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Scientific Reports Mar 2021Detailed understanding of the innervation of the hip capsule (HC) helps inform surgeons' and anaesthetists' clinical practice. Post-interventional pain following... (Meta-Analysis)
Meta-Analysis
Detailed understanding of the innervation of the hip capsule (HC) helps inform surgeons' and anaesthetists' clinical practice. Post-interventional pain following radiofrequency nerve ablation (RFA) and dislocation following total hip arthroplasty (THA) remain poorly understood, highlighting the need for more knowledge on the topic. This systematic review and meta-analysis focuses on gross anatomical studies investigating HC innervation. The main outcomes were defined as the prevalence, course, density and distribution of the nerves innervating the HC and changes according to demographic variables. HC innervation is highly variable; its primary nerve supply seems to be from the nerve to quadratus femoris and obturator nerve. Many articular branches originated from muscular branches of the lumbosacral plexus. It remains unclear whether demographic or anthropometric variables may help predict potential differences in HC innervation. Consequently, primary targets for RFA should be the anterior inferomedial aspect of the HC. For THA performed on non-risk patients, the posterior approach with capsular repair appears to be most appropriate with the lowest risk of articular nerve damage. Care should also be taken to avoid damaging vessels and muscles of the hip joint. Further investigation is required to form a coherent map of HC innervation, utilizing combined gross and histological investigation.
Topics: Arthroplasty, Replacement, Hip; Cadaver; Femoral Nerve; Hip Joint; Humans; Joint Capsule; Obturator Nerve; Pain, Postoperative; Radiofrequency Ablation; Sciatic Nerve
PubMed: 33674621
DOI: 10.1038/s41598-021-84345-z -
Bioscience Trends Nov 2020The human immune system has evolved to recognize and eradicate pathogens, a process that is known as "host defense". If, however, the immune system does not work... (Review)
Review
The human immune system has evolved to recognize and eradicate pathogens, a process that is known as "host defense". If, however, the immune system does not work properly, it can mistakenly attack the body's own tissues and induce autoimmune diseases. Rheumatoid arthritis (RA) is such an autoimmune disease in which the synovial joints are predominately attacked by the immune system. Moreover, RA is associated with bone destruction and joint deformity. Although biologic agents have propelled RA treatment forward dramatically over the past 30 years, a considerable number of patients with RA still experience progressive bone damage and joint disability. That is to be expected since current RA therapies are all intended to halt inflammation but not to alleviate bone destruction. A better understanding of bone erosions is crucial to developing a novel strategy to treat RA-associated erosions. This review provides insights into RA-associated bone destruction and perspectives for future clinical interventions.
Topics: Arthritis, Rheumatoid; Biological Factors; Bone Density Conservation Agents; Cadherins; Humans; Joint Capsule; Osteoblasts; Osteoclasts; Osteogenesis; Osteoporosis; Proteins; RANK Ligand; Recombinant Proteins; Signal Transduction; Synovial Fluid
PubMed: 32908076
DOI: 10.5582/bst.2020.03253 -
Frontiers in Immunology 2024Osteoarthritis (OA) is the most common form of arthritis, characterized by osteophyte formation, cartilage degradation, and structural and cellular alterations of the... (Review)
Review
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.
Topics: Humans; Osteoarthritis; Fibroblasts; Animals; Phenotype; Fibrosis; Synoviocytes; Synovial Membrane
PubMed: 38895122
DOI: 10.3389/fimmu.2024.1385006 -
Seminars in Arthritis and Rheumatism Feb 2023Synovial fibroblasts and their role in juvenile idiopathic arthritis have received limited attention compared to other immune mediated disease such as rheumatoid... (Review)
Review
Synovial fibroblasts and their role in juvenile idiopathic arthritis have received limited attention compared to other immune mediated disease such as rheumatoid arthritis. Furthermore, no review exists regarding synovial fibroblasts, their interaction with immune cells and their potential involvement in juvenile idiopathic arthritis pathogenesis. This scoping review set out to identify and compile the current knowledge of all peer-reviewed studies on synovial fibroblasts from patients with juvenile idiopathic arthritis. The aim was to map the current knowledge and to produce a tool to assist future studies. The entire MEDLINE, EMBASE and Web of Science databases were used to identify all published studies in English regarding synovial fibroblasts from patients with juvenile idiopathic arthritis. We identified 18 eligible studies out of a total of 1778 screened entries. The majority of studies identified synovial fibroblast subsets or functional characteristics that may be involved in disease pathogenesis. We identified mechanisms of cell-cell interaction with leukocytes, pro-inflammatory signaling and unfavorable connective tissue homeostasis that may contribute to cartilage damage or bony overgrowth. All included studies identified mechanisms potentially linking synovial fibroblasts to specific disease traits in juvenile idiopathic arthritis. Most findings were similar to mechanisms also described in synovial fibroblast from adults with arthritis. However, the limited number of studies found identifies an unmet need for additional studies on synovial fibroblasts and their potential role in juvenile idiopathic arthritis.
