ライフサイエンスコーパス: bone erosion

1 ate (MSU) crystals may promote cartilage and bone erosion.

2 g joint tissue destruction and periarticular bone erosion.

3 ges in synovium and bone that precede actual bone erosion.

4 One knee had a bone erosion.

5 umulation of leukocytes, joint swelling, and bone erosion.

6 RANKL) are abundant in sites of inflammatory bone erosion.

7 ing shows sinonasal involvement or paranasal bone erosion.

8 tected against inflammatory bone disease and bone erosion.

9 specifically inhibit osteoclastogenesis and bone erosion.

10 age degradation, and protected the mice from bone erosion.

11 C)-treated cohort was largely protected from bone erosion.

12 severity, synovial tissue OC abundance, and bone erosion.

13 are therapeutic targets for inflammation and bone erosion.

14 mation and cartilage destruction, and halted bone erosion.

15 L-27 plays a homeostatic role in restraining bone erosion.

16 es and neutrophils to the joint and promotes bone erosion.

17 ent arthritis and almost completely prevents bone erosion.

18 a potent inhibitory effect on RANKL-mediated bone erosion.

19 lastogenesis, thereby resulting in decreased bone erosion.

20 shortly after the onset of inflammation and bone erosion.

21 oint cellularity, cartilage destruction, and bone erosion.

22 ynovial lining, macrophage infiltration, and bone erosion.

23 ependent systemic inflammation, and cortical bone erosion.

24 ovial angiogenesis, as well as cartilage and bone erosion.

25 induced weight loss as well as cartilage and bone erosion.

26 or full progression of chronic synovitis and bone erosion.

27 umber, surface area, and size) and increased bone erosion.

28 tion, radiographic soft tissue swelling, and bone erosion.

29 herapeutic targets in states of inflammatory bone erosion.

30 se-positive multinucleated cells at sites of bone erosion.

31 ored for inflammation, cartilage damage, and bone erosion.

32 f bone resorbing cells associated with focal bone erosions.

33 ate these cells in the pathogenesis of focal bone erosions.

34 a role in the initiation and progression of bone erosions.

35 vere disease, as assessed by the presence of bone erosions.

36 cal computed tomography was used to evaluate bone erosions.

37 FNalpha transcriptome were protected against bone erosions.

38 Periarticular bone erosion and bone edema were scored according to the

39 CT scans were evaluated for bone erosion and calcification; MR images, for signal in

40 hronic inflammatory disease characterized by bone erosion and cartilage destruction in the joints.

41 5 decreased synovitis in the joints; reduced bone erosion and cartilage destruction; reduced in situ

42 mmatory arthritis, associated with prominent bone erosion and higher articular expression of Rankl.

43 Bone erosion and joint-space narrowing were measured rad

44 he aim of exploring the relationship between bone erosion and new bone formation in enthesitis.

45 in mice with bacterial infection-stimulated bone erosion and periapical inflammation, which confirms

46 mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/B

47 The presence of bone erosion and spur formation was recorded at 3 sites:

48 lly discharging ears, especially to look for bone erosion and the integrity of the ossicles.

49 ional method of detecting the characteristic bone erosions and an important adjunct in establishing a

50 utoimmune disease that leads to severe focal bone erosions and generalized systemic osteoporosis.

51 in particular, failed to develop subchondral bone erosions and were completely protected from this ch

52 k in vivo osteoclastogenesis, inhibits focal bone erosion, and ameliorates inflammatory responses in

53 es not have a required role in inflammation, bone erosion, and cartilage damage in the K/BxN serum-tr

54 evented neutrophil infiltration into joints, bone erosion, and cartilage damage; furthermore, the pro

55 us involvement, bone expansion and thinning, bone erosion, and extension of disease into the adjacent

56 ovial cell proliferation, cartilage erosion, bone erosion, and fibroproliferative pannus) or frozen,

57 r of inflammation, cartilage catabolism, and bone erosion, and highlight APO866 as a promising therap

58 can inhibit endodontic disease development, bone erosion, and immune response.

