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      Cell signalling and bone remodelling: The skeleton as an endocrine relay organ - Part 1

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          Abstract

          As knowledge on the signalling pathways involved in bone remodelling unfolds, maintenance of skeletal health and the management of skeletal diseases will increasingly focus on the manipulation of the autocrine, paracrine and endocrine mechanisms involved in the process. This overview is aimed at providing practitioners with an update on recent advances on cell signalling in bone remodelling and highlights the role of the skeleton in systemic metabolism.

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          Self-renewing osteoprogenitors in bone marrow sinusoids can organize a hematopoietic microenvironment.

          Benedetto Sacchetti, Alessia Funari, Stefano Michienzi … (2007)
          The identity of cells that establish the hematopoietic microenvironment (HME) in human bone marrow (BM), and of clonogenic skeletal progenitors found in BM stroma, has long remained elusive. We show that MCAM/CD146-expressing, subendothelial cells in human BM stroma are capable of transferring, upon transplantation, the HME to heterotopic sites, coincident with the establishment of identical subendothelial cells within a miniature bone organ. Establishment of subendothelial stromal cells in developing heterotopic BM in vivo occurs via specific, dynamic interactions with developing sinusoids. Subendothelial stromal cells residing on the sinusoidal wall are major producers of Angiopoietin-1 (a pivotal molecule of the HSC "niche" involved in vascular remodeling). Our data reveal the functional relationships between establishment of the HME in vivo, establishment of skeletal progenitors in BM sinusoids, and angiogenesis.
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            Vascular endothelial growth factor stimulates bone repair by promoting angiogenesis and bone turnover.

            John N. Street, Min Hang Bao, Leo deGuzman … (2002)
            Several growth factors are expressed in distinct temporal and spatial patterns during fracture repair. Of these, vascular endothelial growth factor, VEGF, is of particular interest because of its ability to induce neovascularization (angiogenesis). To determine whether VEGF is required for bone repair, we inhibited VEGF activity during secondary bone healing via a cartilage intermediate (endochondral ossification) and during direct bone repair (intramembranous ossification) in a novel mouse model. Treatment of mice with a soluble, neutralizing VEGF receptor decreased angiogenesis, bone formation, and callus mineralization in femoral fractures. Inhibition of VEGF also dramatically inhibited healing of a tibial cortical bone defect, consistent with our discovery of a direct autocrine role for VEGF in osteoblast differentiation. In separate experiments, exogenous VEGF enhanced blood vessel formation, ossification, and new bone (callus) maturation in mouse femur fractures, and promoted bony bridging of a rabbit radius segmental gap defect. Our results at specific time points during the course of healing underscore the role of VEGF in endochondral vs. intramembranous ossification, as well as skeletal development vs. bone repair. The responses to exogenous VEGF observed in two distinct model systems and species indicate that a slow-release formulation of VEGF, applied locally at the site of bone damage, may prove to be an effective therapy to promote human bone repair.
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              Coupling the activities of bone formation and resorption: a multitude of signals within the basic multicellular unit.

              Natalie Sims, T John Martin (2014)
              Coupling between bone formation and bone resorption refers to the process within basic multicellular units in which resorption by osteoclasts is met by the generation of osteoblasts from precursors, and their bone-forming activity, which needs to be sufficient to replace the bone lost. There are many sources of activities that contribute to coupling at remodeling sites, including growth factors released from the matrix, soluble and membrane products of osteoclasts and their precursors, signals from osteocytes and from immune cells and signaling taking place within the osteoblast lineage. Coupling is therefore a process that involves the interaction of a wide range of cell types and control mechanisms. As bone remodeling occurs at many sites asynchronously throughout the skeleton, locally generated activities comprise very important control mechanisms. In this review, we explore the potential roles of a number of these factors, including sphingosine-1-phosphate, semaphorins, ephrins, interleukin-6 (IL-6) family cytokines and marrow-derived factors. Their interactions achieve the essential tight control of coupling within individual remodeling units that is required for control of skeletal mass.
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                Author and article information

                Contributors
                EJ Raubenheimer: Role: ND
                HD Hendrik: Role: ND
                Journal
                Journal ID (publisher): saoj
                Title: SA Orthopaedic Journal
                Abbreviated Title: SA orthop. j.
                Publisher: Champagne Media (Pty) Ltd (Pretoria )
                ISSN: 2309-8309
                Publication date (Print): November 2015
                Volume: 14
                Issue: 4
                Pages: 16-21
                Affiliations
                [1 ] SMU South Africa
                Article
                Publisher ID: S1681-150X2015000400002
                DOI: 10.17159/2309-8309/2015/v14n4a1
                SO-VID: a61b4f76-468e-4503-abae-bbf3a7916f3b
                License:

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO South Africa

                Self URI (journal page): http://www.scielo.org.za/scielo.php?script=sci_serial&pid=1681-150X&lng=en
                Categories
                Subject: Health Care Sciences & Services
                Subject: Orthopedics

                ScienceOpen disciplines: Orthopedics,Health & Social care
                Keywords: bone metabolism,cell signalling,skeletal remodelling
                Data availability:
                ScienceOpen disciplines: Orthopedics, Health & Social care
                Keywords: bone metabolism, cell signalling, skeletal remodelling

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