Nowa wersja platformy jest już dostępna.
Przejdź na


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników
2014 | 10 | 1 |
Tytuł artykułu

Relation between bone mineral density and IL-17 serum levels in Serbian patients with early Rheumatoid arthritis

Treść / Zawartość
Warianty tytułu
Języki publikacji
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial inflammation and destruction of joint cartilage and bone. Different cytokines play important role in the processes that cause articular destruction and extra-articular manifestations in RA. The contribution of cytokines representing the Th1 (INF-γ), Th2 (IL-4) and IL-17A to the pathogenesis of early RA and bone mineral density (BMD) loss in still poorly understood. Serum samples of 38 early RA patients were evaluated for erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), C-reactive protein (CRP), anti-cyclic citrullinated peptide antibodies (anti-CCP) and for the tested cytokines (IL-17A, IL-4 and INF-γ). BMD was evaluated by dualenergyX-ray absorptiometry (DXA). Disease activity score (DAS28) calculation was assessed for all patients. Control serum samples were obtained from 34 healthy volunteers. The levels of tested cytokines were significantly higher (IL-17A, p<0.001; INF-γ, P<0.001; IL-4, P<0.01) in patients with early RA, compared to the healthy controls. In early RA patients, strong correlation of serum IL-17A was found with DAS28, ESR and CRP. Also, a significant negative correlation was found between serum INF-γ levels and the DAS28 score. Significantly positive correlation of BMD values and CRP, DAS28 IL-17A were also demonstrated. DXA analysis revealed that the most common site for osteoporosis was the lumbar spine followed by the femoral neck. BMD values significantly correlated with CRP, DAS28 score and IL-17A serum levels. The mean serum IL-17A levels, in patients with early RA, corresponded with disease activity, severity and BMD loss, indicating the potential usefulness of serum IL-17A in defining the disease activity and bone remodeling.
Słowa kluczowe

Opis fizyczny
  • Institute of Physiology, Medical Faculty University of Nis, Nikole Uzunovica 67, 18000 Nis, Serbia
  • Institute for Treatment and Rehabilitation “Niska Banja”, Niska Banja, Serbia
  • Institute for Treatment and Rehabilitation “Niska Banja”, Niska Banja, Serbia
  • Faculty of Medicine, University of Nis, Serbia
  • Institute for Treatment and Rehabilitation “Niska Banja”, Niska Banja, Serbia
  • [1] Clifton O, Bingham 3rd. The pathogenesis of rheumatoidarthritis: pivotal cytokines involved in bone degradation andinflammation. J Rheumatol, 2002, 65, 3-9.
  • [2] Brennan FM, McInnes IB. Evidence that cytokines play a role inrheumatoid arthritis. J Clin Invest, 2008, 118, 3537-3541.[WoS]
  • [3] Firestein GS. Evolving concepts of rheumatoid arthritis. Nature,2003, 423, 356-361.
  • [4] Lubberts E. IL-17/Th17 targeting: on the road to prevent chronicdestructive arthritis? Cytokine, 2008, 41, 84-91.[WoS]
  • [5] Dong W, Zhu P. Functional niche of inflamed synovium forTh17-cell expansion and activation in rheumatoid arthritis:Implication to clinical therapeutics. Autoimmun Rev, 2012, 12,844-851.[Crossref][WoS]
  • [6] Van Hamburg JP, Asmawidjaja PS, Davelaar N, Mus AM, ColinEM, Hazes JM, Dolhain RJ, Lubberts E. Th17 cells, but not Th1cells, from patients with early rheumatoid arthritis are potentinducers of matrix metalloproteinases and proinflammatorycytokines upon synovial fibroblast interaction, includingautocrine interleukin-17A production. Arthritis Rheum, 2011,63, 73-83.[WoS]
  • [7] Lubberts E, Koenders MI, van den Berg WB. The role of T cellinterleukin-17 in conducting destructive arthritis: lessons fromanimal models. Arthritis Res Ther, 2005, 7, 29-37.[Crossref]
  • [8] Metawi SA, Abbas D, Kamal MM, Ibrahim MK. Serum andsynovial fluid levels of interleukin- 17 in correlation withdisease activity in patients with RA. Clin Rheumatol, 2011, 130,1201-1207.[WoS]
  • [9] Melis L, Vandooren B, Kruithof E, Jacques P, De Vos M,Mielants H, Verbruggen G, De Keyser F, Elewaut D. Systemiclevels of IL-23 are strongly associated with disease activity inrheumatoid arthritis but not spondyloarthritis. Ann Rheum Dis,2010, 69, 618-623.[WoS]
  • [10] Kokkonen H, Söderström I, Rocklöv J, Hallmans G, LejonK, Rantapaa Dahlqvist S. Upregulation of cytokines andchemokines predates the onset of rheumatoid arthritis.Arthritis Rheum, 2010, 62, 383-391.
  • [11] Pavlovic V, Dimic A, Milenkovic S, Krtinic D. Serum levels ofIL-17, IL-4, and INF- γ in Serbian patients with early rheumatoidarthritis. J Med Res Sci, 2014, 19, 18-22.
