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• W3147487504 abstract "On behalf of all authors, I really thank Dr. Stocco, Dr. Porzionato, Dr. De Caro, and Dr. Macchi for sharing their important observations with us.1 I agree that characterization of osteoarthritis-infrapatellar fat pad (OA-IFP) stem cells and analyses of physiological functions of those cells are quite important subjects to understand OA pathogenesis. We also consider that fibroblasts residing in OA-IFP (some of them might be OA-IFP stem cells) play important roles during disease progression, since these cells have central roles in tissue fibrosis. Synovial fibroblasts are shown to express type I collagen and proteoglycan-degrading enzymes, such as ADAMTS-4, 5, 7, and 12(a disintegrin and metalloprotease with thrombospondin motifs) under the pathological condition.2 As described in our manuscript, we showed that fibrotic changes in IFP after acute joint inflammation are closely associated with persistent knee pain in rats. Although the underlying molecular mechanism of persistent pain after acute joint inflammation is yet to be elucidated, we consider that the process of tissue fibrosis may play important roles. As we showed, new vessel formation was observed in the fibrotic lesion in IFP. Calcitonin gene-related peptide (CGRP)-positive nerve fiber endings looked selectively accumulated near the new vessels in the fibrotic lesion. Based on these observations, we consider that fibrosis may induce both neovascularization and invasion of nerve fiber endings into IFP, which may decrease the pain threshold in the knee joint. Previous studies supported this hypothesis, bdecause inflammatory synovial fibroblasts are reported to induce angiogenesis through the hypoxia-inducible transcription factor 1a/vascular endothelial growth factor-mediated pathway.3 Vascular endothelial cells are reported to express a neurotrophic factor, NGF.4, 5 CGRP, which is produced by the sensitized nerve cells, is reported to activate the proliferation of endothelial cells.6 Thus, we expect that the positive feedback loop between vascular endothelial cells and sensory nerve cells might help to activate each other. Since this positive feedback loop seemed to selectively occur in the fibrotic lesion in IFP, we consider that anti-fibrotic drugs might effectively inhibit persistent pain in the joint. To test this hypothesis, we have tested the effects of anti-fibrotic reagents on persistent pain in the rat MIA model. In our current studies, we examine the effects of C-type natriuretic peptides (CNP), which is shown to ameliorate fibrotic changes in various tissues.7, 8 In these studies, thirty-two male Wistar rats were used. Monoiodoacetic acid (MIA) was injected intra-articularly to induce IFP fibrosis and persistent pain. CNP was injected after acute inflammatory phase (Days 4, 6, and 8) in the same knee joint. Time-course pain-avoidance behavior tests and histological analyses were performed. Histological evaluations indicated that intra-articular injection of CNP inhibited fibrotic changes in IFP after acute inflammation. Incapacitance tests (weight bearing asymmetry) indicated that MIA injection into rat knee joint quickly decreased the percent weight on ipsilateral limb. In the vehicle group, the decrease was continued up to Day 28, suggesting that pain persistence occurred after acute inflammation. In contrast, the pain was alleviated in the CNP group after Day 14. In addition, we observed significant improvement in the degree of articular cartilage degeneration at Day 14 in the CNP group. These data strongly suggest that controlling the biological functions of synovial fibroblasts and/or OA-IFP stem cells may be a new target for OA treatment. These data were just published in Osteoarthritis and Cartilage (DOI: 10.1016/j. joca.2020.12.014).9 Japan Society for the Promotion of Science, Grant/Award Numbers: 16K10813, 16K15657 and 18K09097; Japan Agency for Medical Research and Development, Grant/Award Numbers: 122013A109 and 18lm0203003j0002" @default.
• W3147487504 created "2021-04-13" @default.
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• W3147487504 date "2021-03-29" @default.
• W3147487504 modified "2023-09-23" @default.
• W3147487504 title "Reply: Letter to the editor" @default.
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• W3147487504 doi "https://doi.org/10.1002/jor.25028" @default.
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