Cartilage

Part 1 · General anatomy

No vessels, no nerves, no lymphatics — and everything difficult follows from that

The one sentence that organises the chapter

Cartilage is avascular, aneural and alymphatic.

Hold that sentence and you can derive almost everything else. No blood vessels means nutrition by diffusion, which means slow metabolism, which means slow healing and a strict dependence on movement to circulate nutrients. No nerves means articular cartilage cannot hurt — so pain in an osteoarthritic joint must be coming from somewhere else, and knowing where changes how you treat it. No lymphatics and no blood supply means immune privilege, which is why osteochondral allografts can be transplanted between unrelated donors without matching.

Bone rebuilds itself; cartilage largely does not. That asymmetry is the reason cartilage injury dominates long-term musculoskeletal disability while bone injury usually resolves.

Learning outcomes

By the end of this chapter you should be able to:

• Describe the general structure of cartilage and name its cells, matrix constituents and covering.
• Compare hyaline, elastic and fibrocartilage in structure, location and function.
• Describe the molecular architecture of the aggrecan–hyaluronan aggregate and explain how it generates compressive stiffness.
• Describe the zonal organisation of articular cartilage, including the Benninghoff collagen arcades, the tidemark and the calcified zone.
• Explain biphasic (poroelastic) behaviour, interstitial fluid pressurisation and the modes of joint lubrication.
• Explain how cartilage is nourished, and justify early mobilisation on that basis.
• Explain why cartilage heals poorly, and distinguish partial-thickness from full-thickness defect behaviour.
• Describe the structure, vascular zones and healing capacity of the menisci, labra and other fibrocartilages.
• Outline the pathophysiology of osteoarthritis as an active disease of the whole joint rather than passive wear.
• State where osteoarthritic pain actually arises, and use that to justify a rehabilitation strategy.
• Describe the principal cartilage repair procedures and their rehabilitation implications.

General structure

Cartilage is a specialised connective tissue consisting of cells (chondrocytes) embedded in an extensive extracellular matrix, with the unusual property that the matrix, not the cells, does virtually all of the work.

Growth

• Interstitial growth — chondrocytes divide within the matrix, expanding the tissue from within. Occurs in young cartilage and, critically, at the epiphyseal plate.
• Appositional growth — new chondroblasts differentiate from the inner perichondrium and add matrix to the surface. This is how cartilage thickens, and it is impossible where there is no perichondrium.

The three types of cartilage

Figure 1 · The three types compared

Figure 2 · The three types of cartilage under the microscope

Two examination points follow: the epiglottis and auricle are elastic (they must spring back), and the intervertebral disc is a hybrid — an outer fibrocartilaginous anulus surrounding a gelatinous nucleus pulposus that is a notochordal remnant and behaves as a fluid-filled pressure vessel rather than as cartilage proper.

The extracellular matrix of articular cartilage

By wet weight, articular cartilage is approximately 65–80% water, 10–20% collagen, and 4–7% proteoglycan, with chondrocytes occupying only 1–5% of the volume. The mechanical behaviour is entirely a property of how those first three interact.

3.4.1 Collagen — the tensile network

Type II collagen forms roughly 90–95% of the collagen, arranged in fine fibrils cross-linked into a three-dimensional mesh. Minor collagens (IX, XI, VI, X) organise, stabilise and anchor it: type IX cross-links fibrils to one another and to proteoglycans, type XI regulates fibril diameter, type VI forms the pericellular shell, and type X appears only in the calcified zone and the hypertrophic zone of the physis — its presence anywhere else indicates chondrocyte hypertrophy and matrix degeneration.

The collagen network provides tensile strength and, crucially, restrains the swelling of the proteoglycans. It is the pressure vessel; the proteoglycans are the pressure.

3.4.2 Proteoglycans — the compressive engine

Aggrecan is the dominant proteoglycan: a core protein carrying about 100 chondroitin sulphate and 30 keratan sulphate glycosaminoglycan (GAG) chains. GAGs are densely sulphated and carboxylated, and therefore carry a very high fixed negative charge density.

Many aggrecan molecules bind non-covalently, via link protein, to a long backbone of hyaluronan, producing a bottle-brush proteoglycan aggregate of enormous molecular size, physically trapped within the collagen mesh.

The mechanics follow directly:

• Fixed negative charges repel each other, and attract counter-ions (Na⁺) into the tissue.
• The resulting excess ion concentration draws water in osmotically — the Donnan osmotic pressure.
• The tissue therefore tries to swell, and is prevented from doing so by the collagen network.
• The result is a pre-stressed, turgid tissue: the collagen is in tension even at rest, and the water is under pressure.