59 opulations are involved in cartilage damage, bone erosion, and resorption processes during osteoarthr

60 ar influx into the joints, protected against bone erosions, and preserved cartilage integrity.

61 niques in detecting both early synovitis and bone erosion; and the value of combination therapy in co

62 Conversely, CIA joint inflammation and bone erosion are alleviated when TLR5 function is blocke

63 tors driving IL-1beta-dependent inflammatory bone erosion are unknown.

64 inally, osteoclastogenesis and periarticular bone erosions are markedly increased in SHIP1(-/-) mice

65 sease, radiographically occult cartilage and bone erosions are uncommonly seen at MR imaging.

66 orated inflammation, lining hypertrophy, and bone erosion as compared with control-treated CIA mice.

67 set, after which scores for inflammation and bone erosion as well as capillary counts were acquired f

68 ticular inflammation, and markedly decreased bone erosions as measured quantitatively through micro-C

69 eated mice had lower levels of synovitis and bone erosion, as well as less myeloperoxidase in synovia

70 5 and correlated with histologic changes and bone erosions assessed on day 65.

71 nesis and can limit the extent of pathologic bone erosion associated with infection and inflammation.

72 B and JNK and to subsequently ameliorate the bone erosion associated with inflammatory arthritis in m

73 rs in inflammation and tissue damage such as bone erosion, but the mechanisms regulating their activa

74 We assessed bone erosions by several methods: histologic evaluation,

75 us formation, mononuclear cell infiltration, bone erosion, cartilage damage at sites adjacent to and

76 oint cellularity, cartilage destruction, and bone erosion despite significantly reduced RANKL (recept

77 disease (i.e., evidence of inflammation and bone erosions) did develop in a small number of DPPI(-/-

78 A) as a key regulator of synovial injury and bone erosion during autoimmune joint inflammation.

79 n autocrine mechanism to limit the degree of bone erosion during joint inflammation.

80 , and a subacute component, which results in bone erosion, even in the absence of FcgammaR signaling.

81 ere is a predilection for both synovitis and bone erosion formation on the radial side of the MCP joi

82 l role of osteoclasts in the pathogenesis of bone erosion in arthritis and demonstrate distinct mecha

83 er evaluate the role of osteoclasts in focal bone erosion in arthritis, we generated inflammatory art

84 Bone erosion in association with Achilles tendon enthesi

85 ficantly diminished RANKL positive cells and bone erosion in CIA mice.

86 revealed a reduction in areas susceptible to bone erosion in DR3(ko) mice, whereas in vitro osteoclas

87 decreases tumor burden as well as associated bone erosion in immune-compromised animals bearing human

88 ation and blocked subchondral and periosteal bone erosion in inflamed joints.

89 Osteoclasts are essential cells for bone erosion in inflammatory arthritis and are derived f

90 BD peptide may hinder osteoclastogenesis and bone erosion in inflammatory arthritis.

91 e as a target candidate for the treatment of bone erosion in inflammatory arthritis.

92 sents a novel approach to the alleviation of bone erosion in inflammatory arthritis.

93 nfiltration, fibrosis, pannus formation, and bone erosion in joints of BLT1/BLT2(+/+) animals and a t

94 -D) measures of outcomes of inflammation and bone erosion in murine arthritis using contrast-enhanced

95 evels of inflammation, cartilage damage, and bone erosion in OPN-sufficient and OPN-deficient mice.

96 Bone erosion in patients with early SpA occurred at eith

97 We examined tissue sections from areas of bone erosion in patients with RA and JRA.

98 vity are rational targets for blocking focal bone erosion in patients with RA and JRA.

99 The origin of osteoclasts at sites of bone erosion in RA is unknown.

100 t in the pathogenesis of osteoclast-mediated bone erosion in RA.

101 on and activation of osteoclasts at sites of bone erosion in RA.

102 The role of osteoclasts in bone erosion in rheumatoid arthritis (RA) has been demon

103 Studies of tissue sections from sites of bone erosion in rheumatoid arthritis and in animal model

104 ts are involved in the pathogenesis of focal bone erosion in rheumatoid arthritis.

105 d increased COMMD1 expression with decreased bone erosion in rheumatoid arthritis.

