Unicompartmental and bicompartmental knee osteoarthritis show different patterns of mononuclear cell infiltration and cytokine release in the affected joints

Moradi, Babak; Rosshirt, Nils; Tripel, Elena; Kirsch, J.; Barié, Alexander; Zeifang, Felix; Gotterbarm, Tobias; Hagmann, Sébastien

doi:10.1111/cei.12486

Cited by 67 publications

(77 citation statements)

References 51 publications

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“…Two recent studies [19■,20■] employ flow cytometry to study synovial membrane infiltration; both found CD14+ macrophages most abundant, followed by CD4+ T lymphocytes. In the second study [20■], pain scores available from a subset of patients correlated with proportions of synovial CD4+ cells, indicating a role for infiltrating T cells in osteoarthritis pain that needs further investigation.…”

Section: Local Infiltration Of Cellsmentioning

confidence: 99%

Role of low-grade inflammation in osteoarthritis

Scanzello

2017

Current Opinion in Rheumatology

209

151

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Purpose of review-Inflammatory changes in joint tissues can be detected by modern imaging techniques in osteoarthritis patients, but may be clinically subtle compared with many other types of arthritis. These changes associate with disease progression and clinical severity, and many inflammatory mediators may have biomarker utility. Moreover, a number of inflammatory mechanisms play a role in animal models of disease, but it is still not clear which mechanisms predominate and might be therapeutically manipulated most effectively. This review highlights specific examples of recent advances published in the past 18 months that have advanced this field.Recent findings-Clinical investigators now show that synovial inflammation is associated with pain sensitization, and similar to knee osteoarthritis, is a common and important feature of hand osteoarthritis. In addition, recent advances in basic studies demonstrate inflammatory markers and mechanisms related to leukocyte activity, innate immune mechanisms, and the chondrocyteintrinsic inflammatory response that might provide better opportunities for early detection, prognosis, or therapeutic intervention.Summary-Inflammation plays a central role in osteoarthritis pathogenesis, but additional translational work in this field is necessary, as are more clinical trials of anti-inflammatory approaches.

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Section: Local Infiltration Of Cellsmentioning

confidence: 99%

Role of low-grade inflammation in osteoarthritis

Scanzello

2017

Current Opinion in Rheumatology

209

151

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“…These findings suggest that activation of synovial macrophage is required for the production of MMPs leading to cartilage damage (82)(83)(84)(85). Natural killer cells have also been obtained from synovial tissues of patients undergoing total joint replacements, but the mechanism of pathogenesis has not yet been elucidated in detail (86).…”

Section: Correlation Between Synovitis and Oamentioning

confidence: 99%

Recent advances in the understanding of molecular mechanisms of cartilage degeneration, synovitis and subchondral bone changes in osteoarthritis

Wei

Bai

2016

Connective Tissue Research

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Osteoarthritis (OA), the most common form of degenerative joint disease, is linked to high morbidity. It is predicted to be the single greatest cause of disability in the general population by 2030. The development of disease-modifying therapy for OA currently face great obstacle mainly because the onset and development of the disease involve complex molecular mechanisms. In this review, we will comprehensively summarize biological and pathological mechanisms of three key aspects: degeneration of articular cartilage, synovial immunopathogenesis, and changes in subchondral bone. For each tissue, we will focus on the molecular receptors, cytokines, peptidases, related cell, and signal pathways. Agents that specifically block mechanisms involved in synovial inflammation, degeneration of articular cartilage, and subchondral bone remodeling can potentially be exploited to produce targeted therapy for OA. Such new comprehensive agents will benefit affected patients and bring exciting new hope for the treatment of OA.

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“…However, in the context of bone lytic diseases involving chronic inflammation, such as periodontitis and rheumatoid arthritis, infiltrations of not only B and T cells but also of macrophages are observed (6,7). It is true that macrophages are the most abundant immune cells found in the synovial membrane in osteoarthritis (8) and in synovial fluid in rheumatoid arthritis (9), outnumbering T and B cells. Therefore, it is plausible that osteoclast differentiation is affected by local factors produced by infiltrating lymphocytes, especially macrophages.…”

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confidence: 99%

Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis

Yamaguchi

Movila²,

Kataoka

et al. 2016

Infect Immun

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In response to a defined panel of stimuli, immature macrophages can be classified into two major phenotypes: proinflammatory (M1) and anti-inflammatory (M2). Although both phenotypes have been implicated in several chronic inflammatory diseases, their direct role in bone resorption remains unclear. The present study investigated the possible effects of M1 and M2 macrophages on RANKL-induced osteoclastogenesis. In osteoclastogenesis assays using RAW264.7 cells or bone marrow cells as osteoclast precursors, addition of M1 macrophages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulated conditions (M0), addition of M2 macrophages, or no macrophage addition (P < 0.05), suggesting that M1 macrophages can downregulate osteoclastogenesis. This effect was maintained when direct contact between M1 and osteoclast precursors was interrupted by cell culture insertion, indicating engagement of soluble factors released from M1. Macrophages which originate from monocytes not only are the key effector cells in innate immunity but also play a pivotal role in the initiation of adaptive immunity (1). It is well documented that polarized macrophages can be classified mainly into two different phenotypes: proinflammatory (M1) and antiinflammatory (M2). The production of inflammatory cytokines, such as tumor necrosis factor alpha (TNF-␣) and interleukin-6 (IL-6), by M1 macrophages promotes inflammation in the context of innate immune response, whereas the production of antiinflammatory cytokines and arginase by M2 macrophages leads to the resolution of inflammation (2). On the other hand, it is also true that osteoclasts that are engaged in bone resorption also belong to monocyte-lineage cells. Although macrophages and osteoclasts share the same precursor, macrophage colony-stimulating factor (M-CSF)-stimulated monocytes, the possible influence of macrophages, and especially the difference between M1 and M2, on osteoclastogenesis is largely unknown.Bone is a unique mineralized tissue which constantly undergoes a physiological remodeling process, and its homeostasis is achieved by the tuned balance between osteoclasts and boneforming cells (osteoblasts). As such, aberrantly promoted osteoclastogenesis is attributed to the bone destruction found in bone lytic diseases such as periodontitis and rheumatoid arthritis, which affects more than 50 million people in the United States alone (3). Of importance to this study, recent research has revealed that osteoclastogenesis is regulated by the immune system. For instance, a recent study (4) revealed that ␥␦-T cells inhibit osteoclastogenesis by their production of interferon gamma (IFN-␥), whereas B and T cells can produce RANKL under inflammatory conditions, thus working toward the promotion of osteoclastogenesis (5). However, in the context of bone lytic diseases involving chronic inflammation, such as periodontitis and rheumatoid arthritis, infiltrations of not only B and T cells but also of macrophages are observed (6, 7). It is true that macrophages are t...

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Unicompartmental and bicompartmental knee osteoarthritis show different patterns of mononuclear cell infiltration and cytokine release in the affected joints

Cited by 67 publications

References 51 publications

Role of low-grade inflammation in osteoarthritis

Role of low-grade inflammation in osteoarthritis

Recent advances in the understanding of molecular mechanisms of cartilage degeneration, synovitis and subchondral bone changes in osteoarthritis

Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis

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