From bone shape to cartilage injury — what actually happens

Most people diagnosed with femoroacetabular impingement (FAI) are told they have a bone-shape problem — and that is true, as far as it goes. The femoral head is not quite round enough (cam type), or the acetabulum overhangs the joint (pincer type), or both. Think of a door hinge whose pin is very slightly off-centre: the door still opens and closes, but over months and years the frame wears unevenly at one spot. FAI works the same way. Each time the hip flexes — getting into a car, climbing stairs, sitting at a desk — the misshapen bone presses against the acetabular rim rather than gliding cleanly past it.

The damage does not arrive all at once. Repetitive friction first strains the labrum, the fibrocartilage ring that seals the joint. As micro-trauma accumulates, it disrupts the chondrolabral junction — the point where the labrum meets the articular cartilage surface. From there, the cartilage itself begins to lift away from the underlying bone, a process called chondral delamination. Arthroscopic studies confirm that delamination is present in roughly 43% of FAI patients by the time surgery is performed, underlining how frequently the condition has already crossed this threshold at diagnosis.

The pattern of injury has a characteristic shape: FAI produces a centrally anchored cartilage flap with disruption at the periphery — an 'outside-in' lesion. This differs from the damage seen in hip dysplasia and carries a positive predictive value of 91% for FAI specifically. Cam morphology tends to concentrate damage anterosuperiorly at the femoral head-neck junction; when a pincer element is also present, posteroinferior acetabular cartilage is additionally at risk.

Recognising where a patient sits along this progression is the central clinical decision. While the hip is still in the labral-strain phase, the goal is mechanical correction. Once chondral delamination is established, the priority shifts — correction of the bone shape remains necessary, but it is no longer sufficient on its own. Salvaging and rebuilding the cartilage surface becomes an equally important part of any treatment plan.

How common is cartilage damage in FAI, and can imaging detect it?

Knowing that cartilage injury is already present in a large proportion of FAI patients at the point of assessment raises a practical question: can it be reliably detected on a scan before going further?

Standard 3.0-Tesla MRI — the imaging most patients receive — performs reasonably well. In a 2025 study of 233 FAI patients with arthroscopic confirmation as the reference, preoperative 3.0-T MRI achieved a sensitivity of 83.7% and specificity of 82% for acetabular chondral delamination, with a negative predictive value of 89.1%. That NPV is clinically useful: a clearly negative MRI makes delamination less likely, though it does not exclude it with certainty. Roughly one in six cases of genuine cartilage damage may not appear on a standard scan — which is why a scan result should be read alongside symptoms and clinical examination, not treated as a verdict on its own.

When diagnostic precision carries higher stakes — for example before a complex treatment decision, or when clinical findings and imaging reports do not align — MR arthrography offers a step up. Introducing contrast into the joint distends the capsule and outlines the chondrolabral interface more clearly, and published comparisons confirm it detects more labral and cartilage lesions than conventional MRI alone.

Arthroscopy remains the definitive reference standard; a 'normal' MRI cannot rule out chondral damage.

There is also an indirect imaging signal worth noting. Radiographic FAI markers — elevated alpha angle, raised lateral centre-edge angle (LCEA), greater acetabular coverage — correlate with lower T2 cartilage mapping values on both the femoral and acetabular surfaces. This provides an imaging bridge between bone shape and the likely state of the cartilage beneath it, even when direct visualisation of the cartilage is equivocal.

The tipping point — why treating FAI early protects cartilage

Timing matters more than most patients realise — and there is molecular evidence to explain why.

RNA sequencing studies comparing FAI cartilage at different stages of damage have identified something clinically important: early in the disease, the joint is still mounting a repair response. Growth-signalling proteins FGF18 and WNT16 — both involved in cartilage maintenance — are measurably elevated in low-grade FAI tissue. The joint has not given up; it is still trying to stabilise itself.

As the damage worsens, that repair signal weakens. Catabolic enzymes — most notably MMP13 (which breaks down collagen in the cartilage matrix) and ADAMTS4 (which degrades the scaffold proteins between cartilage cells) — begin to dominate instead. This pattern mirrors what researchers see in end-stage hip osteoarthritis, suggesting that late FAI and early OA may share the same destructive biology, not merely the same clinical appearance.

The joint's synovium — its inner lining — adds a further complication. Biochemical studies show that inflammatory signals including IL-1β and TGF-β1 are already active in FAI synovial tissue before visible inflammation appears on a scan or under a microscope. Cartilage may be under chemical attack before structural damage becomes detectable by conventional imaging.

This body of evidence — drawn from cohort and laboratory studies rather than randomised trials — supports a tipping-point model: once the balance tips from repair to destruction, the goal shifts from restoring cartilage to slowing its loss. Intervening while repair signals are still active, before that shift consolidates, offers the widest window for meaningful cartilage salvage.

Treatment options once cartilage is involved

Severity and stage determine where treatment begins — and whether it can stay conservative.

For mild-to-moderate chondral damage without full-thickness involvement, physiotherapy remains the appropriate first step. A supervised programme targeting hip stabilisers and reducing impingement-provoking load patterns can meaningfully reduce symptoms, and the long-term cohort data show that many patients managed conservatively do not progress to surgery. Anti-inflammatory support — oral or injected — may assist symptom control during this phase, though it does not address the underlying bone morphology.

Once full-thickness chondral defects are confirmed, the surgical decision-making becomes more detailed.