This is exactly the mechanism of a car tyre, and it is why loss of proteoglycan — the earliest measurable change in osteoarthritis, detectable on delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) and T1ρ mapping before any structural loss — softens cartilage long before it thins.

Other matrix molecules: decorin and biglycan (small leucine-rich proteoglycans regulating fibrillogenesis), fibronectin, COMP (cartilage oligomeric matrix protein, a biomarker of turnover), and lubricin / PRG4 (superficial zone protein), secreted by superficial chondrocytes and synoviocytes and responsible for boundary lubrication.

Zonal architecture of articular cartilage

Figure 3 · The zones of articular cartilage

Articular cartilage is only 2–4 mm thick, yet it is organised into four distinct zones. Cartilage is thickest where contact stress is highest — up to 5–7 mm on the patella, the thickest in the body.

The classic description of the fibre arrangement is Benninghoff’s arcades: collagen fibres arise perpendicular from the calcified zone, arch through the middle zone, and run parallel at the surface, forming a series of leaf-spring arches. Whether these are literal continuous arcades or a statistical description remains debated, but the model correctly predicts the tissue’s behaviour: vertical fibres resist compression and anchor, horizontal fibres resist shear.

Clinical corollary. Because the deep zone is anchored through the calcified layer to bone but the calcified layer is not crossed by fibres from bone, the osteochondral junction is a plane of mechanical weakness. Shear injury therefore produces either a superficial fibrillation or a full osteochondral flap, but rarely a clean mid-substance tear.

Nutrition — and why movement is not optional

Articular cartilage has no blood supply of its own. Its nutrition comes from two sources:

• Synovial fluid, by diffusion — the dominant route for adult articular cartilage, supplying the superficial and middle zones.
• Subchondral bone, by diffusion across the calcified zone — significant in immature cartilage, and progressively limited in adults as the subchondral plate becomes less permeable, though it becomes more important again in osteoarthritis when vascular channels breach the tidemark.

Diffusion alone is slow across 2–4 mm of dense matrix. What makes it adequate is convection: cyclical loading and unloading squeezes interstitial fluid out of the cartilage and draws it back in with dissolved nutrients — a pumping action driven by joint movement.

This produces the most important clinical statement in the chapter:

Joint movement is the nutritional supply route of articular cartilage. Immobilisation starves it.

The experimental evidence is unambiguous:

• joint immobilisation produces proteoglycan loss, softening, thinning and chondrocyte death within weeks
• static compression is catabolic
• cyclical, moderate-magnitude, intermittent loading is anabolic, up-regulating aggrecan and type II collagen synthesis. Excessive or impact loading is catabolic again. The dose–response curve is an inverted U, and identifying where a given patient sits on it is much of what cartilage rehabilitation consists of

It is also the rationale for continuous passive motion after certain cartilage procedures, for early protected range after joint surgery, and for the advice that a patient with knee osteoarthritis should keep moving rather than rest.

Biomechanics of articular cartilage

3.7.1 Biphasic (poroelastic) theory

Cartilage is modelled as a biphasic material: a porous, permeable solid phase (collagen–proteoglycan matrix) saturated by an interstitial fluid phase (water and ions).

When load is applied:

• Instantaneously, the fluid cannot escape (permeability is very low, ~10⁻¹⁵ m⁴/N·s). It becomes pressurised, and interstitial fluid pressurisation carries up to 90–95% of the applied load. The tissue behaves almost incompressibly and very stiffly.
• Over seconds to minutes, fluid exudes, load transfers progressively to the solid matrix, and the tissue creeps to a new equilibrium. Equilibrium compressive modulus is only ~0.5–1.5 MPa — soft — but the instantaneous behaviour is far stiffer.
• On unloading, osmotic pressure from the fixed charges draws fluid back in and the tissue recovers.

Two important consequences:

• Cartilage is viscoelastic: it shows creep, stress relaxation and hysteresis. Loading rate matters enormously — cartilage tolerates rapid loading better than sustained loading.
• Prolonged static loading is dangerous because fluid pressurisation dissipates, transferring load directly to the solid matrix and to the chondrocytes. This is the mechanical explanation for cartilage damage under sustained posture or unrelieved joint compression, and it is why diurnal variation in stature (1–2 cm, from intervertebral disc fluid exudation) exists at all.

3.7.2 Lubrication

The coefficient of friction of a healthy synovial joint is approximately 0.002–0.02 — lower than ice on ice, and lower than any engineered bearing. Several mechanisms operate together:

Clinical relevance. In inflammatory arthritis, lubricin production is suppressed by IL-1 and TNF-α, and hyaluronan is depolymerised — friction rises before structural damage appears. This is part of the rationale for intra-articular hyaluronan injection, whose clinical effect size in osteoarthritis nonetheless remains small and contested.

Why cartilage heals badly

Figure 4 · Why cartilage heals badly

Five reasons, and they compound:

• No blood supply — no haematoma, no inflammatory cascade, no delivery of stem cells or growth factors, no clot scaffold. The normal wound-healing sequence cannot begin.
• No perichondrium on articular surfaces — no reservoir of chondroprogenitor cells for appositional repair.
• Chondrocytes are post-mitotic and immobile — they are individually entombed in lacunae, cannot migrate to a defect, and divide minimally in adults.
• Low metabolic rate and low oxygen tension — matrix turnover is slow at baseline (the half-life of type II collagen in human cartilage is measured in decades).
• A hostile mechanical environment — the defect is loaded, sheared and bathed in synovial fluid throughout the attempted repair.

The critical distinction: partial-thickness versus full-thickness

This paradox — that the deeper injury heals better — is the entire basis of marrow stimulation techniques, which deliberately convert a non-healing chondral defect into a healing osteochondral one.

Cartilage repair procedures and their rehabilitation

The general rehabilitation principle across all of them: motion early, load late. Movement feeds and organises the repair tissue; premature compressive and shear loading destroys it.

Fibrocartilage: menisci, labra and discs

3.10.1 The menisci of the knee

Two semilunar wedges of fibrocartilage, triangular in cross-section, thicker peripherally.

• Functions: increase congruence between the convex femoral condyles and the near-flat tibial plateau; distribute load over a larger area (transmitting 50–70% of the load in extension, and up to 85–90% of the load in the lateral compartment in deep flexion); shock absorption; secondary stability (the posterior horn of the medial meniscus is a critical secondary restraint to anterior tibial translation, which is why medial meniscal tears accompany chronic ACL deficiency); proprioception; lubrication.
• Collagen orientation: predominantly circumferential fibres, converting compressive load into hoop stress resisted at the anterior and posterior root attachments, with radial “tie” fibres preventing longitudinal splitting.
• Consequence: a root tear functionally equals a total meniscectomy, because hoop stress can no longer be contained and the meniscus extrudes. This is why root repair is now pursued aggressively.
• Vascular zones (Arnoczky and Warren): the red–red peripheral third is vascularised by the perimeniscal capillary plexus and can heal; the red–white middle third heals variably; the white–white inner third is avascular and does not heal.
• Total meniscectomy produces radiographic osteoarthritis in the great majority of patients over 15–20 years (the Fairbank changes). This is the single strongest argument for meniscus-preserving surgery and for the modern preference for structured exercise therapy over arthroscopic partial meniscectomy in degenerative tears.

3.10.2 The labra

• Glenoid labrum: deepens the shallow glenoid by roughly 50%, increasing surface area and contributing to the concavity–compression stability mechanism and to the suction-seal effect. It is the anchor for the long head of biceps superiorly (hence SLAP lesions) and for the inferior glenohumeral ligament (hence the Bankart lesion in anterior dislocation).
• Acetabular labrum: deepens the acetabulum, and — more importantly — forms a fluid seal that maintains intra-articular fluid pressurisation. Labral tearing destroys the seal, allows fluid extrusion under load, and accelerates cartilage degeneration. This is the mechanism linking femoroacetabular impingement to early hip osteoarthritis.

3.10.3 Other fibrocartilages

• Intervertebral disc: anulus fibrosus (15–25 concentric lamellae, fibres at ~30° to the horizontal and alternating in direction between lamellae — an arrangement that resists torsion in both directions but with only half the fibres engaged in each) enclosing the nucleus pulposus. The adult disc is the largest avascular structure in the body, nourished by diffusion through the vertebral endplates; it is treated fully in Chapter 18.
• TFCC at the wrist; articular discs of the sternoclavicular, acromioclavicular and temporomandibular joints; pubic symphysis.
• Fibrocartilaginous entheses, where tendon meets bone through four graded zones — tendon, uncalcified fibrocartilage, tidemark, calcified fibrocartilage, bone. This gradual stiffness gradient dissipates stress concentration, and its degeneration is central to insertional tendinopathy.

Osteoarthritis: what is actually happening

Osteoarthritis is not passive wear and tear of an inert bearing surface. It is an active, cell-mediated disease of the whole joint as an organ — cartilage, subchondral bone, synovium, capsule, ligament, meniscus, fat pad and periarticular muscle.

The sequence

• Initiation. Abnormal load on normal cartilage, or normal load on abnormal cartilage. Chondrocytes are mechanosensitive; injurious loading and inflammatory cytokines shift them to a catabolic phenotype.
• Matrix degradation. Aggrecanases (ADAMTS-4 and -5) cleave aggrecan — the earliest change. Matrix metalloproteinases (MMP-1, -3, -13) subsequently cleave type II collagen — the point of irreversibility, because the collagen network cannot be rebuilt.
• Proteoglycan loss → water content paradoxically rises early (the swollen, softened cartilage of early OA), then falls as the collagen network fails.
• Surface change: softening (chondromalacia) → fibrillation → fissuring → erosion → full-thickness loss with eburnated bone.
• Chondrocyte response: initially proliferative clustering and attempted repair; later hypertrophic differentiation with type X collagen expression, calcification and apoptosis.
• Subchondral bone: sclerosis, thickening, subchondral cysts, and bone marrow lesions — which on MRI correlate with pain far better than cartilage loss does.
• Osteophytes form at the joint margin by endochondral ossification, an attempt to redistribute load.
• Synovitis: matrix fragments (fibronectin fragments, hyaluronan fragments) act as damage-associated molecular patterns, activating synovial macrophages via toll-like receptors → IL-1β, TNF-α, IL-6, prostaglandins — sustaining the catabolic loop. Low-grade inflammation is present in most symptomatic OA.
• Whole-joint failure: capsular fibrosis, ligament laxity, meniscal extrusion, fat pad fibrosis, muscle weakness and altered neuromuscular control.

Grading

Where does the pain come from?

Articular cartilage is aneural. It cannot generate pain. Osteoarthritic pain arises from:

• Subchondral bone — bone marrow lesions, raised intraosseous pressure, microfracture; richly innervated
• Synovium and capsule — inflammation and stretch; type IV free nerve endings
• Periosteum at osteophyte sites
• Ligaments, menisci (peripheral third) and the infrapatellar fat pad — the fat pad is one of the most densely innervated structures in the knee
• Muscle — spasm, weakness, altered load-sharing
• Central mechanisms — peripheral and central sensitisation, which explain much of the notoriously weak correlation between radiographic severity and reported pain

This is the single most useful fact in the chapter for a physiotherapist, because none of those sources is cartilage, and every one of them is modifiable. It is why exercise therapy improves pain and function in osteoarthritis despite doing nothing to reverse cartilage loss, and it is the basis of the GLA:D and comparable structured exercise programmes recommended as first-line care in every major OA guideline (NICE, OARSI, ACR).

Loading and cartilage health

Contrary to lay belief and much clinical folklore, moderate loading is protective, not destructive. Long-distance recreational running is not associated with an increased incidence of knee osteoarthritis in the available cohort data, and is associated with a lower incidence than sedentary living; the risk lies with elite-level volume, with previous joint injury (particularly ACL rupture and meniscectomy, which carry a large increase in post-traumatic OA risk), and with obesity, whose effect is both mechanical and metabolic (adipokines, systemic low-grade inflammation). Advising an osteoarthritic patient to “save the joint” by resting is not neutral advice; it removes the nutritional and anabolic stimulus the tissue depends on.

Where students consistently go wrong

• Saying “cartilage pain”. It is aneural. Name the actual source.
• Confusing collagen types. Hyaline and elastic = type II. Fibrocartilage and bone = type I. Type X = hypertrophic/calcified cartilage only.
• Forgetting that articular cartilage has no perichondrium. This is why the cartilage of the ear can regenerate a surface and the cartilage of the knee cannot.
• Assuming deeper injury is worse. Full-thickness defects heal (with fibrocartilage); partial-thickness ones do not heal at all.
• Treating meniscal tissue as uniform. Red–red heals, white–white does not, and root tears functionally destroy the whole meniscus.
• Equating radiographic OA severity with symptoms. The correlation is weak; treat the patient, not the film.
• Advising rest for osteoarthritis. Cartilage is fed by movement.
• Loading a cartilage graft when the patient feels well. Repair tissue is mechanically weakest at 6–12 weeks, precisely when symptoms resolve.
• Prolonged static positioning. Sustained compression dissipates interstitial fluid pressurisation and transfers load to the solid matrix.
• Forgetting elastic cartilage does not calcify. A reliable one-mark question.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 3 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 4 — Joints: how they are classified, what makes them stable, and what stops them moving.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents