anatomy and physiology of cornea

1. APPLIED ANATOMY
AND PHYSIOLOGY OF
CORNEA
Moderator: Presenters:
Gauri S. Shrestha Aayush Chandan
Aastha Subedi
IOM,TUTH

2. PRESENTATION LAYOUT
 Introduction
 Embryology & clinical significance
 Dimensions with applied aspects
 Histology & applied aspects
 Vascular Supply
 Nerve Supply
 Corneal Physiology
 References

3. INTRODUCTION
 Transparent, avascular, watch glass like
structure
 Anterior 1/6th of outer fibrous coat is protective
(due to collagenous components of stroma).
 A powerful refracting surface of the eye (3/4 of
total refracting power).
 Area 1.3cm2 or 1/14 of the total area of globe.
3

4. 4

5. Embryologic origin of Cornea

6. Embryology contd.

7. Clinical significance
 Cell line originating from surface ectoderm
(e.g. corneal epithelium) has regenerative
capacity
 Cells originating from neural crest
(e.g.,stroma,DM,endothelium) has little
regenerative capacity
 Disease affecting other organ (e.g. atopic
dermatitis) may cause keratitis
 similar embryonic origin

8. Dimensions
Anterior surface
 Elliptical
 Convex
 Average horizontal diameter -
11.75mm
 Average vertical diameter-
11.0mm
Posterior Surface
 Concave
 Circular
 Average diameter – 11.5mm

9. Microcornea
Horizontal diameter
<10mm(in adults)
<9mm(birth-2yrs)
E.g.Blue Diaper
syndrome
Cytomegalovirus
(CMV) infection
Megalocornea
Horizontal diameter
 >13mm(in adult)
 >12mm(birth-2yrs)
 E.g.Marfan’s syndrome
 Ehlers Danlos syndrome

10. Corneal Thickness
Central: 0.52mm
Peripheral:0.67mm
Applied:
IOP estimation (5µm=0.1mmhg)

11. Corneal curvature
Central 5mm area → optical zone
Anterior r1= 7.8 mm
Posterior r2 = 6.5 mm
Flatter in men than in women
Refractive power
Anterior surface = +48D
Posterior surface = -5D
Net = +43D
Refractive index = 1.376
Keratometric Index=1.3375
Reflecting power=-257 D

12. Uses of Corneal curvature Measurement
-Determine astigmatism
-Fitting CL
-IOL power calculation
-Monitor keratoconus and keratoglobus
progression
Measurement of corneal curvature
 keratometer or opthalmometer(anterior)
 handheld keratoscope or placido’s disc(anterior)

13. Applied :
1. Keratoconus :
 Thinning & forward
conical bulging of
cornea
 Progressive and non
inflammatory eye
condition.
 Irregular myopic
astigmatism(scissor
reflex)
13
2.keratoglobus
 Hemispherical
protrusion of whole
cornea
 Generalised steeping &
thinning with globular
shape.
 Non-progressive,non-
inflammatory.
 Irregular myopic
astigmatism

14. 3. Pellucid marginal degeneration
 corneal thinning affecting the
inferior cornea 4 ‘o’ clock to
8 o’ clock
 Ectasia(dilation) above thinning
 Irregular astigmatism
 Also called as “beer belly” appearance.
4 Cornea plana :
 flat cornea
 results in high hypermetropia
 Congenital ,hereditary deformity.
14

15. HISTOLOGY
 Anterior epithelium
 Bowman’s layer
 Central stroma
 Descemet’s membrane
 Endothelium
 Dua’s layer(pre- Descemet’s
membrane.
15

16. 1.Epithelium
 Stratified, squamous, non-keratinized
 continuous with bulbar epithelium at limbus( lacks
goblet cells)
 50-90µm thick, 10% of total cornea
 5-6 layers of nucleated cells
 Hydrophobic
 Sheds at regular interval
 Replaced by growth of basal cells
 Entire epithelium replaced in 6-8 days
16

17. Layers of Epithelium
1. Basal cells
2. Wing/ umbrella cells
3. Flattened cells
17

18. Epithelium contd.
1.1 Basal cell layer:
 Tall, columnar, polygonal cells
 Stand in palisade-like manner on basal lamina
 Basal cells have density of approx. 6000 cells per square
mm.
 Oval nuclei, few organelles
 Germinative layer of epithelium
Epithelial stem cells located at superior & inferior
limbus possibly in the palisades of Vogt
Source of new corneal epithelium.
18

