Normal cell
(Homeostasis)
Stress
Increased demand
injurious stimulus
Cell injury
cell death
Adaptation
Inability to adapt
 Increase
in tissue or organ size due to
increase in the number of component cells
 It takes place if the cellular population is
capable of synthesizing DNA, thus permitting
mitotic division
 Occurs in tissues with labile and stable
cells
Two types of hyperplasia
1. Physiological hyperplasia
Hormonal – eg: proliferation of glandular
epithelium of breast at puberty and
pregnancy
Compensatory hyperplasia – eg: following
resection of part of liver, hyperplasia of
connective tissue cells in wound healing
2. Pathological hyperplasia
Hormonal – endometrial hyperplasia, adrenal
hyperplasia, thyroid hyperplasia, bone
marrow hyperplasia, lymph node hyperplasia,
benign prostatic hyperplasia
Growth factors – skin wart – papilloma virus
and transcription factors
Mechanisms of physiological
hyperplasia
Increased local production of growth factors
Increased levels of growth factor receptors on
the responding cells
Activation of intracellular signaling pathways
 Increase
in tissue or organ size due to
increase in the size of the cell
 Cell size increased due to increased synthesis
of structural proteins and organels
 Usually occurs in tissues with permanent
cells.
Hypertrophy may be physiological or pathological
and caused either by
1. Increased functional demand or
2. Specific hormonal stimulation
Eg.
1. Uterus in pregnancy – oestrogenic stimulation
causing hyperplasia of endometrium, smooth
muscle hypertrophy
2. Body builders – hypertrophy of skeletal muscle
3. Cardiomegaly – hypertension/aortic valve
disease
4. Post myocardial infarct enlargement of residual
viable cardiac myocytes hypertrophy
Mechanisms of hypertrophy
Signal transduction pathways -- induction of
genes -- synthesis of numerous cellular
protiens
Trigger factors
Mechanical triggers eg. Strech
Trophic triggers eg. Polypeptide growth
factor


Hyperplasia is induced by known stimuli
It stops when the stimulus which provoked it,
is removed


Decrease in tissue size due to decrease in
size of a sufficient number of cells,
secondary to protein degradation
Cell metabolism and function are reduced
to a level at which survival is possible
 Two
types of atrophy
1. Physiologic atrophy – During early
development some embryonic structures
undergo atrophy, Uterus after parturition
2. Pathologic atrophy – Local or generalized
1. Decreased work load –immobilisation of a
limb after fracture
2. Loss of innervation
3. Decreased blood supply
4. Loss of endocrine stimulation – in
menopause
5. Lack of nutrients
6. Ageing
 Proteolytic
pathways of protein degradation are
activated
 Lysosomes containing proteases are activated

Replacement of one type of mature (specialised)
tissue by another type of mature (specialised)
tissue, not normally found at that site.

Can occur in epithelium and connective tissue.


Occurs as an adaptive response to a stimulus
Although new mature cell type is better able to
withstand the adverse conditions (adaptive advantage) ,
protective mechanisms, like mucus secretion and ciliary
clearance can be lost eg resp tract of smokers

Structurally normal

is potentially reversible
1.
2.
Squamous metaplasia – Excretory ducts of
salivary glands, pancreas, bile ducts, cervix
-Ciliated epithelium of resp tract of smokers
-Respiratory tract in Vitamin A deficiency
Glandular metaplasia –
Intestinal or gastric metaplasia of oesophagus in
chronic gastric reflux
 Osseous
 Usually
metaplasia of fibrous scars
no adverse effects but rarely
some functional defects
Mechanisms of metaplasia
No change in phenotype of a differentiated
cell type.
Result of reprogramming of stem cells which
exist in normal tissue, or of undifferentiated
mesenchymal cells in connective tissue