🦵 Cartilage Degradation Biomechanics Simulator

Healthy Cartilage Matrix — Normal Load Distribution

Healthy hyaline cartilage spreads joint load evenly across the surface.

• 2.2–2.5 mm: Cartilage thickness (tibial plateau, typical adult)
• ~100%: Proteoglycan content (aggrecan-saturated matrix)
• 0.001–0.02: Friction coefficient (synovial-lubricated surface)
• ~80%: Tissue water content (swelling pressure resists load)

Structure of healthy articular cartilage

Collagen II fibers arch over proteoglycan-rich ground substance.

Cartilage has no blood supply, nerves, or lymphatics.

Load distribution across the joint surface

Fluid pressurization lets cartilage bear load without solid-phase stress.

Chondrocytes and matrix maintenance

Sparse chondrocytes slowly balance matrix synthesis and turnover.

Repetitive Mechanical Loading Begins

Years of repeated impact start to outpace matrix repair capacity.

• 3–7 MPa: Peak joint contact stress (walking, running gait cycles)
• ~1M: Daily loading cycles (steps per year, average adult)
• weeks: Matrix repair lag (chondrocyte turnover is slow)
• <5%: Early collagen microdamage (fiber network still intact)

Cumulative microtrauma from cyclic loading

Repeated peak stress gradually fatigues the collagen network.

Body weight as a load multiplier

Excess body weight multiplies peak stress at every step.

Each extra kilogram adds several kilograms of knee load.

Early biochemical stress response

Chondrocytes upregulate catabolic enzymes under sustained mechanical stress.

Proteoglycan Loss & Matrix Softening

Aggrecan loss lets the matrix swell, soften, and lose compressive strength.

• ~50–60%: Proteoglycan content (of healthy baseline)
• MMP-13, ADAMTS-5: Key degrading enzymes (aggrecanases and collagenases)
• 85–90%: Matrix water content (swelling from lost restraint)
• ~30%: Compressive stiffness loss (relative to healthy tissue)

Aggrecanase-driven proteoglycan depletion

ADAMTS enzymes cleave aggrecan faster than chondrocytes replace it.

Osmotic swelling and softening

Unrestrained water uptake swells and weakens the tissue.

Softened cartilage bears more concentrated local stress.

Inflammatory feedback in the joint

Matrix fragments trigger cytokines that accelerate further breakdown.

Progressive Cartilage Thinning & Fibrillation

The collagen surface frays into vertical clefts as the layer thins.

• 0.8–1.3 mm: Cartilage thickness (roughly half of healthy)
• to mid-zone: Surface fibrillation depth (Outerbridge grade II–III)
• ~25–35%: Proteoglycan content (severely depleted matrix)
• ~0.1–0.3: Friction coefficient (lubrication starting to fail)

Fibrillation — the fraying surface

Vertical clefts split the collagen network into loose fronds.

Focal thinning and cartilage loss

Thinning concentrates at the highest-load contact zones first.

Thinned zones shift load onto adjacent healthier cartilage.

Subchondral bone remodeling response

Underlying bone stiffens and forms early osteophytes.

Full-Thickness Loss & Bone-on-Bone Friction

Cartilage is gone; exposed subchondral bone grinds directly on bone.

• ~0 mm: Cartilage thickness (full-thickness loss, exposed bone)
• 0.5–0.8+: Friction coefficient (unlubricated bone-on-bone)
• ~100%: Joint space narrowing (radiographic end-stage OA)
• ~595M: Global OA prevalence (people affected worldwide)

Eburnation — polished bone-on-bone contact

Exposed bone surfaces polish and grind against each other.

Friction rises roughly 40-fold versus healthy cartilage.

Pain, stiffness, and loss of function

Bone friction drives pain, stiffness, and reduced mobility.

Clinical management at end stage

Options narrow to pain control or joint replacement surgery.