Its collagen barely does, on most measurements. Radiocarbon dating of knee cartilage from 23 people found virtually no replacement of the collagen network after the skeleton finished growing, and another study put the half-life of cartilage collagen at 117 years. Some researchers argue cartilage repairs more than that, pointing to faster turnover in ankle cartilage and to repair after knee joint distraction. The cushioning aggrecan is a different story.
Nuclear bomb tests in the mid-20th century raised the carbon-14 in the atmosphere, so the carbon-14 level in a protein shows roughly when it was made. Heinemeier and colleagues used this bomb-pulse method to date the collagen in shin-bone cartilage from the knees of 23 people born between 1935 and 1997. Fifteen had damaged cartilage and eight healthy (Heinemeier 2016).
The result was blunt. Virtually no replacement of the collagen matrix happened after skeletal maturity, and neither joint disease nor tissue damage changed the turnover rate (Heinemeier 2016). The team concluded that the collagen network of adult human cartilage is an essentially permanent structure with no significant turnover, even with disease.
An earlier study reached a similar answer by a different route. Proteins slowly change one of their amino acids, aspartic acid, into its mirror-image form as they age, so the proportion of the mirror form shows how long a protein has been in place. From that, Verzijl and colleagues calculated the half-life of cartilage collagen at 117 years. Skin collagen came out at 15 years (Verzijl 2000).
Virginia Kraus opened one talk with an even longer estimate, as the view generally held, before presenting her own lab's results that cut against it.
It's generally believed that the articular cartilage has very little intrinsic repair capacity, with collagen half-lives estimated to be between 200 and 400 years. So your collagen lives longer than you do.
The radiocarbon authors linked cartilage's poor capacity to regenerate with this limited turnover of its collagen matrix (Heinemeier 2016). The cells inside cartilage keep a small zone of activity around themselves. In healthy ankle cartilage, signs of new type II collagen were found in all zones, and synthesis and breakdown were balanced in the matrix next to the cells (Aurich 2002). Whether that local upkeep can rebuild the main network once it is lost is where researchers disagree. A 2021 review noted that there were no interventions available to restore degraded cartilage (Hu 2021).
Virginia Kraus and colleagues at Duke used a different molecular clock, the slow chemical ageing of proteins, to measure turnover in cartilage from human ankles, knees and hips. Turnover ran on a gradient, highest in the ankle and lowest in the hip, which they read as a limited capacity for repair (Hsueh 2019). In a 2022 talk Kraus gave half-lives of 3.9 years for type II collagen in the ankle and 8.6 years in the hip. Her group measured the soluble part of the collagen, she pointed out, while the radiocarbon study dated the insoluble network, so the two results may be describing different parts of the same tissue.
The second line of evidence comes from knee joint distraction, where a frame holds the joint slightly apart for a period. A Utrecht study followed 20 people under 60 whose knee osteoarthritis was bad enough for them to be considered for knee replacement. The authors reported an initial boost of cartilage-like tissue repair. Five years on, the narrowest part of the joint space was still wider than at the start, though mean cartilage thickness was no longer significantly above baseline, and the knees had lost less cartilage than comparison data on untreated osteoarthritis predicted (van der Woude 2017). It was a small study with no control group of its own.
Neither result overturns the radiocarbon finding for the knee's collagen network. They do suggest that cartilage, in some joints and some conditions, can repair more than the essentially permanent picture allows.
Tonia Vincent bases her view on small cartilage defects that heal on their own and on the joint-distraction studies.
I think there's really compelling evidence from the literature that cartilage is able to repair itself.
Cartilage has two main building materials, and they behave differently. Aggrecan, the water-holding molecule that resists squashing, is thought to be lost early and reversibly. Type II collagen loss is considered irreversible (Li 2011). In mice without MMP13, cartilage still lost aggrecan after injury but eroded less, which fits the idea that the collagen cut is the decisive one (Little 2009).
A few boswellia extract trials in people with knee osteoarthritis have measured cartilage or its markers. In one, 80 people took 100 mg a day of a standardised extract or placebo for 180 days, and MRI showed cartilage volume, thickness and joint space width increased in the extract group compared with placebo (Kumar 2025). In another, 62 people took boswellia with celery seed extract for 90 days, and blood markers linked to making type II collagen rose against placebo (Vaidya 2025).
These are single trials of specific extracts at specific doses. They don't show that cartilage collagen regrows in general, and their results belong to the extracts tested.
One reason is how fast their collagen turns over. One study estimated the half-life of skin collagen at 15 years and cartilage collagen at 117.
Not in the radiocarbon study. It found that neither joint disease nor tissue damage changed the very low collagen turnover in adult knee cartilage.
A little, close to the cells. Healthy ankle cartilage showed signs of new type II collagen in all zones, balanced against breakdown in the matrix next to the cells.
No. A Duke group found faster protein turnover in ankle cartilage than in the hip, and a small Utrecht study reported cartilage-like tissue repair after knee joint distraction. The radiocarbon study found almost no turnover in the collagen network of the knee.
It depends which part is damaged. Reviews describe losing aggrecan, the water-holding molecule in cartilage, as an early and reversible step, and losing type II collagen...
Type II collagen is the main collagen in joint cartilage. Collagen makes up about two-thirds of adult cartilage's dry mass, and type II is its principal molecule, woven...
MMP13 cuts type II collagen, the rope-like fibre that gives cartilage its strength. It cleaves each three-stranded collagen molecule at one spot, leaving a three-quarter...
In animal and lab studies, yes. AKBA, the lead boswellic acid, suppressed MMP13 in rats with chemically induced knee damage, and a frankincense extract lowered MMP13...