Ophthalmology anatomy of cornea Final.ppt

ANATOMY AND PHYSIOLOGY OF
CORNEA

 The cornea is front part of the eye that
covers the iris, pupil, and anterior
chamber.
 Cornea is the transparent, avascular
structure forming the anterior 1/6th of
the outer fibruos coat of eyeball.
 Smooth convex outer surface and
concave inner surface : resembles the
small watch glass
 Prolate in shape , flatter in the periphery
and steeper centrally, which creates an
aspheric optical system.

• Anterior surface of the cornea is elliptical whereas
posterior surface is sperical.
• Average diameter of cornea is 11.5mm.
• Horizontal diameter of the anterior surface is 11.7 mm and
vertical diamter is 11mm.
• The radius of curvature of cornea is 8mm.

•Corneal Epithelium = Surface
Ectoderm
•Stroma = Paraxial Mesoderm
•Descemets membrane = Paraxial
Mesoderm
•Endothelium = Paraxial Mesoderm

 Anomalies of size and shape of cornea
 Microcornea
 Megalocornea
 Cornea plana
 Congenital anterior staphyloma
 Anomalies of corneal structure and clarity
 Anterior embryotoxon
 Posterior embryotoxon
 Corneal keloids
 Dermoids
 Axenfeld and Rieger anomaly
 Peters anomaly
 Circumscribed posterior keratoconus
 Sclerocornea
 Congenital hereditary endothelial /congenital stromal corneal dystrophy

corneal horizontal diameter
< 10 mm (adult)
< 9 mm (newborn-2yrs)
Cause: arrest in the growth of cornea
in 5th month or overgrowth of
anterior tips of optic cup
• Autosomal dominant inheritence
• Equal sex predilection
 Ocular association: angle closure
glaucoma, congenital cataract,
microphakia, optic nerve
hypoplasia, anterior segment
dysgenesis, hypermetropia
 Systemic association: myotonic
dystrophy, fetal alcohol syndrome,
achondroplasia, ehler’s danlos
syndrome.

• corneal horizontal diameter > 13 mm (adult) and > 12 mm (birth-2yrs)
Cause:
failure growth of the optic cup X-linked recessive inheritance rarely AR
Males>female.
Ocular association: iris translucency ( diaphany), miosis, goniodysgenesis,
cataract, ectopia lentis, arcus juvenilis, and glaucoma ,High myopia, astigmatism
Systemic associations : craniosynostosis, frontal bossing, hypertelorism,
facial anomalies, dwarfism, facial hemiatrophy, intellectual disability, hypotonia,
Down syndrome, Marfan syndrome, Alport syndrome, osteogenesis imperfecta,
mucolipidosis type II,

 Very rare unilateral conditions
 both characterized by protrusion of the
opaque cornea between the eyelids at
birth.
 Differ only in the presence of a uveal lining
of the cornea in congenital anterior
staphyloma
 Congenital broad limbus superiorly with an
otherwise normal anterior segment
representing merely a broad transition
from sclera to cornea.
 The term also is used to describe an
appearance similar to arcus senilis (arcus
juvenilis) present at birth.
 often sporadic, autosomal dominant and
autosomal recessive pedigrees have been

 Most frequently seen anomaly, with the prevalence being
reported as high as 24% in a random population
 It consists of thickening and anterior displacement of
Schwalbe’s line, seen in slit lamp in temporal cornea
 when present alone, this has no functional significance.

 white, glistening, protuberant lesions that involve all or part of the
cornea.
 result from trauma / ocular inflammation, may be present at birth.
 Histopathologically: irregular array of collagen bundles, fibroblasts,
and capillaries arising in the corneal stroma.
 In otherwise healthy eyes, keratoplasty is appropriate.
 dissection of the lesion from the cornea followed by covering with
a conjunctival flap may halt progression.


 Usually at the inferotemporal limbus
but may involve larger areas of the
cornea, the entire limbus, the entire
cornea, or the interior of the eye.
 It is round, domed, and pink to white
to yellow in color.
 Induced astigmatism, even amblyopia,
may be present.
 Histopathology : skin-like collagen with
skin adnexal appendages, which
include hair follicles, sweat and
sebaceous glands, and fat.
 Treatment consists of simple excision.
 lesion is of sufficient depth to warrant
concurrent lamellar keratoplasty to fill
the defect.


