Articular cartilage is specialized connective tissue covering the articulating surfaces of bones in most synovial joints. It provides a smooth, low-friction surface, distributes mechanical loads, absorbs compressive forces, and protects the underlying subchondral bone.
Articular cartilage is the specialized connective tissue covering the opposing bony surfaces of most synovial joints. It creates a smooth, resilient surface that allows bones to move against one another with very little friction while distributing mechanical loads across the joint.
In most synovial joints, articular cartilage is a specialized form of hyaline cartilage. Unlike many other forms of hyaline cartilage, however, mature articular cartilage is not covered by perichondrium. It is also avascular, aneural, and alymphatic.
Articular cartilage is composed primarily of chondrocytes embedded within a highly organized extracellular matrix containing water, collagen, proteoglycans, and other matrix molecules. Its microscopic architecture varies from the joint surface toward the underlying subchondral bone, producing distinct structural zones.
Articular cartilage covers the articular surfaces of bones participating in most synovial joints. Examples include the head of the femur at the hip, femoral and tibial surfaces at the knee, humeral head at the shoulder, and articular surfaces of the elbow, wrist, ankle, and numerous smaller joints.
The thickness and geometry of the cartilage vary considerably among joints and even across different regions of the same articular surface. These variations reflect local loading patterns and joint mechanics.
| Function | Importance |
|---|---|
| Low-friction movement | Allows opposing joint surfaces to move smoothly |
| Load distribution | Spreads forces across the articular surface |
| Compression resistance | Deforms under load and recovers after unloading |
| Protection of bone | Reduces focal stresses transmitted to subchondral bone |
| Joint congruence | Contributes to the geometry of articulating surfaces |
Articular cartilage contains relatively few cells compared with the large volume of extracellular matrix surrounding them. The major components are chondrocytes, collagen, proteoglycans, water, and smaller quantities of additional matrix proteins and glycoproteins.
Chondrocytes are the only mature cellular component of articular cartilage. They are responsible for producing, maintaining, and remodeling the extracellular matrix.
Chondrocytes synthesize collagen, proteoglycans, and other matrix molecules. They also respond to mechanical loading, biochemical signals, inflammatory mediators, and changes in their surrounding matrix.
Chondrocyte shape, density, and orientation vary according to depth. Cells near the articular surface are relatively flattened, while deeper chondrocytes become more rounded and may form columns oriented toward the subchondral bone.
The extracellular matrix gives articular cartilage most of its mechanical properties. It consists primarily of water and a solid matrix containing collagen fibers and proteoglycans.
| Component | Major Role |
|---|---|
| Water | Supports deformation, lubrication, and load distribution |
| Type II collagen | Provides tensile strength and structural framework |
| Proteoglycans | Bind water and contribute to compression resistance |
| Chondrocytes | Produce and maintain extracellular matrix |
Collagen forms the fibrous framework of articular cartilage. Type II collagen is the predominant collagen type, although smaller quantities of other collagen types contribute to matrix organization and interactions.
The collagen network provides tensile strength and restrains the expansion of the highly hydrated proteoglycan-rich matrix during compression.
Collagen fibers are not arranged uniformly throughout articular cartilage. Their orientation changes with depth and is closely related to the mechanical demands placed on different regions of the tissue.
Near the articular surface, collagen fibers are predominantly oriented parallel to the surface. In deeper regions they become increasingly perpendicular to the surface and ultimately anchor the cartilage toward the calcified zone.
Proteoglycans are large matrix molecules consisting of core proteins associated with glycosaminoglycan chains. Their negatively charged components attract cations and water, creating a highly hydrated matrix.
This water-binding capacity is fundamental to the ability of articular cartilage to resist compression.
Aggrecan is a major proteoglycan of articular cartilage. Large aggrecan molecules interact with hyaluronan to form aggregates capable of retaining substantial quantities of water within the extracellular matrix.
Water forms a major proportion of the wet weight of articular cartilage. It moves within the porous extracellular matrix when the tissue is loaded and unloaded.
