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      Changes in expression of Wnt signaling pathway inhibitors dickkopf-1 and sclerostin before and after total joint arthroplasty

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          Abstract

          The aim is to study how serum concentration of Dickkopf-1 (DKK1) and Sclerostin (SOST) varies in patients before and after undergoing total joint arthroplasty (TJA). A total of 104 patients undergoing TJA were included in this study. Serum DKK1 and SOST were measured at 1 day before and 1, 3, and 5 days after surgery. DKK1 levels were highest at 5 days’ postoperation, increasing to 25.17% above preoperation levels ( P < .01), while SOST levels were lowest at 3 days’ postoperation, falling to 18.71% below preoperation levels ( P < .05). Serum levels of DKK1 and SOST showed opposite trends in the days following TJA. Our research describes for the first time the perioperative changes observed in serum DKK1 and SOST levels of osteoarthritis (OA) patients undergoing TJA. Increased DKK1 and decreased SOST levels may help maintain the equilibrium of the WNT pathway in OA patient's postsurgery.

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          WNT signaling in bone homeostasis and disease: from human mutations to treatments.

          Roland Baron, Michaela Kneissel (2013)
          Low bone mass and strength lead to fragility fractures, for example, in elderly individuals affected by osteoporosis or children with osteogenesis imperfecta. A decade ago, rare human mutations affecting bone negatively (osteoporosis-pseudoglioma syndrome) or positively (high-bone mass phenotype, sclerosteosis and Van Buchem disease) have been identified and found to all reside in components of the canonical WNT signaling machinery. Mouse genetics confirmed the importance of canonical Wnt signaling in the regulation of bone homeostasis, with activation of the pathway leading to increased, and inhibition leading to decreased, bone mass and strength. The importance of WNT signaling for bone has also been highlighted since then in the general population in numerous genome-wide association studies. The pathway is now the target for therapeutic intervention to restore bone strength in millions of patients at risk for fracture. This paper reviews our current understanding of the mechanisms by which WNT signalng regulates bone homeostasis.
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            Regulation of bone mass by Wnt signaling.

            Venkatesh Krishnan, Henry Bryant, Ormond A Macdougald (2006)
            Wnt proteins are a family of secreted proteins that regulate many aspects of cell growth, differentiation, function, and death. Considerable progress has been made in our understanding of the molecular links between Wnt signaling and bone development and remodeling since initial reports that mutations in the Wnt coreceptor low-density lipoprotein receptor-related protein 5 (LRP5) are causally linked to alterations in human bone mass. Of the pathways activated by Wnts, it is signaling through the canonical (i.e., Wnt/beta-catenin) pathway that increases bone mass through a number of mechanisms including renewal of stem cells, stimulation of preosteoblast replication, induction of osteoblastogenesis, and inhibition of osteoblast and osteocyte apoptosis. This pathway is an enticing target for developing drugs to battle skeletal diseases as Wnt/beta-catenin signaling is composed of a series of molecular interactions that offer potential places for pharmacological intervention. In considering opportunities for anabolic drug discovery in this area, one must consider multiple factors, including (a) the roles of Wnt signaling for development, remodeling, and pathology of bone; (b) how pharmacological interventions that target this pathway may specifically treat osteoporosis and other aspects of skeletal health; and (c) whether the targets within this pathway are amenable to drug intervention. In this Review we discuss the current understanding of this pathway in terms of bone biology and assess whether targeting this pathway might yield novel therapeutics to treat typical bone disorders.
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              Identification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease.

              W. Balemans (2002)
              Van Buchem disease is an autosomal recessive skeletal dysplasia characterised by generalised bone overgrowth, predominantly in the skull and mandible. Clinical complications including facial nerve palsy, optic atrophy, and impaired hearing occur in most patients. These features are very similar to those of sclerosteosis and the two conditions are only differentiated by the hand malformations and the tall stature appearing in sclerosteosis. Using an extended Dutch inbred van Buchem family and two inbred sclerosteosis families, we mapped both disease genes to the same region on chromosome 17q12-q21, supporting the hypothesis that van Buchem disease and sclerosteosis are caused by mutations in the same gene. In a previous study, we positionally cloned a novel gene, called SOST, from the linkage interval and identified three different, homozygous mutations in the SOST gene in sclerosteosis patients leading to loss of function of the underlying protein. The present study focuses on the identification of a 52 kb deletion in all patients from the van Buchem family. The deletion, which results from a homologous recombination between Alu sequences, starts approximately 35 kb downstream of the SOST gene. Since no evidence was found for the presence of a gene within the deleted region, we hypothesise that the presence of the deletion leads to a down regulation of the transcription of the SOST gene by a cis regulatory action or a position effect.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Wolters Kluwer Health
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: September 2017
                Publication date (Electronic): 29 September 2017
                Volume: 96
                Issue: 39
                Electronic Location Identifier: e8082
                Affiliations
                [a ]Department of Sports Medicine and Adult Reconstructive Surgery, Drum Tower Hospital, School of Medicine
                [b ]Joint Research Center for Bone and Joint Disease, Model Animal Research Center (MARC), Nanjing University, Nanjing, Jiangsu, China.
                Author notes
                [∗ ]Correspondence: Qing Jiang, Department of Sports Medicine and Adult Reconstructive Surgery, Drum Tower Hospital, School of Medicine, Nanjing University, Zhongshan Road 321, Nanjing 210008, Jiangsu, PR China (e-mails: qingj@ 123456nju.edu.cn , jiangqing112@ 123456hotmail.com ); Hua-Jian Teng, Joint Research Center for Bone and Joint Disease, Model Animal Research Center (MARC), Nanjing University, Nanjing 210093, Jiangsu, China (e-mail: tenghj@ 123456nicemice.cn ).
                Article
                Publisher ID: MD-D-17-02180 Accession ID: 08082
                DOI: 10.1097/MD.0000000000008082
                PMC ID: 5626270
                PubMed ID: 28953627
                SO-VID: d19bcf21-a9ac-4c0d-a90e-e7f3dda65129
                Copyright © Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc.
                License:

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                Date received : 19 April 2017
                Date revision received : 3 July 2017
                Date accepted : 24 August 2017
                Categories
                Subject: 7100
                Subject: Research Article
                Subject: Observational Study
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: osteoarthritis,serum dickkopf-1,serum sclerostin,total joint arthroplasty
                Data availability:
                Keywords: osteoarthritis, serum dickkopf-1, serum sclerostin, total joint arthroplasty

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