Standardised Nomenclature, Abbreviations, and Units for the Study of Bone Marrow Adiposity: Report of the Nomenclature Working Group of the International Bone Marrow Adiposity Society

Over the last two decades, increased interest of scientists to study bone marrow adiposity (BMA) in relation to bone and adipose tissue physiology has expanded the number of publications using different sources of bone marrow adipose tissue (BMAT). However, each source of BMAT has its limitations in the number of downstream analyses for which it can be used. Based on this increased scientific demand, the International Bone Marrow Adiposity Society (BMAS) established a Biobanking Working Group to identify the challenges of biobanking for human BMA-related samples and to develop guidelines to advance establishment of biobanks for BMA research. BMA is a young, growing field with increased interest among many diverse scientific communities. These bring new perspectives and important biological questions on how to improve and build an international community with biobank databases that can be used and shared all over the world. However, to create internationally accessible biobanks, several practical and legislative issues must be addressed to create a general ethical protocol used in all institutes, to allow for exchange of biological material internationally. In this position paper, the BMAS Biobanking Working Group describes similarities and differences of patient information (PIF) and consent forms from different institutes and addresses a possibility to create uniform documents for BMA biobanking purposes. Further, based on discussion among Working Group members, we report an overview of the current isolation protocols for human bone marrow adipocytes (BMAds) and bone marrow stromal cells (BMSCs, formerly mesenchymal), highlighting the specific points crucial for effective isolation. Although we remain far from a unified BMAd isolation protocol and PIF, we have summarized all of these important aspects, which are needed to build a BMA biobank. In conclusion, we believe that harmonizing isolation protocols and PIF globally will help to build international collaborations and improve the quality and interpretation of BMA research outcomes.

Download Full-text

Reporting Guidelines, Review of Methodological Standards, and Challenges Toward Harmonization in Bone Marrow Adiposity Research. Report of the Methodologies Working Group of the International Bone Marrow Adiposity Society

Frontiers in Endocrinology ◽

10.3389/fendo.2020.00065 ◽

2020 ◽

Vol 11 ◽

Cited By ~ 1

Author(s):

Josefine Tratwal ◽

Rossella Labella ◽

Nathalie Bravenboer ◽

Greet Kerckhofs ◽

Eleni Douni ◽

...

Keyword(s):

Bone Marrow ◽

Working Group ◽

Reporting Guidelines ◽

Research Report ◽

Marrow Adiposity

Download Full-text

Faculty Opinions recommendation of Growth hormone regulates the balance between bone formation and bone marrow adiposity.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.3123960.2807059 ◽

2010 ◽

Author(s):

Chantal Chenu

Keyword(s):

Bone Marrow ◽

Growth Hormone ◽

Bone Formation ◽

Marrow Adiposity

Download Full-text

Association between Visceral and Bone Marrow Adipose Tissue and Bone Quality in Sedentary and Physically Active Ovariectomized Wistar Rats

Life ◽

10.3390/life11060478 ◽

2021 ◽

Vol 11 (6) ◽

pp. 478

Author(s):

Hélder Fonseca ◽

Andrea Bezerra ◽

Ana Coelho ◽

José Alberto Duarte

Keyword(s):

Physical Activity ◽

Bone Marrow ◽

Adipose Tissue ◽

Bone Mass ◽

Bone Quality ◽

Wistar Rats ◽

Biomechanical Properties ◽

Physically Active ◽

Bone Formation Rate ◽

Marrow Adiposity

Background: Obesity is considered protective for bone mass, but this view has been progressively challenged. Menopause is characterized by low bone mass and increased adiposity. Our aim was to determine how visceral and bone marrow adiposity change following ovariectomy (OVX), how they correlate with bone quality and if they are influenced by physical activity. Methods: Five-month-old Wistar rats were OVX or sham-operated and maintained in sedentary or physically active conditions for 9 months. Visceral and bone marrow adiposity as well as bone turnover, femur bone quality and biomechanical properties were assessed. Results: OVX resulted in higher weight, visceral and bone marrow adiposity. Visceral adiposity correlated inversely with femur Ct.Th (r = −0.63, p < 0.001), BV/TV (r = −0.67, p < 0.001), Tb.N (r = −0.69, p < 0.001) and positively with Tb.Sp (r = 0.58, p < 0.001). Bone marrow adiposity also correlated with bone resorption (r = 0.47, p < 0.01), bone formation rate (r = −0.63, p < 0.01), BV/TV (r = −0.85, p < 0.001), Ct.Th (r = −0.51, p < 0.0.01), and with higher empty osteocyte lacunae (r = 0.39, p < 0.05), higher percentage of osteocytes with oxidative stress (r = 0.64, p < 0.0.01) and lower femur maximal stress (r = −0.58, p < 0.001). Physical activity correlated inversely with both visceral (r = −0.74, p < 0.01) and bone marrow adiposity (r = −0.92, p < 0.001). Conclusions: OVX increases visceral and bone marrow adiposity which are associated with inferior bone quality and biomechanical properties. Physical activity could contribute to reduce adipose tissue and thereby improve bone quality.

Download Full-text

Allogeneic bone marrow transplantation for chronic myelomonocytic leukemia in childhood: a report from the European Working Group on Myelodysplastic Syndrome in Childhood.

Journal of Clinical Oncology ◽

10.1200/jco.1997.15.2.566 ◽

1997 ◽

Vol 15 (2) ◽

pp. 566-573 ◽

Cited By ~ 77

Author(s):

F Locatelli ◽

C Niemeyer ◽

E Angelucci ◽

C Bender-Götze ◽

S Burdach ◽

...

