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By:
Dr/ Walid Zedan
Dr/ Basant Hamdy
1433القعدة، ذو 17الثالثاء،
By the end of this lecture
students should be able to:
Describe & enumerate the
causes of atrophy.
Define hyperplasia,
hypertrophy & metaplasia.
Differentiate physiologic from
pathologic hyperplasia.
Differentiate physiologic from
pathologic hypertrophy.
To get some knowledge about
the developmental disorders
Definition: Reversible changes in size, number,
phenotype, metabolic activity, or functions of cells
in response to changes in their environment
Types:
1- physiologic (response to normal stimulation by
hormones or endogenous chemical mediators)
2- pathologic (response to stresses to escape
injury)
Forms: hypertrophy, hyperplasia, atrophy,
metaplasia
Stimulus or stress
Normal cell Adaptation
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Injury
Reversible
Irreversible
Cell death
Apoptosis
Necrosis
Definition: increase in the size of cells increase in
the size of the organ (with increased functional
capacity)
No new cells, just larger cells
Hyperplasia (will be discussed later), entails increase
in the cell number
Types & causes:
1- physiologic:
Increased functional demand
Skeletal muscles
heart (within limit)
Specific hormonal stimulation
Pregnant uterus
(estrogen stimulates s.m.
hypertrophy & hyperplasia)
2- pathologic:
a) Adaptive hypertrophy
(wall of hollow muscular
organs)
- Stomach in case of pyloric
obstruction
- Left ventricle in case of
aortic valve disease or
hypertension
- Urinary bladder in case of
urethral stricture
b) Compensatory hypertrophy:
In paired organs as in kidney:
when one kidney is absent or
removed surgically, the other
kidney is enlarged in size
c) Hormonal hypertrophy:
eg: excessive growth hormone
leads to gigantism or acromegaly
* Selective hypertrophy (eg: smooth ER
in hepatocytes of patients treated with
barbiturates)
Definition: increase in the number of cells
increase in the size of the organ.
It may occur with hypertrophy & often in
response to the same stimuli.
Types: physiologic & pathologic
1- physiologic hyperplasia
a) Hormonal (glandular epithelium of female
breast at puberty & pregnancy)
a) Compensatory (when a portion of tissue is
resected or diseased, eg. Liver)
2- Pathologic hyperplasia
a) Excessive hormonal or
growth factor stimulation
• Endometrial hyperplasia: due to
loss of balance between
estrogen & progesterone
hormones. This results
in abnormal menstrual
bleeding
• Thyroid gland: due to increased thyroid stimulating hormone (TSH) in thyrotoxicosis.
• Adrenal gland: due to adreno-corticotropic hormone (ACTH) in Cushing’s syndrome.
b) Hyperplasia is an important response of CT
cells in wound healing. Growth factors are
produced by WBCs responding to injury & by
cells in ECM.
c) Hyperplasia due to viral infection. e.g.: HPV
that causes skin warts & squamous cell
papilloma of m.m. Here, growth factors may
be produced by virus or by infected cells.
Sebaceous hyperplasia
Papillary hyperplasia of the palate
Gingival hyperplasia
Hyperplasia & CANCER !!
Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise.
• Endometrial hyperplasia increased risk of endometrial cancer
• Certain HPV infections predisposes to cervical cancers
Definition: shrinkage in the size of cell by loss of cell
substance. When a sufficient number of cells involved,
the entire tissue/organ diminishes in size.
The cells retreats to a smaller size at which survival is still possible.
New equilibrium is achieved between cell size & diminished blood supply
or trophic stimulation.
Mechanism: Reduction in structural components of cell
Protein
synthesis
Protein
catabolism
Mitochondria &
myofilaments
Endoplasmic
reticulum
Atrophy
Types & causes:
1) Physiological
- Atrophy of thymus gland atrophy after puberty
& thyroglossal duct after birth (involution)
- Decreased workload
“disuse”:
immobilized limb to
permit healing of
fracture
- Loss of hormone
stimulation: atrophy
of ovaries & uterus
after menopause
2) Pathological
1. Loss of innervation.
2. Starvation (lack of
food & its
absorption) &
malnutrition.
Unilateral tongue
atrophy following
hypoglossal nerve
damage
4. Pressure atrophy: as tumor pressure on
surrounding tissue.
- In many situations, atrophy is accompanied by
increased autophagy “self-eating”: a process
in which starved cell eats its own components
in an attempt to find nutrients & survive.
3. Senile atrophy: in old
age “brown atrophy of
the heart”
Definition: transformation of one type of tissue into
another type of the same differentiation.
Cells sensitive to a particular stress are replaced by
other cell types better able to withstand the adverse
environment.
