The Histological Features of Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis is an autoimmune condition where the body’s own immune system attacks the thyroid gland. This chronic inflammation impairs the gland’s ability to produce hormones, often leading to hypothyroidism. To understand how this disease affects the thyroid, doctors rely on histology, the microscopic study of biological tissues. By examining thyroid tissue under a microscope, they can identify the specific cellular changes caused by the autoimmune assault, which is fundamental for confirming a diagnosis.

Preparing Thyroid Samples for Histological Analysis

The process begins with Fine Needle Aspiration (FNA), where a thin needle is used to withdraw cells and tissue fragments from the thyroid. While less common for an initial diagnosis, a surgical biopsy, which removes a larger piece of tissue, may also be performed if there are suspicious nodules.

Once obtained, the tissue must be preserved through fixation by immersing the sample in a 10% buffered formalin solution. Following fixation, the tissue undergoes processing, which involves dehydrating it through alcohol solutions, clearing it with a solvent like xylene, and embedding it in paraffin wax. This wax block provides the support needed to cut extremely thin sections, around 4 to 5 micrometers thick, using a microtome.

The final preparatory step is staining. These translucent tissue slices are mounted on glass slides and stained to make different cellular components visible. A common staining method is Hematoxylin and Eosin (H&E), where Hematoxylin stains cell nuclei a purplish-blue, while eosin stains the cytoplasm and connective tissue in varying shades of pink and red.

Core Histological Characteristics of Hashimoto’s Thyroiditis

Under the microscope, Hashimoto’s thyroiditis is defined by several distinctive features. The most prominent is a widespread infiltration of the gland by immune cells, specifically lymphocytes and plasma cells. These lymphocytes often organize themselves into structured arrangements not normally present in the thyroid.

These organized immune structures are known as lymphoid follicles, which contain germinal centers. Germinal centers are active sites where B-lymphocytes mature and multiply, a process normally confined to lymph nodes. Their formation within the thyroid gland itself is a hallmark of the chronic, localized immune response.

Another feature is Hürthle cell metaplasia, where the thyroid’s follicular cells transform into larger cells with abundant, granular, pink-staining cytoplasm. These altered cells, also called Askanazy cells, are a response to the chronic inflammatory environment. While striking in appearance, they are less functional than the original follicular cells they replace.

The immune attack leads to the destruction of the thyroid follicles, which are responsible for producing and storing thyroid hormone. This follicular atrophy causes the gland’s declining hormone output. In response to this chronic injury, the body develops fibrosis, which is the formation of excess fibrous connective tissue, or scarring.

Distinguishing Hashimoto’s Through Microscopy

The specific combination of histological findings allows a pathologist to diagnose Hashimoto’s thyroiditis and separate it from other thyroid disorders. For instance, Graves’ disease, another autoimmune thyroid condition, also shows lymphocytic infiltration, but it is more diffuse. Graves’ disease is characterized by the overstimulation of follicular cells, causing them to become tall and crowded, creating scalloped edges in the colloid.

In contrast, subacute (de Quervain’s) thyroiditis presents a different microscopic picture. It is characterized by granulomas and multinucleated giant cells that form around pools of leaked colloid. The type of inflammatory cells and their organization differ from the dense lymphocytic sheets and germinal centers seen in Hashimoto’s.

Even among other forms of lymphocytic thyroiditis, the features in Hashimoto’s are distinct. The prominent formation of germinal centers and extensive Hürthle cell metaplasia are particularly indicative of Hashimoto’s thyroiditis. Other conditions may show some lymphocytic infiltration but lack this specific combination.

Histology is also used to evaluate any nodules that may arise within a thyroid affected by Hashimoto’s. The chronic inflammation is associated with a slightly increased risk of developing certain thyroid cancers, like papillary thyroid carcinoma or lymphoma. A pathologist will examine tissue from any suspicious nodule for features of malignancy.

Progressive Tissue Alterations in Hashimoto’s

The microscopic appearance of Hashimoto’s thyroiditis evolves as the disease progresses. In the early stages, lymphocytic infiltration may be patchy and focal, with less follicular destruction and minimal fibrosis. Areas of normal-appearing thyroid tissue can often be identified between zones of inflammation.

In later stages, the histological landscape changes dramatically, and the gland may shrink in an atrophic phase. This is represented by extensive fibrosis, with scar tissue replacing functional thyroid tissue. Follicular atrophy becomes widespread, and the intense lymphocytic infiltrate might lessen as the target tissue diminishes, a phenomenon called “burn-out.”

Hashimoto’s can also manifest in a nodular variant where distinct nodules form. Microscopically, tissue within these nodules shows the characteristic features of Hashimoto’s, including lymphocytic infiltration and Hürthle cell changes. The surrounding, non-nodular thyroid tissue displays the more diffuse changes of the disease.

These progressive alterations correlate with the gland’s function. The destruction of thyroid follicles and their replacement with scar tissue and Hürthle cells explain the common outcome of hypothyroidism. As hormone production is eroded, the patient experiences the effects of an underactive thyroid.