Microfracture is the established baseline for focal, contained lesions. Technique is demanding: perforations must be 4 mm deep and 3–4 mm apart, the labrum requires repair to contain the forming clot, and the underlying cam deformity must be corrected simultaneously. Despite correct execution, microfracture carries approximately 22% conversion to total hip arthroplasty at medium-term follow-up — a rate that has prompted interest in more durable alternatives.

Autologous membrane-induced chondrogenesis (AMIC) represents the current preferred option for medium-sized grade III/IV defects — broadly defined as 2–4 cm² in patients with Tönnis grade ≤2. A clinical series of 201 patients followed to five years recorded a mean modified Harris Hip Score improvement of 39.1 points, with scores peaking at three years (85.5 ± 7.2) and remaining stable thereafter. THA conversion rates were lower than those reported for microfracture.

For patients with suitable focal defects who are not yet surgical candidates, or who wish to explore non-theatre options first, an injectable collagen scaffold — delivered as an ultrasound-guided outpatient procedure — provides a matrix-induced chondrogenesis pathway. Specialist assessment determines whether defect size, grade, and overall joint status make this approach appropriate.

At the far end of the spectrum, large parafoveal lesions inaccessible by arthroscopy may require open surgical hip dislocation with fresh osteochondral allograft and concomitant cam osteoplasty. This is a salvage intervention reserved for cases where less invasive reconstruction is not feasible.

Who does well — and what the evidence says about realistic outcomes

Stage at presentation is the single strongest predictor of how well a patient fares — and the long-term data put a precise figure on what timely intervention achieves.

A cohort study following 957 patients over a mean of 12.5 years found that those who underwent hip arthroscopy experienced OA progression in 26.5% of cases, compared with 35.2% in the conservatively managed group. Conversion to total hip arthroplasty ran at 6.8% versus 10.5% respectively. These are meaningful gains — equivalent to roughly one-in-four OA progressions averted — but not a guarantee of permanent preservation.

Who does best? The evidence consistently points to three characteristics: younger age, lower BMI, and Tönnis grade I at the time of treatment. Patients with mild-to-moderate chondral damage at surgery tend to achieve functional outcomes close to those with no cartilage injury at all. Severe full-thickness damage before intervention substantially worsens scores across every reported outcome metric — pain, function, and patient satisfaction.

One evidence gap is worth naming plainly: no randomised trial has yet directly compared microfracture, AMIC, and MACI in FAI-specific lesions, and biological repair durability beyond ten years remains limited. What the data do establish is that bone reshaping alone is insufficient once full-thickness loss is confirmed — cartilage-specific intervention changes the trajectory in a way that cam osteoplasty alone cannot.

A 10–25% surgical failure rate with progressive degeneration in that subgroup is real, but it is disproportionately concentrated in patients with advanced damage at presentation — reinforcing the case for earlier assessment rather than waiting for symptoms to become disabling.

When to get a specialist opinion

The evidence reviewed here converges on one practical point: stage at assessment determines what is possible. Cartilage that has crossed from early anabolic repair capacity into catabolic breakdown responds far less predictably to any treatment — conservative or surgical. That makes earlier specialist review the most modifiable factor in long-term outcome.

Symptoms that justify referral sooner rather than later include groin or anterior hip pain that worsens with flexion-loaded activity, a mechanical catching or locking sensation, pain that has not settled after six to eight weeks of structured physiotherapy, or MRI findings of labral or cartilage involvement alongside FAI morphology. A specialist assessment means clinical history, physical examination, and imaging review — not an automatic surgical pathway.

For patients with confirmed focal chondral defects who are not yet surgical candidates, or who wish to explore outpatient options first, the ultrasound-guided ChondroFiller injection — a collagen scaffold that recruits the body's own progenitor cells — is one pathway worth discussing at consultation. Professor Paul Y. F. Lee delivers Liquid Cartilage™ at the London Cartilage Clinic on Harley Street; book an assessment at londoncartilage.com.

1. [1] The 'Outside-In' Lesion of Hip Impingement and the 'Inside-Out' Lesion of Hip Dysplasia: Two Distinct Patterns of Acetabular Chondral Injury. (2019). https://doi.org/10.1177/0363546519871065 https://doi.org/10.1177/0363546519871065
2. [2] Anatomical Mechanisms of FAI and Its Role in the Progression to Hip Osteoarthritis: A Systematic Review. (2025). https://doi.org/10.7759/cureus.86461 https://doi.org/10.7759/cureus.86461
3. [3] CT-based radiographic parameters with hip articular cartilage T2 MRI mapping values in FAI and dysplasia. (2025). https://doi.org/10.1093/jhps/hnaf011.271 https://doi.org/10.1093/jhps/hnaf011.271
4. [4] Accuracy of MRI in the Diagnosis of Acetabular Chondral Delamination in Femoroacetabular Impingement. (2025). https://doi.org/10.1093/jhps/hnaf011.149 https://doi.org/10.1093/jhps/hnaf011.149
5. [5] Surgical Hip Dislocation and Fresh Osteochondral Allograft Transplantation for FAI and Concomitant Chondral Lesion. (2020). https://doi.org/10.1016/j.eats.2020.08.012 https://doi.org/10.1016/j.eats.2020.08.012
6. [6] Biochemical and Histologic Evaluation of Pulvinar Synovium Provides Insight Into OA Progression Secondary to FAI. (2025). https://doi.org/10.1002/jor.26115 https://doi.org/10.1002/jor.26115
7. [7] Progression of OA at Long-term Follow-up in Patients Treated for FAI With Hip Arthroscopy vs Nonsurgical Patients. (2023). https://doi.org/10.1177/03635465231188114 https://doi.org/10.1177/03635465231188114