Topics: Adult; Humans; Arthritis, Juvenile; Arthritis, Rheumatoid; Fibroblasts; Signal Transduction; Musculoskeletal Diseases; Synovial Membrane
PubMed: 36592581
DOI: 10.1016/j.semarthrit.2022.152159 -
Molecular & Cellular Proteomics : MCP May 2023Rheumatoid arthritis (RA) is a typical autoimmune disease characterized by synovial inflammation, synovial tissue hyperplasia, and destruction of bone and cartilage....
Rheumatoid arthritis (RA) is a typical autoimmune disease characterized by synovial inflammation, synovial tissue hyperplasia, and destruction of bone and cartilage. Protein glycosylation plays key roles in the pathogenesis of RA but in-depth glycoproteomics analysis of synovial tissues is still lacking. Here, by using a strategy to quantify intact N-glycopeptides, we identified 1260 intact N-glycopeptides from 481 N-glycosites on 334 glycoproteins in RA synovium. Bioinformatics analysis revealed that the hyper-glycosylated proteins in RA were closely linked to immune responses. By using DNASTAR software, we identified 20 N-glycopeptides whose prototype peptides were highly immunogenic. We next calculated the enrichment scores of nine types of immune cells using specific gene sets from public single-cell transcriptomics data of RA and revealed that the N-glycosylation levels at some sites, such as IGSF10_N2147, MOXD2P_N404, and PTCH2_N812, were significantly correlated with the enrichment scores of certain immune cell types. Furthermore, we showed that aberrant N-glycosylation in the RA synovium was related to increased expression of glycosylation enzymes. Collectively, this work presents, for the first time, the N-glycoproteome of RA synovium and describes immune-associated glycosylation, providing novel insights into RA pathogenesis.
Topics: Humans; Arthritis, Rheumatoid; Glycopeptides; Glycoproteins; Glycosylation; Osteoarthritis; Proteomics; Synovial Membrane; Proteome
PubMed: 37019382
DOI: 10.1016/j.mcpro.2023.100540 -
Arthritis Research & Therapy Apr 2019Rheumatoid arthritis is an immune-mediated inflammatory disease of the synovium. Yet we still lack robust tissue-specific (synovial) biomarkers that are able to guide...
Rheumatoid arthritis is an immune-mediated inflammatory disease of the synovium. Yet we still lack robust tissue-specific (synovial) biomarkers that are able to guide clinical decisions and stratify patients according to their disease subgroup and predicted response to treatment. The EULAR Synovitis Study Group and the OMERACT synovial tissue biopsy (STB) Special Interests Group have undertaken a consensus exercise to identify factors that are important for the standardisation of STB handling and analytical procedures in two situations-clinical practice and translational research.
Topics: Biopsy; Consensus; Humans; Precision Medicine; Rheumatic Diseases; Synovial Membrane; Synovitis
PubMed: 30961644
DOI: 10.1186/s13075-019-1871-5 -
Osteoarthritis and Cartilage Jun 2022
Topics: Humans; Osteoarthritis, Knee; Synovial Fluid
PubMed: 35257863
DOI: 10.1016/j.joca.2022.02.618 -
Aging Feb 2021Joint capsule fibrosis caused by excessive inflammation leading to post-traumatic joint contracture (PTJC). Fibroblasts trigger inflammation under the challenge of...
OBJECTIVES
Joint capsule fibrosis caused by excessive inflammation leading to post-traumatic joint contracture (PTJC). Fibroblasts trigger inflammation under the challenge of various proinflammatory cytokines. Macrophage migration inhibitory factor (MIF) is a prominent proinflammatory cytokine involved in inflammation- and fibrosis-associated pathophysiology, we investigated the role of MIF in PTJC.
METHODS
Using rat PTJC model and fibroblast inflammation model, we detected MIF expression in posterior joint capsule. Primary joint capsule fibroblasts (JFs) were used to investigate the effects of MIF on cell proliferation, migration and proinflammatory cytokines production. The mechanism of JF-mediated events was evaluated by qRT-PCR, western blot and immunoprecipitation. We screened the mRNA expression profile to identify gene candidates that mediate the effect of MIF on JFs.
