More than a century has passed since the first description of Hashimoto 
thyroiditis (HT) as a clinicopathologic entity. HT is an autoimmune disease in 
which a breakdown of immune tolerance is caused by interplay of a variety of 
immunologic, genetic, and environmental factors. Thyrocyte injury resulting from 
environmental factors results in expression of new or hidden epitopes that leads 
to proliferation of autoreactive T and B cells. Infiltration of thyroid by these 
cells results in HT. In addition to the usual type of HT, several variants such 
as the fibrous type and Riedal thyroiditis are also recognized. The most 
recently recognized variant is immunoglobulin G4(+) HT, which may occur as 
isolated thyroid limited disease or as part of a generalized Ig4-related 
sclerosing disease. The relationship between HT and Riedel thyroiditis remains 
unclear; however, recent evidence seems to suggest that it may also be part of 
the spectrum of Ig4-related sclerosing disease. HT is frequently associated with 
papillary thyroid carcinoma and may indeed be a risk factor for developing this 
type of cancer. The relationship between thyroid lymphoma and HT on the other 
hand appears well established.