Necrosis is a form of cell injury which results in the premature death of cells in living tissue by autolysis. The term "necrosis" came about in the mid-19th century and is commonly attributed to German pathologist Rudolf Virchow, who is often regarded as one of the founders of modern pathology. Necrosis is caused by factors external to the cell or tissue, such as infection, or trauma which result in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.
Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. At onset there are usually no symptoms, but if they develop, symptoms generally begin around middle age. In severe cases, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney disorders, depending on which body parts(s) the affected arteries are located in the body.
Bone healing, or fracture healing, is a proliferative physiological process in which the body facilitates the repair of a bone fracture.
A granuloma is an aggregation of macrophages that forms in response to chronic inflammation. This occurs when the immune system attempts to isolate foreign substances that it is otherwise unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as foreign objects, keratin, and suture fragments.
Fibrosis, also known as fibrotic scarring, is a pathological wound healing in which connective tissue replaces normal parenchymal tissue to the extent that it goes unchecked, leading to considerable tissue remodelling and the formation of permanent scar tissue.
Calcinosis cutis is a type of calcinosis wherein calcium deposits form in the skin. A variety of factors can result in this condition. The most common source is dystrophic calcification, which occurs in soft tissue as a response to injury. In addition, calcinosis is seen in Limited Cutaneous Systemic Sclerosis, also known as CREST syndrome. In dogs, calcinosis cutis is found in young, large breed dogs and is thought to occur after a traumatic injury.
Calcinosis is the formation of calcium deposits in any soft tissue. It is a rare condition that has many different causes. These range from infection and injury to systemic diseases like kidney failure.
Calcification is the accumulation of calcium salts in a body tissue. It normally occurs in the formation of bone, but calcium can be deposited abnormally in soft tissue, causing it to harden. Calcifications may be classified on whether there is mineral balance or not, and the location of the calcification. Calcification may also refer to the processes of normal mineral deposition in biological systems, such as the formation of stromatolites or mollusc shells.
Microcalcifications are tiny deposits of calcium salts that are too small to be felt but can be detected by imaging.
Metastatic calcification is deposition of calcium salts in otherwise normal tissue, because of elevated serum levels of calcium, which can occur because of deranged metabolism as well as increased absorption or decreased excretion of calcium and related minerals, as seen in hyperparathyroidism.
Nephrocalcinosis, once known as Albright's calcinosis after Fuller Albright, is a term originally used to describe the deposition of poorly soluble calcium salts in the renal parenchyma due to hyperparathyroidism. The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. It is caused by multiple different conditions and is determined by progressive kidney dysfunction. These outlines eventually come together to form a dense mass. During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray. It may be severe enough to cause renal tubular acidosis or even end stage kidney disease, due to disruption of the kidney tissue by the deposited calcium salts.
Mönckeberg's arteriosclerosis, or Mönckeberg's sclerosis, is a form of arteriosclerosis or vessel hardening, where calcium deposits are found in the muscular middle layer of the walls of arteries. It is an example of dystrophic calcification. This condition occurs as an age-related degenerative process. However, it can occur in pseudoxanthoma elasticum and idiopathic arterial calcification of infancy as a pathological condition, as well. Its clinical significance and cause are not well understood and its relationship to atherosclerosis and other forms of vascular calcification are the subject of disagreement. Mönckeberg's arteriosclerosis is named after Johann Georg Mönckeberg, who first described it in 1903.
Fat necrosis is a form of necrosis that is caused by the action of lipases on adipocytes.
Ectopic calcification is a pathologic deposition of calcium salts in tissues or bone growth in soft tissues. This can be a symptom of hyperphosphatemia. Formation of osseous tissue in soft tissues such as the lungs, eyes, arteries, or other organs is known as ectopic calcification, dystrophic calcification, or ectopic ossification.
Idiopathic scrotal calcinosis is a cutaneous condition characterized by calcification of the skin resulting from the deposition of calcium and phosphorus occurring on the scrotum. However, the levels of calcium and phosphate in the blood are normal. Idiopathic scrotal calcinosis typically affects young males, with an onset between adolescence and early adulthood. The scrotal calcinosis appears, without any symptoms, as yellowish nodules that range in size from 1 mm to several centimeters.
Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location, around joints, outside the joint capsule. They are frequently (0.5–3%) seen in patients undergoing renal dialysis. Clinically also known as hyperphosphatemic familial tumoral calcinosis (HFTC), is often caused by genetic mutations in genes that regulate phosphate physiology in the body. Best described genes that harbour mutations in humans are FGF-23, Klotho (KL), or GALNT3. A zebrafish animal model with reduced GALNT3 expression also showed HFTC-like phenotype, indicating an evolutionary conserved mechanism that is involved in developing tumoral calcinosis.
Pulp stones are nodular, calcified masses appearing in either or both the coronal and root portion of the pulp organ in teeth. Pulp stones are not painful unless they impinge on nerves.
Necroptosis is a programmed form of necrosis, or inflammatory cell death. Conventionally, necrosis is associated with unprogrammed cell death resulting from cellular damage or infiltration by pathogens, in contrast to orderly, programmed cell death via apoptosis. The discovery of necroptosis showed that cells can execute necrosis in a programmed fashion and that apoptosis is not always the preferred form of cell death. Furthermore, the immunogenic nature of necroptosis favors its participation in certain circumstances, such as aiding in defence against pathogens by the immune system. Necroptosis is well defined as a viral defense mechanism, allowing the cell to undergo "cellular suicide" in a caspase-independent fashion in the presence of viral caspase inhibitors to restrict virus replication. In addition to being a response to disease, necroptosis has also been characterized as a component of inflammatory diseases such as Crohn's disease, pancreatitis, and myocardial infarction.
In vitro models for calcification may refer to systems that have been developed in order to reproduce, in the best possible way, the calcification process that tissues or biomaterials undergo inside the body. The aim of these systems is to mimic the high levels of calcium and phosphate present in the blood and measure the extent of the crystal's deposition. Different variations can include other parameters to increase the veracity of these models, such as flow, pressure, compliance and resistance. All the systems have different limitations that have to be acknowledged regarding the operating conditions and the degree of representation. The rational of using such is to partially replace in vivo animal testing, whilst rendering much more controllable and independent parameters compared to an animal model.
Mitral annular calcification (MAC) is a multifactorial chronic degenerative process in which calcium with lipid is deposited (calcified) in the annular fibrosa ring of the heart's mitral valve. MAC was first discovered and described in 1908 by M. Bonninger in the journal Deutsche Medizinische Wochenschrift. In the majority of cases, affected patients are asymptomatic and the condition is only noted incidentally on echocardiography or computed tomography (CT) scans. However, mitral annular calcification remains clinically significant because while in many cases the calcification is limited to the annulus and proximal leaflet bases, it may also extend further into the valve structure. This may potentially cause mitral regurgitation (MR) or more rarely mitral stenosis (MS), which may produce the classic symptoms of these conditions over time. In addition, calcification of the annulus can inhibit electrical conduction of the AV node, consequently causing various degrees of heart block. While MAC does not usually necessitate treatment independently, the degree of calcification present in the annulus is an important factor in choosing the most appropriate treatment modality for several conditions that do require intervention, particularly those that cause symptomatic obstruction of left ventricular outflow (LVOT).
