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The figure illustrates how neovessle-formation is caused by inflammation and that it is an attempt at remedying the immediate consequence of tissue-hypoxia.

In-growth of blood-vessels into previously avascular areas. It occurs as a response to hypoxia in the tissues, which is a common consequence of the inflammatory response. Inflammation is associated with the accumulation of fluid and a loose web of connective tissue around the target tissue, which then facilitates increased immune-cell migration from the humoral system (blood and lymph). Increased presence of active leucocytes and radial expansion of the extracellular space associated with the inflammatory response, causes a drop in tissue gas- and nutrient-exchange. The body then naturally responds by trying to increase capillary penetration and density to meet these changed demands. This response is chiefly mediated by vascular endothelial growth-factor (VEGF). In short, neovascularisation probably acts to negate the hypoxic consequence of inflammation on parenchymal cells.

Supporting Evidence

  • Oedema may increase diffusion distance from the capillaries to end tissues causing hypoxia 1)
  • Hypoxia is a confirmed trigger of angiogenesis2)
  • Synovitis lowers synovial nutrient perfusion and is connected with neovessle-formation3)
  • Angiogenesis counters the hypoxic effect of inflammation.4)

Conflicting Evidence

  • Neo-vessels may form to assist inflammation rather than as a reaction to hypoxia5)

Association with disease

  • Common finding in TP associated with increased levels of VEGF.6)
  • Evident in synovial tissues in OA and RA8)
  • Increased level of neovascularisation in spinal DH, related to level of histological degeneration11)
  • Neovascularisation is shown to occur in atherosclerosis coming from vasa vasorum12)
  • Evidence of vascular remodelling and higher blood-flow scores in focal MPS.13)

References   [ + ]

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