• Axenfeld’s anomaly consists of bilateral posterior embryotoxon with iris strands adherent to
Schwalbe’s line.
 Rieger’s syndrome includes
 changes of Axenfeld’s anomaly
 Iris atrophy
 Corectopia
 Polycoria
 Glaucoma occurs in about half of the patients who have Axenfeld–Rieger syndrome
 Dental anomalies and a flattened midface and nasal bridge are also features.

• localized absence of the corneal
endothelium and Descemet
membrane leading to central
corneal opacity.
 type I: iridocorneal adhesions
 type II: characterized by a
cataractous lens or
corneolenticular adhesions.
• Associated ocular
abnormalities : congenital
glaucoma, microcornea,
aniridia, and PFV (persistent
fetal vasculator)

 Presence of a localized central or paracentral indentation of the posterior
cornea without any protrusion of the anterior surface, as is seen in typical
keratoconus.
 Amount of overlying stromal haze is also usually present.
 Loss of stromal substance can lead to corneal thinning approaching one-third of
normal

 a nonprogressive, noninflammatory scleralization of the cornea.
 may be limited to the corneal periphery, or the entire cornea
may be involved.
 The limbus is usually ill-defined, and superficial vessels that are
extensions of normal scleral, episcleral, and conjunctival vessels
cross the cornea.
 The most common associated ocular finding is cornea plana,
which occurs in 80% of cases.

Anterior surface:
It is elliptical and conces Convex.
Horizontal diameter :11.75mm (11.5 -12 mm)
Vertical diameter :10.6 mm
• Difference in the diameters due to greater overlap of sclera and
conjunctiva above and below than laterally
• Vertical diameter is more curved than the horizontal diameter thus
leading to astigmatism with the rule .
• In contrarary horizontal diameter is more curved than vertical in older
age .

Posterior Surface:
it is Circular and Concave.
Horizontal diameter:11.5mm
Vertical diameter : 11.5 mm

• Since vertical diameter is more curved in younger age group,
corneal incisions at vertical meridian is useful during cataract
surgery.
• But in older age group temporal incision is better during cataract
surgery

central = 0.52 mm
peripheral = 0.67 mm
 Applied anatomy
 Calculation of corneal thickness is important in IOP
estimation.
 High corneal thickness may lead to artifactually elevated IOP
and vice versa.
 Central corneal ulcers are more prone to perforation than
peripheral corneal ulcers.

 Useful in follow up of patients with corneal odema due to
decompensation eg. Fuch’s dystrophy or in cases of corneal
thinning eg. Keratoconus, ulcer.
 Methods of measuring corneal thickness:
 Ultrasonic pachymetry
 Optical pachymetry
 Optical Coherence Tomography (OCT)
 Laser Inferometry
 High resolution ultrasonography

 Central region is also known as optical zone has radius of curvature
Anterior surface = 7.8mm
Posterior surface = 6.5mm
 Periphery region is more flattened.
 Corneal curvature is greater than that of sclera thus slight furrow
(sulcus sclerae) separates it from sclera.
 Corneal apex /cap- a small zone of 2-4 mm with spherical anterior
curvature located decentrally up and out relative to visual axis but
correctly aligned for pupillary aperture varies from apex to limbus.

 Flattening is greater nasally than temporally and above than
below. More steeper in infants. Flatter in men than women.
 Near the limbus, corneal curvature increase before entering
the trough like contour of limbal zone.

A.
 Progressive corneal steepening, most
typically inferior to the center of the
cornea.
 Hallmark is stromal thinning, related to
alterations in enzyme levels in the
cornea, causing stromal degradation
 Primary: congenital
 Secondary: following trauma, VKC,
Down’s syndrome
 Eye rubbing is strongly associated with
the development of keratoconus.

• Thinning of the corneal apex, scarring
at the level of Bowman’s layer, and
deep stromal stress lines(Vogt’s striae)
that clear when pressure is applied to
the globe.
• A ring of iron deposition accumulates
in the epithelium at the base of the
cone (Fleischer ring).
• Protrusion of the lower eyelid on
downgaze (Munson’s sign)
• Focusing of a light beam shone from
temporally across the cornea in an
arrowhead pattern at the nasal limbus
(Rizutti’s sign)

• Dark reflex in the area of the cone
on observation of the cornea with
the pupil dilated using a direct
ophthalmoscope set on plano
Charleaux’s sign (oil droplet sign)
• In addition, a scissoring reflex can
be found on retinoscopy.
• acute corneal hydrops may occur,
in which an abrupt rupture of
Descemet’s membrane results in
acute overhydration of the cornea
and accumulation of lakes of fluid
within the corneal stroma.

