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In healthy ankle cartilage, collagen stays in balance as people age

MMP13 biologyHuman tissue2002

This 2002 study looked at healthy ankle cartilage from 30 donors aged 16 to 75. All four collagen-cutting enzymes were present but did not change with age, and type II collagen was made and broken down at a steady state throughout life. The authors found no sign that ageing alone produces the breakdown seen in diseased joints.

Evidence typeHuman tissue
Who or what was studied30 donors aged 16 to 75, macroscopically normal ankle cartilage
Dose and durationNot stated in the abstract

What they did

The team took ankle cartilage that looked normal from 30 donors aged 16 to 75. They used in situ hybridisation to find the genetic message for type II collagen, antibodies to detect newly made collagen, collagen cut by collagenases and collagen that had unwound, immunoblotting for the four collagenases, and assays for glycosaminoglycans and a marker of aggrecan.

What they found

After age 30 there were no significant changes in type II collagen, glycosaminoglycan content or the aggrecan marker. Signs of new collagen synthesis were present in all zones and did not change significantly with age. All four collagenases were detectable and showed no identifiable change with age. Collagenase-cut collagen showed a trend upward with age while unwound collagen did not, so the ratio of cut to unwound collagen rose with age. The authors concluded that type II collagen synthesis and breakdown stay at a steady state through life.

What it can't tell us

This is ankle cartilage, which may age differently from knee or hip cartilage. Each donor gave a sample at one point in time, so the study compares people of different ages rather than following anyone over years. It measured how much enzyme was present, not how the cells react when provoked, and the abstract does not report MMP13 separately from the other collagenases.

Why it matters

It separates age from damage. If healthy cartilage keeps its collagen in balance into the mid-70s, then getting older is not by itself what lets MMP13 and the other collagenases take over. That shifts the question to what provokes the cells, which is what Forsyth's 2005 study picked up.

The paper

  1. Aurich M, Poole AR, Reiner A et al. Matrix homeostasis in aging normal human ankle cartilage. Arthritis Rheum 2002.

Read next

Last reviewed 3 November 2026Every study cited here is indexed on PubMed. How we read the evidence