FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2898137718> ?p ?o ?g. }

• W2898137718 endingPage "239" @default.
• W2898137718 startingPage "230" @default.
• W2898137718 abstract "Osteoarthritis (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. Osteoarthritis (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. Osteoarthritis (OA) is a chronic degenerative disease of diarthrodial joints, predominantly affecting the spine and peripheral joints of the body, particularly the hands, hips, knees and feet. OA most commonly affects people over the age of forty, with the risk of disease increasing with age. OA is a complex heterogeneous disease with different clinical and biochemical phenotypes. The cause(s) of OA are unknown, and many studies have suggested that the pathobiology of OA is far more complex than a simple cartilaginous or bone disease. It is now acknowledged that OA affects many joint structures, including degeneration of cartilage, abnormal bone remodelling and synovial inflammation1Bendele A.M. Animal models of osteoarthritis.J Musculoskelet Neuronal Interact. 2001; 1: 363-376PubMed Google Scholar, 2Kuyinu E.L. Narayanan G. Nair L.S. Laurencin C.T. Animal models of osteoarthritis: classification, update, and measurement of outcomes.J Orthop Surg Res. 2016; 11: 19Crossref PubMed Scopus (281) Google Scholar. Also, studies have shown that there is a complex interplay between the different joint components, making understanding of the degradative sequence of events involved in OA pathogenesis very difficult to dissect3Amin A.K. Huntley J.S. Simpson A.H. Hall A.C. Chondrocyte survival in articular cartilage: the influence of subchondral bone in a bovine model.J Bone Joint Surg. 2009; 91: 691-699Crossref Scopus (49) Google Scholar, 4Fell H.B. Jubb R.W. The effect of synovial tissue on the breakdown of articular cartilage in organ culture.Arthritis & Rheumatol. 1977; 20: 1359-1371Crossref PubMed Scopus (246) Google Scholar, 5Heinemann C. Heinemann S. Worch H. Hanke T. Development of an osteoblast/osteoclast co-culture derived by human bone marrow stromal cells and human monocytes for biomaterials testing.Eur Cell Mater. 2011; 21: 80-93Crossref PubMed Scopus (72) Google Scholar. The initial onset of OA disease is considered due to an imbalance between the cartilage degradation and repair process6Abramson S.B. Attur M. Developments in the scientific understanding of osteoarthritis.Arthritis Res Ther. 2009; 11: 227Crossref PubMed Scopus (309) Google Scholar, 7Goldring M.B. Marcu K.B. Cartilage homeostasis in health and rheumatic diseases.Arthritis Res Ther. 2009; 11: 224Crossref PubMed Scopus (508) Google Scholar. The exact sequence of events that trigger the onset of the disease is however widely debated throughout the literature. One hypothesis, suggests that secretion of pro-inflammatory cytokines into the synovial joint induces matrix metalloproteinases which cause the fragmentation and degradation of cartilage extracellular matrix leading to bone remodelling and synovitis8Martel-Pelletier J. Pelletier J.P. Is osteoarthritis a disease involving only cartilage or other articular tissues?.Eklem Hastalik Cerrahisi. 2010; 21: 2-14PubMed Google Scholar, 9Helmtrud IS T. Bone and Osteoarthritis.First edn. Springer, London2007Google Scholar, 10Sharma A. Jagga S. Lee S. Nam J. Interplay between cartilage and subchondral bone contributing to pathogenesis of osteoarthritis.Int J Mol Sci. 2013; 14: 19805-19830Crossref PubMed Scopus (193) Google Scholar. Contrary to this theory, some studies suggest that subchondral bone remodelling and synovitis precede articular degeneration in the early stages of OA8Martel-Pelletier J. Pelletier J.P. Is osteoarthritis a disease involving only cartilage or other articular tissues?.Eklem Hastalik Cerrahisi. 