Serum Inflammatory Markers in Patients With Knee Osteoarthritis

Giordano, Rocco; Petersen, Kristian Kjær; Andersen, Hjalte Holm; Simonsen, Ole; Arendt-Nielsen, Lars

doi:10.1097/ajp.0000000000000804

Cited by 31 publications

(36 citation statements)

References 90 publications

(61 reference statements)

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“…IL-6 has been found to serve as pronociceptive mediators which may be directly implicated in pain generation by acting on nociceptive neurons [ 35 , 36 ]. Several clinical studies also have shown that IL-6 in synovial fluid/serum was correlated with pain scores [ 37 , 38 ], but only few studies have investigated the relationship of IL-6 with pain change [ 13 , 39 ]. Higher synovial fluid levels of IL-6 at the time of surgery were found to predict less pain improvement at 2 years following total knee arthroplasty in 28 patients with OA [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Prospective Association Between Inflammatory Markers and Knee Cartilage Volume Loss and Pain Trajectory

et al. 2021

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Introduction: Inflammation has been suggested to be involved in the pathogenesis of osteoarthritis and pain. We sought to explore the associations between inflammatory serum markers and magnetic resonance imaging-defined long-term structural change and pain trajectory. Methods: A total of 169 randomly selected participants (mean age 63 years; 47% female) from a prospective cohort study were included in this study. Circulating levels of interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-a) and high-sensitivity C-reactive protein (CRP) were measured at baseline. A knee MRI scan was performed to measure cartilage volume (CV) and bone marrow lesions (BMLs) at baseline and at 10.7 years. Knee pain at four visits was measured by the WOMAC pain questionnaire, and pain trajectories were identified using groupbased trajectory modelling. Linear, log-binomial and multi-nominal logistic regression were used for the analyses. Results: IL-6 was associated with lateral but not medial tibial CV loss (b = -0.25% per annum, per standard deviation [SD] log pg/ml; P \ 0.05) in the multivariate analysis. IL-6 was also associated with a 'Moderate pain' trajectory (relative risk ratio 1.93 per SD log pg/ml; 95% confidence interval 1.02-3.65) relative to the 'Minimal pain' trajectory group. There was no significant association of TNF-a and CRP with CV loss and pain trajectory groups with the exception of a beneficial relationship between CRP and medial tibial CV loss (b = 0.20% per annum, per SD log mg/l). No association between inflammatory markers and change in BML size was observed. Conclusions: IL-6 was independently associated with compartment-specific CV loss and worse pain trajectory, but the other markers studied were not, suggesting that components of inflammation are implicated in the pathogenesis of cartilage loss and developing a worse pain course.

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Section: Discussionmentioning

confidence: 99%

Prospective Association Between Inflammatory Markers and Knee Cartilage Volume Loss and Pain Trajectory

et al. 2021

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“…Decreased serum levels of Eukaryotic Translation Initiation Factor 4E-Binding Protein 1 (4E-BP1) correlate with pain intensity. Increased levels of IL-6, CSF-1, FGF-21, Monocyte Chemotactic Protein 3 (MCP-3), known as CCL7, and TGF-β1 have been found in the serum of patients with KOA [ 131 ].…”

Section: Pathogenesis and Histology—osteoarthritis As A Whole Joinmentioning

confidence: 99%

“…Apart from their role in the inflammatory process in the joint, a correlation of pain and the concentration of cytokines has been recognized, with IL-6 and IL-8 showing a correlation with pain on movement, and TNF-α correlating with both pain on movement and rest [ 141 ]. Moreover, IL-10, IL-12, IL-13, VEGF, SCGF-β, fibroblast growth factor-21 and Eukaryotic translation initiation factor 4E-binding protein 1 levels were correlated with knee pain and functional impairment in an analysis of knee OA patients [ 131 , 142 ]. Studies comparing patients with knee OA and hip OA have demonstrated that the profile of cytokines differs not only among patients but among joints, suggesting that knee and hip OA have different cytokine release profiles and that hip OA measured higher concentrations of inflammatory cytokines when compared to the knee [ 143 , 144 ].…”

Section: Pathogenesis and Histology—osteoarthritis As A Whole Joinmentioning

confidence: 99%

Knee Osteoarthritis: A Review of Pathogenesis and State-Of-The-Art Non-Operative Therapeutic Considerations

