Articular Cartilage

Functions

Articular cartilage provides a durable, low-friction bearing surface and distributes load over subchondral bone. Its mechanical behaviour depends on the interaction between a collagen network, proteoglycans and interstitial water.

The major functions are:

• low-friction joint movement
• load distribution over a wider contact area
• resistance to compressive loading
• protection of subchondral bone from focal peak stress

Composition

Articular cartilage is mostly extracellular matrix with a small population of chondrocytes.

Water

• forms the largest component of the tissue
• moves through the matrix during loading and unloading
• contributes substantially to time-dependent load support

Collagen

• predominantly type II
• provides tensile strength and constrains swelling of the proteoglycan-rich matrix
• orientation varies by depth

Proteoglycans

• aggrecan is the major large proteoglycan
• glycosaminoglycan side chains carry fixed negative charges
• attract cations and water, producing swelling pressure

Chondrocytes

• maintain the extracellular matrix
• have low turnover and limited capacity for repair
• vary in shape and orientation between zones

Zonal structure

Superficial zone

• flattened chondrocytes
• collagen fibres lie mainly parallel to the surface
• resists shear
• contributes to surface lubrication

Transitional zone

• rounder cells
• collagen fibres become more oblique
• intermediate mechanical properties

Deep zone

• cells are arranged in columns
• collagen fibres are predominantly perpendicular to the joint surface
• high proteoglycan concentration
• important in resisting compression

Calcified cartilage

• anchors cartilage to subchondral bone
• separated from non-calcified cartilage by the tidemark

Mechanical behaviour

Cartilage behaves as a biphasic or multiphasic material. The solid matrix and interstitial fluid share load. Immediately after loading, fluid pressurisation carries much of the load. With sustained loading, fluid gradually leaves the matrix and the solid phase carries a greater proportion.

This explains:

• creep under constant load
• stress relaxation under constant deformation
• recovery after unloading

Nutrition

Adult articular cartilage is avascular, aneural and alymphatic. Nutrition is predominantly by diffusion from synovial fluid, assisted by cyclic loading and unloading.

Why repair is limited

Repair is poor because:

• there is no direct blood supply
• chondrocyte density is low
• cell migration is limited
• mature matrix has low turnover

A defect confined to cartilage has little access to marrow-derived repair cells. A defect that breaches subchondral bone can recruit marrow elements, but the repair tissue is usually fibrocartilage rather than normal hyaline cartilage.

Viva framework

When asked about articular cartilage, answer in this order:

1. function
2. composition
3. zones and collagen orientation
4. biphasic mechanical behaviour
5. nutrition and poor healing capacity
6. clinical relevance to osteoarthritis and focal cartilage defects

Matrix organisation and load transmission

Articular cartilage is a highly specialised, avascular and aneural connective tissue. Its mechanical behaviour depends on the interaction between chondrocytes, extracellular matrix and interstitial water rather than on any one component in isolation.

The superficial zone contains flattened chondrocytes and collagen fibres arranged mainly parallel to the surface. It has the highest collagen concentration and is particularly important in resisting shear. The middle zone contains more randomly arranged collagen and a higher proteoglycan content. The deep zone contains larger chondrocytes arranged in columns and collagen fibres orientated more perpendicular to the joint surface, helping resist compression and anchor the tissue to the calcified zone. The tidemark separates non-calcified from calcified cartilage.

Type II collagen forms the principal fibrillar framework. Aggrecan molecules bind to hyaluronan and carry negatively charged glycosaminoglycan side chains. These fixed negative charges attract cations and water. Under load, fluid is displaced from the matrix; when the load is removed, water is drawn back in. This fluid pressurisation is a major reason normal cartilage can transmit substantial load with very low friction.

Chondrocyte biology

Chondrocytes maintain a balance between matrix synthesis and matrix degradation. They respond to:

• mechanical loading
• cytokines and growth factors
• osmotic changes
• matrix damage
• ageing and oxidative stress

Physiological cyclic loading is beneficial to matrix homeostasis. Prolonged immobilisation and excessive abnormal loading both produce adverse effects. Chondrocytes have limited regenerative capacity because the tissue lacks a vascular supply and has a low cell density.

Important catabolic mediators in degeneration include inflammatory cytokine signalling and matrix-degrading enzymes such as matrix metalloproteinases and aggrecanases. The key concept is not simply “cartilage wears out”; osteoarthritis reflects failure of the whole osteochondral unit with altered cellular and mechanical behaviour.

Synovial lubrication

Very low joint friction is produced by several complementary mechanisms:

• fluid-film lubrication separates surfaces during movement where conditions permit
• boundary lubrication becomes more important when surfaces are close together or movement is slow
• cartilage interstitial fluid supports much of the applied load immediately after loading
• hyaluronan and lubricin contribute to the lubricating environment

A useful viva point is that cartilage is not merely a smooth plastic-like bearing. It is a biphasic, fluid-rich biological material whose performance changes with loading rate and time.

Response to injury

A purely chondral defect has limited intrinsic healing because there is no access to marrow-derived reparative cells. A defect extending into subchondral bone can generate a fibrocartilaginous repair response. Fibrocartilage contains more type I collagen and does not reproduce the organisation or durability of native hyaline cartilage.

The biological rationale behind marrow-stimulation procedures is to create access to subchondral marrow. Cell-based and osteochondral restorative procedures attempt, by different methods, to provide tissue with better structural characteristics or replace the damaged osteochondral unit.

Osteochondral junction

The subchondral plate and trabecular bone contribute to load distribution. In established osteoarthritis, subchondral sclerosis, cyst formation, osteophytes and altered bone remodelling are not simply secondary radiographic changes; they alter the mechanical environment seen by the remaining cartilage.

Applied FRCS points

When discussing cartilage, link structure to function:

• superficial collagen orientation → shear resistance
• proteoglycan charge → water retention and compressive behaviour
• avascularity → poor intrinsic repair
• calcified cartilage/subchondral bone → anchorage and load transfer
• fluid pressurisation → low friction and time-dependent mechanics

In an exam answer, avoid describing osteoarthritis as simple age-related abrasion. Explain the interaction between matrix failure, abnormal mechanics, chondrocyte response, synovial inflammation and subchondral bone change.