2010; 21: 2-14PubMed Google Scholar, 11Benito M.J. Veale D.J. FitzGerald O. van den Berg W.B. Bresnihan B. Synovial tissue inflammation in early and late osteoarthritis.ARD (Ann Rheum Dis). 2005; 64: 1263-1267Crossref PubMed Scopus (703) Google Scholar, 12Zamli Z. Robson-Brown K. Tarlton J. Adams M. Torlot G. Cartwright C. et al.Subchondral bone plate thickening precedes chondrocyte apoptosis and cartilage degradation in spontaneous animal models of osteoarthritis.BioMed Res Int. 2014; 2014: 606870Google Scholar. While other studies suggest that meniscal degeneration evolving through fibrillation of tissue and a decrease in the levels of type I and II collagen within the meniscus, act as a predisposing or contributing factor to OA progression13Sun Y. Mauerhan D.R. Kneisl J.S. James Norton H. Zinchenko N. Ingram J. et al.Histological examination of collagen and proteoglycan changes in osteoarthritic menisci.Open Rheumatol J. 2012; 6: 24-32Crossref PubMed Scopus (58) Google Scholar, 14Braun H.J. Gold G.E. Diagnosis of osteoarthritis: imaging.Bone. 2012; 51: 278-288Crossref PubMed Scopus (215) Google Scholar. In the later stages of OA, formation of subchondral cysts, subchondral sclerosis and osteophytes occur as a direct result of bone remodelling, cartilage degradation and synovitis15Man G. Mologhianu G. Osteoarthritis pathogenesis – a complex process that involves the entire joint.J Med Life. 2014; 7: 37-41PubMed Google Scholar, 16Burr D.B. Gallant M.A. Bone remodelling in osteoarthritis.Nat Rev Rheumatol. 2012; 8: 665-673Crossref PubMed Scopus (563) Google Scholar, 17Cucchiarini M. de Girolamo L. Filardo G. Oliveira J.M. Orth P. Pape D. et al.Basic science of osteoarthritis.J Exp Orthop. 2016; 3Crossref Scopus (58) Google Scholar. Treatment of OA is largely symptomatic due to insufficient understanding of aetiopathogenesis hindering the development of suitable disease-modifying drugs. This makes targeted treatment of OA a distinct challenge. Human OA tissue samples are usually collected for research once end stages of the disease have been reached, for example during joint replacement, by which time destructive changes in the joint are well established. This makes studying the early disease process very challenging18McCoy A.M. Animal models of osteoarthritis: comparisons and key considerations.Vet Pathol. 2015; 52: 803-818Crossref PubMed Scopus (194) Google Scholar. OA pathology, particularly early OA, is therefore very difficult to study, and so researchers turn to in-vivo and ex-vivo preclinical animal models to investigate early pathological changes in OA. These models offer unique advantages as well as limitations for studying human OA. This article will review the different models used for investigation of OA, discuss their advantages and disadvantages, and propose development of a gold standard model for OA that closely reflects natural human disease. OA research models can be categorised into either ex-vivo or in-vivo models. Depending on the research question, different models can be used to address different aspects of OA development and progression. Each model has its advantages, yet it has become clear that no single model provides the opportunity to study the disease as a whole. The different models currently used in OA research are discussed below. Ex-vivo models can be categorised into monolayer culture, co-culture, three-dimensional (3D) culture and explant-based culture. Each model has its advantages and disadvantages and so can be used to answer different questions in OA research. Ex-vivo models such as monolayer culture and co-culture are easier and cheaper to produce than 3D cell cultures and explant-based models. Monolayer cultures are also easy to produce on a large scale and avoid the challenges associated with culturing different cell types at different conditions. However, monolayer and co-cultures are limited in their use