Osteocyte apoptosis and cellular micropetrosis signify skeletal aging in type 1 diabetes.

Cell death Microdamage accumulation Micropetrosis Osteocyte apoptosis Skeletal aging Type 1 diabetes mellitus

Journal

Acta biomaterialia
ISSN: 1878-7568
Titre abrégé: Acta Biomater
Pays: England
ID NLM: 101233144

Informations de publication

Date de publication:
05 2023
Historique:
received: 12 10 2022
revised: 03 02 2023
accepted: 27 02 2023
medline: 1 5 2023
pubmed: 7 3 2023
entrez: 6 3 2023
Statut: ppublish

Résumé

Bone fragility is a profound complication of type 1 diabetes mellitus (T1DM), increasing patient morbidity. Within the mineralized bone matrix, osteocytes build a mechanosensitive network that orchestrates bone remodeling; thus, osteocyte viability is crucial for maintaining bone homeostasis. In human cortical bone specimens from individuals with T1DM, we found signs of accelerated osteocyte apoptosis and local mineralization of osteocyte lacunae (micropetrosis) compared with samples from age-matched controls. Such morphological changes were seen in the relatively young osteonal bone matrix on the periosteal side, and micropetrosis coincided with microdamage accumulation, implying that T1DM drives local skeletal aging and thereby impairs the biomechanical competence of the bone tissue. The consequent dysfunction of the osteocyte network hampers bone remodeling and decreases bone repair mechanisms, potentially contributing to the enhanced fracture risk seen in individuals with T1DM. STATEMENT OF SIGNIFICANCE: Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease that causes hyperglycemia. Increased bone fragility is one of the complications associated with T1DM. Our latest study on T1DM-affected human cortical bone identified the viability of osteocytes, the primary bone cells, as a potentially critical factor in T1DM-bone disease. We linked T1DM with increased osteocyte apoptosis and local accumulation of mineralized lacunar spaces and microdamage. Such structural changes in bone tissue suggest that T1DM speeds up the adverse effects of aging, leading to the premature death of osteocytes and potentially contributing to diabetes-related bone fragility.

Identifiants

pubmed: 36878337
pii: S1742-7061(23)00125-3
doi: 10.1016/j.actbio.2023.02.037
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

254-265

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:

Auteurs

Sofie Dragoun Kolibová (S)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Eva Maria Wölfel (EM)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany; Interdisciplinary Competence Center for Interface Research, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Haniyeh Hemmatian (H)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Petar Milovanovic (P)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany; University of Belgrade, Faculty of Medicine, Center of Bone Biology, Institute of Anatomy, Belgrade, Serbia.

Herbert Mushumba (H)

University Medical Center Hamburg Eppendorf, Institute of Legal Medicine, Hamburg, Germany.

Birgit Wulff (B)

University Medical Center Hamburg Eppendorf, Institute of Legal Medicine, Hamburg, Germany.

Maximilian Neidhardt (M)

Institute of Medical Technology and Intelligent Systems, Hamburg University of Technology, Am-Schwarzenberg-Campus 3, Hamburg 21073, Germany; Interdisciplinary Competence Center for Interface Research, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Klaus Püschel (K)

University Medical Center Hamburg Eppendorf, Institute of Legal Medicine, Hamburg, Germany.

Antonio Virgilio Failla (AV)

University Medical Center Hamburg Eppendorf, UKE microscopy Imaging facility, Hamburg, Germany.

Annegreet Vlug (A)

Leiden University Medical Center (LUMC), Centre for Bone Quality, Leiden, the Netherlands.

Alexander Schlaefer (A)

Institute of Medical Technology and Intelligent Systems, Hamburg University of Technology, Am-Schwarzenberg-Campus 3, Hamburg 21073, Germany; Interdisciplinary Competence Center for Interface Research, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Benjamin Ondruschka (B)

University Medical Center Hamburg Eppendorf, Institute of Legal Medicine, Hamburg, Germany.

Michael Amling (M)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany.

Lorenz C Hofbauer (LC)

Division of Endocrinology, Department of Medicine III, Technische Universität Dresden Medical Center, Diabetes, and Metabolic Bone Diseases, Dresden, Germany.

Martina Rauner (M)

Division of Endocrinology, Department of Medicine III, Technische Universität Dresden Medical Center, Diabetes, and Metabolic Bone Diseases, Dresden, Germany.

Björn Busse (B)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany; Interdisciplinary Competence Center for Interface Research, University Medical Center Hamburg Eppendorf, Hamburg, Germany. Electronic address: b.busse@uke.de.

Katharina Jähn-Rickert (K)

Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg, Germany; Mildred Scheel Cancer Career Center Hamburg, University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany.

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Classifications MeSH