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INTRACELLULAR

ACCUMULATIONS
PATHOLOGIC
CALCIFICATION
Presented by: Dr. Wajiha Alamgir
M.Phil Oral Pathology
Armed Forces Institutue of Pathology,
Raawalpindi, Pakistan

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Dr.Wajiha Alamgir

Definition

Abnormal deposition of calcium


salts with smaller amounts of
iron,magnesium,and other minerals,
is called pathologic calcification.
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Dr.Wajiha Alamgir

TYPES
Dystrophic
Calcification

Metastatic
Calcification

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Dr.Wajiha Alamgir

DYSTROPHIC CALCIFICATION

Deposition of calcium at the sites of cell injury


and necrosis.
It occurs in the absence of calcium metabolism
derangements i.e. with normal serum levels of
calcium.
May also be a cause of organ dysfunction
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Dr.Wajiha Alamgir

EXAMPLES:

Atheromas of advanced atherosclerosis, associated


with intimal injury in the aorta and large arteries.
Characterized by accumulation of lipids. May be an
incidental finding indicating insignificant past cell
injury.
Lymph nodes affected by tuberculosis.
Past injury
Calcification in malignant tumors

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Dr.Wajiha Alamgir

MORPHOLOGY

Calcium salts are grossly seen as fine white


granules or clumps.
Often felt as gritty deposits.

Carotid plaque

Calcific aortic stenosis

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Dr.Wajiha Alamgir

HISTOLOGY

Histologically, calcification appears


as intracellular and/or extracellular
basophilic deposits.
In time, heterotropic bone may be formed in
the focus of calcification.

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Dr.Wajiha

Alamgir

Dystrophic calcification-Breast

Calcifying odontogenic cyst

Dystrophic jaw calcification

METASTATIC CALCIFICATION

Deposition of calcium in normal tissues.


It almost always reflect some derangements in
calcium metabolism (hypercalcemia)

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Dr.Wajiha

Alamgir

CAUSES:

1.

Hypercalcemia may occur due to:

Increased secretion of parathyroid hormone, due to


a) primary parathyroid tumors
b) production of parathyroid tumor
related protein by other malignant tumors.
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Dr.Wajiha

Alamgir

2.

Destruction of bone due to


a) effects of accelerated turnover
e.g. Pagets disease
b) immobilization
c) increased bone catabolism associated with tumors
e.g. multiple myeloma, leukemia, or diffuse skeletal
metastasis.

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Dr.Wajiha

Alamgir

3. Vitamin D-related disorders including vitamin D


intoxication and sarcoidosis (in which macrophages
activate a vitamin D precursor)
4. Renal failure, in which phosphate retention leads to
secondary hyperparathyroidism.

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Dr.Wajiha

Alamgir

MORPHOLOGY
Same as in dystrophic calcification.

SITES
Principally affects interstitial tissues of
Vasculature
Kidneys (e.g. nephrocalcinosis)
Lungs ( respiratory deficits)
Gastric mucosa
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Dr.Wajiha

Alamgir

KIDNEY

LUNGS

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PATHOGENESIS

DYSTROPHIC CALCIFICATION
Two types:
a) Intracellular
b) Extracellular
Pathogenesis involves two steps:
i) Initiation or nucleation
ii) Propagation
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Dr.Wajiha Alamgir

a) Initiation

Extracellular

Calcium

Phosphate
(Action of
(affinity for membrane
membrane-bound
phospholipids)
phosphatases)
Accumulation

Membrane-bound vesicles

Intracellular

Calcium
Accumulation

Mitochondria of dead or
dying cells that have lost
their ability to regulate
intracellular calcium

Matrix vesicles, in normal cartilage and


bone
In pathologic calcification, derived from
degenerating cells

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Dr.Wajiha Alamgir

b) Propagation
It occurs both intracellularly and extracellularly.

Propagation of crystal formation occurs, yielding crystalline


calcium phosphate.
Factors affecting crystallization
1.
Concentration of calcium and phosphate in the extracellular
spaces.
2.
Presence of mineral inhibitors.
3.
Degree of collagenization.

All these factors when present, enhance the rate of crystal


growth.
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Dr.Wajiha Alamgir

THANK YOU

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