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Article ; Online: Changing the outcome of osteoarthritis: still a challenge for cyclooxygenase 2 inhibitors.

Lories, Rik J U

2012 Volume 64, Issue 1, Page(s) 37–39

MeSH term(s)	Animals ; Arthritis, Experimental/enzymology ; Celecoxib ; Cyclooxygenase 2 Inhibitors/pharmacology ; Female ; Humans ; Male ; Osteoarthritis/enzymology ; Osteoarthritis, Knee/enzymology ; Pyrazoles/pharmacology ; Sulfonamides/pharmacology
Chemical Substances	Cyclooxygenase 2 Inhibitors ; Pyrazoles ; Sulfonamides ; Celecoxib (JCX84Q7J1L)
Language	English
Publishing date	2012-01
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	127294-9
ISSN	1529-0131 ; 0004-3591 ; 2326-5191
ISSN (online)	1529-0131
ISSN	0004-3591 ; 2326-5191
DOI	10.1002/art.33330
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Article ; Online: Inflammation and ankylosis: still an enigmatic relationship in spondyloarthritis.

Lories, Rik J U / Dougados, Maxime

Annals of the rheumatic diseases

2012 Volume 71, Issue 3, Page(s) 317–318

MeSH term(s)	Female ; Humans ; Male ; Ossification, Heterotopic/etiology ; Spine/pathology ; Spondylitis, Ankylosing/complications
Language	English
Publishing date	2012-03
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/annrheumdis-2011-200842
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Article ; Online: Pathophysiology of new bone formation and ankylosis in spondyloarthritis.

Lories, Rik J U / Schett, Georg

Rheumatic diseases clinics of North America

2012 Volume 38, Issue 3, Page(s) 555–567

Abstract: The outcome of patients suffering from spondyloarthritis is determined by chronic inflammation and new bone formation leading to ankylosis. The latter process manifests by new cartilage and bone formation leading to joint or spine fusion. This article ... ...

Abstract	The outcome of patients suffering from spondyloarthritis is determined by chronic inflammation and new bone formation leading to ankylosis. The latter process manifests by new cartilage and bone formation leading to joint or spine fusion. This article discusses the main mechanisms of new bone formation in spondyloarthritis. It reviews the key molecules and concepts of new bone formation and ankylosis in animal models of disease and translates these findings to human disease. In addition, proposed biomarkers of new bone formation are evaluated and the translational current and future challenges are discussed with regards to new bone formation in spondyloarthritis.
MeSH term(s)	Ankylosis/metabolism ; Ankylosis/pathology ; Ankylosis/physiopathology ; Biomarkers/metabolism ; Chronic Disease ; Humans ; Inflammation/metabolism ; Osteogenesis/physiology ; Spine/pathology ; Spondylarthritis/metabolism ; Spondylarthritis/pathology ; Spondylarthritis/physiopathology ; Spondylitis, Ankylosing/metabolism ; Spondylitis, Ankylosing/pathology ; Spondylitis, Ankylosing/physiopathology
Chemical Substances	Biomarkers
Language	English
Publishing date	2012-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	92118-x
ISSN	1558-3163 ; 0889-857X
ISSN (online)	1558-3163
ISSN	0889-857X
DOI	10.1016/j.rdc.2012.08.003
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Article ; Online: Targets, models and challenges in osteoarthritis research.

Thysen, Sarah / Luyten, Frank P / Lories, Rik J U

Disease models & mechanisms

2015 Volume 8, Issue 1, Page(s) 17–30

Abstract: Osteoarthritis is a chronic degenerative disorder of the joint and represents one of the most common diseases worldwide. Its prevalence and severity are increasing owing to aging of the population, but treatment options remain largely limited to ... ...

