Cartilage

What it is

Cartilage (a firm, rubbery body tissue, softer than bone) has cells called chondrocytes. They sit in small spaces called lacunae inside the cartilage matrix (the material around the cells)¹. Cartilage’s distinctive appearance comes from sugar chains called chondroitin sulfates, which bind with proteins to form proteoglycans (large protein-and-sugar molecules that hold water)¹. Articular cartilage has no blood vessels or nerves². In cartilage without blood vessels, nutrients must seep through the matrix to reach the cells¹.

Three kinds of cartilage

The three main kinds differ in what runs through their matrix¹:

• Hyaline cartilage, the most common, has short, scattered fibres of collagen (a strong, rope-like protein) and a lot of proteoglycan. It is found in the nose and rib cage and on bone ends at movable joints¹.
• Fibrocartilage is tough because thick bundles of collagen run through it. It can absorb pressure, and the knee’s menisci (pads of cartilage in the knee) and the spine’s intervertebral discs are made of it¹.
• Elastic cartilage also holds elastic fibres, so it is stiff but springy. The outer ear contains it¹.

The knee holds two of these kinds. The articular cartilage (the hyaline layer on bone ends in a joint) covers the bone surfaces, and the menisci are fibrocartilage¹. Each spinal disc has a tough outer ring around a soft, gel-like centre whose water resists squeezing and helps bear weight¹.

Cartilage and the growing skeleton

Hyaline cartilage forms a model of the skeleton in the embryo before bone forms¹. Once the fetal skeleton has formed, this cartilage model remains only at joint surfaces and at the growth plate¹. The growth plate sits between a long bone’s shaft and end¹. That growth plate lets bones keep growing until adulthood¹.

How it responds to load

Chondrocytes renew the cartilage matrix, and mechanical forces strongly shape whether cartilage is kept up, breaks down or rebuilds⁷. The cells respond to growth factors, mechanical loads and fluid pressure².

A review of ion channels (pores in a cell’s outer layer) in chondrocytes describes two paths⁷. Physiological (normal) loading, at 10% strain (stretch as a share of resting length), opens a channel called TRPV4⁷. This drives a building pathway that raises production of collagen II and aggrecan (a proteoglycan)⁷. Injurious loading, at 50% strain, works through a channel called Piezo1 to switch on a breakdown pathway⁷.

Use and disuse

A review states that joint motion and load are important for keeping articular cartilage normal, and that joint inactivity leads to cartilage breakdown². In people with complete spinal cord injury, knee cartilage was thinner than in healthy volunteers, and the gap widened over time⁸. At 24 months it was 23% to 25% thinner at the kneecap and inner shinbone⁸. In 20 people with ankle fractures who bore only partial weight for 7 weeks, knee cartilage thinned by 2.9% to 6.6%⁹. A review of meniscus research states that feeding the meniscus by diffusion needs repeated loading and unloading¹⁰.

What one run does

A meta-analysis of 24 MRI studies found knee cartilage thickness and volume fell right after running³. Volume fell by 3.3% in the weight-bearing thigh-bone cartilage and 4.9% behind the kneecap³. Its authors rated this evidence very low certainty and judged the changes small and apparently short-lived³. T2 (an MRI measure that changes when tissue is damaged or swollen) in the main knee joint’s cartilage was back to baseline within 91 minutes³.

A second review, of 43 MRI studies, concluded that cartilage changes after running are short-lived and likely reflect normal fluid movement¹¹. It found moderate evidence that running does not lead to new cartilage lesions (areas of damaged tissue)¹¹. The evidence on existing knee lesions was conflicting¹¹.

How it gets injured

Articular cartilage injury and wear are frequent in synovial joints (joints with a fluid-filled space between the bones)¹². Impact and twisting loads can injure it, and the injuries fall into three classes¹³:

• damage inside the cartilage under an intact surface¹³;
• a break limited to the cartilage¹³;
• a break through both the cartilage and the bone beneath¹³.

A review of 11 studies of 931 athletes found full-thickness cartilage defects in 36% of athletes’ knees overall¹⁴. This ranged from 2.4% to 75% between studies¹⁴. It concluded such defects are more common in athletes than in the general population¹⁴.

Why it heals poorly

Articular cartilage has a limited ability to heal and repair itself². It cannot rebuild to its original quality¹². Drilling or piercing the bone beneath prompts a repair process that forms fibrocartilage¹². This fibrocartilage is weaker than normal hyaline cartilage and cannot stand up to long-term repeated use¹⁵.

Articular cartilage collagen has a calculated half-life of 117 years, against 15 years for skin collagen¹⁶.

Articular cartilage collagen has a calculated half-life of 117 years, against 15 years for skin collagen.

Osteoarthritis

Osteoarthritis is the most common type of arthritis, and is associated with ageing and wear of joint cartilage¹. It is linked to chondrocytes’ breakdown and building of matrix falling out of balance². A draft definition from OARSI, a research society, describes it as starting with small and large injuries that trigger faulty repair¹⁷.

The Global Burden of Disease study estimated 595 million people had osteoarthritis in 2020, 7.6% of the world’s population⁶. The knee was the most common site⁶. High body mass index (weight for height) contributed an estimated 20.4% of all osteoarthritis, though this estimate was very uncertain⁶. A review of 53 studies found the odds of knee osteoarthritis about 4 times higher after an ACL (anterior cruciate ligament) injury¹⁸. After a meniscus injury, alone or with an ACL injury, the odds were about 6 times higher¹⁸.