This fluid movement contributes to lubrication, nutrient transport, and the time-dependent mechanical behavior of cartilage.
The extracellular matrix can also be described according to its relationship to individual chondrocytes. It is commonly divided into pericellular, territorial, and interterritorial matrix.
The pericellular matrix immediately surrounds individual chondrocytes. Together, the chondrocyte and its immediate matrix environment form a functional unit involved in sensing and responding to mechanical loads.
The territorial matrix surrounds the pericellular region and differs in composition and organization from the more distant interterritorial matrix.
The interterritorial matrix forms much of the bulk extracellular matrix between chondrocytes and provides a major contribution to the mechanical properties of the tissue.
From the joint surface toward the underlying bone, articular cartilage is commonly divided into four zones: the superficial zone, middle zone, deep zone, and calcified cartilage zone.
| Zone | Chondrocytes | Collagen Orientation | Major Feature |
|---|---|---|---|
| Superficial | Flattened | Predominantly parallel to surface | Resists shear and contributes to low-friction surface |
| Middle | More rounded | Less organized, oblique arrangement | Transitional mechanical region |
| Deep | Rounded, often arranged in columns | Predominantly perpendicular to surface | Strong resistance to compression |
| Calcified | Relatively sparse | Anchored toward bone | Connects uncalcified cartilage to subchondral bone |
The superficial zone, also called the tangential zone, forms the outermost region facing the joint cavity. Chondrocytes are relatively flattened and collagen fibers are densely arranged primarily parallel to the articular surface.
This orientation helps the superficial zone resist tensile and shear forces generated during joint movement.
The surface of healthy articular cartilage is smooth at the macroscopic level and is adapted for repeated contact with the opposing articular surface. Its structural organization contributes to extremely low friction during movement.
The middle zone, or transitional zone, lies beneath the superficial layer. Chondrocytes are more rounded, collagen fibers have a less uniform orientation, and proteoglycan concentration generally increases compared with the superficial region.
This zone forms a structural transition between the shear-resistant superficial layer and the compression-adapted deep cartilage.
The deep zone, also called the radial zone, contains relatively large, rounded chondrocytes that may be arranged in columns. Collagen fibers are predominantly oriented perpendicular to the articular surface.
The deep zone contains a relatively high concentration of proteoglycans and is strongly adapted to withstand compressive loading.
The deepest portion of articular cartilage is the calcified cartilage zone. Mineralization of its extracellular matrix creates a transition between the flexible uncalcified cartilage above and the much stiffer subchondral bone below.
The boundary separating uncalcified deep cartilage from calcified cartilage is known as the tidemark. It can be identified histologically as a distinct line within the osteochondral interface.
The transition from articular cartilage to subchondral bone is called the osteochondral junction. This region allows mechanical forces generated at the articular surface to be transferred progressively into underlying bone.
Subchondral bone lies beneath the calcified cartilage. It supports the articular cartilage and participates in transmission and distribution of forces through the joint.
Cartilage and subchondral bone therefore function together as a mechanically integrated osteochondral unit.
| Structure | Mechanical Role |
|---|---|
| Uncalcified cartilage | Provides resilient low-friction load-bearing surface |
| Calcified cartilage | Provides transitional attachment to bone |
| Subchondral bone | Provides rigid structural support and transmits loads |
Cartilage thickness varies according to joint, location, age, and mechanical loading. Regions exposed to different patterns of pressure and movement can have distinct cartilage thickness profiles.
Unlike many regions of hyaline cartilage elsewhere in the body, mature articular cartilage lacks a perichondrium. Its superficial surface is exposed directly to the synovial environment.
The absence of perichondrium is one factor contributing to the limited regenerative capacity of articular cartilage.
Articular cartilage is avascular. Blood vessels do not normally extend through its extracellular matrix.
The absence of direct vascular supply has major implications for cartilage nutrition, metabolism, and healing.
Chondrocytes receive nutrients largely through diffusion from synovial fluid. Exchange of fluid during cyclic loading and unloading assists transport of nutrients and metabolic products through the matrix.
