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Journal ArticleDOI

The Emerging Role of Dickkopf-1 in Bone Biology: Is It the Main Switch Controlling Bone and Joint Remodeling?

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TLDR
DKK-1 is a regulator of bone mass with increased expression linked to osteopenia and decreased expression to high bone mass and appears to actively participate in joint remodeling in animal models of arthritis, with increased levels related to bone resorption and decreased levels to new bone formation.
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This article is published in Seminars in Arthritis and Rheumatism.The article was published on 2011-10-01. It has received 95 citations till now. The article focuses on the topics: Bone disease & Bone resorption.

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The bone remodelling cycle.

TL;DR: The remodelling process and its regulation is described, osteoporosis is discussed and the commonest pharmacological interventions used in its management are summarized.
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Osteoporosis and vertebral fractures in ankylosing spondylitis.

TL;DR: Although bisphosphonates and tumor necrosis factor-&agr; inhibitors look promising, further prospective trials on the treatment of osteoporosis in AS are needed.
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The coupling of bone and cartilage turnover in osteoarthritis: opportunities for bone antiresorptives and anabolics as potential treatments?

TL;DR: Known bone therapies, namely oestrogens, selective oestrogen receptor modifiers (SERMs), bisphosphonates, strontium ranelate, calcitonin and parathyroid hormone, might prove useful for treating two critical tissue components of the OA joint, the bone and the cartilage.
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Diffuse idiopathic skeletal hyperostosis: clinical features and pathogenic mechanisms

TL;DR: In this Review, the reader is provided with an up-to-date discussion of the epidemiological, aetiological and clinical aspects of DISH, together with the need for modified criteria that enable timely identification of early phases in the development of DISh.
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Wnt signaling pathway in rheumatoid arthritis, with special emphasis on the different roles in synovial inflammation and bone remodeling.

TL;DR: New advances of the Wnt signaling pathway in RA pathogenesis are discussed, with special emphasis on its different roles in synovial inflammation and bone remodeling.
References
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Wnt/beta-catenin signaling in development and disease.

TL;DR: A remarkable interdisciplinary effort has unraveled the WNT (Wingless and INT-1) signal transduction cascade over the last two decades, finding that Germline mutations in the Wnt pathway cause several hereditary diseases, and somatic mutations are associated with cancer of the intestine and a variety of other tissues.
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Metastatic patterns of prostate cancer: an autopsy study of 1,589 patients.

TL;DR: It is shown that bone, lung, and liver are the most frequent sites of distant prostate cancer metastases and there are strong arguments for the existence and clinical significance of a backward venous spread to the spine, which is likely to occur early in the metastatic process.
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High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5

TL;DR: The LRP5V171 mutation causes high bone density, with a thickened mandible and torus palatinus, by impairing the action of a normal antagonist of the Wnt pathway and thus increasing Wnt signaling.
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Secreted antagonists of the Wnt signalling pathway

TL;DR: The extracellular antagonists of the Wnt signalling pathway can be divided into two broad classes: members of the sFRP (secreted Frizzled-related protein) family, WIF (Wnt inhibitory factor)-1 and Cerberus, primarily bind to Wnt proteins; the second class comprises certainMembers of the Dickkopf (Dkk) family; these families have as-yet-undiscovered functions.
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Canonical Wnt Signaling in Differentiated Osteoblasts Controls Osteoclast Differentiation

TL;DR: Findings demonstrate that beta-catenin, and presumably Wnt signaling, promote the ability of differentiated osteoblasts to inhibit osteoclast differentiation and broaden the knowledge of the functions Wnt proteins have at various stages of skeletogenesis.
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