[1] Shiozawa S, Tsumiyama K, Yoshida K,et al.Pathogenesis of joint destruction in rheumatoid arthritis.Arch Immunol Ther Exp (Warsz). 2011;59(2):89-95.[2] Kawabata K, Yamamoto K.Recent advances in the pathogenesis of rheumatoid arthritis.Clin Calcium. 2009 ; 19(3):303-309.[3] Pratt AG, Isaacs JD, Mattey DL.Current concepts in the pathogenesis of early rheumatoid arthritis.Best Pract Res Clin Rheumatol. 2009;23(1):37-48.[4] Bromley M, Woolley DE.Chondroclasts and osteoclasts at subchondral sites of erosion in the rheumatoid joint. Arthritis Rheum. 1984;27(9):968-975.[5] Gravallese EM, Manning C, Tsay A,et al.Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor.Arthritis Rheum. 2000;43(2):250-258.[6] Fox DA.Cytokine blockade as a new strategy to treat rheumatoid arthritis: inhibition of tumor necrosis factor.Arch Intern Med. 2000 ;160(4):437-444.[7] Kmie? Z, Soko?owska I.Role of tumor necrosis factor family ligands in the pathogenesis of rheumatoid arthritis--new therapeutical opportunities.Pol Merkur Lekarski. 2007;22 (130):300-304.[8] Yamamura M.Tumor necrosis factor alpha and beta (TNF-alpha and -beta) in pathogenesis of rheumatoid arthritis.Nihon Rinsho. 2005;63 Suppl 1:145-152.[9] Hussein YM, Mohamed RH, Pasha HF,et al.Association of tumor necrosis factor alpha and its receptor polymorphisms with rheumatoid arthritis in female patients.Cell Immunol. 2011;271(1):192-196.[10] Colucci S, Brunetti G, Cantatore FP,et al.Lymphocytes and synovial fluid fibroblasts support osteoclastogenesis through RANKL, TNFalpha, and IL-7 in an in vitro model derived from human psoriatic arthritis.J Pathol. 2007;212(1):47-55.[11] Kobayashi N, Kadono Y, Naito A,et al.Segregation of TRAF6-mediated signaling pathways clarifies its role in osteoclastogenesis.EMBO J. 2001;20(6):1271-1280.[12] David JP, Sabapathy K, Hoffmann O,et al. JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation- dependent and -independent mechanisms.J Cell Sci. 2002; 115(Pt 22):4317-4325.[13] Asagiri M, Takayanagi H.The molecular understanding of osteoclast differentiation.Bone. 2007;40(2):251-264. [14] Takayanagi H.Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems.Nat Rev Immunol. 2007;7(4):292-304.[15] Koga T, Inui M, Inoue K,et al.Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis. Nature. 2004;428(6984):758-763.[16] Takayanagi H, Kim S, Koga T,et al.Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.Dev Cell. 2002;3(6):889-901.[17] Pageau SC.Denosumab.MAbs. 2009;1(3):210-215. [18] Wei S, Kitaura H, Zhou P,et al.IL-1 mediates TNF-induced osteoclastogenesis.J Clin Invest. 2005;115(2):282-290.[19] Hase H, Kanno Y, Kojima H,et al.Coculture of osteoclast precursors with rheumatoid synovial fibroblasts induces osteoclastogenesis via transforming growth factor beta-mediated down-regulation of osteoprotegerin.Arthritis Rheum. 2008;58(11):3356-3365.[20] Yago T, Nanke Y, Kawamoto M,et al.IL-23 induces human osteoclastogenesis via IL-17 in vitro, and anti-IL-23 antibody attenuates collagen-induced arthritis in rats.Arthritis Res Ther. 2007;9(5):R96.[21] Abe M, Hiura K, Wilde J, et al. Role for macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in the development of osteolytic lesions in multiple myeloma.Blood. 2002;100(6):2195-2202.[22] Kwak HB, Ha H, Kim HN,et al.Reciprocal cross-talk between RANKL and interferon-gamma-inducible protein 10 is responsible for bone-erosive experimental arthritis.Arthritis Rheum. 2008;58(5):1332-4132.