Hyperplasia

It is common knowledge that nodules develop in normal thyroid glands with aging.67 In growing thyroids, the development of the goiter is almost invariably accompanied by the development of multiple nodules of varying size.68 The nodules are generally softer than normal tissue. The surface of a sectioned hyperplastic gland appears granular, and the histopathologic picture shows a dysplastic arrangement with wide variation of follicle size and areas with increased cell density (Fig. 28-3). Follicles in hyperplastic tissue display a heterogenic expression of both functional characteristics (iodination, peroxidase activity, thyroglobulin synthesis, and endocytosis) and proliferative potential.69 Surprisingly, this variation is observed among thyrocytes in the same follicle in both experimental animals and in human thyroid glands.70,71 Thyrocytes with a high replication rate stay adjacent to each other in the follicle wall, indicating that increased growth propensity is inherited from mother to surrounding daughter cells.70 With time, the goitrous gland is composed of a large population of thyrocytes with this abnormal growth pattern.

FIGURE 28-3. Thyroid gland hyperplasia. The cut surface of a hyperplastic nodule (A) in a human thyroid gland shows the smooth and gel-like appearance of the colloid-rich parenchyma. A section of the corresponding tissue (B) reveals numerous large follicles and areas with high cellular density (hematoxylin and eosin).

FIGURE 28-3. Thyroid gland hyperplasia. The cut surface of a hyperplastic nodule (A) in a human thyroid gland shows the smooth and gel-like appearance of the colloid-rich parenchyma. A section of the corresponding tissue (B) reveals numerous large follicles and areas with high cellular density (hematoxylin and eosin).

Three mechanisms have been proposed to explain nodule formation in multinodular goiters69:

1. The aforementioned tendency of cells with higher growth potential to stay adjacent to each other results in the formation of multiple growth centers and uneven proliferation in the gland, with subsequent nodule formation in different parts of the thyroid gland.

2. A somatic mutation may confer an inheritable growth advantage to a subset of thyrocytes. This mechanism may be operative in clonal tumor formation.70"74

3. The presence of fibrous strands in most thyroid tissue results from scarring, necrosis, and hemorrhage in growing goiters and, with time, disturbs the normal thyroid architecture.75

Growth stimulation can be caused by external growth signals such as TSH during iodine deficiency, by growth-stimulating immunoglobulins, or by any other growth-promoting factors.73"78 In patients with multinodular goiter, serum TSH levels are usually normal. A possible growth-promoting effect of TSH may be due to an inherited subset of thyroid cells that have increased sensitivity to TSH. An increased growth propensity toward TSH (or other external growth-promoting factors) may also be induced by mutations that alter cell cycle intervals (i.e., shorten G0 or decrease apop-tosis, leading to an increased number of cell multiplication cycles before cell death).

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