Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis

Damerau A., Rosenow E., Alkhoury D., Buttgereit F., Gaber T.

Narrative Review on Osteoarthritis, Chronic Wound, published in Front Immunol (2024) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Front Immunol (2024)
Reported sample size
—
Source database
Europe PMC
PMID
38895122
PMCID
PMC11183113
DOI
10.3389/fimmu.2024.1385006
Citations
46

Abstract (original English)

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

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Synovial MembraneFibroblastsAnimalsHumansOsteoarthritisFibrosisPhenotypeSynoviocytes

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research