NON NEOPLASTIC

DISORDERS OF
TISSUE GROWTH AND
REGENERATION
DR WALE TITILOYE

 Normal cells have a narrow range

of function/structure regulated by
various factors- genetic, nutrients,
neighboring cells.
Normal cells can handle
physiologic demands at a steady
state- homeostasis

 Increasing physiologic stresses or

pathologic stimuli cause physiologic
and morphologic changes called
cellular adaptation.
If the limits of adaptive responses are
exceeded cellular injury result
Cellular adaptive responses include
Hyperplasia
Hypertrophy

Atrophy
metaplasia

HYPERPLASIA
This is increase in the number of cells in
an organ/tissue
It occurs in tissues capable of mitotic
division
It may be physiologic or pathologic

physiologic hyperplasia
May be hormonal hyperplasia- when increased
functional capacity is required e.g.female breast
at puberty and uterus in pregnancy
May be compensatory when tissues are
damaged or partially resected e.g. liver after
partial hepatectomy
Mechanism involves increased local production
of growth factors, GF receptors.

pathologic hyperplasia
Due to excessive hormonal/ growth factor
stimulation on target organs e.g.
endometrial hyperplasia, benign prostatic
hyperplasia
A fertile ground for development of cancer

HYPERTROPHY
Increase in the size of cells leading to increase in
the size of an organ
This is due to synthesis of more structural
components
May be
physiologic e.g. skeletal muscle hypertrophy in weight
lifters, uterus in pregnancy
pathologic e.g.cardiac muscle in hypertension and
valvular heart disease

Hypertrophic cells do not grow forever : a critical

point is reached after which cellular injury occurs

mechanism
Involves signal transduction pathways
leading to activation of genes that
stimulate synthesis of cellular proteins
Transcription factors
Growth factors
Vasoactive agents

Involves switch of proteins from adult to

fetal types e.g. -MHC to -MHC
Re-expression of embryonic genes

ATROPHY
Decrease in cell size due to loss of cell
substance which may result in reduction in organ
size
May be associated with cell loss
May be
physiologic e.g. early embryogenesis, uterus after
parturition, female genital organs after menopause
pathologic e.g. ischaemic disease

Accompanied by increase in autophagic

vacuoles containing cellular components which
may persist as residual bodies e.g. lipofuscin

 Causes include:
Decreased work load
Loss of innervation
Diminished blood supply
Poor nutrition
Loss of endocrine stimulation
Aging
Pressure

Mechanism
Due to increased cellular protein
degradation via lysosomes or ubiquitinproteosome pathway

METAPLASIA
Reversible change in which one adult cell
type is replaced by another adult cell type
Squamous metaplasia of the respiratory tract in
habitual smokers, vit A deficiency,
Barrett esophagus- columnar metaplasia
Connective tissue metaplasia- formation of bone,
cartilage adipose tissue in areas where they are
not normally found e.g. myositis ossificans

Usually a change into a more resistant cell

type
May come with undesirable effects and
possibility of malignant transformation

mechanism
It is the result of reprogramming of stem
cells/undifferentiated mesenchymal cells
to differentiate along a new line

DISORDERS OF GROWTH
AGENESIS- congenital complete absence
HYPOPLASIA- congenital failure to develop
to mature size
HETEROTOPIA- normal tissue in an
abnormal location
HAMARTOMA- haphazard proliferation of
indigenous tissues

AGENESIS

HAMARTOMA

HAMARTOMA

HAMARTOMA

ATROPHY
REDUCED CELL SIZE / CELL NUMBER
Pressure
Disuse
Blood supply
Age
Radiation
Nutrition
Hormone withdrawal

NON-NEOPLASTIC
PROLIFERATION
Hypertrophy Size
Hyperplasia Number
Metaplasia Change
Dysplasia Disordered

HYPERTROPHY

HYPERPLASIA

HYPERPLASIA

DYSPLASIA - MORPHOLOGIC
SPECTRUM

NEOPLASTIC
PROLIFERATION

Uncontrolled & Irreversible

Benign
Localized, non-invasive.
Malignant (Cancer)
Spreading, Invasive.