• Cornea becomes extremely thin
changes to globular shape.
• Degenerative non-inflammatory
disorder.
• Causes corneal thinning (margins)
resulting in a spherical, slightly
enlarged eye.
 Ocular association: blue sclera,
Leber congenital amaurosis

 Corneal radius of curvature reading 33-35
D is common, producing high
hypermetropia with astigmatism, myopic
astigmatism, poor acuity.
 AD and AR forms are related with
mutation on KERA gene which codes for
keratin sulfate proteoglycan.
 Occular association Shallow anterior
chamber, angle closure glaucoma,
sclerocornea, microcornea,
microphthalmos, Peter’s anomaly, iris
abnormality.

• Most of the refraction of the eye occurs at the front surface of the cornea at the
air-tear interface.
• Cornea contributes to the 70% ( 43D) of the total refractive power of eye i.e
58.60D
Refractive power
 Anterior surface : +48 D
 Posterior surface : -5 D
 Net refractive power: +43 D
 Central 5 mm area forms the powerful refractive surface
Refractive index =1.37
Refractive surgeries aim to correct refractive errors by changing the corneal
curvature and shape.

 Makes up approximately 5%–10% of
the total corneal thickness. The
epithelium and tear film form an
optically smooth surface.
 It is stratified, squamous, non-
keratinised type.
 50 - 90 micrometer thick and 5 -6
layers of cells.
 Corneal epithelium becomes
continous with bulbar epithelium at
the limbus (differs: has no goblet cells)
 Sheds and germinate at regular
interval replaced by growth of basal
cells.
 Entire epithelium is replaced in 6-8
days.

• Superficial/Apical cell layer-
• 2 layers of flattened cells. Broad
and flattened cells: 4 to 5 µm thick,
40 to 50 µm in diameter.
• Freshly emerged surface cells are
bright, darken when mature.
• Exhibit surface microvilli or
microplicae, exaggeration of the
plasma membrane infoldings,
which stabilize the deep precorneal
tear film.

• Tight junctions surrounding the cell circumference near the apical
margin.
• The lateral and basal membranes of the apical cells have
, , and numerous membrane-
bound vesicles.

• Intermediate layer/ layers of
Wing or Umbrella cells
• Polygonal shapes with large ovoid
nuclei. 12 to 15 µm in diameter.
• Cytoplasm contains few rough
endoplasmic reticulum cisternae,
mitochondria, Golgi's complexes.
• Desmosomal and gap junctions are
seen between adjacent wing cells
and between basal and apical cells.

 Deepest layer / Basal cells
 Elongated polygonal cells, 10 µm
width and 15 to 20 µm height,
prominent ovoid nuclei.
 Palisade-like manner on basal lamina.
 Germinative layer of the epithelium.
 Mitosis occurs in irregular clumps of
three to six cells, more numerous in
the periphery.

 Superficial flattened cells are attached to each other by
• Zonula occludentes (tight junctions)
• Desmosomes
• Maculae occludentes
 Wing cells: Desmosomes and large gap junctions
 Basal columnar cells: Desmosomes
Maculae occludentes
Hemidesmosomes
 Tight intercellular junction acts as the barrier to entry of water,
electrolytes,glucose,etc. thus maintains the epithelial transparency.

At limbus
 CORNEA-stratified,
nonkeratinised squamous
epithelium –
 CONJUNCTIVA-stratified,
nonkeratinised columnar
epithelium with mucin secreting
goblet cells
 The limbal stem cells probably
reside in the basal layer of the
alisades of Vogt

• The corneal epithelium undergoes a constant process of cell
renewal and regeneration.
• Regenerates approximately every 7 days.
• Proliferative reserve is in the form of multipotent stem cells
• Hypothesis- Stem cells flourish only in limbal area because
of rich in - vascularity.

 X vector - combination of proliferation and centripetal migration of the
basal epithelial cells.
 Y vector- As the basal epithelial cells divide they give rise to
suprabasal cells that form the stratified layers of the cornea.
 Z vector - shedding of squamous epithelial cells from the surface of
cornea into the tear film.

 Irregularity of the corneal epithelium
disrupts the smoothness of cornea-air
interface affecting the visual acuity (eg:
post LASIK surgery)
 In vitamin A deficiency, corneal
epithelium expresses keratins (normally
found only in cornified epithelium or
epidermis of skin)

 Epithelial defect
• loss of epithelium can be;
 Superficial without inflammation-
abrasion or erosion
 Deep with inflamation in surrounding
cornea- ulcer
 Stained with fluorescein green
 Epithelial odema
Impairs vision more than the stromal
oedema
 Epithelial deposition of iron occurs in
keratoconus forming Fliescher ring

 Secreted by basal cells
 0.5 – 1 micrometer wide
 Consist of superficial lamina lucida and deep lamina densa
 Blends indistinctly into Bowman’s membrane via array of short
anchoring fibrils.
 Adhered with basal cells via hemidesmosomes.
 Composed of collagen and glycoproteins.