due to the fact that they isolate only one or two tissue components at a time. Many studies have shown that there is a strong interplaying network of communication between different joint components that help regulate and maintain a healthy joint, and so isolation of specific joint components hinders this communication3Amin A.K. Huntley J.S. Simpson A.H. Hall A.C. Chondrocyte survival in articular cartilage: the influence of subchondral bone in a bovine model.J Bone Joint Surg. 2009; 91: 691-699Crossref Scopus (49) Google Scholar, 19Radin E.L. Rose R.M. Role of subchondral bone in the initiation and progression of cartilage damage.Clin Orthop Relat Res. 1986; : 34-40PubMed Google Scholar, 20Sophia Fox A.J. Bedi A. Rodeo S.A. The basic science of articular cartilage: structure, composition, and function.Sport Health. 2009; 1: 461-468Crossref PubMed Scopus (1368) Google Scholar. For example, healthy articular cartilage is dependent upon the release of soluble factors by subchondral bone, and interactions between chondrocytes and synovial fluid ensures the flow of growth factors, regulatory peptides and nutrients between them19Radin E.L. Rose R.M. Role of subchondral bone in the initiation and progression of cartilage damage.Clin Orthop Relat Res. 1986; : 34-40PubMed Google Scholar, 20Sophia Fox A.J. Bedi A. Rodeo S.A. The basic science of articular cartilage: structure, composition, and function.Sport Health. 2009; 1: 461-468Crossref PubMed Scopus (1368) Google Scholar. When injured cartilage is co-cultured with synovium, a protective effect is produced on the synoviocytes21Lee C. Kisiday J. McIlwraith C. Grodzinsky A. Frisbie D. Synoviocytes protect cartilage from the effects of injury in vitro.BMC Muscoskel Disord. 2013; 14: 54Crossref Scopus (20) Google Scholar. Similarly, culture of subchondral bone and cartilage separately results in increased chondrocyte death and cartilage degradation as well as decreased protein content in culture media compared to when cultured together3Amin A.K. Huntley J.S. Simpson A.H. Hall A.C. Chondrocyte survival in articular cartilage: the influence of subchondral bone in a bovine model.J Bone Joint Surg. 2009; 91: 691-699Crossref Scopus (49) Google Scholar, 19Radin E.L. Rose R.M. Role of subchondral bone in the initiation and progression of cartilage damage.Clin Orthop Relat Res. 1986; : 34-40PubMed Google Scholar, 22Malinin T. Ouellette E.A. Articular cartilage nutrition is mediated by subchondral bone: a long-term autograft study in baboons.Osteoarthritis Cartilage. 2000; 8: 483-491Abstract Full Text PDF PubMed Scopus (101) Google Scholar. Explant models and 3D cell cultures allow for this inter-tissue communication and so are arguably more useful models available to OA researchers to reproduce natural in-vivo environments. Despite this, these models are more difficult to produce in terms of tissue volume and maintaining cell viability over extended periods of time. Some of the advantages, disadvantages and applications of various ex-vivo models used in OA research are summarised in Table I.Table IA summary of the advantages and disadvantages of different ex-vivo models used in OA researchEx-vivo ModelAdvantagesDisadvantagesExample of the application of the model in OA researchMonolayer culture-A large number of cells can be easily produced from a single sample23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-The configuration of cells cultured in a monolayer layout allows homogenous spread of nutrients and growth factor from the culture medium24Edmondson R. Broglie J.J. Adcock A.F. Yang L. Three-dimensional cell culture systems and their applications in drug discovery and cell-based biosensors.Assay Drug Dev Technol. 