When cartilage is compressed, fluid is displaced within and from the matrix. During unloading, fluid is drawn back into the tissue. Repeated loading cycles facilitate movement of dissolved substances between cartilage and synovial fluid.
Healthy articular cartilage is essentially aneural. It does not contain the sensory nerve endings responsible for pain perception.
Joint pain associated with cartilage disease therefore usually arises from innervated structures such as synovium, capsule, ligaments, periosteum, or subchondral bone rather than directly from the cartilage matrix.
Articular cartilage lacks a conventional lymphatic vascular network. Movement of molecules through its extracellular matrix occurs primarily through diffusion and fluid movement.
Articular cartilage behaves as a complex material in which a porous solid matrix interacts with interstitial fluid. This allows it to withstand repeated mechanical loading while maintaining a smooth articulating surface.
When articular cartilage is compressed, pressure increases within its interstitial fluid and the proteoglycan-rich matrix tends to deform. The collagen network restrains excessive expansion of the matrix.
The interaction between fluid pressure, proteoglycans, and collagen allows cartilage to support substantial compressive loads.
The collagen network provides tensile strength. This is particularly important in the superficial zone, where collagen fibers resist forces generated parallel to the joint surface.
Shear forces develop when opposing surfaces move relative to one another. The highly organized superficial collagen network helps resist these forces.
Articular cartilage exhibits viscoelastic behavior, meaning its mechanical response depends partly on the magnitude, duration, and rate of loading.
Under a sustained load, cartilage gradually deforms as fluid redistributes through the matrix. Following removal of the load, the tissue gradually recovers.
Creep describes the progressive deformation of cartilage when a constant load is applied over time. Fluid movement through the matrix contributes substantially to this response.
Stress relaxation occurs when cartilage is maintained at a constant deformation and the force required to maintain that deformation gradually decreases as fluid and matrix stresses redistribute.
| Property | Structural Basis |
|---|---|
| Compression resistance | Proteoglycans, water, collagen restraint, and fluid pressure |
| Tensile strength | Collagen network |
| Shear resistance | Superficial collagen architecture and matrix organization |
| Viscoelasticity | Interaction of solid matrix and interstitial fluid |
| Recovery after loading | Rehydration and elastic properties of extracellular matrix |
The extremely low friction of synovial joints depends on interactions between articular cartilage and synovial fluid. Several lubrication mechanisms can operate depending on load and movement.
In fluid-film lubrication, a layer of fluid separates opposing articular surfaces and reduces direct surface-to-surface contact during movement.
Boundary lubrication becomes particularly important when opposing surfaces are in close contact or moving slowly under load. Molecules associated with the cartilage surface and synovial fluid reduce friction between surfaces.
Lubricin is a glycoprotein associated with the articular surface and synovial fluid. It contributes to boundary lubrication and helps reduce friction at the cartilage surface.
Hyaluronan is an important component of synovial fluid and contributes to its rheological properties. It also participates in the molecular environment surrounding articular cartilage.
Articular cartilage is adapted to regular physiological loading. Mechanical forces influence chondrocyte metabolism and extracellular matrix turnover.
Both excessive mechanical loading and prolonged absence of normal loading can adversely affect cartilage structure and function.
Mechanotransduction refers to the process by which chondrocytes detect mechanical stimuli and convert them into cellular and biochemical responses.
Changes in matrix deformation, fluid pressure, osmotic environment, and other mechanical factors can influence chondrocyte activity.
Healthy articular cartilage depends on a balance between synthesis and degradation of extracellular matrix components. Chondrocytes regulate this balance in response to mechanical and biochemical signals.
Chondrocytes synthesize collagen, aggrecan, and other matrix molecules required to maintain cartilage structure and mechanical properties.
Normal cartilage undergoes controlled matrix turnover. Excessive activity of matrix-degrading enzymes can contribute to loss of cartilage structure in disease.
Articular cartilage develops in association with formation of synovial joints. During skeletal development, cartilage at the future articular ends of bones is retained while much of the surrounding cartilage model is replaced by bone through endochondral ossification.
