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1 may be an effective strategy for treating OA cartilage damage.
2 nd is hypothesized to play a pivotal role in cartilage damage.
3 opes was always seen in areas with extensive cartilage damage.
4 NPs inhibit inflammation and protect against cartilage damage.
5  fostering tissue regeneration and repairing cartilage damage.
6 cerbating knee joint stress distribution and cartilage damage.
7 mined that chondrocyte death did not lead to cartilage damage.
8 in DBA/1J mice and protects against bone and cartilage damage.
9 Dickkopf-1 reduced the Wnt-signaling-induced cartilage damage.
10 nonical Wnt signaling, resulted in increased cartilage damage.
11 bited no effect on blood-induced (prolonged) cartilage damage.
12  enable physicians to detect and grade early cartilage damage.
13 thological parameters of bone resorption and cartilage damage.
14  other factors include knee malalignment and cartilage damage.
15 and incidence as well as the risk of lateral cartilage damage.
16 emented on knees exhibiting close to grade 1 cartilage damage.
17 els of distinct mechanisms, without inducing cartilage damage.
18  progression of the disease and irreversible cartilage damage.
19 , the more likely was the presence of severe cartilage damage.
20 rge osteophytes, 54 (80.6%) exhibited severe cartilage damage.
21 >/=5 on a 0-7 scale) but lacking substantial cartilage damage.
22 t is poorly known about their selectivity in cartilage damage.
23  strains could lead to chondrocyte death and cartilage damage.
24 a function of increased DDR-2 expression and cartilage damage.
25                        Joint injury leads to cartilage damage, a known determinant for subsequent dev
26 s ratios for the likelihood of having severe cartilage damage according to osteophyte size were estim
27 ples) and good performance in the grading of cartilage damage (accuracy, 0.74; 32 of 43 samples).
28 ed excellent performance in the detection of cartilage damage (accuracy, 0.95; 41 of 43 samples) and
29 ted OR 4.7 [95% CI 1.1-19.5]), and prevalent cartilage damage (adjusted OR 15.3 [95% CI 4.9-47.4]).
30                                    Moreover, cartilage damage after surgical destabilization of the m
31 arthritis (OA) is a disease characterized by cartilage damage and abnormal remodeling of subchondral
32 armacological blockade of CaMKII exacerbated cartilage damage and bone remodelling.
33 nkles and identified temporal progression of cartilage damage and bone resorption.
34      Overall prevalence of knees with severe cartilage damage and concomitant osteophyte status were
35                       Although the degree of cartilage damage and joint cyst formation was comparable
36  including arthritis indices, paw thickness, cartilage damage and neutrophil infiltration in both CIA
37                           We defined lateral cartilage damage and progressive meniscal damage as incr
38                     CM-MSC treatment reduces cartilage damage and suppresses immune responses by redu
39 g tryptases are MMP convertases that mediate cartilage damage and the proteolytic loss of aggrecan pr
40 rest in radiographic methods to detect early cartilage damage and to assess progressive cartilage cha
41 onstrated comparable levels of inflammation, cartilage damage, and bone erosion in OPN-sufficient and
42  toluidine blue and scored for inflammation, cartilage damage, and bone erosion.
43   Scores for inflammation, pannus formation, cartilage damage, and bone resorption returned to normal
44 ibiofemoral subregions but exhibiting severe cartilage damage, and the hypertrophic phenotype being d
45 nisms whereby calcium crystals contribute to cartilage damage are highlighted in this review.
46 ession, MMP-13 expression, and the degree of cartilage damage, are linked, such that DDR-2 promotes t
47  body weight, tissue source, and the type of cartilage damage as critical properties that significant
48 primary outcome was the incidence of bone or cartilage damage as detected in index joints (ankles, kn
49 Intra-articular corticosteroids could reduce cartilage damage associated with synovitis but might hav
50 bregions (1.6%) showed incident or worsening cartilage damage at followup.
51 mononuclear cell infiltration, bone erosion, cartilage damage at sites adjacent to and distal from pa
52                       However, the extent of cartilage damage at the initiation of GTW may be an impo
53 eral immune cell populations are involved in cartilage damage, bone erosion, and resorption processes
54 f tibiofemoral cartilage loss were prevalent cartilage damage, bone marrow lesions, and meniscal extr
55  groups were found for incident or worsening cartilage damage, bone marrow lesions, and osteophytes a
56                  MR images were assessed for cartilage damage, bone marrow lesions, meniscal damage,
57 ammation such as ankle swelling, paw volume, cartilage damage, bone resorption, and body weight decre
58 ve suggested that chondrocyte death precedes cartilage damage, but how the loss of chondrocytes affec
59                             The reduction in cartilage damage corresponded with a significant reducti
60 s for inflammation, pannus, bone damage, and cartilage damage decreased in parallel with the DAS.
61 verlay enabled good anatomic localization of cartilage damage defined with a T2* threshold of 28 msec
62 is a common feature of arthritis, leading to cartilage damage, deterioration of the joint architectur
63 to stimulate the repair of acute and chronic cartilage damage even though there is no definitive evid
64 e majority of knees with severe tibiofemoral cartilage damage exhibited moderate to large osteophytes
65 icin evaluated in this study, a reduction in cartilage damage following ACLT was evident, combined wi
66 abolism, not death, contributes to articular cartilage damage following injury.
67       Lipodystrophic mice are protected from cartilage damage following joint injury.
68  infiltration into joints, bone erosion, and cartilage damage; furthermore, the production of type II
69 MIA in which GTW regimens were started after cartilage damage had progressed to grade 1 or grade 2.
70  agonist, CGS21680, significantly reduced OA cartilage damage in a murine model of obesity-induced OA
71 urther, critical thresholds at 6% and 64% of cartilage damage in area, and 22% and 56% in depth were
72 his kind may be of value in the treatment of cartilage damage in arthritis.
73                  Mechanical loading promoted cartilage damage in both age groups of mice, and the sev
74 nflammation and prevents structural bone and cartilage damage in collagen antibody-induced arthritis.
75       These findings, along with findings of cartilage damage in dogs, raise serious doubts about sel
76 n another study found that eprotirome causes cartilage damage in dogs.
77  ligand, type II collagen, may contribute to cartilage damage in hereditary OA.
78 n is elevated and accompanied by accelerated cartilage damage in humans and mice that have genetic de
79 ease were used to characterize the extent of cartilage damage in infection and investigate the potent
80  play an important role in the modulation of cartilage damage in inflammatory arthritis.
81                              GTW accelerated cartilage damage in knees with close to grade 2 damage.
82 s matrix synthesis to prevent progression of cartilage damage in MIA-affected knees.
83 eral genes of interest involved in articular cartilage damage in OA have been identified.
84 din domain receptor 2 (DDR-2) expression and cartilage damage in osteoarthritis (OA).
85  and may soon lead to drugs that safely halt cartilage damage in patients.
86 n, and migration, which might be involved in cartilage damage in RA.
87                     10a effectively prevents cartilage damage in rabbit animal models of osteoarthrit
88 esting that chondrocyte death does not drive cartilage damage in response to injury.
89  inflammatory arthritis and reduced bone and cartilage damage in the joints as demonstrated by histol
90 ired role in inflammation, bone erosion, and cartilage damage in the K/BxN serum-transfer model.
91 and 17% (20 of 115) of knees showed incident cartilage damage in the lateral tibiofemoral joint, and
92 and 13% (15 of 115) of knees showed incident cartilage damage in the medial tibiofemoral joint, 11% (
93 nd 8% (nine of 115) of knees showed incident cartilage damage in the patellofemoral joint.
94                         ALS 1-0635 modulated cartilage damage in the rat MIA model (mean +/- SEM dama
95 for knees to develop incident or progressing cartilage damage in the root tear group and the meniscal
96 xtrusion, synovitis, effusion, and prevalent cartilage damage in the same subregion were evaluated as
97 ce interval [95% CI] 1.3-9.4), and prevalent cartilage damage in the same subregion with an adjusted
98 l cartilage loss were effusion and prevalent cartilage damage in the same subregion.
99 ssociated with both osteophyte formation and cartilage damage in the STR/Ort joints.
100 ive MMP13 inhibitor that effectively reduces cartilage damage in vivo and does not induce joint fibro
101                           The risk of severe cartilage damage increased markedly with increasing oste
102 ntiviral Wnt7a strongly attenuated articular cartilage damage induced by destabilization of the media
103      Osteoarthritis (OA) is characterized by cartilage damage, inflammation, and pain.
104 ector in an orthotopic large animal model of cartilage damage is reported here.
105 iscal tears, knee malalignment, tibiofemoral cartilage damage, knee effusion, and body mass index wit
106 ading on a focal area, to the level at which cartilage damage may occur.
107 lignment >3 degrees was also associated with cartilage damage on MR imaging in knees without OA (e.g.
108                                              Cartilage damage on safranin O histologic slides was qua
109 ntly decreased inflammatory cell infiltrate, cartilage damage, pannus formation, and bone damage.
110 s, and VEGF, inflammatory cell infiltration, cartilage damage, pannus formation, and bone erosion in
111                                The articular cartilage damage present in the knee joints of the mice
112 by increased arthritic bone erosion, whereas cartilage damage remained unaffected.
113 ling increased protease activity and induced cartilage damage shortly after overexpression.
114        To follow osteoarthritis progression, cartilage damage, synovial thickening, and osteophyte fo
115 ha in the pathogenesis of this blood-induced cartilage damage, the effect of antagonizing these cytok
116  of the protection from structural articular cartilage damage, the postnatal growth plates of IKKalph
117        In participants with minimal baseline cartilage damage, the presence of high BMI, meniscal dam
118  SF was obtained from patients with early OA cartilage damage undergoing arthroscopic meniscal proced
119                            Clear evidence of cartilage damage was also seen in CHIKV-infected CCR2(-/
120 f DT imaging in the diagnosis and grading of cartilage damage was assessed with logistic regression a
121 n knee joints were obtained and the grade of cartilage damage was evaluated according to the Mankin s
122  use of a modified Beck scale for acetabular cartilage damage was performed by an orthopedic surgeon
123                                              Cartilage damage was semiquantitatively assessed by usin
124 f the nailbed and diffuse bone edema without cartilage damage, was also typical of PsA.
125  arthritis in quantities sufficient to cause cartilage damage, we evaluated the effect of tetracyclin
126 and gene expression patterns associated with cartilage damage were also evaluated.
127 lly, meniscal tears, varus malalignment, and cartilage damage were associated with meniscal extrusion
128 ly, meniscal tears, valgus malalignment, and cartilage damage were associated with meniscal extrusion
129 verity of osteophyte formation and extent of cartilage damage were determined in the corresponding fe
130 SA model, cellular infiltrates and articular cartilage damage were mild in the PKC-theta-deficient mi
131 rtilage health and slowed the development of cartilage damage, whereas ALN primarily attenuated subch
132 tionship between the gut microbiota and knee cartilage damage while controlling for adiposity, high f
133 (-) fibroblasts selectively mediate bone and cartilage damage with little effect on inflammation, whe
134                      The frequency of severe cartilage damage (WORMS >/= 5) was higher in the group w
135             Only knees with minimal baseline cartilage damage (WORMS < or = 2.5) were included.

 
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