  • [12] Kotake S, Udagawa N, Takahashi N, Matsuzaki K, Itoh K,Ishiyama S, et al. IL-17 in synovial fluids from patients withrheumatoid arthritis is a potent stimulator of osteoclastogenesis.J Clin Invest, 1999, 103, 1345–1352.
  • [13] Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, CooperNS, Healey LA, Caplan SR, Liang MH, Luthra HS, et al. TheAmerican Rheumatism Association 1987 revised criteria for theclassification of rheumatoid arthritis. Arthritis Rheum, 1998,31, 315-324.
  • [14] Prevoo ML, van’t Hof MA, Kuper HH, van Leeuwen MA, L.B. vande Putte, van Riel PL. Modified disease activity scores thatinclude twenty-eight-joint counts. Development and validationin a prospective longitudinal study of patients with rheumatoidarthritis. Arthritis Rheum, 1995, 38, 44-48.[Crossref]
  • [15] Van der Heijde DM, van ‘t Hof MA, van Riel PL, Theunisse LA,Lubberts EW, van Leeuwen MA, van Rijswijk MH, van de PutteLB. Judging disease activity in clinical practice in rheumatoidarthritis: first step in the development of a disease activityscore. Ann Rheum Dis, 1990, 49, 916-920.
  • [16] Cummings SR, Bates D, Black DM. Clinical use of bonedensitometry: scientific review. JAMA, 2002, 288, 1889-1897.
  • [17] Haugeberg G, Uhlig T, Falch JA, Halse JI, Kvien TK. Bone mineraldensity and frequency of osteoporosis in female patients withrheumatoid arthritis: results from 394 patients in the OsloCounty Rheumatoid Arthritis register. Arthritis Rheum, 2000,43, 522-530.[Crossref]
  • [18] Tedesco A, D’Agostino D, Soriente I, Amato P, Piccoli R, SabatiniP. A new strategy for the early diagnosis of rheumatoidarthritis: a combined approach. Autoimmun Rev, 2009, 8,233-237.[WoS][Crossref]
  • [19] Laan M, Prause O, Miyamoto M, Sjostrand M, HytonenAM, Kaneko T, Lotvall J, Linden A. A role of GM-CSF in theaccumulation of neutrophils in the airways caused by IL-17 andTNF alpha. Eur Respir, 2003, 21, 387-393.[Crossref]
  • [20] Rosu A, Margaritescu C, Stepan A, Musetescu A, Ene M. IL-17patterns in synovium, serum and synovial fluid from treatmentnaïve,early rheumatoid arthritis patients. Rom J MorpholEmbryol, 2012, 53, 73-80.
  • [21] Gullick NJ, Evans HG, Church LD, Jayaraj DM, Filer A, KirkhamBW, Taams LS. Linking power Doppler ultrasound to thepresence of Th17 cells in the rheumatoid arthritis joint. PLoSOne, 2010, 5, e12516.[WoS][Crossref]
  • [22] Leipe J, Grunke M, Dechant C, Reindl C, Kerzendorf U, Schulze-Koops H, Skapenko A. Role of Th17 cells in human autoimmunearthritis. Arthritis Rheum, 2010, 62, 2876- 2885.[Crossref][WoS]
  • [23] Tukaj S, Kotlarz A, Jóźwik A, Smolenska Z, Bryl E, WitkowskiJM, Lipinska B. Cytokines of the Th1 and Th2 type in sera ofrheumatoid arthritis patients; correlations with anti- Hsp40immune response and diagnostic markers. Acta Biochim Pol,2010, 57, 327-332.
  • [24] Machold KP, Neumann K, Smolen JS. Recombinant humaninterferon gamma in the treatment of rheumatoid arthritis:double blind placebo controlled study. Ann Rheum Dis, 1992,51, 1039-1043.[Crossref]
  • [25] Morita Y, Yamamura M, Kawashima M, Harada S, Tsuji K,Shibuya K, Maruyama K, Makino H. Flow cytometric single-cellanalysis of cytokine production by CD4+ T cells in synovialtissue and peripheral blood from patients with rheumatoidarthritis. Arthritis Rheum, 1998, 41, 1669-1676.
  • [26] Raza K, Falciani F, Curnow SJ, Ross EJ, Lee CY, Akbar AN, Lord JM,Gordon C, Buckley CD, Salmon M. Early rheumatoid arthritis ischaracterized by a distinct and transient synovial fluid cytokineprofile of T cell and stromal cell origin. Arthritis Res Ther, 2005,7, R784- 795.[Crossref]
  • [27] Colin EM, Asmawidjaja PS, van Hamburg JP, Mus AM, vanDriel M, Hazes JM, van Leeuwen JP, Lubberts E. 1,25-dihydroxyvitaminD3 modulates Th17 polarization and interleukin-22expression by memory T cells from patients with earlyrheumatoid arthritis. Arthritis Rheum, 2010, 62, 132-142.[WoS]
  • [28] Lubberts E, Joosten LA, Chabaud M, van Den Bersselaar L,Oppers B, Coenen-De Roo CJ, Richards CD, Miossec P, van DenBerg WB. IL-4 gene therapy for collagen arthritis suppressessynovial IL-17 and osteoprotegerin ligand and prevents boneerosion. J Clin Invest, 2000, 105, 1697-1710.