2014; 12: 207-218Crossref PubMed Scopus (1453) Google Scholar-Limited for certain tissue types such as cartilage, whose phenotype changes once in a monolayer culture environment, introducing inter-experimental variability25Nicholson I.P. Gault E.A. Foote C.G. Nasir L. Bennett D. Human telomerase reverse transcriptase (hTERT) extends the lifespan of canine chondrocytes in vitro without inducing neoplastic transformation.Vet J. 2007; 174: 570-576Crossref Scopus (10) Google Scholar, 26Zien A. Aigner T. Zimmer R. Lengauer T. Centralization: a new method for the normalization of gene expression data.Bioinformatics. 2001; 17: S323-S331Crossref PubMed Scopus (94) Google Scholar-Chondrocytes are very sensitive to their molecular environment and so need to remain in contact with the extracellular matrix to ensure that they reflect natural in-vivo samples23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Cartilage has low cellularity, therefore, a large sample of cartilage is required to ensure sufficient numbers of cells are present to carry out a reliable experiment23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Isolating a tissue in culture removes all systemic influences on that tissue, which does not reflect natural joint tissue-Cells in monoculture traditionally grow on a flat surface in glass or plastic flasks and so do not allow for growth in all directions, as seen in the natural 3D in-vivo environment24Edmondson R. Broglie J.J. Adcock A.F. Yang L. Three-dimensional cell culture systems and their applications in drug discovery and cell-based biosensors.Assay Drug Dev Technol. 2014; 12: 207-218Crossref PubMed Scopus (1453) Google Scholar-Monolayer cultures can be used to study the effects of cytokine stimulation and osmotic pressure23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Synovial cell cultures useful to study the role of the synovium in OACo-culturing cells-Co-culturing cells of different lineages is important to allow for changes in cell-specific physiology and cell–cell interactions that are important in regulating cell and tissue physiology23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar, 27Hendriks J. Riesle J. van Blitterswijk C.A. Co-culture in cartilage tissue engineering.J Tissue Eng Regen Med. 2007; 1: 170-178Crossref PubMed Scopus (109) Google Scholar-Different conditions are required for culturing each cell type23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Co-culturing cells can result in alterations of phenotype when cells are isolated23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Co-cultures traditionally grow on a flat surface in glass or plastic flasks and so do not allow for growth in all directions, as seen in the natural 3D in-vivo environment24Edmondson R. Broglie J.J. Adcock A.F. Yang L. Three-dimensional cell culture systems and their applications in drug discovery and cell-based biosensors.Assay Drug Dev Technol. 2014; 12: 207-218Crossref PubMed Scopus (1453) Google Scholar-Co-culturing cells can be used to study the effects of cytokine stimulation and osmotic pressure23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Osteoblast-chondrocyte co-culture useful in understanding bone-cartilage cross-talk28Thysen S. Luyten F.P. Lories R.J.U. Targets, models and challenges in osteoarthritis research.Dis Model Mech. 2015; 8: 17-30Crossref PubMed Scopus (172) Google Scholar-Co-culturing chondrocytes and osteoblasts results in greater cell growth, matrix production and deposition as well as reduced glycosaminoglycan deposition compared to culturing chondrocytes alone29Spalazzi J. Dionisio K. Jiang J. Lu H. Osteoblast and chondrocyte interactions during co-culture on scaffolds examining matrix and substrate-dependent effects on the formation of functional bone-cartilage interfaces.Eng Med Biol Mag. 2003; 22: 27-34Crossref PubMed Scopus (42) Google Scholar, 30Jiang J. Nicoll S.B. Lu H.H. Co-culture of osteoblasts and chondrocytes modulates cellular differentiation in vitro.Biochem Biophys Res Commun. 