ライフサイエンスコーパス: cartilage damage

1 els of distinct mechanisms, without inducing cartilage damage.

2 mined that chondrocyte death did not lead to cartilage damage.

3 may be an effective strategy for treating OA cartilage damage.

4 nd is hypothesized to play a pivotal role in cartilage damage.

5 opes was always seen in areas with extensive cartilage damage.

6 in DBA/1J mice and protects against bone and cartilage damage.

7 t is poorly known about their selectivity in cartilage damage.

8 Dickkopf-1 reduced the Wnt-signaling-induced cartilage damage.

9 nonical Wnt signaling, resulted in increased cartilage damage.

10 bited no effect on blood-induced (prolonged) cartilage damage.

11 enable physicians to detect and grade early cartilage damage.

12 thological parameters of bone resorption and cartilage damage.

13 other factors include knee malalignment and cartilage damage.

14 and incidence as well as the risk of lateral cartilage damage.

15 emented on knees exhibiting close to grade 1 cartilage damage.

16 progression of the disease and irreversible cartilage damage.

17 , the more likely was the presence of severe cartilage damage.

18 rge osteophytes, 54 (80.6%) exhibited severe cartilage damage.

19 >/=5 on a 0-7 scale) but lacking substantial cartilage damage.

20 strains could lead to chondrocyte death and cartilage damage.

21 a function of increased DDR-2 expression and cartilage damage.

22 Joint injury leads to cartilage damage, a known determinant for subsequent dev

23 s ratios for the likelihood of having severe cartilage damage according to osteophyte size were estim

24 ples) and good performance in the grading of cartilage damage (accuracy, 0.74; 32 of 43 samples).

25 ed excellent performance in the detection of cartilage damage (accuracy, 0.95; 41 of 43 samples) and

26 ted OR 4.7 [95% CI 1.1-19.5]), and prevalent cartilage damage (adjusted OR 15.3 [95% CI 4.9-47.4]).

27 Moreover, cartilage damage after surgical destabilization of the m

28 nkles and identified temporal progression of cartilage damage and bone resorption.

29 Overall prevalence of knees with severe cartilage damage and concomitant osteophyte status were

30 Although the degree of cartilage damage and joint cyst formation was comparable

31 including arthritis indices, paw thickness, cartilage damage and neutrophil infiltration in both CIA

32 We defined lateral cartilage damage and progressive meniscal damage as incr

33 CM-MSC treatment reduces cartilage damage and suppresses immune responses by redu

34 g tryptases are MMP convertases that mediate cartilage damage and the proteolytic loss of aggrecan pr

35 rest in radiographic methods to detect early cartilage damage and to assess progressive cartilage cha

36 onstrated comparable levels of inflammation, cartilage damage, and bone erosion in OPN-sufficient and

37 toluidine blue and scored for inflammation, cartilage damage, and bone erosion.

38 Scores for inflammation, pannus formation, cartilage damage, and bone resorption returned to normal

39 ibiofemoral subregions but exhibiting severe cartilage damage, and the hypertrophic phenotype being d

40 nisms whereby calcium crystals contribute to cartilage damage are highlighted in this review.

41 ession, MMP-13 expression, and the degree of cartilage damage, are linked, such that DDR-2 promotes t

42 primary outcome was the incidence of bone or cartilage damage as detected in index joints (ankles, kn

43 Intra-articular corticosteroids could reduce cartilage damage associated with synovitis but might hav

44 bregions (1.6%) showed incident or worsening cartilage damage at followup.

45 mononuclear cell infiltration, bone erosion, cartilage damage at sites adjacent to and distal from pa

46 However, the extent of cartilage damage at the initiation of GTW may be an impo

47 eral immune cell populations are involved in cartilage damage, bone erosion, and resorption processes

48 f tibiofemoral cartilage loss were prevalent cartilage damage, bone marrow lesions, and meniscal extr

49 MR images were assessed for cartilage damage, bone marrow lesions, meniscal damage,

50 ammation such as ankle swelling, paw volume, cartilage damage, bone resorption, and body weight decre

51 ve suggested that chondrocyte death precedes cartilage damage, but how the loss of chondrocytes affec

52 The reduction in cartilage damage corresponded with a significant reducti

53 s for inflammation, pannus, bone damage, and cartilage damage decreased in parallel with the DAS.

54 verlay enabled good anatomic localization of cartilage damage defined with a T2* threshold of 28 msec

55 to stimulate the repair of acute and chronic cartilage damage even though there is no definitive evid

56 e majority of knees with severe tibiofemoral cartilage damage exhibited moderate to large osteophytes

57 icin evaluated in this study, a reduction in cartilage damage following ACLT was evident, combined wi

58 abolism, not death, contributes to articular cartilage damage following injury.

