Brunetti G, D'Amato G, De Santis S, Grano M, Faienza MF. Mechanisms of altered bone remodeling in children with type 1 diabetes. World J Diabetes 2021; 12(7): 997-1009 [PMID: 34326950 DOI: 10.4239/wjd.v12.i7.997]
Corresponding Author of This Article
Giacomina Brunetti, PhD, Academic Research, Department of Biosciences, Biotechnologies and Biopharmaceutics, University "A. Moro" of Bari, Via Orabona 4, Bari 70125, Italy. giacomina.brunetti@uniba.it
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jul 15, 2021; 12(7): 997-1009 Published online Jul 15, 2021. doi: 10.4239/wjd.v12.i7.997
Mechanisms of altered bone remodeling in children with type 1 diabetes
Giacomina Brunetti, Gabriele D'Amato, Stefania De Santis, Maria Grano, Maria Felicia Faienza
Giacomina Brunetti, Department of Biosciences, Biotechnologies and Biopharmaceutics, University "A. Moro" of Bari, Bari 70125, Italy
Gabriele D'Amato, Department of Women’s and Children’s Health, ASL Bari, Neonatal Intensive Care Unit, Di Venere Hospital, Bari 70124, Italy
Stefania De Santis, Department of Pharmacy-Drug Science, University of Bari Aldo Moro, Bari 70126, Italy
Maria Grano, Department of Emergency and Organ Transplantation, Univ Bari, Bari 70124, Italy
Maria Felicia Faienza, Department of Biomedical Sciences and Human Oncology, Pediatric Unit, University "A.Moro", Bari 70124, Italy
Author contributions: Faienza MF and Brunetti G equally contributed to this paper with conception and design of the article; Faienza MF drafted and revised the paper; D'Amato G and De Santis S performed literature review; Grano M critically revised the final version.
Conflict-of-interest statement: No potential conflicts of interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Giacomina Brunetti, PhD, Academic Research, Department of Biosciences, Biotechnologies and Biopharmaceutics, University "A. Moro" of Bari, Via Orabona 4, Bari 70125, Italy. giacomina.brunetti@uniba.it
Received: January 29, 2021 Peer-review started: January 29, 2021 First decision: March 1, 2021 Revised: March 17, 2021 Accepted: May 22, 2021 Article in press: May 22, 2021 Published online: July 15, 2021
Abstract
Bone loss associated with type 1 diabetes mellitus (T1DM) begins at the onset of the disease, already in childhood, determining a lower bone mass peak and hence a greater risk of osteoporosis and fractures later in life. The mechanisms underlying diabetic bone fragility are not yet completely understood. Hyperglycemia and insulin deficiency can affect the bone cells functions, as well as the bone marrow fat, thus impairing the bone strength, geometry, and microarchitecture. Several factors, like insulin and growth hormone/insulin-like growth factor 1, can control bone marrow mesenchymal stem cell commitment, and the receptor activator of nuclear factor-κB ligand/osteoprotegerin and Wnt-b catenin pathways can impair bone turnover. Some myokines may have a key role in regulating metabolic control and improving bone mass in T1DM subjects. The aim of this review is to provide an overview of the current knowledge of the mechanisms underlying altered bone remodeling in children affected by T1DM.
Core Tip: Bone fragility is a well-known complication related to type 1 diabetes mellitus, and it can manifest from the disease onset, already in childhood. The mechanisms underlying this relationship, and the precise role of metabolic control in preventing bone impairment, are not yet fully understood. Future studies are needed to clarify better the factors responsible for bone damage in diabetic subjects, and to identify strategies for avoiding and managing osteopenia/osteoporosis in these subjects.