Abstract	Osteoarthritis is a chronic degenerative disorder of the joint and represents one of the most common diseases worldwide. Its prevalence and severity are increasing owing to aging of the population, but treatment options remain largely limited to painkillers and anti-inflammatory drugs, which only provide symptomatic relief. In the late stages of the disease, surgical interventions are often necessary to partially restore joint function. Although the focus of osteoarthritis research has been originally on the articular cartilage, novel findings are now pointing to osteoarthritis as a disease of the whole joint, in which failure of different joint components can occur. In this Review, we summarize recent progress in the field, including data from novel 'omics' technologies and from a number of preclinical and clinical trials. We describe different in vitro and in vivo systems that can be used to study molecules, pathways and cells that are involved in osteoarthritis. We illustrate that a comprehensive and multisystem approach is necessary to understand the complexity and heterogeneity of the disease and to better guide the development of novel therapeutic strategies for osteoarthritis.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Bone and Bones/pathology ; Cartilage, Articular/pathology ; Clinical Trials as Topic ; Disease Models, Animal ; Epigenomics ; Genomics ; Humans ; Inflammation ; Joints/pathology ; Mice ; Osteoarthritis/pathology ; Osteoarthritis/physiopathology ; Proteomics ; Transcriptome
Chemical Substances	Biomarkers
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.016881
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Article: Joint homeostasis, restoration, and remodeling in osteoarthritis.

Lories, Rik J U

Best practice & research. Clinical rheumatology

2008 Volume 22, Issue 2, Page(s) 209–220

Abstract: Osteoarthritis is the major cause of joint failure. The outcome of the disease process is determined by complex interactions between cells and molecules steering homeostasis, destruction, restoration, and remodeling. The articular cartilage has a limited ...

Abstract	Osteoarthritis is the major cause of joint failure. The outcome of the disease process is determined by complex interactions between cells and molecules steering homeostasis, destruction, restoration, and remodeling. The articular cartilage has a limited restoration and repair capacity. Genetic studies in humans and the development of mouse models have identified the role of signaling pathways that are important for skeletal development in the postnatal biology and pathology of articular cartilage. These include bone morphogenetic protein, transforming growth factor beta, fibroblast growth factor, wingless-type signaling, and their respective antagonists such as noggin and frizzled related protein. The synovium is prone to inflammation and emerging evidence suggests that innate and adaptive immune responses are important. Bone and cartilage form a biomechanical unit; stiffer bones might impair cartilage homeostasis. The biology of frizzled related protein provides a basis for the hypothesized inverse relationship between osteoarthritis and osteoporosis.
MeSH term(s)	Bone Remodeling/physiology ; Cartilage, Articular/physiopathology ; Homeostasis/physiology ; Humans ; Joints/physiopathology ; Osteoarthritis/physiopathology ; Signal Transduction/physiology ; Synovial Membrane/physiopathology
Language	English
Publishing date	2008-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052323-3
ISSN	1521-6942
ISSN	1521-6942
DOI	10.1016/j.berh.2007.12.001
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Article: Animal models of spondyloarthritis.

Lories, Rik J U

Current opinion in rheumatology

2006 Volume 18, Issue 4, Page(s) 342–346

Abstract: Purpose of review: The aim of this article is to review new insights into spondyloarthritis obtained in animal models during the last year.: Recent findings: HLA-B27 misfolding has been demonstrated in HLA-B27/human beta2-microglobulin transgenic ... ...

Abstract	Purpose of review: The aim of this article is to review new insights into spondyloarthritis obtained in animal models during the last year. Recent findings: HLA-B27 misfolding has been demonstrated in HLA-B27/human beta2-microglobulin transgenic rats. HLA-B27 misfolding is associated with a typical unfolded protein stress response and with an interferon-response signature. Prebiotic treatment of these rats reduced colitis and arthritis. Proteoglycan-induced spondylitis is distinct from proteoglycan-induced arthritis. Specific susceptibility loci for proteoglycan-induced spondylitis have been demonstrated. Bone morphogenetic proteins are important in new cartilage and bone formation in ankylosing enthesitis. Psoriasis and psoriatic arthritis-like disease develops in conditional double JunB/c-Jun knockout mice. Summary: Insights into the molecular signaling pathways driving HLA-B27 associated spondylitis, autoimmune spondylitis, ankylosing enthesitis and psoriasis, resulting from animal models, identify new and specific therapeutic targets in spondyloarthritis.
MeSH term(s)	Animals ; Disease Models, Animal ; Genes, jun ; HLA-B Antigens/immunology ; Humans ; Mice ; Mice, Knockout ; Psoriasis/genetics ; Spondylitis, Ankylosing/genetics ; Spondylitis, Ankylosing/immunology
Chemical Substances	HLA-B Antigens
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1045317-9
ISSN	1531-6963 ; 1040-8711
ISSN (online)	1531-6963
ISSN	1040-8711
DOI	10.1097/01.bor.0000231900.81677.c5
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Article ; Online: Targets, models and challenges in osteoarthritis research

