Moderate Physical Activity as a Prevention Method for Knee Osteoarthritis and the Role of Synoviocytes as Biological Key

Castrogiovanni, Paola; Rosa, Michelino Di; Ravalli, Silvia; Castorina, Alessandro; Guglielmino, Claudia; Imbesi, Rosa; Vecchio, Michele; Drago, Filippo; Szychlinska, Marta Anna; Musumeci, Giuseppe

doi:10.3390/ijms20030511

Cited by 145 publications

(141 citation statements)

References 53 publications

(80 reference statements)

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“…This indicates a beneficial effect of MPA on the synovium likely by rescuing type B synoviocyte dysfunction at the early stages of OA. Yet, pro‐inflammatory cytokine IL‐6 expression in ACLT‐rats performing MPA did not decrease with physical activity. Likewise, Cifuentes et al reported that 8 weeks of running at 13 m/min significantly decreased the oxidative stress markers in OA‐affected joints.…”

Section: The Exercise Effect On Cartilage Bio‐composition and Morpholmentioning

confidence: 97%

“…Both TNF‐alpha and IL1‐beta were similar between exercised and control groups. Yet, significant differences were observed for IL‐4, IL‐6, and lubricin . Musumeci et al demonstrated that moderate physical activity improved lubricative properties of articular cartilage by promoting lubricin synthesis and its increase in the SF in adult (12 months old) and elderly (24 years old) rats compared to the unexercised group.…”

Section: The Exercise Effect On Cartilage Bio‐composition and Morpholmentioning

confidence: 99%

“…Yet, significant differences were observed for IL-4, IL-6, and lubricin. 59 Musumeci et al 60 demonstrated that moderate physical activity improved lubricative properties of articular cartilage by promoting lubricin synthesis and its increase in the SF in adult (12 months old) and elderly (24 years old) rats compared to the unexercised group. Lubricin is a boundary lubricant, present in the SF and articular cartilage superficial layer, essential for the articular cartilage low friction and protection from wear.…”

Section: Effect Of Treadmill Exercise On Healthy Jointsmentioning

confidence: 99%

“…71 Similar results were shown for the mild physical activity where the 6 weeks treadmill run at the speed of 5 m/min acted beneficially on the ACLT-induced OA joints, improving lubricin synthesis, and OARSI scoring. 72 More recently, Castrogiovanni et al (2019) explored the effect of mild (5 m/min) and Moderate (20 m/ min) Physical Activity (MPA) in a rat model. Four groups were tested (control, MPA, Anterior Cruciate Ligament Transection (ACLT) rats with OA, and ACLT-rats performing MPA.…”

Section: Treadmill Exercise and Oa Jointsmentioning

confidence: 99%

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Osteoarthritis biomarker responses and cartilage adaptation to exercise: A review of animal and human models

Mazor

Best

Césaro

et al. 2019

Scandinavian Med Sci Sports

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Regular physical activity has been suggested as having both preventive and therapeutic benefits for individuals with osteoarthritis (OA). However, evidence of whether exercise and which type of exercise constitutes a benefit or a risk in the development and progression of OA remains debatable. This may be due to the evaluation of the effect of physical activity or new disease‐modifying OA drugs which is currently based on radiographic criteria (eg, joint space width) and the lack of correlation with clinical signs and symptoms (eg, pain and loss of function). Moreover, OA typically manifests itself as changes within the joint space and subchondral bone as well as the whole joint structure, including progressive degradation of cartilage, menisci, ligaments, and synovial inflammation. Biomarkers are being developed to quantify joint remodeling and disease progression notably involving the articular cartilage and synovial fluid. The primary purpose of this review was to evaluate the current literature and to provide further insight based on OA biomarkers and the role physical activity plays in the management of OA. Osteoarthritis biomarkers together with radiographic imaging evidence will ideally guide healthcare providers to incorporate exercise recommendations into clinical management and offer patients evidence‐based and individually tailored exercise prescriptions.

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Section: The Exercise Effect On Cartilage Bio‐composition and Morpholmentioning

confidence: 97%

Section: The Exercise Effect On Cartilage Bio‐composition and Morpholmentioning

confidence: 99%

Section: Effect Of Treadmill Exercise On Healthy Jointsmentioning

confidence: 99%

Section: Treadmill Exercise and Oa Jointsmentioning

confidence: 99%

See 2 more Smart Citations

Osteoarthritis biomarker responses and cartilage adaptation to exercise: A review of animal and human models

Mazor

Best

Césaro

et al. 2019

Scandinavian Med Sci Sports

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“…This will be the major cause of morbidity and physical limitation among individuals aged over 40 years (24). Current therapy for OA is directed toward non-pharmacological treatments as physical activity through mechanical stimulation (25) and symptomatic treatment, focusing in pain management, and is not able to promote regeneration of degenerated cartilage or to attenuate joint inflammation (18).…”

