Evidence-based physiotherapy and rehabilitation resources
Editorial & review policy
Evidence-based physiotherapy and rehabilitation resources
Editorial & review policyHuman Anatomy · General anatomy
Cartilage has no blood supply, no nerves and no lymphatics. Every difficult thing about it — why it is silent until it is badly damaged, why it heals so poorly, why movement is its only source of nutrition — follows from those three absences.
Cartilage is a firm connective tissue made of cells called chondrocytes sitting in small spaces called lacunae, surrounded by a matrix they produce themselves. The matrix is what gives cartilage its properties: a mesh of collagen holding a gel that is extremely good at trapping water.
That trapped water is the secret. Press on cartilage and water is squeezed out slowly; release the pressure and it draws back in. This is why cartilage can take repeated load without cracking, and why it feels firm but slightly yielding.
The three absences, and what each one costs
No blood vessels. Nutrients must diffuse in from the surface, so delivery is slow and repair is slower.
No nerves. Cartilage itself cannot hurt. Pain from a worn joint comes from the bone, capsule and synovium around it — which is why damage can be advanced before a patient notices.
No lymphatics. Cartilage clears waste and handles swelling poorly compared with tissue that has drainage.
Figure 1 · Why cartilage heals badly
In almost every other tissue, injury brings a rush of blood carrying inflammatory cells, growth factors and the cells that build repair tissue. In cartilage none of that arrives, because there is nothing to carry it.
Chondrocytes are also comparatively few, they sit trapped in their lacunae, and they do not migrate. A cell a millimetre from a defect cannot travel to it. The result is that damage confined to cartilage often does not heal at all, and where repair does occur the tissue laid down is usually fibrocartilage rather than the original hyaline — mechanically inferior, and it wears faster.
The exception that proves it
A defect that penetrates through the cartilage and into the underlying bone does bleed, and it does produce repair tissue — because it has reached a blood supply. Some surgical techniques work by deliberately drilling into the bone for exactly this reason. The repair is fibrocartilage, not hyaline, but it is better than nothing.
If there are no vessels, nutrition must arrive another way, and it does so by two routes.
Cartilage covered by a perichondrium — a fibrous sheath with its own vessels — is fed by diffusion from it. Most cartilage in the body has one.
Articular cartilage does not. The surface facing the joint is bare, and it is fed from the synovial fluid. Getting nutrients through that fluid and into the tissue depends on the joint being loaded and unloaded: compression squeezes fluid out, release draws it back in with fresh nutrients. Cartilage is nourished by being used.
Why this matters at the bedside
A joint that is never moved is a joint whose cartilage is not being fed. Prolonged immobilisation causes cartilage to thin and soften. This is one of the strongest anatomical arguments for early, controlled movement after injury or surgery — and one you can explain to a patient in a sentence.
Figure 2 · The three types compared
Figure 3 · The three types of cartilage under the microscope
Illustration to be added
Three histology panels side by side at matched magnification. Hyaline: chondrocytes in lacunae, often in isogenous groups, within a smooth glassy matrix; perichondrium at one edge. Elastic: the same cell arrangement but with a dense dark network of elastic fibres throughout the matrix. Fibrocartilage: thick parallel collagen bundles with chondrocytes lying in rows between them, no perichondrium. Beneath each panel, a small body silhouette marking where that type is found. Realistic histology style, labelled with gold leader lines.
| Hyaline | Elastic | Fibrocartilage | |
|---|---|---|---|
| Matrix | Fine collagen, not visible under an ordinary microscope; glassy appearance | Collagen plus a dense network of elastic fibres | Thick, parallel bundles of collagen; clearly visible |
| Chondrocytes | In lacunae, often in small clusters | In lacunae, numerous | In rows between the collagen bundles |
| Perichondrium | Present, except on joint surfaces | Present | Absent |
| Where | Joint surfaces, costal cartilages, nose, larynx, trachea, bronchi, growth plates, the fetal skeleton | External ear, epiglottis, auditory tube, parts of the larynx | Intervertebral discs, menisci of the knee, pubic symphysis, glenoid and acetabular labra, some tendon and ligament insertions |
| Good at | Smooth low-friction movement; spreading load | Returning to shape after being bent | Taking tension and compression at once; absorbing shock |
| Weak at | Repair. Wears under repeated shear. | Bearing heavy load | Providing a smooth gliding surface |
A pattern is worth noticing here. Fibrocartilage turns up wherever a joint has to combine movement with heavy load — between vertebrae, inside the knee, at the pubic symphysis, deepening the shoulder and hip sockets. Whenever you meet it, ask what forces that site is managing, and the answer is usually compression and tension together.
This is the type you will spend your career thinking about, so it earns its own section.
It is hyaline cartilage, a few millimetres thick, covering the ends of bones inside a synovial joint. Its surface is extraordinarily smooth — a healthy joint has less friction than ice sliding on ice — and it spreads load from the joint over a wide area of bone beneath.
