Osteoarthritic cartilage lesions in the bovine patellar groove: A macroscopic, histological and immunohistological analysis

Heinola, T.; Sukura, Antti; Virkki, Liisa; Sillat, Tarvo; Lekszycki, Tomasz; Konttinen, Yrjö T.

doi:10.1016/j.tvjl.2014.01.026

Cited by 4 publications

(10 citation statements)

References 30 publications

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“…coli lipopolysaccharide, IL-1, carrageenan 41 Monosodium iodoacetate40, 41, 48Filipin34, 41, 67Lipopolysaccharide 68 Amphotericin 69 Polyvinyl alcohol foam particles41, 70Papain 40 Intra-articular injection of steroids, collagenase, cytokines 40 Equine models used to study articular cartilage repair, osteochondral defects and naturally occurring bone remodelling 2 ZebrafishGenetic knockout e.g. COL10A1 71 Zebrafish model useful in studying gene related pathology of OA 71 PorcinePost-fracture 72 ACLT, ovariectomy, ACL reconstruction, articular groove model 34 ArthroscopyCartilage resurfacingSurgically in miniature pigs:ACLT and ACL reconstruction 41 Porcine model used to study repair and regeneration of focal cartilage defects 73 BovineNaturally occurring OA in patella74, 75ACLT 34 Non-human primatesNaturally occurring OA1, 34, 76Naturally occurring OA in macaques34, 40, 77, 78Transgenic models 1 Meniscectomy34, 40Ovariectomy in macaques40, 77, 79Ovariectomy in cynomolgus monkeys 34 Collagenase induced in cynomolgus monkeys 80 Naturally occurring and transgenic models of non-human primates used to study general features of OA 1 …”

Section: Current Models Used In Oa Researchmentioning

confidence: 99%

Models of osteoarthritis: the good, the bad and the promising

Cope

Ourradi

et al. 2019

Osteoarthritis and Cartilage

166

131

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SummaryOsteoarthritis (OA) is a chronic degenerative disease of diarthrodial joints most commonly affecting people over the age of forty. The causes of OA are still unknown and there is much debate in the literature as to the exact sequence of events that trigger the onset of the heterogeneous disease we recognise as OA.There is currently no consensus model for OA that naturally reflects human disease. Existing ex-vivo models do not incorporate the important inter-tissue communication between joint components required for disease progression and differences in size, anatomy, histology and biomechanics between different animal models makes translation to the human model very difficult. This narrative review highlights the advantages and disadvantages of the current models used to study OA. It discusses the challenges of producing a more reliable OA-model and proposes a direction for the development of a consensus model that reflects the natural environment of human OA.We suggest that a human osteochondral plug-based model may overcome many of the fundamental limitations associated with animal and in-vitro models based on isolated cells. Such a model will also provide a platform for the development and testing of targeted treatment and validation of novel OA markers directly on human tissues.

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Section: Current Models Used In Oa Researchmentioning

confidence: 99%

Models of osteoarthritis: the good, the bad and the promising

Cope

Ourradi

et al. 2019

Osteoarthritis and Cartilage

166

131

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“…A total of 4376 abstracts were screened, and 168 articles were selected for full‐text article screening (Figure 1). After full‐text article screening, 66 articles were included in the systematic review as they fulfilled all selection criteria 13,15,23‐27,32‐91 . Although most studies focused on either human musculoskeletal disease (n = 31) or animal models of musculoskeletal disease (n = 31), four studies investigated HMGB1 in both human and animal models of musculoskeletal disease (Tables 1 and 2).…”

Section: Resultsmentioning

confidence: 99%

“…HMGB1 expression was increased in animal models of musculoskeletal disease in 22 of 23 studies (Table 3). 13,37,40,44,45,47‐52,54‐56,60,61,63,67,70,83,84,87 …”

Section: Resultsmentioning

confidence: 99%

“…Twenty‐six studies investigated the role of HMGB1 in animal models of arthritis, including OA and RA 13,15,27,34,35,37,40,44,45,47‐56,59‐61,63,65,67,70‐74,78,83,84,86,87 . In all 18 studies, HMGB1 expression was increased in diseased tissues compared to control tissues 35,37,40,44,45,47,49‐52,56,60,61,63,67,70,84,87 . In control tissues, HMGB1 was mainly localized in the nuclei, whereas arthritic tissues showed more cytoplasmic and extracellular HMGB1 expression as the severity increased.…”

Section: Resultsmentioning

confidence: 99%

“…In general, HMGB1 expression is increased in tissues of both human and animal models of musculoskeletal disease compared to control tissues, as well as in early (acute) disease compared to late (chronic) disease 13,24‐26,32,33,35‐52,54‐58,60‐64,66‐71,75‐77,80‐85,87‐89,91 . HMGB1 is expressed by both tissue‐resident stromal cells and infiltrating immune cells 24‐26,32,33,42‐48,50‐52,56‐58,60‐64,66,67,69‐71,75,76,80‐82,85,88 . Local administration of HMGB1 to (cultured cells derived from) arthritic tissues worsened both clinical and histopathologic arthritis, increased synovial angiogenesis, and enhanced chemotaxis 32‐34,42,46,57,62,65,71‐75,78,81,85,92 .…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

The potential roles of high mobility group box 1 (HMGB1) in musculoskeletal disease: A systematic review

et al. 2020

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There is increasing evidence for the involvement of high mobility group box 1 (HMGB1) in inflammation, angiogenesis, and tumorigenesis. However, no studies have reviewed the role of HMGB1 in musculoskeletal disease. This systematic review aimed to evaluate the literature regarding the potential roles of HMGB1 in musculoskeletal disease (joint, tendon, ligament, intervertebral disk, and bone). After searching PubMed, MEDLINE, and EMBASE databases up to 01‐01‐2020, 66 articles that measured HMGB1 expression in musculoskeletal disease were included. Immune and tissue‐resident stromal cells expressed HMGB1, and both diseased human tissues and animal disease models showed increased HMGB1 expression relative to controls. Administration of recombinant HMGB1 to diseased musculoskeletal tissues induced inflammation, whereas blocking HMGB1 ameliorated histopathologic and clinical severity of disease. HMGB1 redox status was investigated in only 3% of the articles: Fully reduced HMGB1 promoted chemotaxis of leukocytes and tissue repair, whereas disulfide HMGB1 acted as a pro‐inflammatory mediator. Our review highlights that while HMGB1 is an important mediator in musculoskeletal disease, its redox status remains understudied. Identification of HMGB1 redox status in musculoskeletal tissues is critical to advance understanding of the diverse biological functions of HMGB1 in musculoskeletal disease. Importantly, this will inform future therapeutic strategies to target HMGB1.

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Diseases of the Musculoskeletal System

2017

Veterinary Medicine

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Osteoarthritic cartilage lesions in the bovine patellar groove: A macroscopic, histological and immunohistological analysis

Cited by 4 publications

References 30 publications

Models of osteoarthritis: the good, the bad and the promising

Models of osteoarthritis: the good, the bad and the promising

The potential roles of high mobility group box 1 (HMGB1) in musculoskeletal disease: A systematic review

Diseases of the Musculoskeletal System

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