CELL INJURY
&
CELL ADAPTATIONS
DR. SALEEM SHAIKH
Introduction
 Cell injury is defined as a variety of stresses a cell encounters as
a result of changes in its internal & external environment.
 The cells of the body have inbuilt mechanism to to resist the
changes.
 The response of a cell to changes depends upon
 The type of cell involved
 The type of injury / stress
 The etiology of cell injury may be broadly classified into


Genetic causes
Acquired causes
Acquired causes
Hypoxia & ischemia – deficiency of oxygen; due to lack of
blood supply. (may be other causes of hypoxia)
2. Physical agents – mechanical, thermal, electrical etc
3. Chemical agents – medications, smoke, drugs etc
4. Microbial agents – bacterial, viral fungi etc
5. Immunologic agents – ‘double edged sword’ hypersensitivity
reactions, anaphylactic shock
6. Nutritional derangements – both reduced and in excess
7. Ageing – decreased ability for cell repair
8. Psychogenic causes
9. Iatrogenic factors
10. Idiopathic diseases
1.
Morphology of cell injury
 Morphology of reversible cell injury – also called as
retrogressive changes
 Types of changes
Hydropic change (cloudy swelling)
 Hyaline change
 Mucoid change

Hydropic change
 This is due to accumulation of water within the cytoplasm of the
cell.
 The most commonest and early form of cell injury resulting from
acute cell injury from bacterial toxins, chemicals, burns etc
 Pathogenesis – defective regulation of sodium and potassium at
the cell membrane, which results in rapid flow of water into the
cell.
 Microscopically the cell appears to be swollen, small clear
vacuoles are seen hence called as vacuolar degeneration.
nucleus appears pale.
Hyaline change
 hyaline - glass.
 This refers to the non
specific homogenous pink
material which is seen in
H&E stained sections.
 It may be intracellular or
extracellular.
 Russels bodies in plasma
cell, hyalinised old scar,
hyaline deposits in blood
vessels in hypertension and
diabetes.
Mucoid change
 Mucus is produced mainly by epithelium and by some cells in
connective tissue.
 Mucin is the main constituent.
 Excess mucin accumulation in connective tissue is known as
myxoid and is seen in tumors of odontogenic and salivary gland
origin.
Morphology of Irreversible Cell Injury
 Irreversible cell injury leads to cell death.
 Types of cell death


Necrosis
Apoptosis
 Changes that follow cell death


Gangrene
Calcification
Finally results in end of life
Necrosis
 Necrosis is defined as a localised area of death of tissue
followed by degradation of tissue by hydrolytic enzymes, it is
always accompanied by inflammatory reaction.
 Can be caused by various agents like hypoxia, physical, chemical
etc
 Two important changes seen are


Cell digestion by lytic enzymes – seen as homogeneous and
eosinophilic cytoplasm
Protein denaturation – seen as changes in the nucleus
(condensation – pyknosis; dissolution – karyolysis;
fragmentation- karyohexsis)
Types of necrosis
 Coagulative necrosis – most common, caused by ischemia. The
cell outlines are retained but the cytoplasmic and nuclear details
are lost.
 Liquefactive necrosis – Also commonly seen, this occurs due to
degradation of tissues by hydrolytic enzymes
 Fat necrosis – seen in pancreas and breasts
 Fibrinoid necrosis – deposition of fibrin like material, seen in
immunologic tissue injury
 Caseous necrosis – Found as center foci in tuberculosis
infections. Combines features of both coagulative and
liquefactive necrosis
Apoptosis
 Apoptosis is a form of ‘coordinated and internally programmed




cell death’
This form of cell death is controlled and regulated and is also
referred as cell suicide
Apoptosis is seen in both physiologic and pathologic conditions
Presence of apoptotic bodies
Physiologic process
 Organized shape modification in development of embryo
 Physiologic involution of tissues
 Involution of thymus
 Pathologic process



Cell death by cytotoxic T cells
Degenerative diseases of CNS – Alzheimer’s
Some types of viral infections
Difference chart
Gangrene
 Gangrene is a advanced stage of necrosis which also shows
putrefaction (production of foul odor).
 Two main forms of gangrene
 Dry - this is seen in the distal part of the limb due to ishemia,
usually in toes and feet of old patients with atherosclerosis.
The blood supply to the part is very less. A line of seperation
is seen between the normal part and the gangrene part


Wet – (gas gangrene) – seen in moist tissues such as mouth,
bowel, lung etc. Diabetic foot and bed sores are also common
examples. This is seen due to blockage of venous blood flow.
No line of demarcation is seen.
Gas gangrene is a variant of wet gangrene formed due to gas
producing bacteria (clostridia). Seen in open and contaminated
wounds.
Pathologic Calcifications
 Deposition of calcium in tissues other than teeth or bone is
called pathologic calcification.
 Two types


Dystrophic – deposition in dead and degenerated tissues, with
normal calcium metabolism and calcium levels. Ex- infarcts,
thrombi, old scars
Metastatic – deposition in normal tissues with deranged
calcium metabolism and hypercalcaemia. Ex – kidney stones,
lung, blood vessels etc.
CELLULAR ADAPTATIONS
 When a cell is exposed to stress, the cells make
adjustments in order to survive.
 This adaptation could be to physiologic or pathologic
adaptation.
 In general the adaptive responses are reversible on
withdrawal of stimulus.
 The cells may change by
 Increase or decrease in number
 Change in appearance and structure
Atrophy
 Reduction in number and size of parenchymal cells of an organ




or its parts which was once normal.
Hypoplasia – developmentally small
Causes –
Physiologic
 Atrophy of thymus
 Atrophy of gonads after menopause
 Atrophy of brain after aging
Pathologic
 Ischaemic atrophy
 Disuse atrophy
 Endocrine atrophy
 Pressure atrophy
Hypertrophy
 Increase in the size of parenchymal cells without any change in
number of the cells
 Physiologic 

enlarged size of uterus during pregnancy
Muscular hypertrophy in athletes
 Pathologic –



Hypertrophy of cardiac muscle
Compensatory hypertrophy
Hypertrophy of smooth muscle
Hyperplasia
 Hyperplasia is an increase in the number of parenchymal cells.
 Very often hyperplasia and hypertrophy occur together
 Hyperplasia persists only till the stimulus is present (different
from neoplasia)
 Physiologic hyperplasia –
 Hormonal hyperplasia – puberty
 Pathologic hyperplasia –



excessive stimulation of hormones
Excess granulation tissue during wound healing
Formation of skin warts
Metaplasia
 It is the change of one type of adult cell to another type of adult
cell, usually as a response to stimulus and reverts back to
normal after removal of stimulus
Types
Epithelial
 Mesenchymal
 Epithelial is the more common type, usually the cell becomes
less specialized
 bronchus of smokers- pseudo stratified ciliated columnar to
squamous.
 sialometaplasia – mucous salivary gland acini to squamous
 Bronchitis – pseudo stratified ciliated to coulmnar
 Mesenchymal metaplasia –
Osseous metaplasia – myositis ossificans; riders
bone
 Cartilaginous metaplasia - healing of fractures

Dysplasia
 Disordered cellular growth (bad growth)
 It is characterized by







Increased layer of epithelial cells
Disordered arrangement of cells
Loss of basal polarity
Cellular and nuclear pleomorphism
Increased nucleocytoplasmic ratio
Nuclear hyperchromatism
Increased and abnormal mitotic activity
Very common in oral cavity
 Classified as mild moderate and severe
CARCINOMA IN SITU

1
2
3
4