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Heterotopic Calcification: Pathology, Pathogenesis and Purpose with Special Reference to Dystrophic Calcification (pp. 31-60) $100.00
Authors:  (Dilip K. Das, Department of Pathology, Faculty of Medicine, Kuwait University, Kuwait)
Abstract:
Heterotopic or pathologic calcification is abnormal deposition of calcium salts in tissues other than osteoid or enamel; it has two distinct forms, dystrophic and metastatic. Whereas metastatic calcification is a form of calcification that reflects disordered metabolism of calcium and phosphate, deposition of calcium salts in degenerated or dead (necrosed) tissue with normal plasma levels of calcium and phosphate is called dystrophic calcification. In dystrophic calcification, examples of deposition of calcium salts in dead tissue include caseous material in tuberculous lesions, dead parasites and their eggs, and foci of fat necrosis. Some examples of deposition of calcium salts in degenerated tissue include healed infective endocarditis, atheroma in blood vessels, and psammoma bodies (PBs) in tumors like meningioma, papillary thyroid carcinoma (PTC) and ovarian papillary cystadenocarcinoma. In PTC, paraffin sections of 40 to 50 % cases and fine needle aspiration (FNA) smears of 11 to 35% cases contain PBs; 45% of meningiomas and one third of serous cystadenocarcinomas of ovary also show PBs.
The calcification involves formation of crystalline phosphate mineral in the form of an apatite similar to hydroxyapatite of bone in two major phases: initiation (enucleation), and propagation. This process can occur intracellularly (in mitochondria of cell) or extra cellularly in matrix vesicles. Several noncollagenous matrix proteins (osteopontin, osteonectin and osteocalcin) regulate the growth of apatite crystals. Whereas the irregularly deposited calcium has a basophilic, granular, or clumped appearance in smears and paraffin sections, in structures like psammoma bodies there is deposition of
calciumhaving similar tinctorial character in an orderly concentric manner. Mineralization of membrane bound vesicles, liberated from tumor cells, is said to play a key role in the process. Ultrastructural study of papillary thyroid carcinoma has shown that thickening of the base lamina in vascular stalk of neoplastic papillae followed by thrombosis, calcification, and tumor cell necrosis leads to formation of PBs. Studies on serous cystadenocarcinoma of ovary and meningioma, however, revealed that collagen production by neoplastic cells and subsequent calcification was responsible for formation of PBs. The existence of some precursor forms of PBs has been reported in meningiomas and papillary thyroid carcinoma; and it is found that nanobacteria promotes crystallization of PBs in ovarian serous cystadenocarcinoma. Cellular degeneration and necrosis leading to the disappearance of neoplastic cells has been noticed around PBs but not around the precursor forms. Most likely, release of collagen and membrane bound vesicles in alternate layers from the neoplastic cells and subsequent calcification of the layers containing these vesicles results in compromise in the supply of nutrients to the neoplastic cells leading to their degeneration and death, and retardation of growth of the neoplasm as well as the formation of a barrier against the spread of neoplasm. Possibly, similar process leads to degeneration of villi in the choroid plexus. PB has been described in benign non-neoplastic conditions like endometrium, Hashimoto‘s thyroiditis, and multinodular goiter or benign hyperplastic thyroid nodules. These PBs may represent left over material or remnants of neoplastic papillae, which once originated in or infiltrated the region of benign lesions. Based on these observations, it has been suggested earlier that rather than being the outcome of dystrophic calcification of dead or dying tissue, PBs may indeed represent an active biologic process in the neoplastic lesions. There is growing evidence that the dystrophic calcification in blood-vessels and to some extent the parasites are also active biologic processes. Metastatic calcification occurs as noncrystalline amorphous deposits or deposition of hydroxyapatite crystals in sites such as kidney (tubules), lung (alveolar wall), stomach (around fundic glands), blood vessels (coronary, cutaneous), and cornea. In sarcoidosis, inclusion bodies like asteroid body and Schaumann body are found in the giant cells of epithelioid granulomas. Calcium and phosphorus with smaller quantities of aluminium and iron are found in Schaumann bodies, which are organized concentric structures. Evidence for the possible developmental pathway of the Schaumann body in the giant cells of sarcoid granuloma is provided by morphological changes within myelinoid figures present. 


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Heterotopic Calcification: Pathology, Pathogenesis and Purpose with Special Reference to Dystrophic Calcification (pp. 31-60)