Basic science / Anatomy
Intervertebral disc Embryology
Vertebral column and discs develop at 4 weeks.
Two adjacent sclerotomes combine to form pre-cartilaginous vertebral body.
Mesenchymal cells lie between the vertebrae.
Notochord forms the nucleus pulposus.
Circular fibers form around this to create the annulus fibrosus.
The disc is a secondary cartilaginous joint.
Structure
Discs get larger more caudally, with the largest being L4/5.
Thicker anteriorly in cervical and lumbar spine, contributing to lordosis.
L5/S1 is the most avascular disc and thickest anteriorly.
Annulus
Outer Annulus
Smaller in size.
Made of Type 1 collagen in lamellae.
Adjacent lamellae are obliquely oriented with respect to each other.
Resists tensile and shear stresses.
Contains fibroblasts and nerves.
Attached to anterior longitudinal ligament (ALL) and posterior longitudinal ligament (PLL).
Inner Annulus
Larger in size.
More Type 2 collagen.
No lamellar organization.
Contains chondrocytes.
Nucleus Pulposus
Made of Type 2 collagen.
Rich in mucoid proteoglycan matrix.
Proteoglycans (PGs) attract water, accounting for 80% content.
PGs provide compressive strength.
The matrix gives visco-elastic and anisotropic properties.
Greater stiffness with rapid loading.
Elasticity and resistance to compression.
Attachment to Vertebrae
Outer 1/3 of the disc connects directly via Sharpey's fibers, forming a ring apophysis.
Inner 2/3 folds in to contribute to the vertebral end plate.
End Plate
Covered with hyaline cartilage in young individuals.
Changes to calcified cartilage with age.
No fibrillar connections between the end plate and vertebra.
Vulnerable to shear stresses.
Collagens Present in the Disc
Type 5 , Type 6 (unique to intervertebral disc), Type 9-12 .
Type 1 in outer annulus.
Transition to Type 2 more centrally.
Type 6 is unique to discs.
Nerve Supply
Only the outer annulus has a nerve supply.
Dorsal: Sinuvertebral nerves (branches of spinal nerves).
Ventral: Sympathetic chain.
Blood Supply and Nutrition
Capillary plexus on the surface of the disc.
Nutrition is via diffusion through the end plates.
Disc becomes dehydrated and fibrotic over time.
Nucleus pulposus is replaced by fibrocartilage.
PG content decreases.
Chondroitin sulfate decreases.
Chondroitin-keratin sulfate ratio decreases.
Water content drops.
Relative collagen content increases.
Disc becomes unable to resist load.
Nucleus starts behaving more like a solid.
Fissures and cracks develop in the annulus.
Alters mechanical properties of the spine.
Destabilizes the spinal motion segment .
Facet joint degeneration.
Risk of disc herniation.
Ligamentum flavum buckling.
Further loss of disc height.
Narrowing of neural foraminae, leading to foraminal/recess stenosis.
Further facet arthrosis.
Flavum hypertrophy.
Canal stenosis.
Degenerative spondylolisthesis.
Disc Function
Primary source of spinal mobility.
Resists tensile, compressive, and shear stresses while maintaining movement.
Anatomic Properties :
Outer annulus resists shear and torsion due to alternating lamellar structure and Type 1 collagen.
Nucleus pulposus and inner annulus better resist compression, converting compression to radial forces.
These forces generate hoop stresses in the annulus.
The disc functions as a biphasic material .
Outer annulus undergoes hoop stresses in compression.
Inner layers act as shock absorbers, dissipating stresses.
Disc Injury and Healing
Herniation
Annular tear starts in the inner annulus due to sudden increases in intradiscal pressure.
Pain arises from the nuclear part bulging through the tear and irritating nerves in the outer annulus.
If the tear propagates to the outer annulus, bulging or herniation occurs, causing pain from the disc and nerve root impingement.
90% of herniations are asymptomatic at 3 months due to:
Resorption of nucleus material.
Annular tear does not repair itself.
Disc Degeneration
Occurs with age due to chronic dehydration of the disc and impaired nutrition.
PG content decreases, reducing water content.
Relative collagen content increases.
Decreased vascularity and progressive calcification of endplates impair diffusion.
End plate microfractures occur, permanently deforming the disc.
The disc loses its elastic properties and behaves like a solid.
Alters mechanics and load distribution, leading to osteophyte formation, facet joint arthrosis, and pain.
Related FRCS revision notes Written/reviewed by Kishore Puthezhath
Professor of Orthopaedics and Consultant Paediatric Orthopaedic Surgeon
FRCS (Tr & Orth) revision resource
Reviewed: September 2026
Core revision references: Miller's Review of Orthopaedics; Campbell's Operative Orthopaedics; Orthobullets . Current specialty guidelines are linked within individual notes where applicable.
Prefer studying offline? thinKbox FRCS adds offline personal notes, backlinks, flashcards, spaced review, device-specific capture and private local AI. See the app →