Evidence for a distinctive pattern of bone formation in enthesophytes

Benjamin, Michael; Toumi, Hechmi; Suzuki, Daisuke; Hayashi, Kôji; McGonagle, Dennis

doi:10.1136/ard.2008.091074

Cited by 100 publications

(108 citation statements)

References 13 publications

(14 reference statements)

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“…Bone formation at insertions occurs at sites of maximal entheseal tension and histologically may exhibit endochondral, intramembranous or chondroidal metaplasia [4]. The basis for the post inflammatory new bone formation at entheses in SpA remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies

et al. 2016

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Article:El-Zayadi, AA, Jones, EA orcid.org/0000-0001-9365-2283, Churchman, SM orcid.org/0000-0003-0172-3975 et al. (7 more authors) (2017) Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies. Rheumatology, 56 (3 ReuseUnless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request. This is a Conclusion. This work shows that IL-22 is involved in human MSC proliferation/migration in inflammatory environments with MSC osteogenesis occurring only in IFN-/TNF absence. These effects of IL-22 on MSC function is a novel pathway for exploring pathological, post-inflammation osteogenesis in human SpA.

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Section: Introductionmentioning

confidence: 99%

Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies

et al. 2016

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“…2 On the other hand, Benjamin and McGonagle have thoroughly studied the age-related enthesophyte formation in the Achilles tendon in both rodents and humans. 4,5 Although obviously it remains unclear whether formation of syndesmophytes (which occur in the inflammatory context of AS) and enthesophytes (which may mainly result from mechanical factors during aging 6 ) follow the same molecular pathways, the Achilles tendon is also affected in AS in humans, 7 and is fundamentally similar to the entheses principally affected in AS. 4 Consequently, Benjamin et al 4,5 reasonably assumed that the mechanisms governing syndesmophyte formation in the spine and enthesophyte development in the Achilles tendon may be similar.…”

mentioning

confidence: 99%

“…24 In this hypothesis, cytokines may stimulate ectopic collagen calcification by the mere stimulation of TNAP activity, and this calcified matrix, may in turn induce the ossification process, in the arterial wall, 25 and in entheseal fibro-cartilage during AS. 4,5 MATERIALS AND METHODS Chemicals Cell culture plastic ware was purchased from D Dutscher (Brumath, France). Dulbecco's minimum essential medium (DMEM), a-MEM, fetal calf serum (FCS), insulin, L-glutamine, penicillin, streptomycin (P/S), trypsin/EDTA, and Extract-All reagents were from Eurobio (Les Ulis, France).…”

mentioning

confidence: 99%

Cell-specific effects of TNF-α and IL-1β on alkaline phosphatase: implication for syndesmophyte formation and vascular calcification

Lencel

Delplace

Pilet

et al. 2011

Laboratory Investigation

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Tumor necrosis factor (TNF)-a and interleukin (IL)-1b stimulate tissue non-specific alkaline phosphatase (TNAP) activity and mineralization in cultures of vascular smooth muscle cells (VSMCs). They are, therefore, considered as stimulators of vascular calcification in the context of atherosclerosis and diabetes type 2. In contrast, although ankylosing spondylitis (AS) leads to the formation of syndesmophytes, which are ectopic ossifications from entheses (where ligaments, tendons and capsules are attached to bone), anti-TNF-a therapies fail to block bone formation in this disease. In this context, our aims were to compare the effects of TNF-a and IL-1b on TNAP activity and mineralization in entheseal cells and VSMCs. Organotypic cultures of mouse ankle entheses were treated or not with TNF-a and IL-1b for 5 days. Micro-computed tomography was performed to determine trabecular bone parameters, and histology to assess TNAP activity and mineralization. Human mesenchymal stem cells cultured in pellets in chondrogenic conditions and human VSMCs were also used to determine the effects of cytokines on TNAP activity and expression, measured by quantitative PCR. In organotypic cultures, TNF-a and IL-1b significantly reduced the tibia BV/TV ratio. They also inhibited TNAP activity in entheseal chondrocytes in situ, and in mouse and human chondrocytes in vitro. In contrast, TNF-a stimulated TNAP expression and activity in human VSMCs. These differences were likely due to cell-specific effects of peroxisome proliferator-activated receptor g (PPARg), which is inhibited by TNF-a. Indeed, in human chondrocytes and VSMCs, the PPARg inhibitor GW-9662 displayed the same opposite effects as TNF-a on TNAP expression. In conclusion, whereas TNF-a and IL-1b stimulate TNAP activity in VSMCs, they inhibit it in entheseal cells in situ and on chondrocytes in vitro. The identification of PPARg as a likely mediator of cytokine effects deserves consideration for future research on the mechanisms of ectopic ossification.

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“…Histological characteristics of the formation of the posterior osteophytes in spine as age advances has been documented in literature [22][23][24][25]. Reviewing the literature we found that Peng et al [26] in the experimental model of cervical spondylosis in rabbits had suggested that vertebral osteophytes arises from proliferation of peripheral articular cartilage which undergoes transformation into cartilaginous osteophytes and then converts into bony osteophytes through an endochondral calcification and ossification.…”

Section: Experimental Evidence Showing the Development Of The Posterimentioning

confidence: 86%

Posterior Osteophyte Evolution and its Impact in Cervical Spondylosis: A Literature Review

Lawrence¹

2013

J Spine

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Introduction: In cervical disc disease, the exact location of the posterior osteophyte with relationship to the bodies of the adjacent cervical vertebra at each disc space level, as observed during surgery under operating microscope and correlating it with the histopathological development of the posterior osteophyte has not been documented in literature. A detailed review of literature on the development of posterior osteophytes and its impact on cervical spinal cord is also being reviewed.

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Evidence for a distinctive pattern of bone formation in enthesophytes

Cited by 100 publications

References 13 publications

Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies

Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies

Cell-specific effects of TNF-α and IL-1β on alkaline phosphatase: implication for syndesmophyte formation and vascular calcification

Posterior Osteophyte Evolution and its Impact in Cervical Spondylosis: A Literature Review

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