2005; 338: 762-770Crossref PubMed Scopus (116) Google Scholar-Co-culturing sclerotic osteoarthritic osteoblasts and chondrocytes from osteoarthritic articular cartilage results in an increased shift towards chondrocyte hypertrophy and release of matrix metalloproteinases and aggrecanases31Sanchez C. Deberg M.A. Piccardi N. Msika P. Reginster J.Y. Henrotin Y.E. Subchondral bone osteoblasts induce phenotypic changes in human osteoarthritic chondrocytes.Osteoarthritis Cartilage. 2005; 13: 988-997Abstract Full Text Full Text PDF PubMed Scopus (152) Google Scholar, 32Prasadam I. Crawford R. Xiao Y. Aggravation of ADAMTS and matrix metalloproteinase production and role of ERK1/2 pathway in the interaction of osteoarthritic subchondral bone osteoblasts and articular cartilage chondrocytes -- possible pathogenic role in osteoarthritis.J Rheumatol. 2012; 39: 621-634Crossref PubMed Scopus (64) Google Scholar-Culturing synovium and cartilage together produce very different results in terms of the break-down of proteoglycan and matrix structure compared to when cultured alone4Fell H.B. Jubb R.W. The effect of synovial tissue on the breakdown of articular cartilage in organ culture.Arthritis & Rheumatol. 1977; 20: 1359-1371Crossref PubMed Scopus (246) Google Scholar-Co-culturing synovium and injured cartilage produces a protective effect on synoviocytes21Lee C. Kisiday J. McIlwraith C. Grodzinsky A. Frisbie D. Synoviocytes protect cartilage from the effects of injury in vitro.BMC Muscoskel Disord. 2013; 14: 54Crossref Scopus (20) Google Scholar-Synovium-cartilage cultures useful to study the role of the synovium in OA-Co-culture of bone components ensure balanced bone remodelling5Heinemann C. Heinemann S. Worch H. Hanke T. Development of an osteoblast/osteoclast co-culture derived by human bone marrow stromal cells and human monocytes for biomaterials testing.Eur Cell Mater. 2011; 21: 80-93Crossref PubMed Scopus (72) Google Scholar3D cell culture-3D cell culture allows for culture of different cell lines and important cell–cell interactions-3D cell cultures grow as aggregates or spheroids in a matrix, allowing growth in all directions, similar to the natural in-vivo environment24Edmondson R. Broglie J.J. Adcock A.F. Yang L. Three-dimensional cell culture systems and their applications in drug discovery and cell-based biosensors.Assay Drug Dev Technol. 2014; 12: 207-218Crossref PubMed Scopus (1453) Google Scholar-The 3D structure provides structural strength to sensitive cells23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-The proliferation rate of cells tends to be slower in 3D cell cultures compared to 2D cultures33Chitcholtan K. Sykes P.H. Evans J.J. The resistance of intracellular mediators to doxorubicin and cisplatin are distinct in 3D and 2D endometrial cancer.J Transl Med. 2012; 10: 38Crossref PubMed Scopus (104) Google Scholar-The structural strength provided to cultured cells depends on the scaffold used23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-3D cell culture can be used to study the effects of cytokine stimulation and osmotic pressure, as well as the effects of physical injury and loading on tissue23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-A matrix structure of collagens and proteoglycans favours phenotypically normal cartilage28Thysen S. Luyten F.P. Lories R.J.U. Targets, models and challenges in osteoarthritis research.Dis Model Mech. 2015; 8: 17-30Crossref PubMed Scopus (172) Google ScholarExplant based models-Simple, cheap and easy to produce23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Explant models allow for the natural processes that occur within the extracellular matrix environment to be observed26Zien A. Aigner T. Zimmer R. Lengauer T. Centralization: a new method for the normalization of gene expression data.Bioinformatics. 