Why cartilage damage can stay silent for a long time

Cartilage damage can be present for months — sometimes years — before it makes itself known. The reason lies in the tissue itself: hyaline articular cartilage contains no nerve fibres and no blood vessels, so even a developing defect sends no pain signal of its own.

Symptoms tend to emerge once the lesion grows large enough, or deep enough, to disturb the mechanics of the joint or irritate the surrounding tissue. When they do appear, the pattern is recognisable. Pain is usually activity-related and compartment-specific — felt most keenly during running, squatting, or descending stairs, and often easing at rest. The knee may swell after exertion (a joint effusion), and many patients notice catching, clicking, locking, or a grating sensation (crepitus) during movement. Early on, these symptoms are often intermittent; a bad day followed by a week of near-normality can make the problem easy to dismiss.

One important nuance: the degree of structural damage visible on a scan does not map neatly onto how much pain a patient experiences. Some people carry significant cartilage loss with modest symptoms; others report disabling discomfort from a lesion that looks relatively minor on imaging. Symptoms and imaging together — not either one alone — are what guide the clinical assessment of severity.

Why the symptoms rarely point to cartilage damage alone

Rarely does a focal cartilage defect present as the only finding in an affected knee. According to published evidence, articular cartilage damage in the knee is more often found alongside injury to the ligaments or menisci than on its own — and that coexistence makes the symptom picture genuinely difficult to read.

Take locking as an example. A knee that catches and locks mid-movement could reflect a displaced fragment of damaged cartilage, a torn meniscus flap, or both at once. No single symptom reliably separates one from the other. The same is true of pain: a consistent ache on the inner (medial) side of the joint points towards that compartment, which narrows the picture, but medial pain can arise from the cartilage surface, the meniscus, the collateral ligament, or some combination of these structures.

Concomitant injuries can also mask each other — one source of discomfort drowning out another or making it seem less severe than it is. This is why self-diagnosis at this stage almost always falls short, and why GP triage alone may not unravel the picture completely. A thorough clinical history needs to screen actively for associated injury rather than treating the cartilage as an isolated problem. Specialist assessment is often what brings the full picture into focus.

What a specialist wants to know from your history

By the time a specialist sits down to take a history, they are already building a differential that goes beyond cartilage. The first thing they want to understand is mechanism: was there a discrete traumatic event — a sporting collision, an awkward landing — or has discomfort crept up over months without a single defining moment? A traumatic origin and a slow-wear pattern carry different prognoses and lead the clinician towards different treatment logics from the outset.

Duration matters next. A defect that has been symptomatic for over a year may have already altered how the patient loads the joint, which in turn affects the surrounding structures. Prior interventions — a course of physiotherapy, a steroid or hyaluronic acid injection, or earlier surgery — are noted carefully. Previous knee surgery is particularly significant: altered joint mechanics following any procedure independently raises the risk of further cartilage damage, so it changes how the current picture is interpreted.

Finally, patient-specific factors are formally documented: age, sex, body weight relative to height (BMI), and habitual activity level. These are not administrative details. A 2.9-year cohort study by Carnes et al. (2012) confirmed that these variables influence how quickly a defect progresses — higher BMI and lower activity level being associated with faster deterioration in older adults. Taken together, this history tells the clinician how urgently formal imaging is needed and whether a period of structured conservative management is realistic before any intervention is considered.

What MRI shows and why it is the central imaging step

Once the history points towards a structural cartilage problem, imaging is the next decisive step — and MRI is the tool that answers the patient's most pressing question: how bad is it?

A baseline MRI scan maps the defect in three dimensions. The radiologist and surgeon are looking at depth (how far the damage penetrates towards or through the subchondral bone), surface area in square centimetres, and precise compartmental location. The scan also picks up what is happening around the lesion: bone marrow changes immediately beneath the defect, the condition of the menisci, and whether any ligamentous structures show signs of concurrent injury. All of this feeds directly into treatment planning — a point established in the pre-treatment literature that uses baseline MRI as the reference against which subsequent repair tissue is measured.