Sarah Thysen / Frank P. Luyten / Rik J. U. Lories

Disease Models & Mechanisms, Vol 8, Iss 1, Pp 17-

2015 Volume 30

Abstract	Osteoarthritis is a chronic degenerative disorder of the joint and represents one of the most common diseases worldwide. Its prevalence and severity are increasing owing to aging of the population, but treatment options remain largely limited to painkillers and anti-inflammatory drugs, which only provide symptomatic relief. In the late stages of the disease, surgical interventions are often necessary to partially restore joint function. Although the focus of osteoarthritis research has been originally on the articular cartilage, novel findings are now pointing to osteoarthritis as a disease of the whole joint, in which failure of different joint components can occur. In this Review, we summarize recent progress in the field, including data from novel ‘omics’ technologies and from a number of preclinical and clinical trials. We describe different in vitro and in vivo systems that can be used to study molecules, pathways and cells that are involved in osteoarthritis. We illustrate that a comprehensive and multisystem approach is necessary to understand the complexity and heterogeneity of the disease and to better guide the development of novel therapeutic strategies for osteoarthritis.
Keywords	Osteoarthritis ; Cartilage ; Bone ; Animal models ; Medicine ; R ; Pathology ; RB1-214
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: WNT Signaling in osteoarthritis and osteoporosis: what is the biological significance for the clinician?

Lodewyckx, Liesbet / Lories, Rik J U

Current rheumatology reports

2009 Volume 11, Issue 1, Page(s) 23–30

Abstract: Osteoporosis and osteoarthritis are common musculoskeletal disorders in which cause and outcome are determined by genetic and environmental factors. The WNT signaling pathway plays an important role in skeletal development and growth. Polymorphisms in a ... ...

Abstract	Osteoporosis and osteoarthritis are common musculoskeletal disorders in which cause and outcome are determined by genetic and environmental factors. The WNT signaling pathway plays an important role in skeletal development and growth. Polymorphisms in a number of genes that belong to this pathway are associated with osteoarthritis and/or osteoporosis. This suggests a role for this molecular signaling pathway in postnatal joint and bone homeostasis and pathology. Increased activity of WNT signaling strengthens the bone but may have adverse effects on the articular cartilage. Frizzled related protein (FRZB) plays a role in both bone and cartilage. Better understanding of the WNT pathway and its modulators may lead to specific therapeutics for both osteoarthritis and osteoporosis. This review focuses on recent studies in human genetics and animal models and highlights the potential clinical relevance of this rapidly evolving field of research.
MeSH term(s)	Animals ; Disease Models, Animal ; Glycoproteins/genetics ; Glycoproteins/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Osteoarthritis/genetics ; Osteoarthritis/metabolism ; Osteoporosis/genetics ; Osteoporosis/metabolism ; Signal Transduction ; Wnt Proteins/genetics ; Wnt Proteins/metabolism
Chemical Substances	Glycoproteins ; Intracellular Signaling Peptides and Proteins ; WD repeat containing planar cell polarity effector ; Wnt Proteins
Language	English
Publishing date	2009-01-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057357-1
ISSN	1534-6307 ; 1523-3774
ISSN (online)	1534-6307
ISSN	1523-3774
DOI	10.1007/s11926-009-0004-6
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Article: Osteoarthritis, a disease bridging development and regeneration.

Lories, Rik J U / Luyten, Frank P

BoneKEy reports

2012 Volume 1, Page(s) 136

Abstract: The osteoarthritic diseases are common disorders characterized by progressive destruction of the articular cartilage in the joints, and associated with remodeling of the subchondral bone, synovitis and the formation of bone outgrowths at the joint ... ...

