When the deposition occurs in dying tissue/
degenerated tissue
Normal serum levels of calcium
Absence of derangement of calcium metabolism
Occurs in areas of necrosis→coagulative, caseous,
liquefactiveor in enzymatic necrosis of fat
Aortic valve in heart with
calcificaortic stenosis
Occurs in atheromasof
atherosclerosis
In aging or damaged heart
valves
Grossly:
fine, white granules or
clumps, often felt as gritty
deposits
DYSTROPHIC CALCIFICATION
Histolgically:
the calcium salts have a basophilic, amorphous
granular, sometimes clumped, appearance
can be intracellular, extracellular, or in both
locations.
Heterotopicbone formation may occur
Psammomabodies:-The progressive
acquisition of outer layers may create
lamellatedconfigurations.
Asbestos bodies:-calcium and iron salts gather
about long slender spiculescreating exotic,
beaded dumbbell shape and found asbestos in
the lung,
DYSTROPHIC CALCIFICATION
Single necrotic cells as seed crystal
progressive acquisition by the
mineral deposits in outer layer
lamellated configurations
Psammoma bodies
crystalline calcium phosphate mineral
in the form of an apatite similar to the
hydroxyapatite of bone.
Intracellular/
extracellular
EXTRACELLULAR
•Phospholipids in membrane
bound vesicles
•Dead & dying cells
INITIATION:-
➢Following cell injury (i.e. degeneration or
necrosis), there is membrane damage and
release of membrane phospholipids.
➢Phosphatases associated with phospholipids
generate phosphate ions.
➢there is excess uptake of calcium by injured
mitochondria in degeneration and necrosis.
➢ calcium and phosphate so generated
➢form precipitates of calcium phosphate.
PATHOGENESIS OF DYSTROPHIC
CALCIFICATION
Ca
2+
ion binds to the
phospholipids present
in the vesicle
membrane
phosphatases associated with
the membrane generate
phosphate groups, which bind
to the calcium
the cycle of calcium and
phosphate binding is
repeated
structural change occurs in
the arrangement of calcium
and phosphate groups
microcrystal
CALCIFICATION
CAUSES OF HYPERCALCAEMIA:
1.↑
ed
secretion of parathyroid hormone (PTH) with
subsequent bone resorption. Eg. In
hyperparathyroidism due to parathyroid tumors, and
ectopic secretion of PTH-related protein by malignant
tumors
2.Destruction of bone tissue:
→primary tumorsof bone marrow (e.g., multiple myeloma,
leukemia) or
→diffuse skeletal metastasis (e.g., breast cancer), accelerated
bone turnover (e.g., Paget disease), or
→immobilization;
3)Vitamin D-related disorders:
→vitamin D intoxication,
→sarcoidosis (in which macrophages activate a
vitamin D precursor), and
→idiopathic hypercalcemia of infancy (Williams
syndrome), characterized by abnormal sensitivity to
vitamin D;
4) Renal failure →retention of Po4 →secondary
hyperparathyroidism
5) aluminumintoxication, which occurs in patients on
chronic renal dialysis, and
6) milk-alkali syndrome, which is due to excessive
ingestion of calcium and absorbable antacids such as
milk or calcium carbonate.
SITE:
Interstitial tissues of
gastric mucosa,
kidneys,
lungs,
systemic arteries, and
pulmonary veins
occurs due to excessive binding of inorganic
phosphate ions with elevated calcium ions
due to underlying metabolic derangement.
precipitates of calcium phosphate at the
preferential sites, due to presence of acid
secretions or rapid changes in pH levels
Metastatic calcification is reversible upon
correction of underlying metabolic disorder.