The Genesis of Pain in Osteoarthritis: Inflammation as a Mediator of Osteoarthritis Pain

Wood, Matthew J.; Miller, Rachel E.; Malfait, Anne‐Marie

doi:10.1016/j.cger.2021.11.013

Cited by 79 publications

(28 citation statements)

References 120 publications

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“…Therefore, it is unlikely that the destruction of articular cartilage directly causes OA pain. OA pain has been reported to be associated with synovitis and bone marrow lesion, 76 , 77 as well as alterations in subchondral bone, osteophyte formation, abnormalities of infrapatellar fat pads, and lesion of ligaments, in which tissues have highly distributed sensory nerves. 78 Molecular mechanisms underlying OA pain have been comprehensively updated and discussed in two recent review articles.…”

Section: Clinical Symptomsmentioning

confidence: 99%

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

Yao

Tao

et al. 2023

Sig Transduct Target Ther

417

147

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Osteoarthritis (OA) is a chronic degenerative joint disorder that leads to disability and affects more than 500 million population worldwide. OA was believed to be caused by the wearing and tearing of articular cartilage, but it is now more commonly referred to as a chronic whole-joint disorder that is initiated with biochemical and cellular alterations in the synovial joint tissues, which leads to the histological and structural changes of the joint and ends up with the whole tissue dysfunction. Currently, there is no cure for OA, partly due to a lack of comprehensive understanding of the pathological mechanism of the initiation and progression of the disease. Therefore, a better understanding of pathological signaling pathways and key molecules involved in OA pathogenesis is crucial for therapeutic target design and drug development. In this review, we first summarize the epidemiology of OA, including its prevalence, incidence and burdens, and OA risk factors. We then focus on the roles and regulation of the pathological signaling pathways, such as Wnt/β-catenin, NF-κB, focal adhesion, HIFs, TGFβ/ΒΜP and FGF signaling pathways, and key regulators AMPK, mTOR, and RUNX2 in the onset and development of OA. In addition, the roles of factors associated with OA, including MMPs, ADAMTS/ADAMs, and PRG4, are discussed in detail. Finally, we provide updates on the current clinical therapies and clinical trials of biological treatments and drugs for OA. Research advances in basic knowledge of articular cartilage biology and OA pathogenesis will have a significant impact and translational value in developing OA therapeutic strategies.

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Section: Clinical Symptomsmentioning

confidence: 99%

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

Yao

Tao

et al. 2023

Sig Transduct Target Ther

417

147

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“…Pro-inflammatory Cytokines TNF-α, IL-1β, and IL-6 are potent pro-inflammatory cytokines exerting pleiotropic effects on various cell types and play a critical role in the pathogenesis of chronic inflammatory diseases, such as OA and rheumatoid arthritis (RA). These molecules are released into the joint, and synovial inflammation is associated with pain in OA [26,27]. These cytokines facilitate the firing of joint nociceptors, leading to nociception and the initiation of OA pain [12,[28][29][30].…”

Section: Molecules Involved In Ps and Cs In Oamentioning

confidence: 99%

Mechanisms of Peripheral and Central Sensitization in Osteoarthritis Pain

Ohashi¹,

Uchida²,

Fukushima³

et al. 2023

Cureus

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Pain, the primary symptom of osteoarthritis (OA), reduces both the quality and quantity of life for patients. The pathophysiology of OA pain is complex and often difficult to explain solely by radiological structural changes. One reason for this discrepancy is pain sensitization (peripheral sensitization [PS] and central sensitization [CS]) in OA. Thus, an understanding of pain sensitization is important when considering treatment strategies and development for OA pain. In recent years, pro-inflammatory cytokines, nerve growth factors (NGFs), and serotonin have been identified as causative agents that induce peripheral and central sensitization and are becoming therapeutic targets for OA pain. However, the characteristics of the clinical manifestations of pain sensitization elicited by these molecules remain unclear, and it is not well understood who among OA patients should receive the therapeutic intervention. Thus, this review summarizes evidence on the pathophysiology of peripheral and central sensitization in OA pain and the clinical features and treatment options for this condition. While the majority of the literature supports the existence of pain sensitization in chronic OA pain, clinical identification and treatment of pain sensitization in OA are still in their infancy, and future studies with good methodological quality are needed.

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“…Эти субстанции вызывают возбуждение и сенситизацию ноцицепторов. Повреждение хряща, субхондральной кости и элементов связочного аппарата сопровождается фиброзом, неоангиогенезом и гетеротопической оссификацией -дегенеративными процессами, усиливаю щими механический стресс и снижаю щими болевой порог [29,30].…”

Section: что является причиной появления боли при поражении фасеточны...unclassified

Joint pathology in musculoskeletal lumbar pain: a dialogue between a neurologist and a rheumatologist

Editorial¹

2022

Medicinskij sovet

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Skeletal-muscular (nonspecific) lumbar pain (lumbodynia), often with spread to the leg (lumboishialgia), is one of the most common causes of consultations with a physician and temporary disability in the population. In many cases, the development of pain is associated with lesions of the lumbar facet joints (LFJ) and sacroiliac joint (SI). What are the causes, clinical features, and diagnosis of lumbar pain caused by lesions of the LFJ and SI? What should be the medical tactics for lumbar pain caused by LFJ and SI lesions? What is the actual practice of treating such patients? Leading experts discuss the problem of managing patients with lumbar musculoskeletal pain:Parfenov Vladimir Anatolievich – Dr. Sci. (Med.), Professor, Neurologist, Head of the Department of Nervous Diseases and Neurosurgery, Sklifosovskiy Institute of Clinical Medicine? First Moscow State Medical University (Sechenov University)Karateev Andrey Evgenyevich – Dr. Sci. (Med.), Head of the Laboratory of Pathophysiology of Pain and Clinical Polymorphism of Musculoskeletal Diseases Nasonova Research Institute of Rheumatology.

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The Genesis of Pain in Osteoarthritis: Inflammation as a Mediator of Osteoarthritis Pain

Cited by 79 publications

References 120 publications

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

Mechanisms of Peripheral and Central Sensitization in Osteoarthritis Pain

Joint pathology in musculoskeletal lumbar pain: a dialogue between a neurologist and a rheumatologist

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