This document provides an overview of cellular adaptations and developmental disorders. It begins by defining cellular adaptations as reversible changes in cells in response to environmental changes, which can be physiological or pathological. The main cellular adaptations discussed are hypertrophy, hyperplasia, atrophy, and metaplasia. Causes, types, and examples of each are described. Developmental disorders summarized include hemifacial atrophy, hemihypertrophy, agnathia, micrognathia, and macrognathia. Key features and causes of each condition are highlighted. The document concludes by differentiating between congenital and hereditary conditions.

1. By:
Dr/ Walid Zedan
Dr/ Basant Hamdy
1433 ،‫الثالثاء، 71 ذو القعدة‬

2. 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

3. 
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,
metaplasia
hyperplasia,
atrophy,

4. Stimulus or stress
Adaptation
Normal cell
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Cell death
Apoptosis
Necrosis
Injury
Reversible
Irreversible

5. 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


7. Types & causes:
1- physiologic:
 Increased functional
demand
Skeletal muscles
heart (within limit)
 Specific hormonal
stimulation
Pregnant uterus
(estrogen stimulates s.m.
hypertrophy & hyperplasia)

8. 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

9. 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)

10. 


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)

11. 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

12. •
Thyroid
gland:
•
Adrenal
gland:
due to
increased
thyroid
stimulating hormone (TSH)
in thyrotoxicosis.
due
adreno-corticotropic
hormone
(ACTH)
Cushing’s syndrome.
to
in
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.

13. 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.

14. Sebaceous
hyperplasia
Papillary hyperplasia
of the palate

15. Gingival hyperplasia

16. 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

17. 
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.

Mechanism:
Reduction in structural components of cell
Protein
synthesis
Mitochondria &
myofilaments
Atrophy
Protein
catabolism
Endoplasmic
reticulum
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.

18. 
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
-

19. 2)
Pathological
1.
Loss of innervation.
Starvation (lack of
food
&
its
absorption)
&
malnutrition.
2.
Unilateral tongue
atrophy following
hypoglossal nerve
damage

20. 3.
Senile atrophy: in old
age “brown atrophy of
the heart”
4.
Pressure atrophy:
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.
as tumor pressure on

21. 
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)

22. 
1)
2)
Types:
Epithelial metaplasia
Connective tissue metaplasia
1- Epithelial
metaplasia
Squamous metaplasia
- In the respiratory
epithelium of
habitual cigarette
smokers & in
vitamin A
deficiency

23. Squamous metaplasia
- Transitional epithelium of urinary bladder to stratified
squamous epithelium in urinary bilharziasis
a)

24. 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”
b)

25. 
1)
2)
Types:
Epithelial metaplasia
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
“

27. 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.

28. 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%

29. Organ–specific malformations
Agenesis : refers to the complete absence of an
organ or its primordium
Aplasia : indicates incomplete development of an
organ
Hypoplasia : means underdevelopment of an
organ
Atresia : 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

30. 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

32. 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

33. 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

34. * 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)
b)
c)
d)
e)
Chromosomal abnormalities
Localized chronic infection
Lymphatic & vascular problems
Neurogenic abnormalities
Unknown

35. 
a)
b)
c)
d)
e)
f)
Clinical Features
Mental disturbances
Skin abnormalities such as
nevi
Varicosed veins
Umbilical hernia
Hemangioma
Thick & coarse hair on the
involved side

36. Oral Manifestations
a)
b)
c)
Large permanent teeth in the affected side
Premature eruption of the permanent teeth
Premature shedding of deciduous teeth on the
affected side
Differential Diagnosis:
Neurofibromatosis, Fibrous Dysplasia

37. 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





38. 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

40. 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”

41. 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