RESULTS
MIF increased in posterior joint capsule following PTJC and co-localized with fibroblasts. Injection of MIF inhibitor significantly suppressed joint capsule inflammation and fibrosis. , MIF promoted JF proliferation, migration, and inflammation by regulating mitogen-activated protein kinase/nuclear factor-κB pathway through coupling with CD74. Transcriptome analysis revealed that lipid metabolism-related factors Pla2g2a, Angptl4, and Sgpp2, downstream of MIF/CD74, were potentially implicated in JF inflammation.
CONCLUSION
MIF/CD74 axis elicited JF inflammation and may provide new therapeutic targets for joint capsule fibrosis in PTJC.
Topics: Animals; Contracture; Fibroblasts; Inflammation; Joint Capsule; Macrophage Migration-Inhibitory Factors; Rats
PubMed: 33601337
DOI: 10.18632/aging.202505 -
International Journal of Molecular... Sep 2020Osteoarthritis (OA) is the most common degenerative joint disease, predicted to increase in incidence year by year due to an ageing population. Due to the biological... (Review)
Review
Osteoarthritis (OA) is the most common degenerative joint disease, predicted to increase in incidence year by year due to an ageing population. Due to the biological complexity of the disease, OA remains highly heterogeneous. Although much work has been undertaken in the past few years, underlying molecular mechanisms leading to joint tissue structural deterioration are not fully understood, with only few validated markers for disease diagnosis and progression being available. Discovery and quantitation of various OA-specific biomarkers is still largely focused on the bodily fluids which does not appear to be reliable and sensitive enough. However, with the advancement of spatial proteomic techniques, several novel peptides and proteins, as well as N-glycans, can be identified and localised in a reliable and sensitive manner. To summarise the important findings from OA biomarker studies, papers published between 2000 and 2020 were searched via Google Scholar and PubMed. Medical subject heading (MeSH) terms 'osteoarthritis', 'biomarker', 'synovial fluid', 'serum', 'urine', 'matrix-assisted laser desorption/ionisation', 'mass spectrometry imaging', 'proteomic', 'glycomic', 'cartilage', 'synovium' AND 'subchondral bone' were selectively used. The literature search was restricted to full-text original research articles and written only in English. Two main areas were reviewed for OA biomarker studies: (1) an overview of disease-specific markers detected from different types of OA bio-samples, and (2) an up-to-date summary of the tissue-specific OA studies that have utilised matrix-assisted laser desorption/ionisation mass spectrometry imaging (MALDI-MSI). Overall, these OA biomarkers could provide clinicians with information for better the diagnosis, and prognosis of individual patients, and ultimately help facilitate the development of disease-modifying treatments.
Topics: Biomarkers; Cartilage, Articular; Humans; Osteoarthritis; Proteome; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Synovial Membrane
PubMed: 32899238
DOI: 10.3390/ijms21176414 -
Clinical and Experimental Immunology Feb 2019Osteoarthritis (OA) is the most common joint disease that strongly reduces the quality of life in patients; However, no disease-modifying therapy is available. For a... (Review)
Review
Osteoarthritis (OA) is the most common joint disease that strongly reduces the quality of life in patients; However, no disease-modifying therapy is available. For a long time, OA was considered a non-inflammatory disease that was the result of 'wear-and-tear' and abnormal mechanics, and therefore many considered the term 'osteoarthritis' a misnomer. However, during the last decades the notion arose that inflammation is not only present in the majority of OA patients but, rather, actively involved in the progression of the disease. Influx of immune cells is observed in the synovium and a plethora of inflammatory mediators is present in tissues and fluids from OA patients. These mediators cause the production of degrading enzymes that break down the cartilage matrix, which is the main hallmark of OA. Alarmins, which belong to the group of danger signals, have been implicated in many inflammatory diseases. They are among the first factors to be released upon cell stress due to, for example, infection, damage and inflammation. They attract and activate cells of the immune system and therefore lie at the base of the inflammatory reaction. In this narrative review, an overview of the history of OA, the evolving concept of inflammation as important factor in the OA pathogenesis, and particularly the central role that alarmins play in the initiation and maintenance of the low-grade inflammatory response in OA, is provided. Moreover, the targeting of alarmins as a promising approach to dampen the inflammation in OA is highlighted.
Topics: Alarmins; Humans; Inflammation; Osteoarthritis; Synovial Fluid; Synovial Membrane
PubMed: 30421798
DOI: 10.1111/cei.13237