106 vial fibroblasts (SF) and the development of bone erosion in the collagen-induced arthritis (CIA) mou

107 reduced efficacy of bisphosphonates to stop bone erosion in the inflamed joints of RA patients may r

108 inct mechanisms of cartilage destruction and bone erosion in this animal model of arthritis.

109 cal analysis demonstrated that the degree of bone erosion in TRANCE/RANKL knockout mice was dramatica

110 bit anti-inflammatory properties and prevent bone erosions in models of inflammatory arthritis.

111 understanding the pathogenesis of aggressive bone erosions in PsA.

112 us contribute to antagonize inflammation and bone erosions in RA.

113 ore sensitive than radiography for detecting bone erosions in rheumatoid arthritis (RA).

114 ellular mechanisms and factors implicated in bone erosions in rheumatoid arthritis, and discusses the

115 essive inflammation began with cartilage and bone erosions in the interphalangeal joints, and later e

116 ve osteoclasts were found at sites of active bone erosion, in close proximity to hyperproliferating s

117 itis develop profound osteoclastogenesis and bone erosion independent of stromal cell expression of T

118 formed on teeth #13 to #15, and as there was bone erosion into the maxillary sinus, a biopsy of the s

119 The pathogenesis of focal bone erosions is an area of active investigation.

120 oint inflammation (cellular inflammation and bone erosion) is similar in the i.p. versus s.c. immuniz

121 n extensive and rapid cartilage degradation, bone erosion, joint ankylosis, and deformities in Tnfip6

122 atory cytokine expression, pannus formation, bone erosion, joint swelling, and pain.

123 s potent joint monocyte chemoattractants and bone erosion markers, suggesting that both direct and in

124 Repair of articular bone erosion occurs in the setting of resolving inflamma

125 paB ligand (RANKL) is critically involved in bone erosion of rheumatoid arthritis (RA).

126 al symptoms, sinonasal changes, or paranasal bone erosion on imaging (P < 0.001).

127 is of the kinetics of synovial inflammation, bone erosion, osteoclast formation, and growth of bony s

128 Joint inflammation is characterized by bone erosions, osteopenia, soft-tissue swelling, and uni

129 si sarcoma and associated bilateral alveolar bone erosion presented for dental evaluation subsequent

130 stration also resulted in protection against bone erosion (r(2) = 0.4720, P < 0.01), which was associ

131 e tooth, leading to periapical inflammation, bone erosion, severe pain, and tooth loss.

132 Inflammatory arthritis and bone erosion subside in the presence of antiinflammatory

133 y correlated with the intensity of arthritic bone erosion, suggesting relevance in pathology.

134 cture, including minimal to no cartilage and bone erosions, synovial hyperplasia, and pannus formatio

135 n of CLL cells caused an appreciable compact bone erosion that was prevented by Denosumab.

136 ngly linked to infection-driven inflammatory bone erosion, thrives within a highly inflamed milieu an

137 both anticytokines reduced inflammation and bone erosion to a similar degree.

138 s from PsA patients, particularly those with bone erosions visible on plain radiographs, exhibit a ma

139 Bone erosion was assessed in the joints by histologic an

140 sin K in articular cartilage and subchondral bone erosion was further corroborated by the finding tha

141 Bone erosion was particularly evident in long bone shaft

142 flammation, cartilage degradation, and local bone erosion were assessed at the wrist, knee, and ankle

143 igns of arthritis, osteoclast formation, and bone erosion were assessed.

144 s from the bone-pannus interface at sites of bone erosion were examined for the presence of osteoclas

145 In this model, osteoclastogenesis and bone erosion were prevented by low doses (1 or 0.33 mg/k

146 In patients with early RA in whom bone erosions were present, there was a propensity for i

147 a dose- and schedule-dependent manner, halts bone erosion when given at any point during the course o

148 tis was characterized by increased arthritic bone erosion, whereas cartilage damage remained unaffect

149 , particularly outside sites of cartilage or bone erosion, which dramatically declined by day 35.

150 mages revealed that APO866 protected against bone erosion, while qPCR demonstrated inhibition of RANK

151 rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid art