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1 type II collagen by collagenase, as well as synovial hyperplasia.
2 that a defect in apoptosis may contribute to synovial hyperplasia.
3 NTK-mediated phototherapy notably alleviated synovial hyperplasia and enhanced bone and cartilage reg
5 osteophyte formation, meniscal ossification, synovial hyperplasia and fibrosis, and cruciate ligament
8 articular joints, characterized by invasive synovial hyperplasia and pathological neovascularization
9 s of RA due to the comparisons drawn between synovial hyperplasia and paucity of apoptosis in RA with
10 ds to premature joint failure, hallmarked by synovial hyperplasia and premature articular cartilage f
11 olymer effectively inhibited joint swelling, synovial hyperplasia, and bone destruction in collagen-i
12 , such as increased epiphyseal growth plate, synovial hyperplasia, and increased cellularity in the j
13 severe cellular infiltration in the joints, synovial hyperplasia, and joint erosion, this pathology
14 g minimal to no cartilage and bone erosions, synovial hyperplasia, and pannus formation, and reduced
15 inical inflammation, formation of pannus and synovial hyperplasia, and the erosion of cartilage and b
16 rats with PIA, while DA rats had pronounced synovial hyperplasia, angiogenesis, inflammatory infiltr
18 lowing immunization that is characterized by synovial hyperplasia, cellular infiltration, and cartila
19 filtration of inflammatory cells, edema, and synovial hyperplasia in the joint were significantly att
20 Specifically, OSM + TNFalpha induced marked synovial hyperplasia, inflammation, and cartilage and bo
21 hronic inflammatory disease characterized by synovial hyperplasia, inflammatory cell infiltration, ir
22 rthritis; decreased macrophage infiltration, synovial hyperplasia, osteoclast formation, joint destru
23 ex non-cartilaginous OA conditions including synovial hyperplasia, osteophyte outgrowth and subchondr
24 itic joints from OPN-deficient mice revealed synovial hyperplasia, pannus formation, mononuclear cell
25 with DA, including significant reduction in synovial hyperplasia, pannus, angiogenesis, inflammatory
26 mation, immune reactivity, angiogenesis, and synovial hyperplasia persisted in RA-SCID grafts for 12
27 artilage injury, Gdf5-lineage cells underpin synovial hyperplasia through proliferation, are recruite
28 e to total articular cartilage (CC/TAC), and synovial hyperplasia with increased lining cells was fou
29 days before the onset of arthritis) revealed synovial hyperplasia without leukocytic infiltration.