1. Abnormal basal lamina lead to recurrent erosions and
epithelial defect.
2. Ageing and diabetes : It becomes thick and multilaminated
3. Epithelial oedema- adherence between basal lamina and
basal cells get less firm thus gets readily detached.

 Narrow acellular homogenous zone.
 8-14 micrometer thick.
 Contains condensed collagen fibrils (type V )
 It’s the condensed superficial part of stroma.

 Binds stroma anteriorly with basement membrane of
epithelium.
 Once destroyed, does NOT regenerate but replaced by
coarse scar tissue.
 Relatively resistant to infections and trauma.
 Perforated in many places by unmyelinated nerves in
transit to corneal epithelium.

 Wounds and ulcers penetrating into the bowman’s membrane,
new collagen fibres are produced in irregular pattern during
healing forming corneal opacity.
TYPES
 Nebular opacity
 Faint opacity
 Scars involving superficial stroma along with bowman’s
membrane
 Interferes with vision
 Irregular astigmatism

 Macular opacity
scarring involves bowman’s membrane +1/2 of stroma.
 Leucomatous opacity
scarring involves bowman’s membrane +>1/2 of
stroma.
 Corneal facet
depressed corneal scar.
 Kerectesia
buldging opacity(weak scar).

In normal or raised IOP bowman’s
membrane is under tension and
appears smooth
Series of convex ridges develop at its
surface known as chicken wire
network seen when tension is relaxed
as in corneal indentation, applanation
tonometry, hypotony, corneal
manipulation during surgery and
application of pressure bandage
Responsible for anterior corneal Mosaic
, which may be induced at the surface
of normal cornea by massaging the lid

 Comprises 90% of corneal
thickness.
 0.5 mm thick
 Composed of
i) collagen fibrils /lamellae
ii) cells embedded in the
hydrated matrix of
proteoglycans.

Lamellae
 Many layered : 200-300 centrally
500 peripherally
 Each lamellae comprises of a band of collagen fibrils arranged parallel
to eachother and to the corneal plane.
 Most predominant type I Collagen
Other: Type V,VI, XII, XIV
 Becomes continuous with scleral lamellae at the limbus.
 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: parallely arranged central lamellae adopt
a concentric configuration at limbus forming a weave

Clinical significance
 Corneal transparency is due to regularity and fineness of collagen
fibrils and the closeness and homogeneity of their packing.
 Parallel arrangement of fibrils makes dissection easy during
superficial or lamellar keratoplasty.
 Weave pattern at peripheri=
 Gives strengh to peripheral cornea
 Maintains corneal curvature.

 Lipid deposition in stroma with
ageing results in arcus senilis
and in hypercholesterolemia
leads to arcus juvenilis
 Stromal dystrophy shows
deposition in anterior stroma
 Hyaline (Macular dystrophy)
 Amyloid (lattice dystrophy)
 Mucopolysaccharides (Granular
dystrophy)

1. Keratocytes
 2.5 - 5 % of stromal volume.
 Long, thin and flat cell with eccentric
nucleus parallel to corneal surface.
 long branching processes forming
contacts with other cells in the same
horizontal plane.
 However anterior-posterior connections
between keratocytes in adjacent planes
do not occur.
 Produces ground substance and
collagen during embryogenesis and
after injury.

2. Wandering cells
migrate from marginal loops of corneal blood vessels
3. Histiocytes
4. Lymphocytes
5. Dendritic ( langerhan’s cells ) present in fetal corneal stroma
disappear in the mature cornea except in the peripheri.
However in response to injury they appear in the central
cornea too.

 Strong homogenous layer, Binds stroma posteriorly, unlike bowman’s
membrane it is sharpely defined highly elastic.
 Represents the basement membrane of endothelium
 Made up of i) collagen (type IV )
ii) glycoproteins, proteoglycans (stains brilliant pink Periodic acid
Schiff)
 Thickness varies with age
 at birth: 3-4 micrometer
 children: 5 micrometer
 adults: 10-12 micrometer

 Resistant to chemical agents, trauma, infection, pathological
process.
 Regenerate even if destroyed.
 Remains in a state of tension thus curls if torn,
 In the peripheri ends as Schwalbe’s line, also marks the internal
landmark of corneal limbus.