59 infiltration into joints, bone erosion, and cartilage damage; furthermore, the production of type II

60 MIA in which GTW regimens were started after cartilage damage had progressed to grade 1 or grade 2.

61 his kind may be of value in the treatment of cartilage damage in arthritis.

62 Mechanical loading promoted cartilage damage in both age groups of mice, and the sev

63 nflammation and prevents structural bone and cartilage damage in collagen antibody-induced arthritis.

64 These findings, along with findings of cartilage damage in dogs, raise serious doubts about sel

65 n another study found that eprotirome causes cartilage damage in dogs.

66 ligand, type II collagen, may contribute to cartilage damage in hereditary OA.

67 n is elevated and accompanied by accelerated cartilage damage in humans and mice that have genetic de

68 ease were used to characterize the extent of cartilage damage in infection and investigate the potent

69 play an important role in the modulation of cartilage damage in inflammatory arthritis.

70 GTW accelerated cartilage damage in knees with close to grade 2 damage.

71 s matrix synthesis to prevent progression of cartilage damage in MIA-affected knees.

72 din domain receptor 2 (DDR-2) expression and cartilage damage in osteoarthritis (OA).

73 and may soon lead to drugs that safely halt cartilage damage in patients.

74 n, and migration, which might be involved in cartilage damage in RA.

75 10a effectively prevents cartilage damage in rabbit animal models of osteoarthrit

76 esting that chondrocyte death does not drive cartilage damage in response to injury.

77 inflammatory arthritis and reduced bone and cartilage damage in the joints as demonstrated by histol

78 ired role in inflammation, bone erosion, and cartilage damage in the K/BxN serum-transfer model.

79 ALS 1-0635 modulated cartilage damage in the rat MIA model (mean +/- SEM dama

80 for knees to develop incident or progressing cartilage damage in the root tear group and the meniscal

81 xtrusion, synovitis, effusion, and prevalent cartilage damage in the same subregion were evaluated as

82 ce interval [95% CI] 1.3-9.4), and prevalent cartilage damage in the same subregion with an adjusted

83 l cartilage loss were effusion and prevalent cartilage damage in the same subregion.

84 ssociated with both osteophyte formation and cartilage damage in the STR/Ort joints.

85 ive MMP13 inhibitor that effectively reduces cartilage damage in vivo and does not induce joint fibro

86 The risk of severe cartilage damage increased markedly with increasing oste

87 ntiviral Wnt7a strongly attenuated articular cartilage damage induced by destabilization of the media

88 iscal tears, knee malalignment, tibiofemoral cartilage damage, knee effusion, and body mass index wit

89 ading on a focal area, to the level at which cartilage damage may occur.

90 lignment >3 degrees was also associated with cartilage damage on MR imaging in knees without OA (e.g.

91 Cartilage damage on safranin O histologic slides was qua

92 ntly decreased inflammatory cell infiltrate, cartilage damage, pannus formation, and bone damage.

93 The articular cartilage damage present in the knee joints of the mice

94 by increased arthritic bone erosion, whereas cartilage damage remained unaffected.

95 ling increased protease activity and induced cartilage damage shortly after overexpression.

96 To follow osteoarthritis progression, cartilage damage, synovial thickening, and osteophyte fo

97 ha in the pathogenesis of this blood-induced cartilage damage, the effect of antagonizing these cytok

98 In participants with minimal baseline cartilage damage, the presence of high BMI, meniscal dam

99 SF was obtained from patients with early OA cartilage damage undergoing arthroscopic meniscal proced

100 Clear evidence of cartilage damage was also seen in CHIKV-infected CCR2(-/

101 f DT imaging in the diagnosis and grading of cartilage damage was assessed with logistic regression a

102 n knee joints were obtained and the grade of cartilage damage was evaluated according to the Mankin s

103 use of a modified Beck scale for acetabular cartilage damage was performed by an orthopedic surgeon

104 Cartilage damage was semiquantitatively assessed by usin

105 f the nailbed and diffuse bone edema without cartilage damage, was also typical of PsA.

106 arthritis in quantities sufficient to cause cartilage damage, we evaluated the effect of tetracyclin

107 and gene expression patterns associated with cartilage damage were also evaluated.

108 lly, meniscal tears, varus malalignment, and cartilage damage were associated with meniscal extrusion

109 ly, meniscal tears, valgus malalignment, and cartilage damage were associated with meniscal extrusion

110 verity of osteophyte formation and extent of cartilage damage were determined in the corresponding fe

111 SA model, cellular infiltrates and articular cartilage damage were mild in the PKC-theta-deficient mi

112 The frequency of severe cartilage damage (WORMS >/= 5) was higher in the group w

113 Only knees with minimal baseline cartilage damage (WORMS < or = 2.5) were included.