Compiled by:

Abdul Saboor
MBBS batch 2028
CMH Institute of Medical Sciences Bahwalpur
Any errors, e-mail at:

[email protected]
Chapter 20 (Eye embryology) into
high-yield, exam-ready tables 📝

🔑 High-Yield Tables — Eye Embryology

1. Timeline of Eye Development ⏳

Week Event Key Notes
Early diencephalic
3rd Optic grooves form on neural folds
outpocketings
Optic vesicles evaginate; contact surface
4th Induces lens placode
ectoderm
Double-layered cup (retina
5th Optic vesicle invaginates → optic cup
layers)
Reciprocal induction with optic
5th–6th Lens placode → lens pit → lens vesicle
cup
Choroid (optic) fissure allows hyaloid artery
6th–7th Failure of closure → coloboma
entry
>7th Hyaloid vessels regress Persistence → PFV
2nd–3rd Retinal differentiation, eyelid fusion &
Eyelids reopen ~26–28 weeks
trimester reopening
2. Tissue Contributions 🧬
Embryonic Origin Derivatives in Eye
Neuroectoderm Retina (neural & RPE), optic nerve, ciliary body epithelium, iris
(diencephalon) epithelium
Surface ectoderm Lens, corneal epithelium, eyelid epidermis, conjunctival epithelium
Corneal stroma & endothelium, sclera, choroid, iris stroma,
Neural crest mesenchyme
trabecular meshwork, uveal melanocytes
Mesoderm Extraocular muscles, vascular endothelium

3. Morphogenesis of Eye Structures

Structure Developmental Origin Key Features
Inner → neural retina; Outer
Optic cup Invagination of optic vesicle
→ RPE
Lens fibers elongate, fill
Lens Surface ectoderm placode → pit → vesicle
cavity
Surface ectoderm (epithelium) + neural crest Transparent due to
Cornea
(stroma, endothelium) avascularity
Choroid
Ventral groove of optic cup Closes normally by week 7
fissure
Hyaloid Regresses → hyaloid canal
Branch of ophthalmic artery
system (Cloquet’s)

4. Molecular Regulation ⚙️
Factor Role Clinical Defect if Mutated
Master gene of eye field; lens & retina
PAX6 Aniridia, panocular malformations
induction
SHH (Sonic Splits eye field into two; regulates Holoprosencephaly, cyclopia,
hedgehog) fissure closure coloboma
FGF Lens induction, fiber differentiation Lens aplasia, congenital cataract
Patterning of retina & anterior
BMP/Wnt Anterior segment dysgenesis
structures

5. Clinical Correlates 🏥
 Malformation Embryologic Cause Clinical Presentation
Anophthalmia / Failure of optic vesicle
Absent/small globe
Microphthalmia outgrowth
Incomplete closure of optic Keyhole defect in
Coloboma
fissure iris/retina/choroid/ON
PAX6 mutation → iris fails
Aniridia Absence of iris, glaucoma risk
to form
Persistent Fetal Vasculature
Hyaloid artery fails to regress Leukocoria, microphthalmia
(PFV / PHPV)
Lens induction/fiber
Congenital cataract Lens opacity
differentiation defect
Anterior segment dysgenesis Neural crest migration defect Iris/cornea anomalies, glaucoma

6. High-Yield MCQ-style Pearls 📝

Question Answer
Master control gene of eye development? PAX6
Failure of choroid fissure closure → ? Coloboma
Origin of lens? Surface ectoderm
Retina layers origin? Neuroectoderm
Anterior chamber structures derived from? Neural crest cells
Remnant of hyaloid artery in adult eye? Cloquet’s canal

✅ Explanation (if time):

Chapter 20 — Eye (Langman’s, 15th ed.)
Below is a solid, exam-ready, and clinically useful walkthrough of what Chapter 20: Eye
covers.
It begins with a definition/introduction, then a glossary of terms, then explanatory answers
first from Sadler (Langman’s 15th ed.), then from Moore, Persaud & Torchia (The
Developing Human, 12th ed.), followed by integration of recent authoritative reviews and
articles.
Finally, it closes with clinical mapping, high-yield pearls, study tips, and references.

1) Basis — Definition & Brief Introduction

 Definition / Scope:
Eye embryology is the study of how the visual system (eyeball + adnexa) develops from
early embryonic primordia.
It begins during the 3rd–4th week of development with optic grooves in the forebrain
(diencephalon).
These grooves → evaginate into optic vesicles, which interact with surface ectoderm →
form the lens placode.
Through reciprocal inductive signaling and morphogenetic events, the optic cup forms,
and tissues differentiate into the retina, lens, cornea, sclera, and associated structures.
 Clinical Relevance:
Many ocular malformations (e.g., coloboma, aniridia, persistent fetal vasculature,
microphthalmia/anophthalmia) arise from discrete errors in these developmental
events. Understanding the timeline helps correlate embryology with ophthalmic disease
and pathology.

