 Telangiectasias and arteriovenous malformations in HHT are thought to arise because of changes in angiogenesis , the development of blood vessels out of existing ones . The development of a new blood vessel requires the activation and migration of various types of cells , chiefly endothelium , smooth muscle and <unk> . The exact mechanism by which the HHT mutations influence this process is not yet clear , and it is likely that they disrupt a balance between pro- and <unk> signals in blood vessels . The wall of telangiectasias is unusually friable , which explains the tendency of these lesions to bleed . 
