Abstract
Osteoporosis stems from an unbalance between bone mineral resorption and deposition. Among the numerous cellular players responsible for this unbalance bone marrow (BM) monocytes/macrophages, mast cells, T and B lymphocytes, and dendritic cells play a key role in regulating osteoclasts, osteoblasts, and their progenitor cells through interactions occurring in the context of the different bone compartments (cancellous and cortical). Therefore, the microtopography of immune cells inside trabecular and compact bone is expected to play a relevant role in setting initial sites of osteoporotic lesion. Indeed, in physiological conditions, each immune cell type preferentially occupies either endosteal, subendosteal, central, and/or perisinusoidal regions of the BM. However, in the presence of an activation, immune cells recirculate throughout these different microanatomical areas giving rise to a specific distribution. As a result, the trabeculae of the cancellous bone and endosteal free edge of the diaphyseal case emerge as the primary anatomical targets of their osteoporotic action. Immune cells may also transit from the BM to the depth of the compact bone, thanks to the efferent venous capillaries coursing in the Haversian and Volkmann canals. Consistently, the innermost parts of the osteons and the periosteum are later involved by their immunomodulatory action, becoming another site of mineral reabsorption in the course of an osteoporotic insult. The novelty of our updating is to highlight the microtopography of bone immune cells in the cancellous and cortical compartments in relation to the most consistent data on their action in bone remodeling, to offer a mechanist perspective useful to dissect their role in the osteoporotic process, including bone damage derived from the immunomodulatory effects of endocrine disrupting chemicals.
Highlights
Osteoporosis is a worldwide public health problem, primarily as a result of increasing survival in aging [1], involves an estimated 200 million people worldwide [2], and has a global economic impact estimated up to more than 20 billion euros per year during the 5 years on the health care systems of Western countries [3]
B cells remaining attached to the central bone marrow (BM) region may act as a source of RANKL to cause endosteal OC activation and bone resorption [51]; in postmenopausal osteoporotic patients, they release granulocyte-macrophage colonystimulating factor (CSF) to promote differentiation of OCs precursors [52]
A peculiar in vivo feature of the bone immune cells is their quite selective segregation in specific BM regions and areas of the cortical bone, both in steady state and upon an inflammatory or endocrine-disrupting chemicals (EDs)-dependent insult. This cellular distribution is aimed at ensuring functional niches for hematopoiesis and myelopoiesis [23, 50]
Summary
Osteoporosis is a worldwide public health problem, primarily as a result of increasing survival in aging [1], involves an estimated 200 million people worldwide [2], and has a global economic impact estimated up to more than 20 billion euros per year during the 5 years on the health care systems of Western countries [3]. Osteoporotic changes worsen in postmenopausal females and can variably affect any bone, but more frequently the femoral neck, vertebrae, and distal radius where unique patterns of bone derangement emerge. This lesional microtopography is gaining particular interest in bones traditionally considered less affected by osteoporosis such as the jaw (Figures 1A,B) because of the increased request of prosthetic implants [5] and as a unique site for chronic inflammation and aseptic osteonecrosis during antiresorptive therapy [6]. We offer a mechanistic and space-related perspective of the action of immune cells involved in the osteoporotic process
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