19. 19
Division of slow cycling stem
cells
Transient amplifying cells
Migrate centripetally
Cell division
Terminal differentiation
Ultimate shedding

20.  Basal cells firmly attached to other basal cells and
anterior wing cell layer by desmosomes and maculae
occludentes respectively forming tight junction
Transparency and
barrier function of
corneal epithelium
20

21. 1.2Wing cell layer:
 Comprises of 2-3 layers of polyhedral cells
 Flattened nuclei
 Lesser organelles than basal layer
1.3 Flattened cell layer:
 Constitutes 2 most superficial layers
 Long, thin cells, flattened nuclei
 Numerous desmosomes and maculae occludentes
 Zonulae occludentes present in this layer only
21

22.  Anterior cell wall of the most
superficial cells has many microvilli
and microplicae
 Coated with charged glycocalyx
Allows
hydrophilic
spread of tear
film with blink
22
Maintains
tear film
stability

23.  Basement membrane
 Secreted by basal cells
 Composed of collagen(type –VII) & glycoprotein
 Adhered with basal cells via hemi desmosomes
 Posteriorly, blends indistinctly with bowman’s
membrane
 Becomes thick with Age, Diabetes ,corneal
pathology
23

24. Applied anatomy of Epithelium
 Healthy epithelium repels dyes such as fluorescein and
rose bengal due to tight junctional complexes
 Basal hemidesmosomal system prevents detachment of
the multilayer epithelial sheet from the cornea
o Abnormalities result in recurrent corneal erosion or
ulcers
24

25. Flourescein stain in Cornea
 Fluorescein doesn’t actually stain tissues,it merely
colors the tear film.
 The normal corneal epithelium is impermeable to the
tear film & substances dissolved in it because lipid
membranes at surface of eye act as an effective barrier
against polar, water soluble substances.
 If this barrier is breached, tear film gains access to
deeper layers.
 There is pH difference between surface & deeper
tissue causing green color in the area of
desquamation.
25

26.  In vit.A deficiency, corneal
epithelium becomes
keratinized
 Keratinized cells produce an
epithelial keratitis with
subsequent vascularization of
the cornea
 Fleischer rings are pigmented
rings in peripheral cornea due
to iron deposition in basal
epithelial cells .
 Usually yellowish to dark
brown may be complete or
broken.
26

27. Iron deposition located at corneal edge of
regressive pterygium: Stocker’s Line which
is punctate ,brownish,subepithelial line
passing vertically in front of invasive apex of
pterygium.
27

28. Microorganisms invading intact
cornea
28

29. 2.Bowman’s Membrane
 Acellular homogeneous zone
 Condensed superficial part
of stroma
 condensed collagen fibrils
 8-14µm thick
 Binds stroma anteriorly with
BM of epithelium
 Resistant to infection and
injury
 Does not regenerate
29

30. Applied anatomy of Bowman’s m/m
 Corneal opacity
Mechanism:
Wound and ulcers penetrating
Bowman’s m/m
New collagen fibers produced in
irregular pattern
Wound is healed by fibrosis
leaving behind opacity
30

31. Types of corneal opacity
1. Nebular opacity:
 Faint opacity
 Scars involving superficial stroma
along with bowman’s membrane
 Interferes with vision
 Irregular astigmatism
2. Macular opacity:
 Semi dense opacity
 Scarring involves bowman’s m/m
+ ½ of stroma
31

32. 3.leucomatous opacity
 Scarring involves bowman’s m/m +
>½ of stroma
32

33. 4.Adherent Leucoma:
results when healing occurs after perforation of
cornea with incarceration of iris
33

35.  BM appears smooth, is under
tension .By releasing
tension,reproducible polygonal
ridge pattern becomes manifest.
 Convex ridges can be seen when
tension is relaxed – POLYGONAL /
CHICKEN WIRE PATTERN
 In prolonged hypotony and
atrophia bulbi,degenerative
changes in the ridges projecting
into epithelium contribute to
secondary anterior crocodile
shagreen.
35

36. 3.Stroma (Substantia Propria)
 0.5mm thick, 90% of total cornea
 Composed of :
–Collagen fibrils(type I) (lamellae)
–cells (keratocytes)
– ground substance
(proteoglycans)
36

37. Lamellae
 Arranged in many layers
-(200-300 centrally)
-(500 peripherally)
 Parallel to each other and corneal surface
 Continuous with scleral lamellae at limbus
37