Although both are forms of hyaline cartilage, articular cartilage and growth plate cartilage have different organizations and functions. Growth plate cartilage is specialized for longitudinal bone growth, whereas articular cartilage is retained as a permanent joint surface.
| Feature | Articular Cartilage | Growth Plate Cartilage |
|---|---|---|
| Primary function | Joint movement and load bearing | Longitudinal bone growth |
| Persistence | Normally persists throughout life | Normally ossifies at skeletal maturity |
| Location | Articular ends of bones | Between epiphysis and metaphysis in growing long bones |
| Relationship to joint cavity | Faces synovial cavity | Does not form the articular surface |
Articular cartilage should also be distinguished from fibrocartilage, which is found in structures such as menisci and intervertebral discs.
| Feature | Articular Cartilage | Fibrocartilage |
|---|---|---|
| Predominant collagen | Type II | Prominent type I with additional collagen components |
| Typical location | Synovial joint surfaces | Menisci, intervertebral discs, symphyses |
| Primary mechanical emphasis | Low-friction load bearing and compression resistance | Resistance to combined compression and tension |
Articular cartilage is not mechanically identical throughout the body. Its thickness, matrix composition, cellular organization, and mechanical properties vary according to the requirements of each joint.
The knee contains articular cartilage covering the femoral condyles, tibial plateaus, and articular surface of the patella. These surfaces experience substantial compressive and shear forces during standing, walking, running, and stair climbing.
Articular cartilage covers the femoral head and the lunate articular surface of the acetabulum. The hip transmits substantial forces between the trunk and lower limb.
Articular cartilage covers the humeral head and glenoid articular surface. The shoulder combines a large range of motion with relatively limited bony constraint compared with the hip.
The articular cartilage of the talocrural joint covers the trochlea of the talus and corresponding distal tibial and fibular articular surfaces. These surfaces transmit substantial loads through a relatively compact joint area.
Articular cartilage has a limited capacity for spontaneous repair. Important contributing factors include its lack of blood vessels, absence of perichondrium, low cellular density, and restricted ability of mature chondrocytes to restore large areas of damaged matrix.
A partial-thickness defect remains confined to articular cartilage without penetrating the subchondral bone. Because the lesion does not reach a vascular source of reparative cells, spontaneous healing is generally limited.
A full-thickness defect extends through the articular cartilage toward or into subchondral bone. Penetration of vascularized bone can produce a repair response involving blood and marrow-derived cells.
Repair tissue formed after penetration of subchondral bone frequently differs from native hyaline articular cartilage. It may contain more fibrocartilaginous characteristics and generally does not reproduce all of the mechanical properties of normal articular cartilage.
Focal articular cartilage defects can result from trauma, repetitive mechanical injury, osteochondral lesions, or degenerative processes. Their effects depend on size, depth, location, joint mechanics, and the condition of surrounding tissues.
A chondral injury involves articular cartilage. Damage can range from superficial matrix disruption to deep defects extending through most or all of the cartilage thickness.
An osteochondral injury involves both articular cartilage and the underlying subchondral bone.
Osteoarthritis is a disorder of synovial joints involving changes in articular cartilage, subchondral bone, synovium, and other joint tissues. Cartilage changes can include matrix disruption, surface fibrillation, fissuring, progressive tissue loss, and altered chondrocyte activity.
Fibrillation describes disruption and fraying of the normally smooth cartilage surface. Progressive structural deterioration can extend into deeper cartilage layers.
Advanced structural loss can produce thinning or complete absence of cartilage in focal regions, increasing mechanical loading of the underlying subchondral bone.
Because cartilage and subchondral bone form an integrated mechanical unit, disease affecting articular cartilage is frequently accompanied by changes in underlying bone.
Articular cartilage itself lacks sensory innervation. Consequently, isolated cartilage damage does not necessarily generate pain directly from the cartilage. Symptoms can develop when associated changes affect innervated joint structures.
