Molecular Interaction of BMAT with Bone

Abstract

Bone marrow adipose tissue (BMAT) is a distinct adipose tissue with diverse local and systemic effects, affecting both physiological processes and pathological conditions, including hematopoiesis, bone remodeling, osteoporosis, obesity, anorexia nervosa, diabetes, and cancer. BMAT increases with age and bone loss, while the significance of this phenomenon has been neglected until recently. Bone cells and BMAT are mutually connected in terms of bone remodeling and energy metabolism. It has been suggested that high BMAT is caused by a shift in bone marrow mesenchymal stromal cell (BMSC) differentiation in favor of adipogenesis, and BMAT promotes bone loss through direct or indirect interaction with bone cells. However, it remains unclear why osteoporosis accelerates BMAT accumulation and what is the role of BMAT in bone remodeling and particularly in bone loss. The purpose of this review is to present the latest published data on the role of BMAT in physiological bone processes and during osteoporosis progression. BMAT secretes numerous endocrine factors designated as adipokines as well as pro-inflammatory cytokines, which affect bone homeostasis through the regulation of osteoblast and osteoclast function. Most clinical data from osteoporotic patients demonstrate a negative relationship between BMAT and bone mass. Through technological advances in BMAT imaging, investigators are now able to quantify BMAT in humans and animal models. Pharmaceutical interventions targeting either bone loss or BMA expansion shed light in the understanding of the possible interactions between BMAT and bone cells. A neglected feature of osteoporosis progression is BMAT development. BMAT appears as a “new tissue” with unique properties, which undoubtedly plays important physiological and pathological roles, but which remains insufficiently understood.