Primorac

Molnar

Rod

et al. 2020

Genes

256

176

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Being the most common musculoskeletal progressive condition, osteoarthritis is an interesting target for research. It is estimated that the prevalence of knee osteoarthritis (OA) among adults 60 years of age or older is approximately 10% in men and 13% in women, making knee OA one of the leading causes of disability in elderly population. Today, we know that osteoarthritis is not a disease characterized by loss of cartilage due to mechanical loading only, but a condition that affects all of the tissues in the joint, causing detectable changes in tissue architecture, its metabolism and function. All of these changes are mediated by a complex and not yet fully researched interplay of proinflammatory and anti-inflammatory cytokines, chemokines, growth factors and adipokines, all of which can be measured in the serum, synovium and histological samples, potentially serving as biomarkers of disease stage and progression. Another key aspect of disease progression is the epigenome that regulates all the genetic expression through DNA methylation, histone modifications, and mRNA interference. A lot of work has been put into developing non-surgical treatment options to slow down the natural course of osteoarthritis to postpone, or maybe even replace extensive surgeries such as total knee arthroplasty. At the moment, biological treatments such as platelet-rich plasma, bone marrow mesenchymal stem cells and autologous microfragmented adipose tissue containing stromal vascular fraction are ordinarily used. Furthermore, the latter two mentioned cell-based treatment options seem to be the only methods so far that increase the quality of cartilage in osteoarthritis patients. Yet, in the future, gene therapy could potentially become an option for orthopedic patients. In the following review, we summarized all of the latest and most important research in basic sciences, pathogenesis, and non-operative treatment.

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“…In addition, the recent single-cell sequencing work in chondrocytes demonstrated differential expression of translation initiation factors 4E-BP1 [in proliferative chondrocytes (ProCs)] and EIF4A1, EIF4A2, EIF4A3, EIF1 and EIF5 [in homeostatic chondrocytes (HomCs)] [ 16 ▪ , 29 ]. Interestingly, in an osteoarthritis serum biomarker study, patients with knee osteoarthritis had significantly lower serum levels of 4E-BP1, which was found be positively correlated with osteoarthritis pain intensity [ 34 ]. Together, this suggests that the mechanisms and involvement of deregulated ribosome protein translation activity in osteoarthritis chondrocytes are far more complex and depend on the stage of osteoarthritis progression and the chondrocyte phenotype, warranting further studies to dissect its complexity.…”

Section: The Ribosome In Osteoarthritismentioning

confidence: 99%

“…1). Multiple studies have gathered compelling evidence of major proteomic changes in fluids, cells and tissues of the osteoarthritis joint [32][33][34][35][36][37][38][39]. For a long time, it was assumed that these changes originate from major mRNA transcriptomic changes only.…”

Section: Altered Ribosome Activity In Osteoarthritismentioning

confidence: 99%

Ribosome dysfunction in osteoarthritis

Akker

Caron

Peffers

et al. 2022

Current Opinion in Rheumatology

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Purpose of review Translation of genetic information encoded within mRNA molecules by ribosomes into proteins is a key part of the central dogma of molecular biology. Despite the central position of the ribosome in the translation of proteins, and considering the major proteomic changes that occur in the joint during osteoarthritis development and progression, the ribosome has received very limited attention as driver of osteoarthritis pathogenesis. Recent findings We provide an overview of the limited literature regarding this developing topic for the osteoarthritis field. Recent key findings that connect ribosome biogenesis and activity with osteoarthritis include: ribosomal RNA transcription, processing and maturation, ribosomal protein expression, protein translation capacity and preferential translation. Summary The ribosome as the central cellular protein synthesis hub is largely neglected in osteoarthritis research. Findings included in this review reveal that in osteoarthritis, ribosome aberrations have been found from early-stage ribosome biogenesis, through ribosome build-up and maturation, up to preferential translation. Classically, osteoarthritis has been explained as an imbalance between joint tissue anabolism and catabolism. We postulate that osteoarthritis can be interpreted as an acquired ribosomopathy. This hypothesis fine-tunes the dogmatic anabolism/katabolism point-of-view, and may provide novel molecular opportunities for the development of osteoarthritis disease-modifying treatments.

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Serum Inflammatory Markers in Patients With Knee Osteoarthritis

Cited by 31 publications

References 90 publications

Prospective Association Between Inflammatory Markers and Knee Cartilage Volume Loss and Pain Trajectory

Prospective Association Between Inflammatory Markers and Knee Cartilage Volume Loss and Pain Trajectory

Knee Osteoarthritis: A Review of Pathogenesis and State-Of-The-Art Non-Operative Therapeutic Considerations

Ribosome dysfunction in osteoarthritis

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