Mechanism: it seems to be induced by altered
differentiation pathway of tissue stem cells (genetic
reprogramming of stem cells rather than
transdifferentiation of already differentiated cells)
Types:
1) Epithelial metaplasia
2) Connective tissue metaplasia
1- Epithelial metaplasia
Squamous metaplasia
- In the respiratory
epithelium of
habitual cigarette
smokers & in
vitamin A
deficiency
a) Squamous metaplasia
- Transitional epithelium of urinary bladder to stratified
squamous epithelium in urinary bilharziasis
b) Odontogenic epithelial metaplasia
c) Glandular metaplasia
- In chronic gastric reflux, normal st. sq. epith. of the
lower esophagus may undergo metaplastic
transformation into gastric or intestinal type
“Barrett’s”
Types:
1) Epithelial metaplasia
2) Connective tissue metaplasia
1- cartilage to bone in old age
2- bone occasionally forms at
foci of injury
3- muscle tissue to bone “ in
traumatic myositis ossificans
“
Difference Between Congenital & Hereditary Conditions
Congenital defects/anomalies:
Structural defects that are present at, before, or after
birth but not necessarily inherited “transmitted by genes”. They have either cosmetic or functional
significance. They may be a significant cause of
infant illness, disability & death.
Hereditary defects/Anomalies:
Diseases or conditions transmitted by genes, some
become apparent at birth & others years after birth.
Known causes can be grouped into the following categories:
1. Genetic factors: All chromosomal syndromes are associated with
congenital malformations (10-15%). e.g. Down syndrome & Turner
syndrome.
2. Environmental influences
• Infections: Viral, Rubella, Toxoplasmosis, Syphilis, CMV, HIV to which
the mother was exposed (2- 3% ).
• Drugs: alcohol, Androgens, Phenytoin , Thalidomide & Warfarin (1%)
• Maternal disease states: Diabetes, Phenylketonuria &
Endocrinopathies (6-8%).
• Pregnant smokers
• Irradiation
3. Multifactorial inheritance : which implies the interaction of
environmental influences with two or more genes of small effect, is the
most common genetic cause of congenital malformation representing
20-25%.
4. Unknown: comprises 40-60%
Organ–specific malformations
: refers to the complete absence of an
organ or its primordium
: indicates incomplete development of an
organ
: means underdevelopment of an
organ
: describes the absence of an opening
of a hollow visceral organ or duct such as that of
salivary glands, of intestines or of bile ducts
Agenesis
Aplasia
Hypoplasia
Atresia
Hemifacial - atrophy
Progressive atrophy of tissues on one side of the face
Causes:
1. Atrophic malformation of cervical sympathetic
nervous system
2. Hereditary
3. Trauma or infection
4. Peripheral trigeminal neuritis
5. A form of localized scleroderma
Clinically
Noticed at 1st or 2nd decades of life
Noticed first as a white line or furrow on one side
of the face near midline
Lesion extends progressively to include atrophy of
all tissues on one side of the face
Eye appears depressed in the orbit
Epilepsy & trigeminal neuralgia might occur
Skin on the affected side would look dark &
pigmented with loss of hair on that side
Oral Manifestations
Atrophy of tongue & lips on the
affected side
Underdevelopment of the roots
Retarded eruption of the teeth
Reduced growth of the jaw on
the affected side
* Mild form of facial asymmetry is more common
* Hemihypertrophy might involve:
- entire half of the body
- one or both limbs
- The face & head
Causes:
a) Chromosomal abnormalities
b) Localized chronic infection
c) Lymphatic & vascular problems
d) Neurogenic abnormalities
e) Unknown
Clinical Features
a) Mental disturbances
b) Skin abnormalities such as
nevi
c) Varicosed veins
d) Umbilical hernia
e) Hemangioma
f) Thick & coarse hair on the
involved side
Oral Manifestations
a) Large permanent teeth in the affected side
b) Premature eruption of the permanent teeth
c) Premature shedding of deciduous teeth on the
affected side
Differential Diagnosis:
Neurofibromatosis, Fibrous Dysplasia
1. Agnathia
Extremely rare
Total absence of the jaw
partial absence of the jaw might be seen
In the maxilla: one of the maxillary processes
or premaxilla
In the mandible: one side of the mandible, the
condyle or ramus
2. Micrognathia
Either true or relative
True when the actual jaw is small relative to normal
size
Relative when jaw size is normal & teeth are large
“macrodontia”.
It might be due to:
1. posterior positioning of the mandible relative to
maxilla or
2. agenesis of condyle
Agenesis of the TMJ or ankylosis of the joint might
lead to acquired micognathia
3. Macrognathia
Abnormally large jaw
In both mandible & maxilla in hyper-pituitary gigantism
Mandibular prognathism is considered as a form of Macrognathia
Macrognathia can be true with actual large jaw or
relative when the jaw size is normal whereas the size
of teeth is smaller ” Microdontia”
Causes:
1. increase size of the ramus
2. increase Mandibular length
3. increase the gonial angle
4. anterior position of the glenoid
fossa
5. decreased maxillary length
6. posterior positioning of the maxilla
7. prominent chin button
8. Varying soft tissue contour
