Articular Cartilage: Structure, Components, and Clinical Relevance

Articular Cartilage: Structure, Components, and Clinical Relevance

Prepared by Dr. Alper DUNKI

Spot Knowledge – Articular Cartilage

• Composition: 95% ECM (water, collagen, proteoglycans), 5% chondrocytes
• Water: 65–80%, enables load-bearing, nutrient transport
• Collagen: >50% dry weight, mainly type II (90–95%); tensile strength
• Proteoglycans: 10–15% dry weight; aggrecan + GAGs provide compressive resilience
• Zones:
  Superficial (parallel collagen, friction reduction)
  Transitional (irregular, load distribution)
  Deep (vertical, compressive strength)
  Calcified (anchors to bone)
• Functions: Low-friction motion, load distribution, joint stability, resistance to forces
• Clinical relevance:
  Limited healing (avascular)
  Water/collagen/PG imbalance → osteoarthritis
  Collagen II & X defects → chondrodysplasias
  PG loss → elasticity ↓, cartilage breakdown

Articular Cartilage: Structure, Components, and Clinical Relevance

Overview

Articular cartilage is composed predominantly of extracellular matrix (ECM, ~95%) and a small number of chondrocytes (~5%). Chondrocytes maintain ECM homeostasis throughout life. The main components of ECM are water, collagen, and proteoglycans.

Water

Water accounts for 65–80% of cartilage. It is 80% in the superficial zone and 65% in the deep zone.

• Water      plays a critical role in load-bearing by deforming in response to      compression.
• Its      movement through ECM pores, along with frictional resistance and      pressurization, provides high load-bearing capacity.
• Facilitates      the transport of nutrients and metabolites.
• Alterations      in water content affect permeability, stiffness, and elastic modulus.

Collagen

Collagen constitutes more than 50% of the dry weight and 10–20% of the wet weight.

• Provides      tensile and shear strength.
• Type      II collagen accounts for 90–95% of the total.
• Minor      collagens include types V, VI, IX, X, and XI.
  • Type       VI: increases in early osteoarthritis.
  • Type       X: produced by hypertrophic chondrocytes during endochondral       ossification; associated with calcification.
• The      unique amino acid composition (glycine, proline, hydroxyproline,      hydroxylysine) forms a triple-helix structure.
• Covalent      cross-links between fibrils enhance durability.
• Defects      in collagen type II and X can lead to achondroplasia, spondyloepiphyseal      dysplasia, Kniest dysplasia, and metaphyseal chondrodysplasia.

Proteoglycans

Proteoglycans constitute 10–15% of dry weight and provide compressive strength.

• Synthesized      by chondrocytes and secreted into the ECM.
• Contain      glycosaminoglycans (GAGs) composed of repeating disaccharides: chondroitin      sulfate and keratan sulfate.
  • Chondroitin       sulfate decreases with age, keratan sulfate increases.
• The      most important proteoglycan is aggrecan, which consists of a long protein      core with GAG side chains.
• Aggrecan      molecules aggregate with hyaluronic acid and link proteins, imparting      resilience to the matrix.
• Interact      with collagen fibrils to form a robust network.

Zones

Histologically, articular cartilage is organized into four zones:

1. Superficial      zone: Collagen fibers are aligned parallel; reduces friction.
2. Transitional      zone: Fibers are irregular; distributes load.
3. Deep      zone: Fibers are vertically aligned; provides high compressive      strength.
4. Calcified      zone: Anchors cartilage to bone.

Functions

• Provides      low-friction joint motion.
• Distributes      loads and contributes to joint stability.
• Resists      compressive and tensile forces.
• Maintains      nutrient transport and metabolic homeostasis.

Clinical Relevance

• Cartilage      is avascular, with limited intrinsic healing capacity.
• Alterations      in water, collagen, and proteoglycan content are associated with      degenerative disorders such as osteoarthritis.
• Defects      in type II and X collagen result in genetic chondrodysplasias.
• Loss      of proteoglycans leads to reduced elasticity and cartilage breakdown.

Reference

1. Guo L, Li P, Rong X, Wei X. Key roles of the superficial zone in articular cartilage physiology, pathology, and regeneration. Inflamm Regen. 2024;44:21. doi:10.1186/s41232-022-00202-0

2. Alcaide-Ruggiero L, Cugat R, Domínguez JM. Proteoglycans in Articular Cartilage and Their Contribution to Chondral Injury and Repair Mechanisms. Int J Mol Sci. 2023;24(14):11472. doi:10.3390/ijms241411472

3. Karpiński R, Szczodry M, Zawadzki G. Articular Cartilage: Structure, Biomechanics, and the Potential of Regenerative Medicine. Appl Sci. 2025;15(12):6896. doi:10.3390/app15126896