TY - JOUR
T1 - Immunology of Osteoporosis
T2 - A Mini-Review
AU - Pietschmann, Peter
AU - Mechtcheriakova, Diana
AU - Meshcheryakova, Anastasia
AU - Föger-Samwald, Ursula
AU - Ellinger, Isabella
N1 - Publisher Copyright:
© 2015 S. Karger AG, Basel.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - Osteoporosis is a major cause of fractures and associated morbidity in the aged population. The pathogenesis of osteoporosis is multifactorial; whereas traditional pathophysiological concepts emphasize endocrine mechanisms, it has been recognized that also components of the immune system have a significant impact on bone. Since 2000, when the term 'osteoimmunology' was coined, novel insights into the role of inflammatory cytokines by influencing the fine-tuned balance between bone resorption and bone formation have helped to explain the occurrence of osteoporosis in conjunction with chronic inflammatory reactions. Moreover, the phenomenon of a low-grade, chronic, systemic inflammatory state associated with aging has been defined as 'inflamm-aging' by Claudio Franceschi and has been linked to age-related diseases such as osteoporosis. Given the tight anatomical and physiological coexistence of B cells and the bone-forming units in the bone marrow, a role of B cells in osteoimmunological interactions has long been suspected. Recent findings of B cells as active regulators of the RANK/RANKL/OPG axis, of altered RANKL/OPG production by B cells in HIV-associated bone loss or of a modulated expression of genes linked to B-cell biology in response to estrogen deficiency support this assumption. Furthermore, oxidative stress and the generation of advanced glycation end products have emerged as links between inflammation and bone destruction.
AB - Osteoporosis is a major cause of fractures and associated morbidity in the aged population. The pathogenesis of osteoporosis is multifactorial; whereas traditional pathophysiological concepts emphasize endocrine mechanisms, it has been recognized that also components of the immune system have a significant impact on bone. Since 2000, when the term 'osteoimmunology' was coined, novel insights into the role of inflammatory cytokines by influencing the fine-tuned balance between bone resorption and bone formation have helped to explain the occurrence of osteoporosis in conjunction with chronic inflammatory reactions. Moreover, the phenomenon of a low-grade, chronic, systemic inflammatory state associated with aging has been defined as 'inflamm-aging' by Claudio Franceschi and has been linked to age-related diseases such as osteoporosis. Given the tight anatomical and physiological coexistence of B cells and the bone-forming units in the bone marrow, a role of B cells in osteoimmunological interactions has long been suspected. Recent findings of B cells as active regulators of the RANK/RANKL/OPG axis, of altered RANKL/OPG production by B cells in HIV-associated bone loss or of a modulated expression of genes linked to B-cell biology in response to estrogen deficiency support this assumption. Furthermore, oxidative stress and the generation of advanced glycation end products have emerged as links between inflammation and bone destruction.
KW - B-Lymphocytes/immunology
KW - Cytidine Deaminase/immunology
KW - Glycation End Products, Advanced/immunology
KW - Humans
KW - Inflammation/immunology
KW - Osteoporosis/immunology
KW - Osteoprotegerin/immunology
KW - Oxidative Stress/immunology
KW - RANK Ligand/immunology
KW - Receptor Activator of Nuclear Factor-kappa B/immunology
UR - http://www.scopus.com/inward/record.url?scp=84959214876&partnerID=8YFLogxK
U2 - 10.1159/000431091
DO - 10.1159/000431091
M3 - Review article
C2 - 26088283
SN - 0304-324X
VL - 62
SP - 128
EP - 137
JO - Gerontology
JF - Gerontology
IS - 2
ER -