2001; 17: S323-S331Crossref PubMed Scopus (94) Google Scholar-Cell death often occurs at the explant edge-Only a limited number of cells can be extracted from a single source-Limited tissue availability and significant inter-experimental variability23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar-Explant based models can be used to study the effects of cytokine stimulation and osmotic pressure, as well as the effects of physical injury and biomechanical loading on tissue23Johnson C. Argyle D. Clements D. In vitro models for the study of osteoarthritis.Vet J. 2016; 209: 40-49Crossref PubMed Scopus (119) Google Scholar, 28Thysen S. Luyten F.P. Lories R.J.U. Targets, models and challenges in osteoarthritis research.Dis Model Mech. 2015; 8: 17-30Crossref PubMed Scopus (172) Google Scholar-Synovial tissue explants useful to study the role of the synovium in OA Open table in a new tab Many animal models in at least eighteen different species have been developed to study established pathological features of OA such as pain, synovitis, cartilage degeneration and bone remodelling. Animal models used in OA research (see Table II) can be categorised into either induced or spontaneous models. Induced models refer to models where OA disease (or OA like features) have been induced either chemically or surgically. On the other hand, spontaneous models are subcategorised into naturally occurring and genetically modified models that develop OA.Table IIA summary of the different animal models used in OA researchSpecies/ModelSpontaneousSurgically inducedChemically InducedExamples of the application of the model in OA researchMouseNaturally occurring OA1Bendele A.M. Animal models of osteoarthritis.J Musculoskelet Neuronal Interact. 2001; 1: 363-376PubMed Google Scholar, 2Kuyinu E.L. Narayanan G. Nair L.S. Laurencin C.T. Animal models of osteoarthritis: classification, update, and measurement of outcomes.J Orthop Surg Res. 2016; 11: 19Crossref PubMed Scopus (281) Google Scholar, 34Lampropoulou-Adamidou K. Lelovas P. Karadimas E.V. Liakou C. Triantafillopoulos I.K. Dontas I. et al.Useful animal models for the research of osteoarthritis.Eur J Orthop Surg Traumatol. 2014; 24: 263-271Crossref PubMed Scopus (126) Google Scholar-Genetic models:PAR2−/−, CD4−/−, MMP17−/−, Tenascin C−/-, Ddr2−/−, SulPhatase−/- 1/2, Syndecan 4−/−, Fgf2−/−, Mmp13−/−,Hif2a+/-, GDF5+/−, Osteopontin, Ptges1, Tnfrsf11b+/-, Runx 2+/−, ADAMTS-5/4 −/−, Adamts5−/−, ADAMTS4−/−, MMP3−/−, ICE−/-, IL-1β−/-, iNOS −/−35Vincent T.L. Williams R.O. Maciewicz R. Silman A. Garside P. Mapping pathogenesis of arthritis through small animal models.Rheumatology. 2012; 51: 1931-1941Crossref PubMed Scopus (87) Google Scholar-Transgenic models2Kuyinu E.L. Narayanan G. Nair L.S. Laurencin C.T. Animal models of osteoarthritis: classification, update, and measurement of outcomes.J Orthop Surg Res. 2016; 11: 19Crossref PubMed Scopus (281) Google Scholar, 36Fang H. Beier F. Mouse models of osteoarthritis: modelling risk factors and assessing outcomes.Nat Rev Rheumatol. 2014; 10: 413-421Crossref PubMed Scopus (123) Google ScholarMutations in type II collagen gene1Bendele A.M. Animal models of osteoarthritis.J Musculoskelet Neuronal Interact. 2001; 1: 363-376PubMed Google ScholarBrtl mouse37Blair-Levy J.M. Watts C.E. Fiorentino N.M. Dimitriadis E.K. Marini J.C. Lipsky P.E. A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model.Arthritis Rheum. 2008; 58: 1096-1106Crossref PubMed Scopus (46) Google ScholarMouse Del1: Short deletion in type II collagen18McCoy A.M. Animal models of osteoarthritis: comparisons and key considerations.Vet Pathol. 2015; 52: 803-818Crossref PubMed Scopus (194) Google ScholarCol9a1 knockout36Fang H. Beier F. Mouse models of osteoarthritis: modelling risk factors and assessing outcomes.Nat Rev Rheumatol. 