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Figure 1

Figure 1. The TNF-induced OCP vicious cycle in inflammatory-erosive arthritis. From: The Role of Bone Marrow Edema and Lymphangiogenesis in Inflammatory-Erosive Arthritis.

(1) The pathogenesis commences with an unknown event that leads to chronic TNF over expression in the joint. (2) This TNF has endocrine effects on the bone marrow where it stimulates M-CSF production by stromal cells and differentiation of hematopoietic progenitors to CD11bhi/cFmshi OCPs. (3) M-CSF stimulates the proliferation of CD11bhi/cFmshi OCP, which (4) leads to their migration from the bone marrow to the blood via a mechanism that is involves the down-regulation of stromal cell derived factor −1 (CXCL12). (5) PBMC/OCPs are recruited into the inflamed synovium, and are stimulated by RANKL to become bone resorbing osteoclasts. (6) This RANKL stimulation also induces the expression of lymphangiogenic factor, VEGF-C and perhaps other yet to be defined angiogenic and lymphangiogenic factors that complete the vicious cycle through paracrine/endocrine effects on inflammation and myelopoiesis.

Edward M. Schwarz, et al. Adv Exp Med Biol. ;658:1-10.

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