38.  Anterior 1/3rd stroma: oblique orientation
 Posterior 2/3rd stroma: alternating layer of
lamellae at right angle to each other
 X-ray diffraction study shows: parallelly
arranged central lamellae adopt a concentric
configuration at limbus forming a weave
38

39. Keratocytes
 Occupy 2.5-5% of stromal volume
 Long, thin, flattened cells running
parallel to corneal surface
 eccentric nucleus
 long branching processes
 Synthesis of stromal collagen and
proteoglycan during development and
injury
39

40. Besides keratocytes, some other cells are also
found in corneal stroma:
 Wandering macrophages
 Histiocytes
 Lymphocytes
 Polymorphonuclear leucocytes (very rarely)
40

41. Applied anatomy of stroma:
 Regular arrangement of lamellae accounts
for transparency of cornea
 Weave pattern at periphery :
- provides strength to peripheral cornea
- maintains corneal curvature
41

42.  Arcus senilis: lipid
deposition in
peripheral cornea with
ageing
 Cornea farinata : flour-
like deposits in the
deep stroma
42

43. Primary lipid keratopathy:
white or yellowish stromal
deposits consisting of
cholesterol, fats and
phospholipids.
VOGT Striae ;:Very fine,
vertical, deep stromal lines
(keratoconous)
43

44. Sclerocornea
 Primary anomaly in which scleralization of
the pheripheral part of cornea,or of the
entire tissue occurs.
 A type of mesodermal dysgenesis
 Precise arrangement of stromal lamellae
is absent
 Non-progreesive,usually
bilateral,asymmetric

46. 4.Descemet’s membrane (Posterior limiting
layer):
 Basal lamina of corneal endothelium
 Strong homogenous layer
 Binds stroma posteriorly
 Thickness varies with age:
-3µm at birth
-10-12µm in adults
 Posteriorly endothelium & DM are attached by
modified hemidesmosomes
46

47. Descemet’s membrane contd..
 Composed of: -collagen (type IV)
-glycoproteins
 Resistant to trauma, chemical agents & pathological
processes( barrier to perforation in deep corneal ulcer)
 Normally, it stays in tension & curls if torn
 Regenerable
47

48. Descemet’s membrane contd..
 Peripherally, ends as schwalbe’s line
 With age, round wart like excrescences are seen in posterior
periphery called – Hassel-Henle bodies
48
Internal landmark of corneal limbus.
Anterior limit of Trabecular meshwork
Prominent and anteriorly displaced in Posterior
embryotoxon(seen in slit lamp as a irregular white
line just concentric with and anterior to limbus)

50. Applied anatomy of DM:
 remains intact even in severe corneal ulceration
 maintains the integrity of eyeball even when the whole
stroma is sloughed off by the descemetocele
 Descemet’s folds are seen in corneal edema
 Haab’s striae: break in descemet’s m/m, seen in
congenital glaucoma
50

51.  Copper pigment deposition in
descemet membrane: Wilson’s
disease:
51
It is a genetic disorder in which
copper builds up in the body;
typically affecting brain and liver.
Kayser-Fleischer’s rin

52. Corneal guttata of vogt:
 Drop-like excrescences in posterior surface o f DM
similar to Hassal-Henle bodies
 May occur independently or in Fuch's
dystrophy(endothelial cells die off ,fluid fills up and
cornea gets swollen and puffy)
52

53. Dua’s layer
53
15 um thick
Between corneal stroma and
Descemet’s membrane
Strong and impervious to air.
It doesn’t extend to the periphery.
Primararily type –I collagen.

54. Clinical significance
 Involved in posterior
corneal pathology
 Acute hydrops
 Pre- decemet’s
dystrophies.
 Significant in DALK
54
Also called leaking of
aqueous.
A build up fluid in cornea
,common in patient with
keratoconus
Caused by tear in Dua’s layer.
It is due to
Dua’s layer
,the cornea
doean’t
perforate in
hydrops even
after
Descemet’s

55. 5.Endothelium
 Hexagonal nonreplicating monolayer
 Cell density at birth:- 6000/mm3
falls by 26% in 1st year
further 26% lost in 11 year
rate slows down, stabilizes in
mid-age
 Defect left by dying cells is filled
by enlargement of remaining
cells : polymegathism
 Considerable functional reserve:75%
of adult age cell (500 cells/mm2)
55

