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      Calcitonin and vitamin D 3 have high therapeutic potential for improving diabetic mandibular growth

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          Abstract

          The goal of this study was to assess the effect of the intermittent combination of an antiresorptive agent (calcitonin) and an anabolic agent (vitamin D 3) on treating the detrimental effects of Type 1 diabetes mellitus (DM) on mandibular bone formation and growth. Forty 3-week-old male Wistar rats were divided into four groups: the control group (normal rats), the control C+D group (normal rats injected with calcitonin and vitamin D 3), the diabetic C+D group (diabetic rats injected with calcitonin and vitamin D 3) and the diabetic group (uncontrolled diabetic rats). An experimental DM condition was induced in the male Wistar rats in the diabetic and diabetic C+D groups using a single dose of 60 mg·kg −1 body weight of streptozotocin. Calcitonin and vitamin D 3 were simultaneously injected in the rats of the control C+D and diabetic C+D groups. All rats were killed after 4 weeks, and the right mandibles were evaluated by micro-computed tomography and histomorphometric analysis. Diabetic rats showed a significant deterioration in bone quality and bone formation (diabetic group). By contrast, with the injection of calcitonin and vitamin D 3, both bone parameters and bone formation significantly improved (diabetic C+D group) ( P < 0.05). These findings suggest that these two hormones might potentially improve various bone properties.

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          Osteoporosis: now and the future.

          Tilman Rachner, Sundeep Khosla, Lorenz Hofbauer (2011)
          Osteoporosis is a common disease characterised by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. With an ageing population, the medical and socioeconomic effect of osteoporosis, particularly postmenopausal osteoporosis, will increase further. A detailed knowledge of bone biology with molecular insights into the communication between bone-forming osteoblasts and bone-resorbing osteoclasts and the orchestrating signalling network has led to the identification of novel therapeutic targets. Novel treatment strategies have been developed that aim to inhibit excessive bone resorption and increase bone formation. The most promising novel treatments include: denosumab, a monoclonal antibody for receptor activator of NF-κB ligand, a key osteoclast cytokine; odanacatib, a specific inhibitor of the osteoclast protease cathepsin K; and antibodies against the proteins sclerostin and dickkopf-1, two endogenous inhibitors of bone formation. This overview discusses these novel therapies and explains their underlying physiology. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            Resurrection of vitamin D deficiency and rickets.

            Michael Holick (2006)
            The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.
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              Bone formation is impaired in a model of type 1 diabetes.

              James Aronson, Lichu Liu, Christopher W. V. Hogue … (2005)
              The effects of type 1 diabetes on de novo bone formation during tibial distraction osteogenesis (DO) and on intact trabecular and cortical bone were studied using nonobese diabetic (NOD) mice and comparably aged nondiabetic NOD mice. Diabetic mice received treatment with insulin, vehicle, or no treatment during a 14-day DO procedure. Distracted tibiae were analyzed radiographically, histologically, and by microcomputed tomography (microCT). Contralateral tibiae were analyzed using microCT. Serum levels of insulin, osteocalcin, and cross-linked C-telopeptide of type I collagen were measured. Total new bone in the DO gap was reduced histologically (P < or = 0.001) and radiographically (P < or = 0.05) in diabetic mice compared with nondiabetic mice but preserved by insulin treatment. Serum osteocalcin concentrations were also reduced in diabetic mice (P < or = 0.001) and normalized with insulin treatment. Evaluation of the contralateral tibiae by microCT and mechanical testing demonstrated reductions in trabecular bone volume and thickness, cortical thickness, cortical strength, and an increase in endosteal perimeter in diabetic animals, which were prevented by insulin treatment. These studies demonstrate that bone formation during DO is impaired in a model of type 1 diabetes and preserved by systemic insulin administration.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Oral Sci
                Journal ID (iso-abbrev): Int J Oral Sci
                Title: International Journal of Oral Science
                Publisher: Nature Publishing Group
                ISSN (Print): 1674-2818
                ISSN (Electronic): 2049-3169
                Publication date (Print): March 2016
                Publication date (Electronic): 18 December 2015
                Publication date PMC-release: 1 March 2016
                Volume: 8
                Issue: 1
                Pages: 39-44
                Affiliations
                [1 ]Orthodontic Department, Faculty of Dentistry, King Abdulaziz University , Jeddah, Saudi Arabia
                [2 ]Department of Orofacial Development and Function, Division of Oral Health Sciences, Graduate School, Tokyo Medical and Dental University , Tokyo, Japan
                [3 ]Alexandria University , Alexandria, Egypt
                [4 ]Conservative Dentistry Department, Faculty of Dentistry, King Abdulaziz University , Jeddah, Saudi Arabia
                [5 ]Cariology and Operative Dentistry Department, Graduate School of Medical and Dental Sciences, Tokyo Medical & Dental University , Tokyo, Japan
                [6 ]Conservative Dentistry Department, Faculty of Dentistry, Alexandria University , Alexandria, Egypt
                Author notes
                [* ]Orthodontic Department, Faculty of Dentistry, King Abdulaziz University , P.O.Box 80209, Jeddah 21589, Saudi Arabia
                Article
                Publisher Item ID: ijos201547
                DOI: 10.1038/ijos.2015.47
                PMC ID: 4822182
                PubMed ID: 27025264
                SO-VID: 5cf447a8-6337-4ff8-b486-f6f9600a57be
                Copyright © Copyright © 2015 West China School of Stomatology
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                Date accepted : 15 July 2015
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Dentistry
                Keywords: type 1 diabetes mellitus,mandibular bone structure,mandibular bone formation,micro-computed tomography,bone,histomorphometry
                Data availability:
                ScienceOpen disciplines: Dentistry
                Keywords: type 1 diabetes mellitus, mandibular bone structure, mandibular bone formation, micro-computed tomography, bone, histomorphometry

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