Hyperplasia in goiter may be associated with altered apoptosis thyrocytes. There are numerous techniques for the detection and quantification of apoptosis. Some of them were light microscopy, electron microscopy, flow cytometry, studying the activities of caspase, DNA fragmentation and so on. In patients with multinodular endemic goiter after six months of iodine load, number of apoptotic thyrocytes increased by ten times, Bcl-2 is missing and Bax appeared in thyrocytes. Excess iodine in molecular form causes apoptosis in thyrocytes creating free radicals, mitochondrial damage and release of cytochrome c. Research shows that the level of sFas in the serum of patients with multinodular goiter increased compared to normal controls, it can still point to the reduced expression of Fas protein on the surface of cells that then leads to increased thyroid cell proliferation. Further study of apoptosis in goiter combined morphological and biochemical methods are important for better diagnosis and treatment of diseases.

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