Sport, activity and osteoarthritis

• A systematic review (a study that sums up all the research on a question) compared sport participants with non-participants¹⁹. It found knee osteoarthritis in 7.7% of 3,759 sport participants and 7.3% of 4,730 non-participants¹⁹.
• The same review found it significantly more common in soccer players, elite long-distance runners, competitive weightlifters and wrestlers¹⁹.
• A meta-analysis of 17 studies found hip and knee osteoarthritis in 3.5% of recreational runners and 13.3% of competitive runners. The figure was 10.2% in non-running controls²⁰.
• A meta-analysis of 14 observational studies (studies that watch people without assigning groups) found 26% higher knee osteoarthritis risk with high than with moderate activity²¹. Neither high nor moderate activity carried lower risk than low activity²¹.

The sport review also looked at players with no past knee injury. Elite soccer and orienteering athletes, and non-elite soccer and American football players, still had more knee osteoarthritis than non-participants¹⁹. Its authors note it is unclear whether any added risk comes from the sport, a sport injury or something else¹⁹. The running review could not tell whether its links were causal or explained by factors such as past injury²⁰.

Reviews of activity and knee structure on MRI also disagree. One found strong evidence that activity goes with fewer cartilage defects but more osteophytes (bone spurs), and limited evidence of more cartilage volume²². A later review of 18 studies in adults without knee osteoarthritis found no strong evidence either way²³.

How training builds it

A review of 9 randomised trials (studies that assign people to groups by chance) studied people with knee osteoarthritis or at raised risk of it⁴. It concluded that knee-loading exercise seems not to harm cartilage, as measured on MRI⁴. The evidence quality was low⁴. In trials of people with knee osteoarthritis, six comparisons found exercise did not thicken cartilage or change its volume or defects⁴.

A study of athletes points the same way. Knee cartilage thickness did not differ significantly between 18 triathletes training over 10 hours a week and 18 people never regularly active⁵.

A review of 29 randomised trials in healthy animals found moderate daily exercise went with no change or better knee cartilage²⁴. In 19 of 27 high-dose comparisons in these animals, cartilage measures fell²⁴. The authors suggest the link between daily exercise dose and cartilage make-up may not be a straight line²⁴. The authors of the 43-study running review suggest cartilage adapts to repeated running¹¹.

The discs of the spine

A meta-analysis of 39 studies (4,152 people) linked upright loading on two legs, mostly running, with better disc health²⁵. The certainty was very low, and no other kind of loading was linked to better or worse disc health²⁵. In a running review, one 15-year study found no difference in disc change between runners and controls²⁶.

Across the lifespan

Children and adolescents

In 74 children aged 9 to 18 measured about 1.6 years apart, knee cartilage volume grew at every site²⁷. Those above the median for sport intensity gained about twice as much at the tibia (shinbone), though not at the kneecap²⁷.

The growth plate is the cartilage layer near a growing bone’s end. A review of its injuries in young athletes notes it resists stress less than adult joint cartilage²⁸. It also resists shear and tension less than nearby bone²⁸. So forces that might tear a ligament in an adult can injure the growth plate instead²⁸.

• The growth plate is involved in about 15% of children’s fractures²⁸.
• Overuse problems of the apophyses (growth plates where major tendons attach) are common in young athletes²⁸. One is Osgood-Schlatter disease (a painful bump just below the kneecap in growing children)²⁸.
• In eight studies of gymnasts, 10% to 85% had X-ray changes consistent with growth plate stress in the radius (a forearm bone) at the wrist²⁸.

A review of 24 studies looked at overuse growth plate injuries in young athletes²⁹. It named rapid growth, age, body size, training volume and past injury as risk factors²⁹.

Adults and older adults

With age, articular cartilage holds less water and grows stiffer when squeezed². Chondrocytes lose some of their ability to divide and make matrix, but still release substances that drive inflammation and break down matrix³⁰. Sugar-modified proteins build up in the matrix, and aged cartilage copes less well with stress³⁰. MRI studies show knee cartilage thinning with age, mainly on the thigh bone and kneecap³⁰.

Sources differ on cell numbers. One says the total number of chondrocytes stays essentially unchanged with age². Another describes age-related thinning as consistent with falling water content and cell numbers³⁰.

With age, the meniscus becomes stiffer and less elastic¹⁰. The disc’s centre slowly loses water, so the disc becomes thinner and less flexible¹. In 3,110 people without back pain, scans showed disc degeneration (wear-type disc changes) in 37% of 20-year-olds and 96% of 80-year-olds³¹. The review’s authors concluded many such features are likely part of normal ageing³¹.

Osteoarthritis most often occurs after age 40, and becomes steeply more common with age⁶. In Global Burden of Disease estimates for 2020, it affected⁶:

Age group	People with osteoarthritis, per 100,000
25 to 49	29846
50 to 69	232376
70 and over	384196

Knee osteoarthritis peaked at ages 80 to 84⁶.

Connections

The library has entries on two cartilage structures of the knee. Articular cartilage is the hyaline layer on the bone ends¹. The two menisci are C-shaped pads of fibrocartilage between the thigh bone and shinbone¹. Their injury has its own page, meniscus tear. The 43-study running review found no change in foot and ankle cartilage with repeated running¹¹.

Cartilage covers the ends of bones at movable joints, and a cartilage plate lets bones grow in length¹. Injury to the ACL, a ligament, was linked to higher odds of knee osteoarthritis¹⁸. Traction growth plates sit where major tendons attach²⁸.

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Every source the library cites

Changes

• September 30, 2026 First published.