Viscosupplementation for hip osteoarthritis: Does systematic review of patient-reported outcome measures support use?

Acuña, Alexander J.; Samuel, Linsen T.; Jeong, Stacy; Kamath, Atul F.

doi:10.1016/j.jor.2020.03.016

Cited by 11 publications

(40 citation statements)

References 55 publications

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Section: Discussionmentioning

confidence: 99%

“…Hence, resent studies have suggested that the expressions of leptin and its receptor have been considered positively as a risk factor associated with the development of OA [49][50][51]. [52] IL-1 family, including IL-1α and IL-1β, is considered the most key cytokine associated with the pathogenesis of OA that induces the inflammatory catabolic process combined with other catabolic factors such as aging, obesity, and traumatic joint injury [53]. Generally, the level of IL-1 family in the synovial fluid, synovial membrane, articular cartilage, and subchondral bone is elevated in the synovial joint of patients with OA [54].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Lim

Kim

et al. 2021

Oxidative Medicine and Cellular Longevity

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Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Lim

Kim

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Hence, resent studies have suggested that the expressions of leptin and its receptor have been considered positively as a risk factor associated with the development of OA [49][50][51]. [52] IL-1 family, including IL-1α and IL-1β, is considered the most key cytokine associated with the pathogenesis of OA that induce the in ammatory catabolic process combined with other catabolic factors such as aging, obesity, and traumatic joint injury [53]. Generally, the level of IL-1 family in the synovial uid, synovial membrane, articular cartilage, and subchondral bone is elevated in the synovial joint of patients with OA [54].…”

Section: Discussionmentioning

confidence: 99%

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Lim

Kim

et al. 2020

Preprint

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Objectives To verify the anti-catabolic effects of acteoside [α-L-rhamnosyl-(1->3)-β-D-glucoside] against osteoarthritis and its anti-catabolic signaling pathway. Methods Primary rat chondrocytes were isolated enzymatically from the articular cartilage of rat knee joint. Cytotoxicity of acteoside was assessed by MTT and Cell Live/Dead assay. Proteoglycan content was measured by dimethylmethylene blue assay. The proteoglycan loss was assessed by histological analysis using safranin-O & fast green staining after ex vivo organ culture of articular cartilage. The alteration of catabolic factors such as cartilage degrading enzymes, pro-inflammation cytokines, and inflammatory mediators were assessed by qPCR, qRT-PCR, gelatin zymography, western blot, and cytokine array. Cellular signaling pathways were investigated by western blot and nucleus translocation. Acteoside was orally administrated to osteoarthritic animals generated by the destabilization of medial meniscus at the knee joint of mice for 8 weeks. Thereafter, proteoglycan loss was assessed by safranin-O & fast green staining. Results Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as a normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase (MMP)-13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of pro-inflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Conclusion Our findings indicate that acteoside is a promising potential anti-catabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.

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“…[17]. By effectively increasing viscosity and reducing friction, viscosupplementation with hyaluronic acid (HA) has been shown to achieve satisfactory pain relief and improved function in OA [18][19][20]. Furthermore, HA is known to mitigate the activity of pro-inflammatory mediators and stimulate the metabolism of fibroblasts, possibly resulting in analgesic, anti-inflammatory, and chondroprotective effects on the joint [21].…”

Section: Introductionmentioning

confidence: 99%

Hybrid Hyaluronic Acid versus High Molecular Weight Hyaluronic Acid for the Treatment of Hip Osteoarthritis in Overweight/Obese Patients

Scaturro

Vitagliani

Terrana

et al. 2022

JFMK

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Background: Obesity is the main risk factor for hip osteoarthritis, negatively affecting the outcome of the disease. We evaluated the effectiveness of viscosupplementation with hybrid hyaluronic acid compared to that with high molecular weight hyaluronic acid in overweight/obese patients with hip osteoarthritis (OA). Methods: 80 patients were divided into two groups: a treatment group received two ultrasound-guided intra-articular hip injections of hybrid HA 15 days apart; a control group received a single ultrasound-guided infiltration with medium-high molecular weight hyaluronic acid (1500–2000 kDa). We assessed the pain, functional and cardiovascular capacity of the patients at baseline, after 3 months, and after 6 months of the infiltrative sessions. Results: The treatment group showed greater improvements in the scores on the NRS scale (5.4 ± 0.8 vs. 6.3 ± 0.8; p < 0.05) and in the Lequesne index (11.4 ± 2.6 vs. 13.6 ± 2.7; p < 0.05) and in the distance traveled at 6MWT (238.1 ± 53.9 m vs. 210.7 ± 46.2 m; p = 0.02) both at 3 months (T1) and at 6 months (T2). Conclusions: This study underlines the importance of exploiting the anti-inflammatory, analgesic, and chondrogenic properties of hybrid HA for the treatment of hip OA in overweight/obese patients.

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Viscosupplementation for hip osteoarthritis: Does systematic review of patient-reported outcome measures support use?

Cited by 11 publications

References 55 publications

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Hybrid Hyaluronic Acid versus High Molecular Weight Hyaluronic Acid for the Treatment of Hip Osteoarthritis in Overweight/Obese Patients

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