[23] So H, Rho J, Jeong D,et al.Microphthalmia transcription factor and PU.1 synergistically induce the leukocyte receptor osteoclast-associated receptor gene expression.J Biol Chem. 2003;278(26):24209-24216. [24] Kim K, Kim JH, Lee J,et al.MafB negatively regulates RANKL-mediated osteoclast differentiation.Blood. 2007; 109(8): 3253-3259. [25] Herman S, Müller RB, Krönke G,et al.Induction of osteoclast-associated receptor, a key osteoclast costimulation molecule, in rheumatoid arthritis.Arthritis Rheum. 2008; 58(10): 3041-3050.[26] Polzer K, Diarra D, Zwerina J,et al.Inflammation and destruction of the joints--the Wnt pathway.Joint Bone Spine. 2008;75(2):105-107.[27] Baron R, Rawadi G, Roman-Roman S.Wnt signaling: a key regulator of bone mass.Curr Top Dev Biol. 2006;76: 103-127.[28] Sen M, Lauterbach K, El-Gabalawy H,et al.Expression and function of wingless and frizzled homologs in rheumatoid arthritis.Proc Natl Acad Sci U S A. 2000;97(6):2791-2796.[29] Heiland GR, Zwerina K, Baum W,et al. Neutralisation of Dkk-1 protects from systemic bone loss during inflammation and reduces sclerostin expression.Ann Rheum Dis. 2010;69(12): 2152-2159. [30] Fuller K, Kirstein B, Chambers TJ.Murine osteoclast formation and function: differential regulation by humoral agents. Endocrinology. 2006;147(4):1979-1985.[31] Kaji K, Katogi R, Azuma Y,et al.Tumor necrosis factor alpha-induced osteoclastogenesis requires tumor necrosis factor receptor-associated factor 6.J Bone Miner Res. 2001; 16(9):1593-1599.[32] Smolen JS, Han C, Bala M,et al.Evidence of radiographic benefit of treatment with infliximab plus methotrexate in rheumatoid arthritis patients who had no clinical improvement: a detailed subanalysis of data from the anti-tumor necrosis factor trial in rheumatoid arthritis with concomitant therapy study.Arthritis Rheum. 2005;52(4):1020-1030.[33] Catrina AI, Trollmo C, af Klint E,et al.Evidence that anti-tumor necrosis factor therapy with both etanercept and infliximab induces apoptosis in macrophages, but not lymphocytes, in rheumatoid arthritis joints: extended report.Arthritis Rheum. 2005;52(1):61-72.[34] Takasaki W, Kajino Y, Kajino K,et al.Structure-based design and characterization of exocyclic peptidomimetics that inhibit TNF alpha binding to its receptor.Nat Biotechnol. 1997; 15(12): 1266-1270.[35] Aoki K, Saito H, Itzstein C,et al.A TNF receptor loop peptide mimic blocks RANK ligand-induced signaling, bone resorption, and bone loss.J Clin Invest. 2006;116(6):1525-1534.[36] Redlich K, Görtz B, Hayer S,et al.Repair of local bone erosions and reversal of systemic bone loss upon therapy with anti-tumor necrosis factor in combination with osteoprotegerin or parathyroid hormone in tumor necrosis factor-mediated arthritis.Am J Pathol. 2004;164(2):543-555.[37] Saidenberg-Kermanac'h N, Corrado A, Lemeiter D,et al. TNF-alpha antibodies and osteoprotegerin decrease systemic bone loss associated with inflammation through distinct mechanisms in collagen-induced arthritis.Bone. 2004;35(5): 1200-1207.[38] Seriolo B, Paolino S, Sulli A,et al.Are there any positive effects of TNF-alpha blockers on bone metabolism. Reumatismo. 2006;58(3):199-205.[39] Anandarajah AP, Ory P, Salonen D,et al.Effect of adalimumab on joint disease: features of patients with psoriatic arthritis detected by magnetic resonance imaging.Ann Rheum Dis. 2010;69(1):206-209. [40] Musacchio E, Valvason C, Botsios C,et al.The tumor necrosis factor-{alpha}-blocking agent infliximab inhibits interleukin 1beta (IL-1beta) and IL-6 gene expression in human osteoblastic cells.J Rheumatol. 2009;36(8):1575-1579. |