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1 ase Activity Score (DAS), is associated with joint destruction.
2 eposition, formation of bony outgrowths, and joint destruction.
3 re unrecognized role in rheumatoid arthritis joint destruction.
4 ion, antirheumatic treatment, or severity of joint destruction.
5 sting a role for this cytokine in rheumatoid joint destruction.
6 , may amplify local inflammation, leading to joint destruction.
7 thways play a significant role in rheumatoid joint destruction.
8 ic mice, deletion of Lasp1 reduces arthritic joint destruction.
9 lammation, pannus formation, and progressive joint destruction.
10 mprove the efficacy of treatments to prevent joint destruction.
11 ncreased Th1 T cell responses, and increased joint destruction.
12 nts present without radiographic evidence of joint destruction.
13 blematic site, eventually protecting against joint destruction.
14 immune response contributes substantially to joint destruction.
15 s (OA) is a pathology that ultimately causes joint destruction.
16 ance-2 important issues in S. aureus-induced joint destruction.
17 , exacerbate clinical arthritis, and augment joint destruction.
18  quality of life, functional impairment, and joint destruction.
19 e infiltration, angiogenesis, and ultimately joint destruction.
20  able to reduce efficiently paw swelling and joint destruction.
21 d arthritis suppresses both inflammation and joint destruction.
22  for histologic evidence of inflammation and joint destruction.
23 isease, as well as retard the progression of joint destruction.
24 herapeutic interventions designed to prevent joint destruction.
25 s) that function to promote inflammation and joint destruction.
26 omote local T cell activation and consequent joint destruction.
27  both cartilage and synovium, thus promoting joint destruction.
28 s and its response to steroid therapy before joint destruction.
29 lpha (TNF-alpha), which may lead to bone and joint destruction.
30 r of studies to identify novel correlates of joint destruction.
31 s in the periarticular soft tissues, without joint destruction.
32 products important in joint inflammation and joint destruction.
33  arthritis (RA) and are directly involved in joint destruction.
34 c degradation of the joint matrices leads to joint destruction.(4,5) The early phase of RA is charact
35 ies evaluating the risk of accelerated OA or joint destruction after IACS injections are needed.
36  featuring multiple exostoses, enchondromas, joint destruction and bony deformities.
37 dly mitigate synovial inflammation, suppress joint destruction and cartilage matrix degradation, with
38 ate treatment of SA can lead to irreversible joint destruction and disability.
39 immobility caused by inflammatory bone loss, joint destruction and fractures in rheumatoid arthritis
40  a novel susceptibility gene underlying both joint destruction and growth retardation of the KBD.
41 st that the movement strategy may perpetuate joint destruction and impede the long-term success of re
42 e affected joints of Nfat5+/- mice increased joint destruction and macrophage infiltration, demonstra
43                                              Joint destruction and osteoclast differentiation were lo
44  (JRA) have persistently active disease with joint destruction and profound growth delay despite maxi
45 hronic inflammatory disease characterized by joint destruction and severe morbidity.
46 , inflammatory polyarthritis that results in joint destruction and significant disability.
47 by chronic inflammatory synovitis leading to joint destruction and systemic bone loss.
48 inical symptoms, retarded the progression of joint destruction, and delayed disability.
49  significantly increased joint inflammation, joint destruction, and expression of interleukin-6 (IL-6
50                 However, clinical arthritis, joint destruction, and synovial gene expression in the p
51 igher joint compression and could exacerbate joint destruction, and therefore needs to be altered to
52 ncy and severity of arthritis and subsequent joint destruction as compared with Deltafmt mutant strai
53 antibody significantly inhibited SCW-induced joint destruction, as measured by its ability to block i
54 tors on human synoviocytes may contribute to joint destruction by increasing IL-6 expression.
55 arthritis model, including the inflammation, joint destruction, cartilage prostaglandin depletion, os
56  synovial hyperplasia, osteoclast formation, joint destruction, cathepsin activity, and inflammatory
57 edema correlates with inflammation severity, joint destruction, clinical signs and symptoms of rheuma
58 cted gene transfer may ameliorate hemophilic joint destruction, even in the absence of circulating FI
59 hibited joint inflammation and periarticular joint destruction in a dose-dependent manner.
60 lts in potent inhibition of inflammation and joint destruction in a model of autoimmune arthritis in
61 L-1)-induced collagenase gene expression and joint destruction in arthritis.
62 MKK-6 is a crucial regulator of inflammatory joint destruction in CIA.
63 isease, can also be an important mediator of joint destruction in inflammatory bone disorders, such a
64 r selective loss of JNK-2 function decreases joint destruction in JNK-2 knockout mice, in order to de
65 elineate the contribution of aggrecanases to joint destruction in Lyme arthritis.
66 culature is important for the development of joint destruction in RA.
