Correlation between plasma and synovial fluid basic fibroblast growth factor with radiographic severity in primary knee osteoarthritis

Honsawek, Sittisak; Yuktanandana, Pongsak; Tanavalee, Aree; Saetan, Natthaphon; Anomasiri, Wilai; Parkpian, Vinai

doi:10.1007/s00264-011-1435-z

Cited by 28 publications

(18 citation statements)

References 26 publications

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“…The levels of HSPG-2, FGF-2, FGF-18, FGFR-1, and FGFR-3 were consistently decreased in OA cartilage lesions after DMM, whereas staining was maintained in the peripheral cartilage and osteophytes and increased in the synovium. Such tissue and topographic differences have been previously reported in human OA, in which, despite increased FGF-2 levels in the synovium and synovial fluid (40,41), the levels of FGF-2 protein (and mRNA) in OA cartilage have been found to vary between patients according to disease severity and according to whether lesion, perilesion, distant, or marginal/osteophyte tissue is examined (42)(43)(44). The single report on chondrocyte HSPG-2 in OA describes increased staining surrounding chondrocyte clusters only in the perilesion cartilage (45), where FGF-2 is also most strongly localized (42).…”

Section: Discussionsupporting

confidence: 77%

Ablation of Perlecan Domain 1 Heparan Sulfate Reduces Progressive Cartilage Degradation, Synovitis, and Osteophyte Size in a Preclinical Model of Posttraumatic Osteoarthritis

Shu

Jackson

Smith

et al. 2016

Arthritis & Rheumatology

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Objective. To investigate the role of the heparan sulfate (HS) proteoglycan perlecan (HSPG-2) in regulating fibroblast growth factor (FGF) activity, bone and joint growth, and the onset and progression of posttraumatic osteoarthritis (OA) in a mouse gene-knockout model.Methods. Maturational changes were evaluated histologically in the knees of 3-, 6-, and 12-week-old wildtype (WT) mice and Hspg2 D32/D32 mice (Hspg2 lacking domain 1 HS, generated by ablation of exon 3 of perlecan). Cartilage damage, subchondral bone sclerosis, osteophytosis, and synovial inflammation were scored at 4 and 8 weeks after surgical induction of OA in WT and Hspg2 D32/D32 mice. Changes in cartilage expression of FGF-2, FGF-18, HSPG-2, FGF receptor 1 (FGFR-1), and FGFR-3 were examined immunohistochemically. Femoral head cartilage from both mouse genotypes was cultured in the presence or absence of interleukin-1a (IL-1a), FGF-2, and FGF-18, and the content and release of glycosaminoglycan (GAG) and expression of messenger RNA (mRNA) for key matrix molecules, enzymes, and inhibitors were quantified.Results. No effect of perlecan HS ablation on growth plate or joint development was detected. After induction of OA, Hspg2 D32/D32 mice had significantly reduced cartilage erosion, osteophytosis, and synovitis. OA-induced loss of chondrocyte expression of FGF-2, FGF-18, and HSPG-2 occurred in both genotypes. Expression of FGFR-1 after OA induction was maintained in WT mice, while FGFR-3 loss after OA induction was significantly reduced in Hspg2 D32/D32 mice. There were no genotypic differences in GAG content or release between unstimulated control cartilage and IL1a-stimulated cartilage. However, IL-1a-induced cartilage expression of Mmp3 mRNA was significantly reduced in Hspg2 D32/D32 mice. Cartilage GAG release in either the presence or absence of IL-1a was unaltered by FGF-2 in both genotypes. In cartilage cultures with FGF-18, IL-1a-stimulated GAG loss was significantly reduced only in Hspg2 D32/D32 mice, and this was associated with maintained expression of Fgfr3 mRNA and reduced expression of Mmp2/Mmp3 mRNA.Conclusion. Perlecan HS has significant roles in directing the development of posttraumatic OA, potentially via the alteration of FGF/HS/FGFR signaling. These data suggest that the chondroprotection conferred by perlecan HS ablation could be attributed, at least in part, to the preservation of FGFR-3 and increased FGF signaling. Perlecan (heparan sulfate proteoglycan 2 [HSPG-2])is a large proteoglycan found not only in vascularized tissue, but also in the cartilage, meniscus, and intervertebral disc (1). It is a key component of basement membranes and the pericellular matrix surrounding cells in avascular tensional and weight-bearing connective tissue that may serve as an intrinsic basement membrane (2). The pericellular localization of perlecan is consistent with its roles in matrix stabilization, cell binding, and mechano-regulation (3,4). Perlecan is an early marker