Keyword(s):

Bone Marrow ◽

Bone Marrow Transplantation ◽

Myelodysplastic Syndrome ◽

Marrow Transplantation ◽

Working Group ◽

Allogeneic Bone Marrow Transplantation ◽

Chronic Myelomonocytic Leukemia ◽

Allogeneic Bone ◽

European Working ◽

Myelomonocytic Leukemia

PURPOSE To evaluate the role of allogeneic bone marrow transplantation (BMT) in children with chronic myelomonocytic leukemia (CMML). PATIENTS AND METHODS Forty-three children with CMML given BMT and reported to the European Working Group on Myelodysplastic Syndrome in Childhood (EWOG-MDS) data base were evaluated. In 25 cases, the donor was a human leukocyte antigen (HLA)-identical or a one-antigen-disparate relative, in four cases a mismatched family donor, and in 14 a matched unrelated donor (MUD). Conditioning regimens consisted of total-body irradiation (TBI) and chemotherapy in 22 patients, whereas busulfan (Bu) with other cytotoxic drugs was used in the remaining patients. RESULTS Six of 43 patients (14%), five of whom received transplants from alternative donors, failed to engraft. There was a significant difference in the incidences of chronic graft-versus-host disease (GVHD) between children transplanted from compatible/one-antigen-mismatched relatives and from alternative donors (23% and 87%, respectively; P < .005). Probabilities of transplant-related mortality for children given BMT from HLA-identical/one-antigen-disparate relatives or from MUD/ mismatched relatives were 9% and 46%, respectively. The probability of relapse for the entire group was 58%, whereas the 5-year event-free survival (EFS) rate was 31%. The EFS rate for children given BMT from an HLA-identical sibling or one-antigen-disparate relative was 38%. In this latter group, patients who received Bu had a better EFS compared with those given TBI (62% v 11%, P < .01). CONCLUSION Children with CMML and an HLA-compatible relative should be transplanted as early as possible. Improvement of donor selection, GVHD prophylaxis, and supportive care are needed to ameliorate results of BMT from alternative donors.

Download Full-text

Allogeneic bone marrow transplantation in childhood chronic myelomonocytic leukemia. A report on behalf of the European Working group on childhood myelodysplastic syndromes (EWOG-MDS)

Leukemia Research ◽

10.1016/0145-2126(94)90178-3 ◽

1994 ◽

Vol 18 ◽

pp. 25

Author(s):

E.T. van 't Veer-Korthof ◽

W. Ebell

Keyword(s):

Bone Marrow ◽

Bone Marrow Transplantation ◽

Myelodysplastic Syndromes ◽

Marrow Transplantation ◽

Working Group ◽

Allogeneic Bone Marrow Transplantation ◽

Chronic Myelomonocytic Leukemia ◽

Allogeneic Bone ◽

European Working ◽

Myelomonocytic Leukemia

Download Full-text

CCAAT/enhancer binding protein β-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00764.2010 ◽

2011 ◽

Vol 300 (5) ◽

pp. R1250-R1260 ◽

Cited By ~ 20

Author(s):

Katherine J. Motyl ◽

Michelle Raetz ◽

Srinivasan Arjun Tekalur ◽

Richard C. Schwartz ◽

Laura R. McCabe

Keyword(s):

Bone Marrow ◽

Type 1 Diabetes ◽

Bone Resorption ◽

Bone Loss ◽

Wild Type ◽

Bone Stiffness ◽

Bone Phenotype ◽

Enhancer Binding Protein ◽

Marrow Adiposity

Bone loss in type 1 diabetes is accompanied by increased marrow fat, which could directly reduce osteoblast activity or result from altered bone marrow mesenchymal cell lineage selection (adipocyte vs. osteoblast). CCAAT/enhancer binding protein beta (C/EBPβ) is an important regulator of both adipocyte and osteoblast differentiation. C/EBPβ-null mice have delayed bone formation and defective lipid accumulation in brown adipose tissue. To examine the balance of C/EBPβ functions in the diabetic context, we induced type 1 diabetes in C/EBPβ-null (knockout, KO) mice. We found that C/EBPβ deficiency actually enhanced the diabetic bone phenotype. While KO mice had reduced peripheral fat mass compared with wild-type mice, they had 5-fold more marrow adipocytes than diabetic wild-type mice. The enhanced marrow adiposity may be attributed to compensation by C/EBPδ, peroxisome proliferator-activated receptor-γ2, and C/EBPα. Concurrently, we observed reduced bone density. Relative to genotype controls, trabecular bone volume fraction loss was escalated in diabetic KO mice (−48%) compared with changes in diabetic wild-type mice (−22%). Despite greater bone loss, osteoblast markers were not further suppressed in diabetic KO mice. Instead, osteoclast markers were increased in the KO diabetic mice. Thus, C/EBPβ deficiency increases diabetes-induced bone marrow (not peripheral) adipose depot mass, and promotes additional bone loss through stimulating bone resorption. C/EBPβ-deficiency also reduced bone stiffness and diabetes exacerbated this (two-way ANOVA P < 0.02). We conclude that C/EBPβ alone is not responsible for the bone vs. fat phenotype switch observed in T1 diabetes and that suppression of CEBPβ levels may further bone loss and decrease bone stiffness by increasing bone resorption.

Download Full-text