Figure 4 · The zones of articular cartilage
Illustration to be added
A vertical section through articular cartilage on the end of a bone, showing four zones with collagen fibre direction drawn in each: superficial zone with fibres parallel to the surface and flattened chondrocytes; middle zone with oblique arcading fibres and rounded cells; deep zone with fibres perpendicular to the surface and cells in columns; calcified zone below the tidemark, anchoring into subchondral bone. Mark the tidemark and the subchondral bone plate. Include a small companion panel showing the same section with fibrillation and thinning, for comparison. Cartilage pale blue, bone warm ivory, collagen fibres as fine navy lines.
| Zone | Collagen fibres run | What it does |
|---|---|---|
| Superficial | Parallel to the surface | Resists shear as the surfaces slide; the smooth gliding layer |
| Middle | Obliquely, in arcades | Absorbs compression |
| Deep | Perpendicular to the surface | Resists compression and anchors the tissue downwards |
| Calcified | Anchoring into bone | Binds cartilage to the bone beneath, across the tidemark |
The changing fibre direction is not decoration. It means the tissue is built to handle a different kind of force at each depth — shear at the top where surfaces slide, compression deeper down where load passes into bone.
From within. Chondrocytes already in the matrix divide and lay down more matrix around themselves, so the tissue expands from the inside. This is how cartilage grows in young people and how the growth plate lengthens a bone.
From the surface. Cells in the inner layer of the perichondrium become chondrocytes and add new cartilage to the outside, so the tissue thickens. This is the only route available where a perichondrium exists.
Both slow markedly with age. Adult cartilage has limited capacity to grow at all, which is part of why the tissue does not simply replace itself when worn.
You will meet worn cartilage constantly, so it is worth understanding the sequence rather than only the diagnosis.
| Stage | What is happening | What the patient notices |
|---|---|---|
| Early matrix change | Water content rises and the collagen mesh loosens. The surface softens. | Often nothing at all. Cartilage has no nerves. |
| Surface fibrillation | The smooth surface frays and splits vertically. | Perhaps stiffness after rest; perhaps still nothing. |
| Thinning and loss | Cartilage is lost down towards bone. Load concentrates on a smaller area. | Pain on loading, stiffness, reduced range. |
| Bone involvement | Exposed bone thickens, cysts form, osteophytes grow at the margins. | Pain at rest and at night, deformity, marked loss of function. |
Two things this explains
Why the pain arrives late. The cartilage is not what hurts. Symptoms begin when the bone, capsule and synovium beneath and around it become involved — which is well after the cartilage itself has changed.
Why what you see on a scan may not match how the patient feels. Structural change and symptoms come from different tissues, so they do not run in step. Treat the person in front of you, not the report.
It has no nerve supply and cannot generate pain. Name the structure that actually hurts: subchondral bone, capsule, synovium, or the surrounding soft tissue.
Articular cartilage is fed by the loading and unloading cycle. Complete rest starves it. Controlled movement is protective; immobility is not.
Learn what each is good at and the locations follow. Fibrocartilage appears where compression and tension arrive together; elastic cartilage where something must spring back; hyaline where surfaces must glide.
Without vessels there is no inflammatory phase, and without migration there are no cells arriving to rebuild. Repair that does occur is usually fibrocartilage, and it is not as good as what was lost.
The outer third of a meniscus has a blood supply and can heal; the inner two thirds do not. This is why some meniscal tears are repaired and others are trimmed, and it is a favourite examination question.
Ten questions on this chapter. Tap one to see the answer and the reasoning.
Answer: (B) No nerve supply. Pain from a worn joint arises in the subchondral bone, capsule and synovium, which is why cartilage damage can be advanced before symptoms begin.
Answer: (C) It has no perichondrium. Nutrients come from synovial fluid, and the pumping action of loading and unloading is what drives exchange.
Answer: (C) Fibrocartilage. It appears wherever a site must take compression and tension together.
Answer: (B) Reaching bone means reaching blood, so an inflammatory and repair response occurs. The tissue formed is fibrocartilage rather than hyaline.
Answer: (B) Parallel to the surface, which resists the shear generated as the joint surfaces slide over one another.
Answer: (B) Interstitial growth. Appositional growth adds new cartilage at the surface from the perichondrium.
Answer: (C) Articular cartilage. Its free surface faces the joint cavity, which is why it depends on synovial fluid for nutrition.
Answer: (C) Thin and soften. Loading and unloading drive nutrient exchange, so a joint that is not moved is a joint whose cartilage is not being fed.
Answer: (B) The outer third is vascularised and can heal. The inner two thirds are avascular, so tears there are usually trimmed instead.
Answer: (B) Matrix softening comes first, then the surface frays, then the tissue thins, and only then does the bone become involved. Symptoms usually begin at that last stage.
Everything on this page, in one screen
| Book | What it adds here |
|---|---|
| B D Chaurasia's Handbook of General Anatomy Chaurasia and Garg |
Concise coverage of cartilage types and their distribution, in the order used above. |
| BRS Cell Biology and Histology Gartner |
The microscopic detail, including matrix composition and how the three types are told apart down a microscope. |
| Anatomy and Human Movement: Structure and Function Palastanga, Field and Soames |
The mechanical behaviour of articular cartilage under load, which is the part that matters most in practice. |
| Di Fiore's Atlas of Histology Eroschenko |
Photomicrographs, if you want to see the three types rather than read about them. |
Reviewed by the Physiotherapist India Team. · Human Anatomy contents