This document discusses pathological calcification and summarizes its main types: 1) Dystrophic calcification refers to the local deposition of calcium salts in necrotic or degenerate tissues regardless of normal serum calcium levels. 2) Metastatic calcification reflects deranged calcium metabolism and systemic deposition of calcium salts associated with increased serum calcium levels. 3) Pigments that accumulate in tissues include exogenous pigments like carbon and tattoos, as well as endogenous pigments such as lipofuscin, melanin, hemosiderin, and bile.

1. PATHOLOGICAL CALCIFICATION
Definition:-
Abnormal deposition of calcium salts
together with smaller amount of Mg++ ,Fe++ &
other minerals in tissues other than osteoid or
enamel

2. Pathologic calcification
• Dystrophic calcification
• Metastatic calcification

3. • Dystrophic calcification
refers to local deposition of calcium salts in
necrotic or degenerate tissues, whatever the
type of necrosis, in spite of normal serum Ca++

4. Pathologic Calcification
 Dystrophic Calcification
- Area of tissue necrosis
- Aging or damage heart valve
- Atherosclerosis
- Single necrotic cell
“psammoma body”

5. Aortic valve , gross , (calcified aortic stenosis).
5

6. Metastatic calcification
reflects deranged calcium metabolism
in contrast to dystrophic calcification and
is associated with increase serum calcium
level & systemic deposition of Ca++salts
in interstitial tissue of gastric mucosa,
kidney,lungs,systemic arteries&
pulmonary veins.

7. Metastatic calcification
Hypercalcimia
• Increased secretion of parathyroid hormone
• Destruction of bone tissue 2ndry to primary tumor of
bone marrow ( multiple myeloma, leukemia), or diffuse
skeletal metastasis.
• Vitamin D-related intoxication
• Renal failure
•Excessive intake of calcium & absorbable antacids as
milk or calcium carbonate.

8. This is dystrophic calcification in the wall of the stomach. At
the far left is an artery with calcification in its wall

9. “Metastatic calcification" in the lung of a patient with a very
high serum calcium level (hypercalcemia).

10. PIGMENTS
EX-ogenous--- (tattoo, Anthracosis)
END-ogenous--- they all look the
same, (e.g., hemosiderin, melanin,
lipofucsin, bile), in that hey are all
golden yellowish brown on “routine”
Hematoxylin & Eosin (H&E) stains

11. Accumulation of Pigments
• Exogenous pigments
Carbon ( anthracosis)
Coal dust ( pneumoconiosis)
Lung: pick up by alveolar macrophages
regional lymph nods
blackening the tissues of the lungs
(anthracosis)

12. TATTOO, MICROSCOPIC

13. ANTHRACOSIS

14. Pulmonary anathracosis (deposition of carbon particles)

15. Carbon- laden macrophages (black exogenous pigment)

16. Accumulation of Pigments
• Endogenous pigment
:Lipofuscin – aging pigment(fucus=brown)
lipid, phospholipid-protein complex (lipid
peroxidation) ,brown-yellow pigment
accumulated as the atrophic and dying cells
undergo autophagocytosis. Harmless,Sign of free
radical injury & lipid perioxidation, seen in aging patients
severe malnutrition & cancer cachexia.

17. Lipofuscin granules in a cardiac myocyte as shown by A, light microscope (deposits indicated by
arrows) , and B,Electron microscopy (perinuclear ,intralysosomal location).

18. Lipofuscin (wear & tear) pigments in cardiac myocytes

20. Melanin
• Melanin – melas= black
• In melanocytes formed by oxidation of
tyrosine to dihydroxyphenylalanine by
tyyrosinase enzyme

21. Nevus ( melanin pigmentation)

22. :Hemosiderin – aggregates of ferritin micelles (iron + apoferritin =
ferritin)
Hemosiderosis:- Excess of hemosiderin granules in
mononuclear phagocytes without organ dysfunction
Causes:- Local (bruise)
Systemic as
Hemolytic anemia,
Increased absorption of dietary iron
Repeated blood transfusion
Hemochromatosis:- Excess of hemosiderin granules in
mononuclear phagocystic system & paranchymal cells causing
organ dysfunction ( liver fibrosis, DM, heart failure).

23. Hemosiderin granules in liver cells A, H&E section showing golden-brown,finely
granular pigment. B, Prussian blue reaction, specific for iron.

24. Alveolar (hemosiderin-laden) macrophages in patient with heart failure
(heart failure cells)

25. Heart failure cells (hemosiderin-laden macrophages ),Prussian blue reaction

26. Jaundice
Yellowish discoloration of skin &
sclera due to deposition of bilirubin
pigment.

27. Bile pluges in liver of patient with obstructive jaundice

28. Hemosiderin

29. The brown coarsely granular material in macrophages in
this alveolus is hemosiderin

30. These renal tubules contain large amounts of hemosiderin,
as demonstrated by the Prussian blue iron stain

31. • Fig 1-20

32. Ageing:
“Progressive time related loss of
structural and functional
capacity of cells leading to
death”
• Senescence, Senility, Senile
changes.
• Ageing of a person is intimately
related to cellular ageing.

33. Factors affecting Ageing:
• Genetic – Clock genes, (fibroblasts)
• Diet – malnutrition, obesity etc.
• Social conditions -
• Diseases – Atherosclerosis, diabetes etc.
• Werner’s syndrome.

34. Cellular mechanisms of
ageing
• Cross linking proteins &
DNA.
• Accumulation of toxic
by-products.
• Ageing genes.
• Loss of repair
mechanism.
• Free radicle injury
• Telomerase shortening.

35. Telomerase in ageing:
Germ
Cells
Somatic
Cells

36. Ageing –changes:
• Gradual atrophy of tissues and organs.
• Dementia
• Loss of skin elasticity
• Greying and Loss of hair
• BV damage – atherosclerosis/bruising.
• Loss of Lens elasticity  opacity 
vision
• Lipofuscin pigment deposition – Brown
atrophy in vital organs.

37. Pathology
of elderly

38. Factors affecting ageing:
• Stress • Diminished stress
• Infections response.
• Diseases • Diminished immune
• Malnutrition response.
• Accidents • Good health.

39. Conclusions:
• Cellular Injury - Various causes
• Reversible Injury  Adaptations
– Hypertrophy, Hyperplasia, Atrophy
– Accumulations - Hydropic, hyaline,
fat..
• Irreversible Injury - Necrosis
– Coagulative, Liquifactive, Caseous
• Ageing - Causes, Changes, Factors

40. THE END