2) Glossary — Key Terms (Exam-Friendly)

Term Meaning
Optic groove/sulcus Early depression in forebrain → evaginates into optic vesicle
Optic vesicle Outpouching of diencephalon → induces lens placode
Lens placode → pit → Surface ectoderm thickens → invaginates → separates into lens
vesicle vesicle
Optic cup Double-layered cup (inner = neural retina, outer = RPE)
Choroid/optic fissure Ventral groove allowing hyaloid artery entry; failure → coloboma
 Term Meaning
Hyaloid artery Embryonic supply to lens/vitreous; regression failure → PFV
Neuroectoderm Retina, RPE, optic nerve, iris epithelium, ciliary body epithelium
Surface ectoderm Lens, corneal epithelium, eyelid epidermis
Corneal stroma/endothelium, sclera, uveal stroma, trabecular
Neural crest mesenchyme
meshwork
Master transcription factor of eye development; mutation →
PAX6
aniridia

3) Explanatory Answers — From Sadler, Langman’s

Medical Embryology (15th ed.)
(pp. 365–374)

3.1 Timeline & Morphogenesis

 Week 3–4: Optic grooves → evaginate as optic vesicles → contact surface ectoderm →
induce lens placode.
 Week 4–6: Optic vesicle invaginates → optic cup; lens placode → lens pit → lens
vesicle.
 Choroid fissure forms ventrally → hyaloid vessels enter; normally closes ~7th week.

3.2 Tissue Contributions

 Neuroectoderm: Retina (neural + RPE), optic nerve, iris & ciliary body epithelium.
 Surface ectoderm: Lens, corneal epithelium, eyelids.
 Neural crest + mesoderm: Corneal stroma & endothelium, sclera, choroid, trabecular
meshwork, ocular vasculature, extraocular muscles (mesoderm).

3.3 Clinical Correlates

 Coloboma → optic fissure fails to close.

 Aniridia → PAX6 mutations.
 PFV (Persistent Fetal Vasculature) → failure of hyaloid artery regression.

4) Explanatory Answers — From Moore, Persaud &

Torchia (The Developing Human, 12th ed.)
  Eye field & molecular regulation:
Defined by PAX6, RAX, LHX2 in anterior neural plate. SHH splits single eye field →
two lateral fields. Failure → cyclopia/holoprosencephaly.
 Reciprocal induction:
Optic vesicle induces lens placode → lens influences optic cup → coordinated retinal and
lens differentiation. FGF, BMP, Wnt, SHH mediate this.
 Clinical Emphasis:
o Leukocoria: PFV, cataract, retinoblastoma.
o Coloboma: keyhole iris or retinal gap.
o Microphthalmia/Anophthalmia: failure of optic vesicle growth.

5) Explanatory Answers — From Modern Reviews

(Molecular & Mechanistic)
Factor Function Defect if disrupted
Master regulator of eye field, lens & Aniridia, microphthalmia, panocular
PAX6
retina anomalies
Splits eye field, regulates fissure
SHH Cyclopia, coloboma
closure
Lens placode induction & fiber
FGF Lens aplasia, cataract
differentiation
BMP/Wnt Retina & anterior segment patterning Anterior segment dysgenesis
Hyaloid
Involves VEGF & apoptosis PFV with leukocoria
regression

6) Clinical Mapping (Quick Table)

Embryologic Event Defect if Abnormal Clinical Manifestation
Optic vesicle fails to grow Anophthalmia/microphthalmia Absent or small eye
Choroid fissure fails to close Coloboma Keyhole iris, retinal gap
Lens induction defective Congenital cataract Leukocoria
Hyaloid artery fails to regress PFV Leukocoria, retinal traction
Neural crest migration abnormal Anterior segment dysgenesis Glaucoma, iris/cornea defects

7) High-Yield Exam/Viva Pearls 📝

 Optic cup layers: inner = neural retina, outer = RPE.
 Master gene: PAX6.
 Failure of fissure closure = coloboma.
  Lens origin = surface ectoderm.
 Anterior chamber structures = neural crest.
 Remnant of hyaloid artery = Cloquet’s canal.

8) Diagram Suggestion
👉 For exams, draw 3 panels:

1. Optic vesicle contacting ectoderm (lens placode).

2. Invagination → optic cup + lens pit.
3. Lens vesicle separating; optic cup layered; hyaloid artery entering fissure.

9) References (APA, Clickable)

 Sadler, T. W. (2022). Langman’s Medical Embryology (15th ed., Chapter 20: Eye, pp.
365–374). Wolters Kluwer.
https://integratedsciences.lwwhealthlibrary.com/book.aspx?bookid=3221
 Moore, K. L., Persaud, T. V. N., & Torchia, M. G. (2024). The Developing Human:
Clinically Oriented Embryology (12th ed.). Elsevier.
https://www.us.elsevierhealth.com/the-developing-human-9780443116988.html
 Cunha, D. L., et al. (2019). The spectrum of PAX6 mutations in aniridia and related
malformations. Frontiers in Genetics.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947179/
 Gestri, G., et al. (2018). Cell behaviors during choroid fissure closure in vertebrates.
Developmental Biology.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5826230/
 Cavodeassi, F., et al. (2018). Hedgehog signaling in ocular development. Frontiers in
Cell and Developmental Biology.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6710239/
 Garcia, C. M., et al. (2011). Role of FGF in lens placode/lens development.
Developmental Biology.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3053579/
 Harding, P., et al. (2019). Molecular basis of anophthalmia and microphthalmia. Eye.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787759/
 Thomas, D. M., et al. (2021). Genes & pathways in persistent fetal vasculature. Frontiers
in Medicine.
https://www.frontiersin.org/articles/10.3389/fmed.2021.690594/full