Morphologic and morphometric studies on human C cells in disorders of calcium metabolism.

Abstract

The distribution of immunohistochemically detectable C cells in 49 human thyroid glands obtained at autopsy was investigated by determining the percentage of single-lying and grouped C cells. Eight patients suffered from primary, and 7 from secondary hyperparathyroidism; 2 had a hypercalcemia due to osteolytic bone metastases. Thirty two thyroids from normocalcemic patients (aged 0–76 years) served as controls. Innormocalcemic controls, two different C cells were found. Non-autolyzed tissue contained large, polygonal C cells with big, round nuclei. The orientation of the cytoplasm was such that its calcitonin-laden granules were adjacent to capillaries (type Ia). Autolyzed tissue displayed rounded C cells with small, pyknotic nuclei. The cytoplasm in proximity to the colloid appeared light-optically empty (type Ib). Sections passing through such cellular portions rendered their recognition as C cells impossible. Consequently, larger populations of C cells seemed to be subdivided into smaller cell groups. From birth to the age of 14 years, the number of visible C cells increased exponentially with a constant of 0.02/year. Inhypercalcemic patients (serum calcium >14mg%), neither immunohistochemical methods nor silver stains permitted the demonstration of C cells. They were obviously devoid of granules. Instates of uremia, hypocalcemia, and secondary hyperparathyroidism, a third type of C cells appeared (type II). The calcitonin-containing granules were scattered diffusely through the cytoplasm. Even when the nuclei were pyknotic, the cytoplasm did not display light-optically empty areas. Such cells retained their coherent, even follicular arrangement. A division into smaller subgroups was therefore lacking. In cases withprimary hyperparathyroidism whose calcium level had been lowered therapeutically prior to death, the overall distribution pattern of C cells corresponded to that in chronic hypocalcemia. The fall in serum calcium induced C cells to store calcitonin and the histologically empty forms were therefore absent. We conclude that the distinct cellular arrangement of demonstrable C cells as seen in different disturbances of calcium metabolism need not necessarily result from their cellular proliferation, but may well reflect their varying morphologic forms induced in part by autolysis and in part due to their functional state.