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As a result, TNF- orchestrates a process of local (expressed as bone erosions and juxta-articular osteoporosis) and systemic bone loss in patients with inflammatory arthritis [12, 35, 36]

This lack of significant improvement may be attributed to the activation of VEGF-independent angiogenic pathways, the recruitment of proangiogenic stromal cells, the induction of vasculogenesis or even the dose of the antiangiogenic agent used, which may reduce the size of blood vessel pores, further obstructing the delivery of this antibody [30, 39, 40]

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