Samuels J, Abramson SB. Osteoarthritis in 2007. Bull NYU Hosp Jt Dis 2007; 65: 222–228.

  12.Loeser RF. Aging and osteoarthritis: the role of chondrocyte senescence and aging changes in the cartilage matrix. Osteoarthritis Cartilage 2009; 17: 971–979.

  13.Kim JH, Jeon J, Shin M et al. Regulation of the catabolic cascade in osteoarthritis by the zinc-ZIP8-MTF1 axis. Cell 2014; 156: 730–743.

  14.Hirata M, Kugimiya F, Fukai A et al. C/EBPbeta and RUNX2 cooperate to degrade cartilage with MMP-13 as the target and HIF-2alpha as the inducer in chondrocytes. Hum Mol Genet 2012; 21: 1111–1123.

  15.Little CB, Barai A, Burkhardt D et al. Matrix metalloproteinase 13-deficient mice are resistant to osteoarthritic cartilage erosion but not chondrocyte hypertrophy or osteophyte development. Arthritis Rheum 2009; 60: 3723–3733.

  16.Glasson SS, Askew R, Sheppard B et al. Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis. Nature 2005; 434: 644–648.

  17.Barnholtz-Sloan JS, Severson RK, Stanton B et al. Pediatric brain tumors in non-Hispanics, Hispanics, African Americans and Asians: differences in survival after diagnosis. Cancer Causes Control 2005; 16: 587–592.

  18.Clinical practice. Osteoarthritis of the knee. Felson DT N Engl J Med. 2006 Feb 23; 354(8):841-8.

  19.Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, Gabriel S, Hirsch R, Hochberg MC, Hunder GG, Jordan JM, Katz JN, Kremers HM, Wolfe F, National Arthritis Data Workgroup. Arthritis Rheum. 2008 Jan; 58(1):26-35.

  20.Loeser RF. Aging and osteoarthritis. Curr Opin Rheumatol 2011; 23: 492–496.

  21.Kim J, Xu M, Xo R et al. Mitochondrial DNA damage is involved in apoptosis caused by pro-inflammatory cytokines in human OA chondrocytes. Osteoarthritis Cartilage 2010; 18: 424–432.

  22.Goodwin W, McCabe D, Sauter E et al. Rotenone prevents impact-induced chondrocyte death. J Orthop Res 2010; 28: 1057–1063.

  23.Naik E, Dixit VM. Mitochondrial reactive oxygen species drive proinflammatory cytokine production. J Exp Med 2011; 208: 417–420.

  24.Conde J, Scotece M, Gomez R et al. Adipokines and osteoarthritis: novel molecules involved in the pathogenesis and progression of disease. Arthritis 2011; 2011: 2001.

  25.Das UN. Is obesity an inflammatory condition? Nutrition 2001; 17: 953–966. Fain JN. Release of inflammatory mediators by human adipose tissue is enhanced in obesity and primarily by the nonfat cells: a review. Mediators Inflamm 2010; 2010: 5148.

  26.Radin EL. Who gets osteoarthritis and why? J Rheumatol Suppl, 2004; 70: 10–15.

  27.Andriacchi TP, Mundermann A, Smith RL et al. A framework for the in vivo pathomechanics of osteoarthritis at the knee. Ann Biomed Eng 2004; 32: 447–457.

  28.Miyazaki T, Wada M, Kawahara H et al. Dynamic load at baseline can predict radiographic disease progression in medial compartment knee osteoarthritis. Ann Rheum Dis 2002; 61: 617–622.

  29.Fridén T, Sommerlath K, Egund N et al. Instability after anterior cruciate ligament rupture. Measurements of sagittal laxity compared in 11 cases. Acta Orthop Scand 1992; 63: 593–598. Sernert N, Kartus JT Jr, Ejerhed L et al. Right and left knee laxity measurements: a prospective study of patients with anterior cruciate ligament injuries and normal control subjects. Arthroscopy 2004; 20: 564–571.

  30.Modulating hedgehog signaling can attenuate the severity of osteoarthritis. Lin AC, Seeto BL, Bartoszko JM, Khoury MA, Whetstone H, Ho L, Hsu C, Ali SA, Alman BA Nat Med. 2009 Dec; 15(12):1421-5.

  31.Serra R, Johnson M, Filvaroff EH et al. Expression of a truncated, kinase-defective TGF-beta type II receptor in mouse skeletal tissue promotes terminal chondrocyte differentiation and osteoarthritis. J Cell Biol 1997; 1: 541–552.

  32.Shen J, Li J, Wang B et al. Deletion of the transforming growth factor beta receptor type II gene in articular chondrocytes leads to a progressive osteoarthritis-like phenotype in mice. Arthritis Rheum 2013; 65: 3107–3119.

  33.Wang M, Tang D, Shu B et al. Conditional activation of beta-catenin signaling in mice leads to severe defects in intervertebral disc tissue. Arthritis Rheum 2012; 64: 2611–2623.

  34.Mirando AJ, Liu Z, Moore T et al. RBP-Jkappa-dependent Notch signaling is required for murine articular cartilage and joint maintenance. Arthritis Rheum 2013; 65: 2623–2633.

  35.Lories RJ, Corr M, Lane NE. To Wnt or not to Wnt: the bone and joint health dilemma. Nat Rev Rheumatol 2013; 9: 328–3.

  36.Sassi N, Laadhar L, Allouche M et al. WNT signaling and chondrocytes: from cell fate determination to osteoarthritis physiopathology. J Recept Signal Transduct Res 2014; 34: 73–80.

  37.From the Case Western Reserve University; Division of Rheumatic Diseases, University Hospitals of Cleveland, OH. Roland W. Moskowitz, MD: Professor of Medicine, Case Western Reserve University; Director, Division of Rheumatic Diseases, University Hospitals of Cleveland Dr. Moskowitz was the Principal Investigator and Con-sultant for a study on pharmaceutical collagen hydrolysate for DGF Stoess. doi:10.1053/sarh.2000.9622

  38.Osteoarthritic cartilage fibrillation is associated with a decrease in chondrocyte adhesion to fibronectin By Muriel Piperno,Pascal Reboul†, Marie-Pierre Hellio le Graverand,Mj Peschard †,Marliese Annefeld‡, M. Richard† and Eric Vignon Claude Bernard University. Centre Hospitalier Lyon Sud, 165 chemin du Grand Revoyet, 69495 Pierre Be nite; †Department of Biochemistry, INSERM-CNRS U189, Lyon Sud Medical School, BP 12, 6992

  .Treatment and Rehabilitation of Arthrofibrosis of the KneeScott E. Lawrance MS, PT, ATC, CSCS, K. Donald Shelbourne MD, in Clinical Orthopaedic Rehabilitation: a Team Approach (Fourth Edition), 2018

  40.CALCIFICATION OF HUMAN ARTICULAR KNEE CARTILAGE IS PRIMARILY AN EFFECT OF AGING RATHER THAN OSTEOARTHRITIS. H Mitsuyama,* RM Healey,* RA Terkeltaub,# RD Coutts,* and D Amiel*