Toward defining the role of the synovium in mitigating normal articular cartilage wear and tear

Pellicore, Matthew J.; Gangi, Lianna R.; Murphy, Lance A.; Lee, Andy J.; Jacobsen, Timothy; Kenawy, Hagar M.; Shah, Roshan P.; Chahine, Nadeen O.; Ateshian, Gerard A.; Hung, Clark T.

doi:10.1016/j.jbiomech.2023.111472

Cited by 5 publications

(3 citation statements)

References 57 publications

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“…Despite the extensive work that has been carried out, the challenge we face is to pay attention to cellular mechanisms, integrating various key mechanical induction modules into a complete model to reveal deeper mechanisms. This is similar to how cells integrate different components to coordinate cohesive responses, , as shown in Figure . Many studies have focused on the modules of the topography-induced stem cell differentiation mechanism.…”

Section: Resultssupporting

confidence: 56%

Regulation of Tendon Stem Cell Behavior by Designed Nanoporous Topography of Microfibers

Ye,

Xu,

Hou

et al. 2023

Biomacromolecules

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Section: Resultssupporting

confidence: 56%

Regulation of Tendon Stem Cell Behavior by Designed Nanoporous Topography of Microfibers

Ye,

Xu,

Hou

et al. 2023

Biomacromolecules

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“…While most research in OA in recent decades has focused on the role of cartilage and subchondral bone, synovial tissue and fibroblasts are gaining increasing attention. They are, in particular, recognized for their role in maintaining cartilage homeostasis and mitigating “wear and tear maintenance” ( 153 ). The gathered research demonstrates a nuanced correlation between mechanical stimuli and TGF-β signaling regulating various cellular pathways ( Table 2 ).…”

Section: Metabolic Pathways In Fibroblasts and Myofibroblastsmentioning

confidence: 99%

Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis

Damerau,

Rosenow,

Alkhoury

et al. 2024

Front. Immunol.

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Osteoarthritis (OA) is the most common form of arthritis, characterized by osteophyte formation, cartilage degradation, and structural and cellular alterations of the synovial membrane. Activated fibroblast-like synoviocytes (FLS) of the synovial membrane have been identified as key drivers, secreting humoral mediators that maintain inflammatory processes, proteases that cause cartilage and bone destruction, and factors that drive fibrotic processes. In normal tissue repair, fibrotic processes are terminated after the damage has been repaired. In fibrosis, tissue remodeling and wound healing are exaggerated and prolonged. Various stressors, including aging, joint instability, and inflammation, lead to structural damage of the joint and micro lesions within the synovial tissue. One result is the reduced production of synovial fluid (lubricants), which reduces the lubricity of the cartilage areas, leading to cartilage damage. In the synovial tissue, a wound-healing cascade is initiated by activating macrophages, Th2 cells, and FLS. The latter can be divided into two major populations. The destructive thymocyte differentiation antigen (THY)1─ phenotype is restricted to the synovial lining layer. In contrast, the THY1+ phenotype of the sublining layer is classified as an invasive one with immune effector function driving synovitis. The exact mechanisms involved in the transition of fibroblasts into a myofibroblast-like phenotype that drives fibrosis remain unclear. The review provides an overview of the phenotypes and spatial distribution of FLS in the synovial membrane of OA, describes the mechanisms of fibroblast into myofibroblast activation, and the metabolic alterations of myofibroblast-like cells.

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“…The cross-tissue interaction in subchondral bone and cartilage and a network-based molecular regulation by the synovium are responsible for healthy environments in joints [ 24 , 108 ]. In Table 1 , we collected and represented data focusing on a given healthy condition—molecular activity in each resident or non-resident cell type.…”

Section: Joint As An Organ In a Healthy Statementioning

confidence: 99%

Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk

Semenistaja

Skuja

Kadisa

et al. 2023

IJMS

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Osteoarthritis (OA) is a chronic, progressive, severely debilitating, and multifactorial joint disease that is recognized as the most common type of arthritis. During the last decade, it shows an incremental global rise in prevalence and incidence. The interaction between etiologic factors that mediate joint degradation has been explored in numerous studies. However, the underlying processes that induce OA remain obscure, largely due to the variety and complexity of these mechanisms. During synovial joint dysfunction, the osteochondral unit undergoes cellular phenotypic and functional alterations. At the cellular level, the synovial membrane is influenced by cartilage and subchondral bone cleavage fragments and extracellular matrix (ECM) degradation products from apoptotic and necrotic cells. These “foreign bodies” serve as danger-associated molecular patterns (DAMPs) that trigger innate immunity, eliciting and sustaining low-grade inflammation in the synovium. In this review, we explore the cellular and molecular communication networks established between the major joint compartments—the synovial membrane, cartilage, and subchondral bone of normal and OA-affected joints.

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Toward defining the role of the synovium in mitigating normal articular cartilage wear and tear

Cited by 5 publications

References 57 publications

Regulation of Tendon Stem Cell Behavior by Designed Nanoporous Topography of Microfibers

Regulation of Tendon Stem Cell Behavior by Designed Nanoporous Topography of Microfibers

Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis

Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk

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