Editorial: Osteoarthritis as an autoinflammatory disease caused by chondrocyte‐mediated inflammatory responses

Konttinen, Yrjö T.; Sillat, Tarvo; Barreto, Gonçalo; Ainola, Mari; Nordström, Dan

doi:10.1002/art.33451

Cited by 70 publications

(62 citation statements)

References 11 publications

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“…The characteristic features of OA include knee joint edema, decomposition of cartilage, hyperplasia of synovium and degradation of sub-chondral bones [16]. Various cytokines such as nitric oxide, PG, interleukin-1β, tumor necrosis factor-α, interleukin-6 and interleukin-8 are expressed in higher proportions in the chondrocytes of OA patients [6,9].…”

Section: Discussionmentioning

confidence: 99%

“…Various cytokines such as nitric oxide, PG, interleukin-1β, tumor necrosis factor-α, interleukin-6 and interleukin-8 are expressed in higher proportions in the chondrocytes of OA patients [6,9]. Chondrocytes play an important role in the onset of pain during inflammation by activating the neurons [7,16]. Studies have demonstrated that the expressions of interleukin-4, tumor necrosis factor-α, interleukin-6, and interleukin-13 are promoted by P2X7R activation [17].…”

Section: Discussionmentioning

confidence: 99%

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Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

He¹,

Li²,

Li³

et al. 2018

Trop. J. Pharm Res

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

He¹,

Li²,

Li³

et al. 2018

Trop. J. Pharm Res

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“…Chondrocytes lack the capacity to drive efficient repair and thus in osteoarthritis (OA) articular cartilage is irreversibly damaged. While earlier studies viewed OA as a wear-and-tear condition, there is now a consensus, reviewed by Konitten et al, 1 that chondrocytes both respond to and may themselves produce proinflammatory cytokines which can result in cartilage breakdown through modulating the expression of metalloproteinases including a disintegrin and metalloproteinase with thrombospondin domains (ADAMTS) enzymes, matrix metalloproteinases (MMPs), and serine proteinases. 2 Interplay of pain-related neurovascular peptides with cartilage biology submit your manuscript | www.dovepress.com…”

Section: The Cartilage Environmentmentioning

confidence: 99%

Chondrocyte responses to neurovascular peptides, cytokines, and a 3D environment: focus on ADAMs

Bevan¹,

Baker²,

Goldring

et al. 2016

MNM

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Chondrocyte exposure to inflammatory stimuli in several arthritic conditions, including osteoarthritis, results in the well-characterized induction of extracellular matrix degrading proteinases, notably members of a disintegrin and metalloproteinase (ADAM) with thrombospondin domains and matrix metalloproteinase families. Here we briefly review the less-studied ADAM family of proteinases in chondrocyte and cartilage biology. Following damage, cartilage is exposed to neurovascular peptides, and in this study we hypothesized that substance P and bradykinin, alongside inflammatory cytokines, may modulate chondrocyte steady-state messenger RNA levels for the proteolytic ADAM family members as well as for key cytokines and neuropeptides. We compared chondrocytes cultured in both two-dimensional and three-dimensional (3D) environments and found that 3D culture generally resulted in repression of expression of the genes under investigation, with the exception of anti-inflammatory interleukin 10 which was markedly upregulated in a 3D environment. Substance P and bradykinin had little effect on ADAM family expression, but further investigation revealed that a combination of bradykinin and cytokines led to enhanced expression of ADAM28 and a synergistic upregulation of interleukin 6, also observed under hypoxic conditions. Overall these data reveal wider chondrocyte responses to neurovascular peptides which may have an impact in an osteoarthritis context.

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“…These levels remain high for weeks and even months after trauma (Catterall et al, 2010;Olson et al, 2014;Christiansen et al, 2015). Based on clinical observations, cartilage derived biomarkers increase significantly a month after knee injury (Kramer et al, 2011;Konttinen et al, 2012). This shows that significant cartilage damage takes place weeks after the trauma, hence early intervention can effectively prevent long-term articular destruction (Imamura et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Post-Traumatic Arthritis: The Role of Cytokine Levels in Serum and Synovial Fluid

Sarafan¹,

Fakoor²,

Mehdinasab³

et al. 2017

GJHS

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Background and Objectives: Inflammatory processes play an important role in intra-articular fractures. The present study aimed to examine the relationship between chemerin, high-sensitivity C-reactive protein (hs-CRP), and Interleukin 17 (IL-17) serum and synovial fluid levels of osteoarthritis patients and individuals with intra-articular fractures. Method:In this case-control study, all osteoarthritis patients and individuals with intra-articular fractures who visited the Imam Khomeini Orthopedic Clinic of Ahvaz were examined. Blood samples (5 cc) were collected prior to surgery to measure chemerin Interleukin 17, and hs-CRP serum levels. Synovial fluid samples (2 cc) were collected during the surgery. Results:Measuring the levels of IL-17, chemerin and hs-CRP indicated a significant statistical difference between the serum and synovial fluids of osteoarthritis patients, individuals with intra-articular fractures, and the control group (p < .001). Post-hoc analyses showed statistically significant differences in all conditions except for hs-CRP levels between osteoarthritis patients and individuals with intra-articular fractures.Conclusion: Discovering ways to stop or slow down osteoarthritis is a matter of great concern. The findings on osteoarthritis indicate diverse, complex, and multidimensional processes involving cytokines. Information on cytokines that effect diseases can help develop efficient therapy methods.

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Editorial: Osteoarthritis as an autoinflammatory disease caused by chondrocyte‐mediated inflammatory responses

Cited by 70 publications

References 11 publications

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

Chondrocyte responses to neurovascular peptides, cytokines, and a 3D environment: focus on ADAMs

Post-Traumatic Arthritis: The Role of Cytokine Levels in Serum and Synovial Fluid

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