2014; 10: 413-421Crossref PubMed Scopus (123) Google ScholarSTR/ORT + C57/BL6 strains1Bendele A.M. Animal models of osteoarthritis.J Musculoskelet Neuronal Interact. 2001; 1: 363-376PubMed Google Scholar, 2Kuyinu E.L. Narayanan G. Nair L.S. Laurencin C.T. Animal models of osteoarthritis: classification, update, and measurement of outcomes.J Orthop Surg Res. 2016; 11: 19Crossref PubMed Scopus (281) Google Scholar, 36Fang H. Beier F. Mouse models of osteoarthritis: modelling risk factors and assessing outcomes.Nat Rev Rheumatol. 2014; 10: 413-421Crossref PubMed Scopus (123) Google Scholar, 38Glasson S.S. In vivo osteoarthritis target validation utilizing genetically-modified mice.Curr Drug Targets. 2007; 8: 367-376Crossref PubMed Scopus (114) Google Scholar, 39Longo U.G. Loppini M. Fumo C. Rizzello G. Khan W.S. Maffulli N. et al.Osteoarthritis: new insights in animal models.Open Orthop J. 2012; 6: 558-563Crossref PubMed Google Scholar, 40Little C. Smith M. Animal models of osteoarthritis.Curr Rheumatol Rev. 2008; 4Crossref Scopus (96) Google Scholar-Anterior cruciate ligament transection (ACLT)18McCoy A.M. Animal models of osteoarthritis: comparisons and key considerations.Vet Pathol. 2015; 52: 803-818Crossref PubMed Scopus (194) Google Scholar, 34Lampropoulou-Adamidou K. Lelovas P. Karadimas E.V. Liakou C. Triantafillopoulos I.K. Dontas I. et al.Useful animal models for the research of osteoarthritis.Eur J Orthop Surg Traumatol. 2014; 24: 263-271Crossref PubMed Scopus (126) Google Scholar, 41Teeple E. Jay G.D. Elsaid K.A. Fleming B.C. Animal models of osteoarthritis: challenges of model selection and analysis.AAPS J. 2013; 15: 438-446Crossref PubMed Scopus (146) Google Scholar, 42Kamekura S. Hoshi K. Shimoaka T. Chung U. Chikuda H. Yamada T. et al.Osteoarthritis development in novel experimental mouse models induced by knee joint instability.Osteoarthritis Cartilage. 2005; 13: 632-641Abstract Full Text Full Text PDF PubMed Scopus (420) Google Scholar, 43Lorenz J. Grassel S. Experimental osteoarthritis models in mice.Methods Mol Biol. 2014; 1194: 401-419Crossref PubMed Scopus (71) Google Scholar-Articular groove model34Lampropoulou-Adamidou K. Lelovas P. Karadimas E.V. Liakou C. Triantafillopoulos I.K. Dontas I. et al.Useful animal models for the research of osteoarthritis.Eur J Orthop Surg Traumatol. 2014; 24: 263-271Crossref PubMed Scopus (126) Google Scholar-Intra-articular tibial plateau fracture, cyclic articular cartilage tibial compression, anterior cruciate ligament, rupture via tibial compression overload2Kuyinu E.L. Narayanan G. Nair L.S. Laurencin C.T. Animal models of osteoarthritis: classification, update, and measurement of outcomes.J Orthop Surg Res. 2016; 11: 19Crossref PubMed Scopus (281) Google Scholar-Ovariectomy34Lampropoulou-Adamidou K. Lelovas P. Karadimas E.V. Liakou C. Triantafillopoulos I.K. Dontas I. et al.Useful animal models for the research of osteoarthritis.Eur J Orthop Surg Traumatol. 2014; 24: 263-271Crossref PubMed Scopus (126) Google Scholar-Partial discectomy44Xu L. Polur I. Lim C. Servais J.M. Dobeck J. Li Y. et al.Early-onset osteoarthritis of mouse temporomandibular joint induced by partial discect" @default.
• W2898137718 created "2018-11-02" @default.
• W2898137718 creator A5013899119 @default.
• W2898137718 creator A5057325286 @default.
• W2898137718 creator A5062874020 @default.
• W2898137718 creator A5083187821 @default.
• W2898137718 date "2019-02-01" @default.
• W2898137718 modified "2023-10-12" @default.
• W2898137718 title "Models of osteoarthritis: the good, the bad and the promising" @default.
• W2898137718 cites W103910462 @default.
• W2898137718 cites W1618293427 @default.
• W2898137718 cites W188532228 @default.
• W2898137718 cites W1962462 @default.
• W2898137718 cites W1966532209 @default.
• W2898137718 cites W1967170359 @default.
• W2898137718 cites W1967556007 @default.