56. Endothelium contd..
 Cells of endothelium are firmly bound together by cell
junctions including maculae adhaerentes, maculae
occludentes
 Endothelial cells are attached to DM by
hemidesmosomes
 These linkage maintains barrier function of
endothelium
 Maintains an effective barrier from aqueous humour
56

57. Endothelium contd..
 Maintains the water balance of stroma &
transparency of cornea by active pump mechanism.
 Dysfunction of endothelial pump leads to corneal
oedema
57

58. Applied anatomy of endothelium:
 In Keratoconus or Diabetic patients, endothelial
morphology changes without decrease in cell density
 Disrupted by excrescences of DM
 Loss of Endothelium in Fuch’s dystrophy
(reduction in Na+,K+-ATPase pump activity)
58

59. Keratitis
 Condition in which cornea become inflamed
characterized by
 May be ulcerative or non- ulcerative type
 Ulcerative keratitis leads to corneal ulceration
causing thinning of Cornea.
59
Corneal edema
Cellular infiltration
Ciliary congestion

60. 60
Bacterial keratitis Fungal keratitis
Viral keratitis
Superficial punctate
keratitis

61. Blood Supply
 Avascular Structure
 Small loops derived from anterior cilliary
vessels invade its periphery for about 1mm &
provide nourishment
 Important factor in corneal transparency
 Helps to establish “Immune Privilege” that
gives some protection against rejection of
grafts
 Corneal Neovascularisation : Sproutting of new
vessels from the perilimbal capillaries(in

63. Nerve Supply
 Densely innervated with sensory fibers
70-80 large nerves,branches of
long & short ciliary nerves ,enter
peripheral stroma
Lose their myelin sheath after
passing 2-3mm into cornea,but
covering from schwann cells
remains
Branching occurs and 3 nerve
networks are formed

64. Stomal plexus
• Located in
midstroma
Subepithelial
plexus
• Located in
region of
bowman’s
layer &
anterior
stroma
Intraepithelial
plexus
• Located in
epithelium
• Here nerves
from stromal
and
subepithelial
plexus
meets

66.  As sensory nerves pass through bowman’s
layer,schwann cell covering is lost & fibers
terminate as free nerve endings
 No nerve endings are located in Descemet’s
membrane or the endothelium
 Density of sensory nerve endings in the
epithelium is approx.400 times than that of
epidermis of skin(7000 nocireceptors per
square mm in the cornea)
 Individuals with corneal anesthesia & loss of
nerve endings may have increased epithelial
permeability,reduced mitosis,decreased cell
adhesion & impaired wound healing.

67. Assessing corneal sensitivity
 Can be measured by gently
touching the cornea with a
wisp of cotton from a swab
& initiating a blink response
 Quantitatively by
Esthesiometer

68. Corneal sensitivity
also decreases with:
-Corneal disease (herpes
simplex keratitis,
diabetes, corneal
dystrophies,
keratoconus,exposure
keratitis)
-Following surgical
procedures
-Application of
anesthetics,
-NSAIDs
-Contact lens wear
-Thyroid disease

69. Corneal Physiology

70. Functions:
 Acts as powerful refracting surface
 Protect intraocular contents
 Absorption of topically applied drugs
 Wound repair after anterior segment
surgery or trauma

71.  These functions of cornea are governed by
following physiological processes:
 Biochemical composition of cornea
 Metabolism of cornea
 Corneal transparency
 Drug permeability through the cornea
 Corneal wound healing

72. Biochemical composition of cornea
80
20
-Water 80%
-Solids 20%
water stroma

73. SOLID COMPONENTS
 COLLAGEN 15 %
Type I 50-55 %
Type III <1%
Type IV 8-10 %
Type VI 25-30 %
 OTHER PROTEIN 5%
 KERATAN SULPHATE 0.7%
 CHONDRITIN/ DERMATAN SULPHATE 0.3%
 HYALURONIC ACID &SALTS 1%

74. • 70% of total wet weight
water
• Synthesis is 5X of stroma and 2X of
descemet’s membrane & endothelium
Protein
• 5.4% of dry epithelium
• Mainly present in cell membrane
• Phospholipids and cholesterol
lipids
Epithelium

75. • Necessary for glycolysis,kreb’s cycle
and active transportation
Enzymes
• Na,K,Cl
electrolytes
• Glutathione
• Ascorbic acid
• Ach
• cholinesterase
others

