Summary Treatment with iodine prior to thyroidectomy has been shown to reduce intraoperative bleeding in patients with Graves Disease (GD). However, the molecular interrelation between iodine treatment and reduced bleeding remains unclear. The purpose of this study is to examine whether the described effect results from a reduction of microvessel density. We used immunohistochemical staining to determine the vascular surface density (VSD) and the most important stimulator for angiogenesis, VEGF, in thyroid tissue of patients with GD and non-toxic goiter. Two groups of GD patients were compared: GD patients treated with antithyroid drugs only and GD patients who underwent iodine treatment in addition to antithyroid drugs. Non-toxic goiter patients were used as control group. No significant differences of microvessel density were recorded among all groups. VEGF was detected in all non-toxic goiters, only a small amount of GD goiters with iodine treatment were positive for VEGF and hardly any GD goiters in the group of antithyroid drugs. Within the group of iodine treated GD, the duration of pharmacological therapy longer than 1 year seemed to cause lower VEGF levels than shorter therapy. Due to the fact that untreated GD goiters are more vascularized than non-toxic goiters, we interpret the absence of difference among the groups as a reduction of microvessel density induced by therapy with antithyroid drugs. Under therapy with antithyroid drugs VEGF is reduced significantly. Thus we reason that antithyroid treatment is accountable for lowered levels of vascularization. To analyze the effect of iodine on vascularization separately, it is necessary to investigate GD patients without antithyroid therapy with and without iodine treatment. In our study setting no reduction of microvessel density under iodine treatment was detected. We assume other mechanisms to be responsible for the reduction of intraoperative bleeding in GD goiters after iodine therapy.