• W2898137718 cites W1968374344 @default.
• W2898137718 cites W1969047817 @default.
• W2898137718 cites W1973498895 @default.
• W2898137718 cites W1974813723 @default.
• W2898137718 cites W1979121447 @default.
• W2898137718 cites W1981342213 @default.
• W2898137718 cites W1986996383 @default.
• W2898137718 cites W1992252990 @default.
• W2898137718 cites W1993179559 @default.
• W2898137718 cites W1993938593 @default.
• W2898137718 cites W2000391742 @default.
• W2898137718 cites W2002780234 @default.
• W2898137718 cites W2003507235 @default.
• W2898137718 cites W2006850678 @default.
• W2898137718 cites W2007696224 @default.
• W2898137718 cites W2011038175 @default.
• W2898137718 cites W2015716158 @default.
• W2898137718 cites W2021862667 @default.
• W2898137718 cites W2023234477 @default.
• W2898137718 cites W2023592016 @default.
• W2898137718 cites W2025387481 @default.
• W2898137718 cites W2027251634 @default.
• W2898137718 cites W2028885917 @default.
• W2898137718 cites W2028920679 @default.
• W2898137718 cites W2039590395 @default.
• W2898137718 cites W2040730853 @default.
• W2898137718 cites W2043834774 @default.
• W2898137718 cites W2050606344 @default.
• W2898137718 cites W2056406997 @default.
• W2898137718 cites W2056717312 @default.
• W2898137718 cites W2056942201 @default.
• W2898137718 cites W2057853539 @default.
• W2898137718 cites W2058435889 @default.
• W2898137718 cites W2059103432 @default.
• W2898137718 cites W2074367519 @default.
• W2898137718 cites W2088657142 @default.
• W2898137718 cites W2089566404 @default.
• W2898137718 cites W2093665893 @default.
• W2898137718 cites W2095417845 @default.
• W2898137718 cites W2096734017 @default.
• W2898137718 cites W2098756499 @default.
• W2898137718 cites W2101454456 @default.
• W2898137718 cites W2101471525 @default.
• W2898137718 cites W2104146295 @default.
• W2898137718 cites W2104653602 @default.
• W2898137718 cites W2106616036 @default.
• W2898137718 cites W2107894170 @default.
• W2898137718 cites W2112073300 @default.
• W2898137718 cites W2113727407 @default.
• W2898137718 cites W2117040516 @default.
• W2898137718 cites W2117748540 @default.
• W2898137718 cites W2122674110 @default.
• W2898137718 cites W2123452676 @default.
• W2898137718 cites W2128509275 @default.
• W2898137718 cites W2129531706 @default.
• W2898137718 cites W2137567737 @default.
• W2898137718 cites W2141363952 @default.
• W2898137718 cites W2143730163 @default.
• W2898137718 cites W2148313037 @default.
• W2898137718 cites W2149953008 @default.
• W2898137718 cites W2150916874 @default.
• W2898137718 cites W2152333225 @default.
• W2898137718 cites W2153745500 @default.
• W2898137718 cites W2155109953 @default.
• W2898137718 cites W2160719250 @default.
• W2898137718 cites W2162197765 @default.
• W2898137718 cites W2166148611 @default.
• W2898137718 cites W2167513470 @default.
• W2898137718 cites W2169461456 @default.
• W2898137718 cites W2170982730 @default.
• W2898137718 cites W2171324043 @default.
• W2898137718 cites W2244116208 @default.
• W2898137718 cites W2269139557 @default.
• W2898137718 cites W2298507390 @default.
• W2898137718 cites W2331628193 @default.
• W2898137718 cites W2404694334 @default.
• W2898137718 cites W2407568408 @default.
• W2898137718 cites W2411450942 @default.
• W2898137718 cites W2415367704 @default.
• W2898137718 cites W2518977853 @default.
• W2898137718 cites W2600599045 @default.
• W2898137718 cites W2753843980 @default.

• next