Abstract	The osteoarthritic diseases are common disorders characterized by progressive destruction of the articular cartilage in the joints, and associated with remodeling of the subchondral bone, synovitis and the formation of bone outgrowths at the joint margins, osteophytes. From the clinical perspective, osteoarthritis leads to joint pain and loss of function. Osteoarthritis is the leading cause of progressive disability. New data from genetic, translational and basic research have demonstrated that pathways with essential roles in joint and bone development also contribute to the postnatal homeostasis of the articular cartilage and are involved in osteoarthritis, making these potential therapeutic targets. Other systems of interest are the tissue-destructive enzymes that break down the extracellular matrix of the cartilage as well as mediators of inflammation that contribute to synovitis. However, the perspective of a durable treatment over years to decades highlights the need for a personalized medicine approach encompassing a global view on the disease and its management, thereby including nonpharmaceutical approaches such as physiotherapy and advanced surgical methods. Integration of novel strategies based on their efficacy and safety with the identification of individuals at risk and optimal individual rehabilitation management remains a major challenge for the medical community in particular, as the incidence of osteoarthritis is likely to further increase with the overall aging of the population.
Language	English
Publishing date	2012-08-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2816308-4
ISSN	2047-6396
ISSN	2047-6396
DOI	10.1038/bonekey.2012.136
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Article ; Online: Blocking p38 signalling inhibits chondrogenesis in vitro but not ankylosis in a model of ankylosing spondylitis in vivo.

Braem, Kirsten / Luyten, Frank P / Lories, Rik J U

Annals of the rheumatic diseases

2012 Volume 71, Issue 5, Page(s) 722–728

Abstract: Objectives: To investigate p38 mitogen activated protein kinase (MAPK) signalling in an in vitro model of bone morphogenetic protein (BMP) and transforming growth factor β (TGFβ)-induced chondrogenesis and in vivo, with specific attention to its ... ...

Abstract	Objectives: To investigate p38 mitogen activated protein kinase (MAPK) signalling in an in vitro model of bone morphogenetic protein (BMP) and transforming growth factor β (TGFβ)-induced chondrogenesis and in vivo, with specific attention to its potential role in ankylosing enthesitis. Methods: Human periosteum-derived cells (hPDCs) were cultured in pellets and stimulated with BMP2 or TGFβ1 in the presence or absence of a p38 inhibitor SB203580 or proinflammatory cytokines. Chondrogenic differentiation was evaluated using quantitative PCR. Male DBA/1 mice from different litters were caged together at the age of 8 weeks and treated with SB203580 in both a preventive and therapeutic strategy. The mice were evaluated for prospective signs of arthritis and the toe joints were analysed histologically to assess disease severity. Results: p38 inhibition by SB203580 and proinflammatory cytokines downregulated chondrogenic markers in pellet cultures stimulated by BMP2 or TGFβ1. In contrast, the in vivo experiments resulted in an increased clinical incidence of arthritis and pathology severity score, reflecting progression towards ankylosis in mice given SB203580. Conclusion: Inhibition of p38 inhibited chondrogenic differentiation of progenitor cells, showing that not only the SMAD signalling pathways and also alternative activation of MAPKs including p38 contribute to chondrogenesis. Such an inhibitory effect is not found in an in vivo model of joint ankylosis and spondyloarthritis. Increased incidence and severity of disease in preventive experiments and shifts in disease stages in a therapeutic experimental set-up suggest that specific inhibition of p38 may have deleterious rather than beneficial effects.
MeSH term(s)	Animals ; Ankylosis/drug therapy ; Ankylosis/genetics ; Ankylosis/physiopathology ; Bone Morphogenetic Proteins/pharmacology ; Cell Proliferation/drug effects ; Cells, Cultured ; Chondrocytes/drug effects ; Chondrocytes/pathology ; Chondrogenesis/drug effects ; Chondrogenesis/genetics ; Disease Models, Animal ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Gene Expression/drug effects ; Imidazoles/pharmacology ; Male ; Mice ; Mice, Inbred DBA ; Periosteum/cytology ; Periosteum/drug effects ; Pyridines/pharmacology ; Signal Transduction/drug effects ; Smad Proteins/genetics ; Smad Proteins/metabolism ; Spondylitis, Ankylosing/drug therapy ; Spondylitis, Ankylosing/metabolism ; Spondylitis, Ankylosing/pathology ; Transforming Growth Factor beta/pharmacology ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/biosynthesis ; p38 Mitogen-Activated Protein Kinases/genetics
Chemical Substances	Bone Morphogenetic Proteins ; Enzyme Inhibitors ; Imidazoles ; Pyridines ; Smad Proteins ; Transforming Growth Factor beta ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; SB 203580 (OU13V1EYWQ)
Language	English
Publishing date	2012-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/annrheumdis-2011-200377
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