Immunology of Osteoporosis: A Mini-Review

Abstract

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.

The Protective Effect of Amphimas pterocarpoides Plant Extract on Bone Mineral Density and Strength in Estrogen Deficient Ovariectomized Wistar Rats

“…Some of these isolated isoflavonoids such as daidzein, clycitein and formononetin have proven anabolic effect on bone metabolism and they prevent bone loss [20,32,[34][35][36][37]. A good correlation between the content of AP extract in isoflavones and its antioxidant activity has already been described [10,11] while the role of oxidative stress in the pathogenesis of osteroporosis is well established [38,39].…”

Chronic Psychological Stress as a Risk Factor of Osteoporosis

“…The effects of inflammatory cytokines on the dynamic balance of bone resorption and bone formation can partially explain the occurrence of osteoporosis in conjunction with chronic inflammatory reactions [48]. Inflammatory cytokines are also potential stimulators of the HPA axis and might contribute to hypercortisolism in depression subjects.…”

“…Inflammatory cytokines are also potential stimulators of the HPA axis and might contribute to hypercortisolism in depression subjects. Chronic psychological stress is associated with dysregulation of inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α [48,49]. Furthermore, oxidative stress and the generation of advanced glycation end products have emerged as links between chronic stress, inflammation and osteoporosis.…”

Hard Tissue Augmentation of Aged Bone by Means of a Tin-Free PLLA-PCL Co-Polymer Exhibiting in vivo Anergy and Long-Term Structural Stability

“…Noteworthy in this context is the fact that treatment with serum-containing culture media caused no apparent reduction of long-term stability. This indicates that PbP can be further useful for studying biological restrictions of long-term biomaterial stability (e.g., interactions with osteoclasts) [37]. PbP may be further expedient in establishing conditions to study activated stroma in combination with cancerous cells or when modeling a proinflammatory condition that would actually propel fibrosis [38].…”