  • [29] Parsonage G, Falciani F, Burman A, Filer A, Ross E, Bofill M,Martin S, Salmon M, Buckley CD. Global gene expressionprofiles in fibroblasts from synovial, skin and lymphoid tissuereveals distinct cytokine and chemokine expression patterns.Thromb Haemost, 2003, 90, 688-697.
  • [30] Jurisic V, Terzic T, Pavlovic S, Colovic N, Colovic M. ElevatedTNF-a and LDH without parathormone disturbance is associatedwith diffuse osteolytic lesions in leukemic transformation ofmyelofibrosis. Pathol Res Pract, 2008, 204, 129-132.[WoS]
  • [31] Jurisic V, Terzic T, Colic S, Jurisic M. The concentration ofTNF-alpha correlate with number of inflammatory cells and degreeof vascularization in radicular cysts. Oral Dis, 2008, 14, 600-605.[WoS][Crossref]
  • [32] Brand C, Lowe A, Hall S. The utility of clinical decision toolsfor diagnosing osteoporosis in postmenopausal women withrheumatoid arthritis. BMC Musculoskelet Disord, 2008, 9, 13.[WoS][Crossref]
  • [33] Laan RF, Buijs WC, Verbeek AL, Draad MP, Corstens FH, van dePutte LB, van Riel PL. Bone mineral density in patients withrecent onset rheumatoid arthritis: influence of disease activityand functional capacity. Ann Rheum Dis, 1993, 52, 21-26.[Crossref]
  • [34] Tourinho TF, Stein A, Castro JA, Brenol JC. Rheumatoid arthritis:evidence for bone loss in premenopausal women. J Rheumatol,2005, 32, 1020-1025.
  • [35] Shenstone BD, Mahmoud A, Woodward R, Elvins D, PalmerR, Ring EF, BHalla AH. Longitudinal bone mineral densitychanges in early rheumatoid arthritis. Br J Rheumatol, 1994,33, 541–545.[Crossref]
  • [36] Gough AK, Lilley J, Eyre S, Holder RL, Emery P. Generalised boneloss in patients with early rheumatoid arthritis. Lancet, 1994,344, 23-27.
  • [37] Book C, Karlsson M, Akesson K, Jacobsson L. Disease activityand disability but probably not glucocorticoid treatmentpredicts loss in bone mineral density in women with earlyrheumatoid arthritis. Scand J Rheumatol, 2008, 37, 248-254.[Crossref][WoS]
  • [38] Kroot EJ, Nieuwenhuizen MG, de Waal Malefijt MC, van Riel PL,Pasker-de Jong PC, Laan RF. Change in bone mineral density inpatients with rheumatoid arthritis during the first decade of thedisease. Arthritis Rheum, 2001, 44, 1254–1260.[Crossref]
  • [39] Dao HH, Do QT, Sakamoto J. Bone mineral density andfrequency of osteoporosis among Vietnamese women withearly rheumatoid arthritis. Clin Rheumatol, 2011, 30, 1353-1361.[Crossref][WoS]
  • [40] Green MJ, Deodhar AA. Bone changes in early rheumatoidarthritis. Best Pract Res Clin Rheumatol, 2001, 15, 105-123.[Crossref]
  • [41] Sato K, Suematsu A, Okamoto K, Yamaguchi A, MorishitaY, Kadono Y, Tanaka S, Kodama T, Akira S, Iwakura Y, Cua DJ,Takanayagi H. Th17 functions as an osteoclastogenic helper Tcell subset that links T cell activation and bone destruction. JExp Med, 2006, 203, 2673-2682.
  • [42] Lubberts E, van den Bersselaar L, Oppers-Walgreen B, SchwarzenbergerP, Coenen-de Roo CJ, Kolls JK, Joosten LA, van DenBerg WB. IL-17 promotes bone erosion in murine collageninducedarthritis through loss of the receptor activator ofNF-kappa B ligand/osteoprotegerin balance. J Immunol, 2003,170, 2655-2662.
  • [43] Kotake S, Udagawa N, Takahashi N, Matsuzaki K, Itoh K,Ishiyama S, Saito S, Inoue K, Kamatani N, Gillespie MT,Martin TJ, Suda T. IL-17 in synovial fluids from patients withrheumatoid arthritis is a potent stimulator of osteoclastogenesis.J Clin Invest, 1999, 103, 1345-1352.
  • [44] Haugeberg G, Emery P. Value of dual-energy X-ray absorptiometryas a diagnostic tool in early rheumatoid arthritis.Rheum Dis Clin Am, 2005, 31, 715-728.[Crossref]
Typ dokumentu
Identyfikator YADDA
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.