Articular cartilage undergoes changes in matrix composition and cellular activity with age. The ability of chondrocytes to maintain and repair the extracellular matrix may become less effective, while mechanical properties can also change.
Cartilage can be evaluated indirectly or directly using imaging and arthroscopic techniques. The optimal method depends on the joint, suspected abnormality, and clinical context.
Normal articular cartilage is not directly visible on conventional radiographs. The distance between opposing bony surfaces produces the radiographic joint space, which can provide an indirect indication of cartilage and other intra-articular structures.
Reduction in radiographic joint space can reflect loss or thinning of articular cartilage, although interpretation depends on the specific joint and imaging technique.
MRI can directly depict articular cartilage and provides information about cartilage thickness, surface integrity, focal defects, subchondral bone, and surrounding soft tissues.
Arthroscopy permits direct visualization of the articular surface through an instrument introduced into the joint. Cartilage defects can be assessed according to their location, size, depth, and appearance.
Several surgical strategies are used for selected focal cartilage defects. Their purpose may include stimulating repair from subchondral bone, transferring osteochondral tissue, or introducing cells or tissue intended to restore the articular surface.
Microfracture involves creating small openings in subchondral bone beneath a cartilage defect to allow marrow-derived elements to enter the lesion and form repair tissue.
Osteochondral grafting transfers units containing articular cartilage and underlying bone into a focal osteochondral defect.
Cell-based cartilage repair approaches use chondrocytes or related techniques with the aim of producing repair tissue within selected articular defects.
Articular cartilage function depends partly on normal joint alignment. Malalignment can redistribute mechanical loads and increase stress within particular regions of an articular surface.
At the knee, the menisci increase contact area and help distribute loads across articular cartilage. Meniscal loss or dysfunction can substantially alter cartilage loading patterns.
Ligaments maintain normal relationships between articular surfaces. Instability can alter joint kinematics and expose cartilage to abnormal patterns of loading and shear.
Muscles crossing a joint help control movement, absorb loads, and maintain alignment. Neuromuscular control therefore influences the mechanical environment experienced by articular cartilage.
| Joint Requirement | Contribution of Articular Cartilage |
|---|---|
| Smooth movement | Provides highly congruent, low-friction surface |
| Weight bearing | Distributes compressive loads |
| Shock management | Deforms and redistributes mechanical stresses |
| Bone protection | Reduces focal stress on subchondral bone |
| Repeated motion | Maintains durable articulating surface under physiological loading |
| Feature | Key Point |
|---|---|
| Tissue type | Specialized hyaline cartilage in most synovial joints |
| Primary cell | Chondrocyte |
| Predominant collagen | Type II collagen |
| Major proteoglycan | Aggrecan |
| Blood vessels | Absent |
| Nerves | Absent from normal cartilage |
| Perichondrium | Absent |
| Major zones | Superficial, middle, deep, and calcified |
| Tidemark | Boundary between uncalcified and calcified cartilage |
| Deep support | Subchondral bone |
| Nutrition | Primarily diffusion associated with synovial fluid and fluid exchange |
| Repair capacity | Limited |
Articular cartilage is a highly specialized component of synovial joints. Its combination of a collagen framework, water-binding proteoglycans, interstitial fluid, and metabolically active chondrocytes creates a surface capable of supporting substantial loads while maintaining exceptionally low friction.
Its organization is closely matched to mechanical function. The superficial zone resists shear and tensile forces, the middle zone provides a transition in matrix architecture, the deep zone is adapted to compression, and the calcified zone anchors the tissue to the underlying subchondral bone.
Articular cartilage does not function independently. Its mechanical environment is influenced by subchondral bone, synovial fluid, joint geometry, ligaments, menisci, labra, muscles, and alignment of the entire articulation.
Its avascular and aneural structure is advantageous for maintaining a smooth uninterrupted articular surface but contributes to its limited capacity for repair after injury. Understanding articular cartilage is therefore fundamental to the anatomy and biomechanics of synovial joints, load transmission, joint lubrication, osteochondral structure, cartilage injury, and degenerative joint disease.