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Section: Discussionsupporting

confidence: 77%

Ablation of Perlecan Domain 1 Heparan Sulfate Reduces Progressive Cartilage Degradation, Synovitis, and Osteophyte Size in a Preclinical Model of Posttraumatic Osteoarthritis

Shu

Jackson

Smith

et al. 2016

Arthritis & Rheumatology

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“…3 Noninvasive biochemical analyses have been developed to evaluate disease progress and severity, and provide a nonradiographical alternative for the early detection of osteoarthritis. [4][5][6] Although the aetiology and pathophysiology of osteoarthritis are both poorly understood, it is believed that secreted inflammatory molecules (such as proinflammatory cytokines) are among the critical mediators of the disturbed processes implicated in osteoarthritis pathophysiology. 7 Proinflammatory cytokines have been reported to contribute to osteoarthritis pathogenesis by increasing cartilage degradation and inducing hyperalgesia via a number of direct and indirect actions.…”

Section: Introductionmentioning

confidence: 99%

Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

et al. 2013

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Objective: To determine interleukin (IL)-17 concentrations in serum and synovial fluid from patients with knee osteoarthritis, and evaluate their correlation with disease severity. Methods: Serum and synovial fluid were collected from patients with primary knee osteoarthritis; age-and sex-matched healthy control subjects provided serum samples. This study was conducted retrospectively. IL-17 was quantified by enzyme-linked immunosorbent assay. Osteoarthritis severity and grade were assessed using the Lequesne index and Kellgren and Lawrence (KL) grading system, respectively. Results: Serum IL-17 concentrations were significantly higher in patients (n ¼ 98) than in controls (n ¼ 50). In the patient group, the synovial fluid IL-17 concentration increased significantly with KL grade and was significantly positively correlated with Lequesne index (r ¼ 0.6232). Conclusions: The synovial fluid IL-17 concentration could represent a useful biochemical marker to reflect knee osteoarthritis severity and progression.

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“…Basic fibroblast growth factor (bFGF, also known as FGF-2) is one of the most well-characterized members of the family and one of the most powerful angiogenic polypeptide with a molecular weight of 18 kD [5]. bFGF secreted by fibroblasts, platelets or other cells is responsible for connective tissue formation and wound healing [6][7][8]. A previous study has demonstrated that bFGF expression was evident in LF degeneration and was involved with calcium pyrophosphate crystal deposition in the LF of degenerated lumbar spine [9].…”

Section: Introductionmentioning

confidence: 99%

Hypertrophy of the ligamentum flavum in lumbar spinal canal stenosis is associated with increased bFGF expression

Honsawek

Poonpukdee

Chalermpanpipat

et al. 2013

International Orthopaedics (SICOT)

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Purpose A prospective study was undertaken to investigate basic fibroblast growth factor (bFGF) expression in hypertrophic ligamentum flavum (LF) from patients with lumbar spinal canal stenosis (LSCS) and to determine whether there was a correlation of bFGF expression with LF thickness. Methods Twenty patients with lumbar spinal canal stenosis were enrolled in this study. bFGF mRNA and protein expressions in LF were analyzed using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA), respectively. The thickness of LF was measured by axial T1-weighted magnetic resonance imaging. Results Expression of bFGF was substantially higher in the hypertrophic LF group than in the control group (P<0.001) as quantified by quantitative real-time PCR. In immunohistochemical study, bFGF was positively stained on the fibroblasts within hypertrophic LF compared to nonpathologic LF of controls. Subsequent ELISA analysis revealed that bFGF concentration in the hypertrophic LF group was remarkably higher than that in the control group (P=0.003). The thickness of LF in the hypertrophic LF was significantly greater than that in the control group (P<0.001). LSCS patients with greater severity of LF hypertrophy had significantly higher bFGF levels in the LF tissues (P<0.001). Furthermore, the bFGF concentration exhibited a positive correlation with the LF thickness (r=0.974, P<0.001). Conclusions These findings suggest that the increased expression of bFGF is associated with the hypertrophy of ligamentum flavum in patients with LSCS.

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Correlation between plasma and synovial fluid basic fibroblast growth factor with radiographic severity in primary knee osteoarthritis

Cited by 28 publications

References 26 publications

Ablation of Perlecan Domain 1 Heparan Sulfate Reduces Progressive Cartilage Degradation, Synovitis, and Osteophyte Size in a Preclinical Model of Posttraumatic Osteoarthritis

Ablation of Perlecan Domain 1 Heparan Sulfate Reduces Progressive Cartilage Degradation, Synovitis, and Osteophyte Size in a Preclinical Model of Posttraumatic Osteoarthritis

Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

Hypertrophy of the ligamentum flavum in lumbar spinal canal stenosis is associated with increased bFGF expression

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