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The Injured Cell
Published in Jeremy R. Jass, Understanding Pathology, 2020
There are two types of calcification: dystrophic and metastatic. Dystrophic calcification occurs in areas of necrosis or in diseased and relatively inert tissues in which there has been extensive fibrosis. Relatively common disorders associated with calcification include tuberculosis, atherosclerosis, and heart valvular disease. Certain neoplasms, particularly those with a papillary architecture, show calcification. The tips of the finger-like papillae are prone to ischaemic necrosis with secondary calcification. Calcifying cancers include papillary carcinoma of thyroid, papillary ovarian neoplasms, and the central nervous system tumours meningioma and oligodendroglioma. Histologically, calcium salts (mainly phosphate) appear as amorphous, granular basophilic material or as crystalline deposits. The calcified bodies in cancers are often quite large and show concentric lamellae. They are called psammoma bodies.
Tissue injury and repair
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The microscopic changes that occur in necrosis reflect these key processes. Necrotic cells stain pink with routine (haematoxylin and eosin) stains, reflecting the presence of denatured proteins produced by the action of lysosomal enzymes. The cells lose definition under the microscope, reflecting the loss of organelles, again because of the effects of phospholipases and proteases. Nuclear changes are an important feature: there may be a loss of staining of the nucleus (karyolysis), shrinkage of the nucleus (pyknosis: more characteristically seen in apoptosis), and fragmentation of the nucleus (karyorrhexis). Eventually, the nucleus disappears completely. Calcium may be deposited in the dead cells, a process referred to as dystrophic calcification. It is important to recognize that the histological changes are only identifiable microscopically several hours after cell death in a surviving host.
Cell and Extracellular Matrix Interactions in a Dynamic Biomechanical Environment:
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
Dystrophic calcification, on the other hand, is caused by cell death, a process involving myofibroblastic VICs (Jian et al. 2003, Yip et al. 2009, Chen et al. 2015). Diseased valves are enriched with TGF-β1, released in part by infiltrating lymphocytes, which in vitro promotes VICs to differentiate into a highly contractile myofibroblastic phenotype that aggregates into apoptotic nodules (Jian et al. 2003). Strikingly, a dramatic shift has been observed in the composition of the resident VIC population from one with low numbers of αSMA-positive myofibroblasts (1%–2%) in healthy valves to one with large numbers of αSMA-positive myofibroblasts (31%–36%) in diseased valves (Rabkin-Aikawa et al. 2004, Pho et al. 2008), which might explain the prevalence of dystrophic calcification. Temporary elevation in myofibroblast count is also seen in valve development, during adaption after valve transplant or in maturing tissue-engineered valves, but it eventually subsides. However, it persists in CAVD (Rabkin-Aikawa et al. 2004), suggesting that dysregulated repair and remodeling mechanisms contribute to the disease.
Leg ulceration with histological features of pseudoxanthoma elasticum
Published in Baylor University Medical Center Proceedings, 2021
Usman Asad, Sheevam Shah, Palak Parekh
PXE-like elastic fibers have also been seen in patients with calciphylaxis.1 However, these fibers tend to be straight with transverse fractures, unlike the crinkled-looking fibers seen in PXE. Often, they are accompanied by luminal thrombi and calcification of vessel walls.1 Lupus-associated renal failure, idiopathic hypercalcemia with secondary calcinosis cutis, necrobiosis lipoidica, exposure to saltpeter, and osteoectasia are other documented conditions of abnormal calcium metabolism showing histological findings of PXE without clinical manifestations.5–8 Hypotheses have included an atypical form of PXE being a predisposing factor to the development of calciphylaxis and chronically elevated levels of calcium saturate fibrillin leading to calcification and fragmentation of elastic fibers. The calcification observed in our patient may also have simply been due to chronic inflammation (dystrophic calcification).
An unusual case of idiopathic calcinosis of the eyelid
Published in Orbit, 2019
Ashlie A. Bernhisel, Brian E. Zaugg, Nick Mamalis, Jonathan J. Dutton, Bhupendra C. K. Patel
Soft tissue calcium deposits are a common clinical finding, which have been classified as dystrophic, metastatic, calciphylaxis, iatrogenic, and idiopathic in nature. There is also calcification that occurs in several dermal diseases of the eyelid including calcifying epithelioma of Malherbe (pilomatrixoma), chalazia, and pilar cysts.1,2 Dystrophic calcification refers to tissue calcification caused by trauma or an underlying medical condition such as CREST syndrome, which causes chronic inflammation and alterations within connective tissue resulting in calcium deposits.3 Metastatic calcification is associated with metabolic disorders that cause elevated blood calcium, phosphorus, or vitamin D levels. Calciphylaxis is small vessel calcification that occurs in end stage renal disease and iatrogenic calcification occurs with use of calcium gluconate or calcium chloride therapy.3
Therapy for prevention and treatment of skin ionizing radiation damage: a review
Published in International Journal of Radiation Biology, 2019
José L. Soriano, Ana C. Calpena, Eliana B. Souto, Beatriz Clares
Late effects of radiation injury are those appearing weeks to years after exposure. It may be that the emergence of these effects is not always preceded by acute effects (Jaschke et al. 2017). These effects may include insidious and variable onset of symptoms such as delayed ulcers, fibrosis, atrophy, pigmentary changes, telangiectasia, loss of skin appendages and hair follicles, sebaceous and sudoriferous glands and development of cutaneous malignancies such as skin tumors (Bray et al. 2016; Spalek 2016). Subcutaneous dystrophic calcification has also been associated with these late adverse effects (Mahomed et al. 2011). Literature suggests that late effects are related to an imbalance of proinflammatory and profibrotic cytokines (Spalek 2016).