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In contrast, dystrophic calcification is caused by abnormalities or degeneration of tissues [2] [3] resulting in mineral deposition, though blood levels of calcium remain normal. These differences in pathology also mean that metastatic calcification is often found in many tissues throughout a person or animal, whereas dystrophic calcification ...
One of the principal causes of arterial stiffening with age is vascular calcification. Vascular calcification is the deposition of mineral in the form of calcium phosphate salts in the smooth muscle-rich medial layer of large arteries including the aorta. DNA damage, especially oxidative DNA damage, causes accelerated vascular calcification. [11]
Pulp stones are not painful unless they impinge on nerves. They are classified: [2] A) On the basis of structure 1) True pulp stones: formed of dentin by odontoblasts 2) False pulp stones: formed by mineralization of degenerating pulp cells, often in a concentric pattern B) On the basis of location 1) Free: entirely surrounded by pulp tissue
Stones can cause disease by several mechanisms: [citation needed] Irritation of nearby tissues, causing pain, swelling, and inflammation; Obstruction of an opening or duct, interfering with normal flow and disrupting the function of the organ in question; Predisposition to infection (often due to disruption of normal flow)
The characteristic radiologic finding of giant cell tumors of bone is a lytic lesion that does not have marginal sclerosis of bone. On histology, giant cells of fused osteoclasts are seen as a response to neoplastic mononucleated cells. Notably, giant cells are not unique among benign bone tumors to giant cell tumors of bone.
Kidney stone disease, also known as renal calculus disease, nephrolithiasis or urolithiasis, is a crystallopathy where a solid piece of material (renal calculus) develops in the urinary tract. [2] Renal calculi typically form in the kidney and leave the body in the urine stream. [2] A small calculus may pass without causing symptoms. [2]
Caseous necrosis in the kidney. In caseous necrosis no histological architecture is preserved (unlike with coagulative necrosis). [5] [6] On microscopic examination with H&E staining, the area is acellular, characterised by amorphous, roughly granular eosinophilic debris of now dead cells, [6] also containing interspearsed haematoxyphilic remnants of cell nucleus contents. [5]
[2] Inflammation or infection of the gland may develop as a result. Sialolithiasis may also develop because of the presence of existing chronic infection of the glands, dehydration (e.g. use of phenothiazines), Sjögren's syndrome and/or increased local levels of calcium, but in many instances the cause is idiopathic (unknown).