1. Descemet’s membrane may remain intact
even in severe corneal ulceration and
maintain the integrity of the eyeball even
when the whole stroma is sloughed off by
forming descemetocele.
2. Descemet folds are seen in corneal
oedema.
3. Descemet’s tears are seen in congenital
glaucoma (Haab striae)
4. Fuch’s dystrophy –abnormal
descemet’s membrane secreted –forms
central wart like excrescences called
guttattae (Increased endothelial
permeability)

 The endothelium is made up of closely interdigitated cells
arranged in a mosaic pattern. It is single layer.
 Contains hexagonal cuboidal cells.
 Diffrentiate from limbal area at earliest developmental
stage.

 Cell density of endothelium:
at birth: 6000 cells/mm2
Count decreases by 26% by age 1 yr
Further decrease by 26% by age 11 yrs
Rate of loss slows and stabilises around middle age
Adults : 2400 (1500-3000 )
Cell number decreases with age because there is NO
mitosis.
Defect caused by dying cells fulfilled by enlargement of the
remaining cells (polymegathism), where cells increase in
area but decrease in size.

• Endothelial cells are attached to the descemets membrane
by hemidesmosomes and laterally to each other by tight
junctional complexes.
• This maintains a barrier from the aqueous humor.
• Endothelial layer is responsible for maintaining the water
balance of stroma and thus the transparencyof cornea by
active pump mechanism.
• If the endothelial pump is dysfunctional, it will result in
corneal edema.

• Endothelial cell count is done by specular microscopy (mosaic
pattern).
• Minimal endothelial cell count for maintainence of normal
corneal function=1000.
• Corneal decompensation occurs if 75% are lost i.e cell count
<500cells/mm2.

CLINICAL SIGNIFICANCE
 Surgeries affect the endothelial cell count (cell loss around 8-10%)
Egs: Cataract surgery( min count 1000-1500), Graft of PK( min
count-2000)
 In Keratoconus or DM patients, it is seen that endothelial
morphology changes without a decrease in cell density.
 Corneas with low cell density do not tolerate intraocular surgery
 Accelerated cell loss seen in Fuch’s endothelial dystrophy.
 Posterior polymorphous dystrophy endothelium gets multilayered
(pseudoepithelium).

 Cornea is avascular.
 Small loops of vessels which are
derived from the anterior ciliary vessels
invade its periphery for about 1 mm.
 Corneal transparency is also due to its
avascularity
 Corneal neovascularization: sprouting
of perilimbal vessels
 Cornea is immunoprivileged site with
respect to graft rejection due to its
avascularity.
 Delayed wound healing after corneal
ulcer, laceration and keratoplasty due
to avascularity.

Trigeminal nerve
Opthalmic division
Nasociliary nerve
Long ciliary nerves
Enter eyeball around optic nerve with short ciliary nerve
Run forward in the suprachoroidal space

• A short distance from limbus, pierce the sclera to leave the
eyeball
• Divide into 2 distinct part and connect with each other and
conjunctival nerves.
 Pericorneal plexus: 60-80 trunks(myelinated)
• Enters the cornea at various levels-sclera, episclera and
conjunctiva
• After going 1-2mm in the stroma, myelin sheath is lost and
brach dichotomously and form stromal plexus
• Some end in mid-stroma and some pass anteriorly and forms
sub-epithelial plexus.

• Fibres from subepithelial plexus penetrate pores in
Bowman’s membrane and lose their Schwann’s sheath then
divide into filaments under basal layer of epithelium
• Filaments extends between the layers of epithelial cells and
form intraepithelial plexus
• Ends as fine beaded filaments.

• Cornea is highly innervated thus corneal erosions and ulcer
are highly painful.
• Loss of corneal sensation can predispose to neurotrophic
ulcers as in leprosy, diabetes.
• Prominent corneal nerves can be seen in;
 Ocular conditions like keratoconus, keratoconjunctivitis
sicca, Fuch’s endothelial dystrophy, trauma, congenital
glaucoma.
 Systemic conditions like leprosy, neurofibromatosis,
Refsum’s disease, ichthyosis, normal variant with increasing
age.
• Perineuritis seen in acanthamoeba keratitis

Ophthalmology anatomy of cornea Final.ppt

Ophthalmology anatomy of cornea Final.ppt

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Ophthalmology anatomy of cornea Final.ppt