For standardised, reproducible documentation across the whole joint, validated scoring tools exist. The MOAKS — MRI Osteoarthritis Knee Score — is one such framework, offering a structured semi-quantitative map of cartilage loss, bone changes, and other features across every knee compartment. Its value lies in consistency: different clinicians reviewing the same scan use the same language and the same severity anchors.

Plain weight-bearing X-rays are used alongside MRI to assess overall limb alignment and any visible joint-space narrowing, though they provide little detail on the cartilage surface itself.

MRI is not infallible. Partial-thickness lesions — those that do not yet reach the subchondral bone — can be difficult to detect reliably, and arthroscopy remains the definitive reference standard for cartilage assessment. In practice, however, arthroscopy is reserved for when treatment is being carried out, not used purely for diagnosis.

The three defect parameters that drive treatment decisions

Three specific measurements emerge from that baseline MRI — and together they determine which repair options are even on the table.

Depth is graded using the ICRS system developed by the International Cartilage Repair Society. Grade 1 describes superficial softening or fissuring that does not penetrate deeply; Grade 2 reaches less than half the cartilage thickness; Grade 3 goes deeper still, with sub-grades (A through D) reflecting how close the damage is to the subchondral bone; Grade 4 means the lesion has breached that bone layer entirely. This progression matters because the biological environment available for repair changes at each grade — a Grade 4 lesion requires a fundamentally different approach from a Grade 2.

Area, measured in cm², is the second critical number. A broad clinical divide sits at roughly 2–4 cm², below which certain marrow-stimulation techniques remain viable and above which cell-based or scaffold-based approaches become more appropriate. The precision of this measurement has direct outcome consequences. The SUMMIT trial, comparing cell-based repair (MACI) with microfracture in patients with defects of 3 cm² or larger, found that MACI produced meaningfully better KOOS pain and function scores at both two and five years. That result means accurate area measurement at the assessment stage is not a bureaucratic formality — it is outcome-predictive.

Containment describes whether an intact cartilage rim surrounds the defect on all sides. When the lesion opens to the joint edge — an uncontained pattern — the structural support needed for a blood clot to stabilise and mature is absent. Large uncontained lesions are associated with 93% of microfracture failures, making containment status one of the most decisive single findings in the entire assessment pathway.

Characterise all three parameters accurately, and the treatment decision largely follows.

The full pre-treatment checklist and what happens next

Imaging and defect parameters answer the 'how bad is it?' question, but they do not answer it alone. Three adjacent findings must be documented before any treatment plan can be finalised.

Limb alignment — specifically varus (bow-legged) or valgus (knock-kneed) deviation — determines whether mechanical load is being channelled abnormally through the damaged compartment. Unaddressed malalignment will overload a repair site regardless of the technique or material used to address the cartilage itself.

Ligamentous stability matters for the same reason: instability redistributes compressive and shear force unpredictably with every step, undermining the biological environment a healing cartilage lesion requires. Where instability is confirmed, it must be addressed concurrently, not deferred.

Meniscal status closes the pre-treatment checklist. The meniscus absorbs a substantial proportion of the compressive load passing through the knee, and a deficient or damaged meniscus amplifies loading directly on the cartilage surface beneath it. Its condition must be factored into any repair strategy from the outset.

Taken together, defect grade, area, containment, alignment, ligament integrity, and meniscal health form the decision matrix a specialist works through before stratifying options. That range extends from supervised physiotherapy and load management for milder presentations through to injectable collagen scaffolds, cell-based repair, and corrective osteotomy for more complex cases — each intervention matched to the specific parameters the assessment has established.

What a completed assessment ultimately delivers is clinical clarity. A patient who understands the grade, size, containment, and mechanical context of their defect is far better placed to weigh the available options and commit meaningfully to a pathway.

1. [1] Hyaline cartilage. https://en.wikipedia.org/?curid=1130627 https://en.wikipedia.org/?curid=1130627
2. [2] Articular cartilage damage. https://en.wikipedia.org/?curid=19057920 https://en.wikipedia.org/?curid=19057920