76. Stroma
 Water (75-80%)
 Solids (20-25%)
-Extracellular collagen(Type I,V,VI,XII & XIV)
-soluble proteins( Albumin, immunoglobulin &
glycoproteins)
-proteoglycans- keratan sulphate(50%)
-chondroitin sulphate(25%)
-chondroitin(25%)
(plays important role in maintenance of corneal
hydration level and transparency)
-Enzymes (glycolytic and kreb cycle’s enzymes)
-Matrix metalloproteinases(maintains normal corneal
framework)
-Electrolytes (Na , Cl )

77. Descemet’s membrane
 Collagen(73%) & glycoprotein
 Collagen is insoluble and extremely resistant
to chemicals and enzymatic actions ,
accounting for resistant to chemical agents ,
infection and barrier perforation in deep
corneal ulcers.
Endothelium
Contains enzymes for glycolysis and Kreb’s
cycle

78. Metabolism of cornea

79. Metabolism is mainly required to
produce energy for the maintenance of
 Transparency
 Relative state of dehydration
 Most active part – Epithelium
 Second most active part -
Endothelium

80. SOURCES OF NUTRIENTS
REQUIRED FOR METABOLISM
Oxyge
n
• Epithelium – dissolved oxygen from
atmosphere into tear film, through limbal
capillaries
• Endothelium – Aqueous humour
glucos
e
• prime source of energy.
• Aqueous is the main source
• Negligible amount comes from tear film and
perilimbal capillaries.
Amino
acids
• Aqueous is the main source –
principally by passive diffusion

82. Metabolic pathways in cornea
 Anaerobic Glycolysis (2 ATP)
 Kreb’s Cycle (36 ATP)
 HMP shunt (NADPH)

83. Corneal Transparency

84. Factors affecting corneal
transparency
 Anatomical factors/physical factors
 Tear film and corneal epithelium
 Arrangement of stromal lamellae
 Corneal vascularization
 Absence of myelinated nerve
lymphatics
 Physiological factors
 Corneal hydration

85. Tear film and corneal
epithelium
 Forms an optically smooth and
homogenous layer over anterior surface
of cornea
 Fills up small irregularities of corneal
surface
 Normal epithelium is transparent –
homogenicity of Refractive Index
 Tight intercellular junctions i.e.
desmosomes and maculae occludentes

86. Arrangement of stromal
lamellae
 Collagen fibrils of Stroma bundled
together in the form of lamellae
 Arranged parallel to each other as well as
to the surface.
 Two theories has been proposed –
 Maurice theory
 Theory of Goldman et al.

87. Maurice theory
 It states that:
Cornea is transparent because the uniform
collagen fibrils are arranged in a regular lattice
so that the scattered light is nullified by
MUTUAL INTERFERENCE.
Fibrils are arranged regularly in a lattice form,
separated by less than a wavelength of visible
light wave ( 4000 to 7000 A ).

88. Electron microscopy suggests
absence of lamellar arrangement

89. Theory of Goldmann et al
 nullifies the need of lattice arrangement to maintain
transparency by DIFFRACTION THEORY
 fibrils are small in relationship to the light and will
not interfere with light tranmission unless they are
larger than half of a wavelength of visible light i.e.
2000A.
 Further confirmed by – ‘LAKES’ – areas devoid of
collagen having dimension more than 2000A, in
edematous hazy cornea, mainly found around

90. Corneal vascularization
Pathological incidents leads to corneal
vascularisation :
 Invite defense mechanism against noxious
agents.
 Nutrition
 Transport of drugs
However, progressive corneal vascularisation is
HARMFUL

91. Theories explaining corneal avascularity
chemical
Role of VIF Role of VSF
mechanical combined

92. Chemical theory
 Role of VIF(meyer and chafre)
-Avascularity of cornea is due to
presence of VIF(sulphate ester of
hyaluronic acid)
 Role of VSF((campbell and
michaelson,1949)
Release of VSF at the site of insult
which diffuses through stroma upto the

93. Mechanical theory(cogan)
 Compact structure of the cornea prevents
vascularisation
 Loosening due to edema causes
neovascularisation
 However, vascularisation is not seen in many
edematous cases such as Fuch’s dystrophy and
aphakic bullous keratopathy

94. Combined theory
 Demonstrated by Maurice et al
Release
of VSF
Structural
loosening of
compact
corneal
stroma by
edema
neovascularisatio
n

95. Absence of myelinated nerve
lymphatics
 Corneal nerves loose their myelin sheaths at
1-2 mm away from limbus
 Thin and sheath-less nerves produces very
little scattering of light.