Section: Articular Cartilage and Inflammationmentioning

confidence: 99%

Macrophage: A Potential Target on Cartilage Regeneration

et al. 2020

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Cartilage lesions and osteoarthritis (OA) presents an ever-increasing clinical and socioeconomic burden. Synovial inflammation and articular inflammatory environment are the key factor for chondrocytes apoptosis and hypertrophy, ectopic bone formation and OA progression. To effectively treat OA, it is critical to develop a drug that skews inflammation toward a pro-chondrogenic microenvironment. In this narrative and critical review, we aim to see the potential use of immune cells modulation or cell therapy as therapeutic alternatives to OA patients. Macrophages are immune cells that are present in synovial lining, with different roles depending on their subtypes. These cells can polarize to pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes, being the latter associated with wound-healing by the production of ARG-1 and pro-chondrogenic cytokines, such as IL-10, IL-1RA, and TGF-b. Emerging evidence reveals that macrophage shift can be determined by several stimuli, apart from the conventional in vitro IL-4, IL-13, and IL-10. Evidences show the potential of physical exercise to induce type 2 response, favoring M2 polarization. Moreover, macrophages in contact with oxLDL have effect on the production of anabolic mediators as TGF-b. In the same direction, type II collagen, that plays a critical role in development and maturation process of chondrocytes, can also induce M2 macrophages, increasing TGF-b. The mTOR pathway activation in macrophages was shown to be able to polarize macrophages in vitro, though further studies are required. The possibility to use mesenchymal stem cells (MSCs) in cartilage restoration have a more concrete literature, besides, MSCs also have the capability to induce M2 macrophages. In the other direction, M1 polarized macrophages inhibit the proliferation and viability of MSCs and impair their ability to immunosuppress the environment, preventing cartilage repair. Therefore, even though MSCs therapeutic researches advances, other sources of M2 polarization are attractive issues, and further studies will contribute to the possibility to manipulate this polarization and to use it as a therapeutic approach in OA patients.

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miR‐122 and the WNT/β‐catenin pathway inhibit effects of both interleukin‐1β and tumor necrosis factor‐α in articular chondrocytes in vitro

Scott

Cohen

Boyan

et al. 2022

J of Cellular Biochemistry

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Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and WNT/β-catenin signaling cause dysregulation of rat primary articular chondrocytes (rArCs), resulting in cartilage extracellular matrix destruction and osteoarthritis (OA) progression. microRNA (miR) miR-122 represses these effects whereas miR-451 exacerbates IL-1β-stimulated matrix metalloproteinase-13 (MMP-13) and prostaglandin E2 (PGE2) production. The goals of this study were to evaluate crosstalk between these signaling pathways and determine if miR-122 and miR-451 exert their protective/destructive effects through these pathways in an in vitro model of OA. Primary rArCs were treated with IL-1β or TNF-α for 24 h and total DNA, MMP-13, and PGE2, as well as expression levels of miR-122 and miR-451 were measured. After 24-h transfection with miR-122, miR-451, miR-122-inhibitor, or miR-451-inhibitor, rArCs were treated with or without TNF-α for 24 h; total DNA, MMP-13, and PGE2 were measured.Similarly, cells were treated with WNT-agonist lithium chloride (LiCl), WNTantagonist XAV-939 (XAV), or PKF-118-310 (PKF) with and without IL-1β or TNF-α stimulation. Both IL-1β and TNF-α-stimulation increased MMP-13 and PGE2 production. Transfection with miR-122 prevented TNF-α-stimulated increases in MMP-13 and PGE2 whereas transfection with miR-451 did not change these levels. No differences were found in MMP-13 or PGE2 production with miR-122 or miR-451 inhibitors. LiCl treatment decreased PGE2 production in cultures treated with TNF-α, but not MMP-13. XAV increased TNF-α-stimulated increases in PGE2 but not MMP-13. LiCl reduced IL-1β-stimulated increases in MMP-13 and PGE2. XAV and PKF increased IL-1β-stimulated increases in MMP-13 and PGE2. In this in vitro OA model, miR-122 protects against both IL-1β and TNF-α stimulated increases in MMP-13 and PGE2 production. miR-451 does not act through the TNF-α pathway. The WNT/β-catenin pathway regulates the effects of IL-1β and TNF-α

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Moderate Physical Activity as a Prevention Method for Knee Osteoarthritis and the Role of Synoviocytes as Biological Key

Cited by 145 publications

References 53 publications

Osteoarthritis biomarker responses and cartilage adaptation to exercise: A review of animal and human models

Osteoarthritis biomarker responses and cartilage adaptation to exercise: A review of animal and human models

Macrophage: A Potential Target on Cartilage Regeneration

miR‐122 and the WNT/β‐catenin pathway inhibit effects of both interleukin‐1β and tumor necrosis factor‐α in articular chondrocytes in vitro

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