Insights into the molecular landscape of osteoarthritis in human tissues

Katsoula, Georgia; Kreitmaier, Peter; Zeggini, Eleftheria

doi:10.1097/bor.0000000000000853

Cited by 21 publications

(11 citation statements)

References 52 publications

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“…The study found that over 140 genes were associated with OA and majority of the variants were localized in the non-coding region which made it inconspicuous. Hence, it is essential to establish the functional link between genomic and diseaserelevant alteration on multimolecular levels (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Obesity, Inflammation, and Immune System in Osteoarthritis

et al. 2022

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Obesity remains the most important risk factor for the incidence and progression of osteoarthritis (OA). The leading cause of OA was believed to be overloading the joints due to excess weight which in turn leads to the destruction of articular cartilage. However, recent studies have proved otherwise, various other factors like adipose deposition, insulin resistance, and especially the improper coordination of innate and adaptive immune responses may lead to the initiation and progression of obesity-associated OA. It is becoming increasingly evident that multiple inflammatory cells are recruited into the synovial joint that serves an important role in pathological changes in the synovial joint. Polarization of macrophages and macrophage-produced mediators are extensively studied and linked to the inflammatory and destructive responses in the OA synovium and cartilage. However, the role of other major innate immune cells such as neutrophils, eosinophils, and dendritic cells in the pathogenesis of OA has not been fully evaluated. Although cells of the adaptive immune system contribute to the pathogenesis of obesity-induced OA is still under exploration, a quantity of literature indicates OA synovium has an enriched population of T cells and B cells compared with healthy control. The interplay between a variety of immune cells and other cells that reside in the articular joints may constitute a vicious cycle, leading to pathological changes of the articular joint in obese individuals. This review addresses obesity and the role of all the immune cells that are involved in OA and summarised animal studies and human trials and knowledge gaps between the studies have been highlighted. The review also touches base on the interventions currently in clinical trials, different stages of the testing, and their shortcomings are also discussed to understand the future direction which could help in understanding the multifactorial aspects of OA where inflammation has a significant function.

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Section: Introductionmentioning

confidence: 99%

Obesity, Inflammation, and Immune System in Osteoarthritis

et al. 2022

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“…Inflammatory response and oxidative stress play key roles in the degenerative course of OA ( Tudorachi et al, 2021 ; Katsoula et al, 2022 ). It has been shown in several investigations that oxidative stress can cause articular cartilage dysfunction ( Ziskoven et al, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

Ginkgolide C slows the progression of osteoarthritis by activating Nrf2/HO-1 and blocking the NF-κB pathway

Jia

Zhao³

et al. 2022

Front. Pharmacol.

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Osteoarthritis (OA) is driven by chronic low-grade inflammation and subsequent cartilage degradation. OA is the most prevalent degenerative joint disease worldwide, and its treatment remains a challenge. The aim of this study was to explore the potential effects and mechanism underlying the anti-OA properties of ginkgolide C (GC). Protective effects of GC on hydrogen peroxide (H2O2)-treated rat chondrocytes were evaluated using ELISA, qPCR, western blot analysis, flow cytometry, ROS detection and immunofluorescence in vitro. Ameliorating effects of GC on cartilage degeneration in rats were evaluated through behavioral assays, microcomputed tomography, histopathological analysis, western blot analysis and ELISA in vivo. In vitro, GC treatment inhibited the release of pro-apoptotic factors induced by H2O2 and promoted the release of the anti-apoptotic proteins. In addition, GC decreased the expression of matrix metalloproteinase (MMP3 and MMP13), thrombospondin motifs 4 (ADAMTS4), and inflammatory mediators inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), and SOX9 thereby inhibiting extracellular matrix (ECM) degradation. Mechanistically, GC exerts its anti-apoptotic and anti-inflammatory effects by upregulating the oxidative stress signaling Nrf2/HO-1 pathway and preventing p65 from binding to DNA. Similarly, In a rat model with post-traumatic OA (PTOA) induced by anterior cruciate ligament transection (ACLT), GC inhibited joint pain, cartilage destruction, and abnormal bone remodeling of subchondral bone. GC inhibited H2O2-induced chondrocyte apoptosis through Nrf2/HO-1 and NF-κB axis, exerted anti-inflammatory effects, and inhibited cartilage degeneration in rat OA. Our findings advanced the concept that GC may contribute to cartilage metabolism through anti-inflammatory and anti-apoptotic effects, and the identified GC is a potential therapeutic agent for the treatment of OA.

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“…The interaction between the tissues that make up the joint, cartilage, the subcondral bone, synovial capsule are essential in the determinism of the pathogenesis of osteoarthritis, characterized by the remodelling of the extracellular matrix in the inflammatory environment. Modern genetic typing approaches have allowed the identification of two types of osteoatritis and have provided the molecular sequence of two different tissue-specific osteoarthritis, allowing a better understanding of the etiopatogenesis of this disease [21]…”

Section: The Fundamental Components Of the Jointmentioning

confidence: 99%

Bone Disease and New Prevention Borders Chapter 2: Osteoarticular Pathology

Riccardi¹,

Resta²,

Resta³

2022

Int J Biomed Res Prac

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In this second chapter, we are going to address the controversial topic of osteoarticular diseases of an inflammatory and degenerative nature that has a high incidence and a frequent feedback in advanced age and high social and health costs. We will focus our attention on the description of the pathogenic processes responsible for osteoarticular diseases, highlighting the fundamental role that collagen degenerations play in these. We are going to examine various options proposed for the prevention and treatment of diseases indicated with medications and food supplements. We are going to present a special description on the effects of Silicon, in particular, Organic Silicon G5, on these pathologies, until now poorly considered, and we will propose our own formulation composed of Silicon G5 plus trace elements. Finally, we are going to show the results obtained with this formulation on a consistent patient case history. Thanks to the results obtained, we propose to adopt our supplement, as an alternative or as an adjuvant treatment, to the drugs most used drugs in these diseases with the double advantage of reducing the dosage and the side effects of the latter, and improving its anti-inflammatory effectiveness with the synergistic activity obtainable with the two principals.

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Insights into the molecular landscape of osteoarthritis in human tissues

Cited by 21 publications

References 52 publications

Obesity, Inflammation, and Immune System in Osteoarthritis

Obesity, Inflammation, and Immune System in Osteoarthritis

Ginkgolide C slows the progression of osteoarthritis by activating Nrf2/HO-1 and blocking the NF-κB pathway

Bone Disease and New Prevention Borders Chapter 2: Osteoarticular Pathology

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