By Peter Pietschmann
Osteoimmunology is a brand new and speedily constructing box of serious significance. It offers with mechanisms and attainable remedies of bone-related ailments, comparable to osteoporosis, rheumatoid arthritis and periodontitis, which are attributable to or linked to a malfunctioning immune method. This booklet describes the fundamentals of bone biology and of the immune approach and gives perception into the molecular mechanisms of bone ailments. furthermore, medical facts is gifted and positioned into context with the most recent study findings. It used to be meant for all scientists and physicians operating in immunology, pathophysiology and osteology.
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Extra resources for Principles of Osteoimmunology: Molecular Mechanisms and Clinical Applications
1998; Al-Fakhri et al. 2005; Rasmussen et al. 2006). After the identification of OPG followed the discovery of RANKL, which does not only have a huge repertoire of names (TRANCE: TNF-related activationinduced cytokine; ODF: osteoclast differentiating factor; OPGL: osteoprotegerin ligand; TNFSF11: TNF superfamily member 11), but also many facets regarding its structure, function and appearance in tissues. The names originated from the four discoverers, each one having used different approaches to identify the protein.
Ann N Y Acad Sci 1116:281–290 Boyden LM, Mao J, Belsky J, Mitzner L, Farhi A, Mitnick MA, Wu D, Insogna K, Lifton RP (2002) High bone density due to a mutation in LDL-receptor-related protein 5. N Engl J Med 346:1513–1521 Bucay N, Sarosi I, Dunstan CR, Morony S, Tarpley J, Capparelli C, Scully S, Tan HL, Xu W, Lacey DL, Boyle WJ, Simonet WS (1998) Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. Genes Dev 12:1260–1268 Canalis E (1986) Interleukin-1 has independent effects on deoxyribonucleic acid and collagen synthesis in cultures of rat calvariae.
Among others, estrogen, bone morphogenetic protein-2, INF-γ, and TGF-β positively regulate OPG, whereas PTH, 1,25(OH)2 vitamin D3, glucocorticoids, prostaglandin E2, IL-6, IL-8 and IL-11 enhance the expression of RANKL (summarized in Khosla (2001) and Leibbrandt and Penninger (2009)). 3 Cytokines and Chemokines Bone remodeling is also critically regulated by various cytokines and chemokines, not only in pathopyhsiological conditions, but also within physiological bone remodeling. Many pro-inflammatory cytokines including TNF-α, interleukin (IL)-1, IL-6, IL-7, IL-11, IL-15, and IL-17 create bone loss either by increasing osteoclast generation and activation or by inducing RANKL expression by the osteoblasts.