MECHANISMS IN ENDOCRINOLOGY: Bone marrow adiposity and bone, a bad romance?

Document type :

Compte-rendu et recension critique d'ouvrage: Autre communication scientifique (congrès sans actes - poster - séminaire...)

DOI :

10.1530/EJE-18-0182

Title :

MECHANISMS IN ENDOCRINOLOGY: Bone marrow adiposity and bone, a bad romance?

Author(s) :

Rharass, Tareck [Auteur]
Marrow Adiposity & Bone Lab - Adiposité Médullaire et Os - ULR 4490 [MABLab]
Lucas, Stéphanie [Auteur]
Université du Littoral Côte d'Opale [ULCO]
Marrow Adiposity & Bone Lab - Adiposité Médullaire et Os - ULR 4490 [MABLab]

Journal title :

EUROPEAN JOURNAL OF ENDOCRINOLOGY

Pages :

R165-R182

Publisher :

Oxford Univ. Press

Publication date :

2018-10

ISSN :

0804-4643

HAL domain(s) :

Sciences du Vivant [q-bio]

English abstract : [en]

Bone marrow adipocytes (BMA-) constitute an original and heterogeneous fat depot whose development appears interlinked with bone status throughout life. The gradual replacement of the haematopoietic tissue by BMA arises ...
Show more >Bone marrow adipocytes (BMA-) constitute an original and heterogeneous fat depot whose development appears interlinked with bone status throughout life. The gradual replacement of the haematopoietic tissue by BMA arises in a well-ordered way during childhood and adolescence concomitantly to bone growth and continues at a slower rate throughout the adult life. Importantly, BM adiposity quantity is found well associated with bone mineral density (BMD) loss at different skeletal sites in primary osteoporosis such as in ageing or menopause but also in secondary osteoporosis consecutive to anorexia nervosa. Since BMA and osteoblasts originate from a common mesenchymal stem cell, adipogenesis is considered as a competitive process that disrupts osteoblastogenesis. Besides, most factors secreted by bone and bone marrow cells (ligands and antagonists of the WNT/β-catenin pathway, BMP and others) reciprocally regulate the two processes. Hormones such as oestrogens, glucocorticoids, parathyroid and growth hormones that control bone remodelling also modulate the differentiation and the activity of BMA. Actually, BMA could also contribute to bone loss through the release of paracrine factors altering osteoblast and/or osteoclast formation and function. Based on clinical and fundamental studies, this review aims at presenting and discussing these current arguments that support but also challenge the involvement of BMA in the bone mass integrity.Show less >

Language :

Anglais

Popular science :

Non

Collections :

Marrow Adiposity & Bone Lab (MABLab) - ULR 4490

Source :

Harvested from HAL

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