67  contribute to synovial lining expansion and joint destruction in RA.
68 roduction and has important implications for joint destruction in RA.
69  antibodies were associated with more severe joint destruction in RA.
70 of potential therapeutic value in inhibiting joint destruction in RA.
71 immune mechanisms that mediate synovitis and joint destruction in rheumatoid arthritis (RA) remain po
72    High expression of galectin 3 at sites of joint destruction in rheumatoid arthritis (RA) suggests
73 viocytes (FLS) play a major role in invasive joint destruction in rheumatoid arthritis (RA).
74  joint are key mediators of inflammation and joint destruction in rheumatoid arthritis (RA).
75 atrix metalloproteinase (MMP) expression and joint destruction in rheumatoid arthritis (RA).
76  important elements in the events leading to joint destruction in rheumatoid arthritis (RA).
77  metalloproteinase (MMP) gene expression and joint destruction in rheumatoid arthritis (RA).
78 signed to suppress synovial inflammation and joint destruction in rheumatoid arthritis.
79 IL-8 as a major mediator of inflammation and joint destruction in rheumatoid arthritis.
80                       IL-15 is a mediator of joint destruction in S. aureus-induced arthritis and con
81 n of c-Jun N-terminal kinase (JNK) decreases joint destruction in the rat adjuvant arthritis model.
82 logy reveals 63 and 77% reduction in overall joint destruction in two independent experiments.
83 conclude that the DR3-TL1A pathway regulates joint destruction in two murine models of arthritis and
84 D-JNKi dramatically reduced inflammation and joint destruction in WT mice.
85 ese interactions finally lead to progressive joint destruction, in a way that is different from all o
86 ulated in RA and contribute significantly to joint destruction, in the present study we investigated
87 ons of pre-existing osteonecrosis, and rapid joint destruction (including bone loss) may be observed
88 e, complications of osteonecrosis, and rapid joint destruction, including bone loss.
89                             The pathology of joint destruction is associated with elevated production
90 matory drugs, may have limited efficacy once joint destruction is complete.
91 ion, time-averaged disease activity fits the joint destruction model better than one-time disease act
92                               In addition to joint destruction, mutant mice also develop aortic root
93     The chronic inflammation and progressive joint destruction observed in rheumatoid arthritis (RA)
94 ough TLR-2 and TLR-4 in the inflammation and joint destruction of RA.
95                     Histological analyses of joint destruction provided evidence for a significant re
96 uvette assay, was positively correlated with joint destruction (r = 0.7) and inflammation (r = 0.8).
97                                        Since joint destruction reflects the history of disease activi
98       Optimal treatment to prevent or reduce joint destruction remains controversial.
99 ll migration and invasion, but their role in joint destruction remains unknown.
100 le it is clear that pigment deposits lead to joint destruction, renal stone formation and cardiac val
101      IL-6 and MMP-1 promote inflammation and joint destruction, respectively.
102   Postmenopausal osteoporosis and rheumatoid joint destruction result from increased osteoclast forma
103 perienced poor long-term outcomes, including joint destruction, severe functional declines, considera
104 ciency suppresses inflammatory arthritis and joint destruction, suggesting it might be a therapeutic
105  arthritis and histological scores measuring joint destruction, synovial lining, macrophage infiltrat
106 disease activity would better correlate with joint destruction than one-time disease activity.
107 to apoptosis and less efficient at promoting joint destruction than were NFAT5-sufficient macrophages
108  (TNF) and interleukin 1 (IL-1), mediate the joint destruction that characterizes rheumatoid arthriti
109 insights into the pathogenesis of autoimmune joint destruction that is reminiscent of JIA.
110           Rheumatoid arthritis culminates in joint destruction that, in mouse models of disease, is s
111 etic markers predicting rapid progression of joint destruction; the role of serology, in particularly
112 nvading cartilage and bone in RA may mediate joint destruction through direct effects on cartilage or
113                                     Although joint destruction was decreased in Jnk2(-/-) mice with C
114                The severity of synovitis and joint destruction was significantly decreased in IL-15 k
115 the joints showed that both inflammation and joint destruction were blocked by the IKK inhibitor.
116 ted course of RA, structural consequences of joint destruction were more pronounced in women.
117 istent synovial inflammation and progressive joint destruction, which are mediated by innate and adap
118 al disorders characterized by osteolysis and joint destruction, which can mimic severe rheumatoid art
119    Complete inhibition of MMP expression and joint destruction will likely require combined JNK-1 and
120 understanding of the molecular mechanisms of joint destruction will pave the way for new therapeutic
121 rthritis (RA) is characterized by autoimmune joint destruction with debilitating consequences.
122 owed statistically significant reductions in joint destruction with PB-145 and PPS treatments (P < 0.

 
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