96. Corneal hydration
 Cornea has the highest water content than
any other connective tissue in the body i.e.
78%
 Four Factors are responsible for keeping the
water content constant
A. Factor which draws in water stromal
swelling pressure
B. Factor preventing inflow of water
Barrier mechanism
C. Factor which pump out water from cornea
Metabolic pump

97. Stromal swelling pressure
 Pressure exerted by GAG in corneal
stroma(60mm Hg)
-These have anionic effect on the tissue & therefore
sucking the fluid with equal negative pressure
IMBIBITION PRESSURE
In vitro : IP=SP
In vivo : IP changes with IOP
IP=IOP-SP(17-60=-43)
Therefore,corneal edema is imminent when IOP>SP

99. Barrier mechanism
-Barrier function is exerted by both Epithelium
and endothelium
-Barrier to excessive flow of water & electrolytes
into stroma due to semipermeable nature.

101. Active pump mechanism
 mainly in endothelium
-Na+/K+ ATPase pump system
-Na+/H+ pump system
-Bicarbonate dependent ATPase
-Carbonic anhydrase enzyme

102. Evaporation of water from corneal
surface
Evaporation leads to increased osmolarity of
precorneal tear film
Hyperosmolarity of pre-corneal tear film draws
in water from cornea
Helps maintaining dehydration of cornea

103. Drug permeability across cornea
 Factors affecting drug penetration through
the cornea are :
1. Lipid and water solubility of the drug
2. Molecular size, weight and concentration of
drug
3. Ionic form of the drug
4. pH of the solution
5. Surface active agents
6. Tonicity of the solution

104. 1. Lipid and water solubility of the drug
Epithelium and endothelium are lipophilic
whereas stroma is hydrophilic , so the drug
should be amphipathic
2. Molecular size, weight and concentration of drug
- lipid soluble molecules can cross irrespective of
size.
- water soluble molecules(less than 4A can only
pass).
- molecular weight of less than 100 can pass readily
whereas that of more than 500 cannot pass.
3. Ionic form of the drug
-must exist in both ionic and non-ionic form.
-only non-ionized can pass through
epithelium.

106. 4.pH of the solution
-Normal range : 4 to 10
-Any solution outside this range increases
Permeability
5. Surface active agents
-Agents which reduce surface tension,increase
corneal wetting and ,therefore ,present more drug
for absorption
Eg.Benzalkonium chloride

107. 6. Tonicity of the solution
-Hypotonic solutions increase permeability
7. Pro-drug form
-Pro-drug forms are lipophilic which after
absorption
through epithelium converted into proper drug
which can easily pass through stroma
Eg. dipivefrine - epinephrine

108. Corneal wound healing
A. Epithelial wound healing
B. Stromal wound healing
C. Endothelial wound healing

109. A. Epithelial wound healing
 Corneal epithelium heals by the
sequence of
-latent/lag phase
-migration
-proliferation

110. Latent/lag phase
Cellular remodeling & changes to tear
composition in preparation for healing
Epithelial cells damaged during injury undergo
apoptosis & are shed into tear film
Adherent junction & gap junction are lost & basal
cells attachment are broken down
Formation of filopodia & lamelliopodia & coating
with fibronectin

111. Migration
Progressive movement of both basal and
suprabasal cell layers that are adjacent to wounded
surface , resurfaces corneal epithelial wound.
Takes over 24-36 hour

112. Proliferation
Monolayer of cells covering the defect
proliferates to restore the normal thickness of
epithelium & fill in the defect
Tight junctions form to re-establish the cornea’s
barrier function & gap junction , adherens junction &
desmosomes reform between cells

113. Epithelial reattachment
Hemidesmosomes reassemble to firmly
attach the epithelial layer
Final formation of attachment and re-
anchoring of cells can take months or longer

114. Stromal wound healing
Deposition of fibrin within the stromal woud
Rapid epithelization of wound
Activation of keratocytes to divide & synthesize collagen &
GAGs
Initial lay out of irregular fibroblast
Production of normal corneal matrix to restore
clarity in small wound

115. Endothelium wound healing
-Does not mitosis in humans
-Defects are repaired by migration and
enlargement of surrounding cells.

116. REFERENCES