Hashimoto thyroiditis is a common autoimmune disorder that impacts the thyroid gland, a butterfly-shaped organ in the neck responsible for producing hormones that regulate metabolism. In this condition, the body’s immune system mistakenly attacks the thyroid cells, leading to inflammation and damage. This immune attack can eventually impair the thyroid’s ability to produce sufficient hormones, often resulting in an underactive thyroid, also known as hypothyroidism.
Understanding Histology in Thyroid Disease
Histology is the microscopic study of tissues, providing a detailed view of cellular structures. In thyroid conditions, it is a valuable diagnostic tool, especially when other findings are inconclusive. Pathologists examine thin tissue slices to identify specific changes characterizing different disorders.
A tissue sample for thyroid histology is typically obtained through a fine needle aspiration (FNA) biopsy or, less commonly, a surgical biopsy. During an FNA biopsy, a very thin, hollow needle collects a small sample of cells and fluid from a thyroid nodule or the gland. This procedure is often guided by ultrasound imaging to accurately target the area. The collected sample is then prepared on slides and sent to a pathology laboratory for microscopic analysis.
The Microscopic Hallmarks of Hashimoto Thyroiditis
Microscopic examination of thyroid tissue in Hashimoto thyroiditis reveals several distinctive features, or “hallmarks,” that pathologists use to confirm diagnosis. The extent and presentation of these features can vary with disease stage and severity.
Lymphocytic infiltration is a prominent feature, characterized by immune cells, primarily lymphocytes and plasma cells, diffusely spreading throughout the thyroid tissue. These infiltrating lymphocytes, including both T and B cells, actively participate in the destruction of thyroid follicular cells.
Within these lymphocytic infiltrates, pathologists often observe the formation of germinal centers. These structures resemble the germinal centers found in lymph nodes, indicating an active immune response within the thyroid gland itself. Germinal centers are sites where B cells proliferate and mature, producing autoantibodies that target thyroid components like thyroid peroxidase (TPO) and thyroglobulin.
Another characteristic change is Hurthle cell (oxyphilic) metaplasia, where the normal thyroid follicular cells transform. These altered cells become larger, polygonal, and acquire an abundant, granular, eosinophilic (pink-staining) cytoplasm. This distinct appearance is attributed to an increased number of mitochondria within the cells, and their nuclei are often enlarged and hyperchromatic.
Thyroid follicular atrophy and destruction are also observed, as chronic inflammation leads to damage and reduction in the number of normal thyroid follicles. In late stages of the disease, the colloid-filled follicles, which are the functional units of the thyroid, may shrink or be largely absent. This destruction of the follicular architecture directly impairs the gland’s ability to produce thyroid hormones.
Fibrosis, or the increase in connective tissue (scarring), is another common finding within the thyroid gland in Hashimoto thyroiditis. This scarring can be patchy or diffuse, depending on the disease stage and severity. In severe cases, dense fibrotic bands of collagen may replace the normal thyroid tissue, contributing to the gland’s firm and rubbery texture often noted during physical examination.
What Histology Reveals About Hashimoto’s
The microscopic findings from a thyroid tissue sample provide insights into Hashimoto thyroiditis. The presence of lymphocytic infiltration, germinal centers, Hurthle cell changes, follicular atrophy, and fibrosis collectively confirms the diagnosis.
Histology is particularly useful in differentiating Hashimoto thyroiditis from other thyroid conditions that might present with similar symptoms. For instance, Graves’ disease, another autoimmune thyroid disorder, typically shows diffuse follicular hyperplasia with columnar follicular cells and reduced colloid content, alongside inflammatory cells, distinguishing it from the destructive changes seen in Hashimoto’s. While both conditions involve inflammation, the specific cellular alterations and architectural disruptions differ significantly under the microscope.
Histological examination also helps distinguish Hashimoto thyroiditis from thyroid cancer. While thyroid cancer can sometimes coexist with Hashimoto’s, the characteristic nuclear features of cancerous cells, such as nuclear grooves and pseudoinclusions found in papillary thyroid carcinoma, are distinct from the changes observed in Hashimoto thyroiditis. The fibrous variant of Hashimoto’s, characterized by extensive fibrosis, must also be carefully differentiated from other conditions that cause a hard, enlarged thyroid, such as Riedel’s thyroiditis, which involves fibrosis extending beyond the thyroid capsule.
The microscopic observations also offer insights into the progression of Hashimoto thyroiditis. The degree of lymphocytic infiltration and fibrosis often correlates with the extent of thyroid dysfunction, indicating that more severe pathological changes are associated with less remaining thyroid function. Histology can reveal the slow, progressive destruction of the thyroid over time, explaining why symptoms like hypothyroidism may develop gradually over many years.