Why defect size is the first question your surgeon asks

A scan report that mentions cartilage damage tends to raise an immediate question: what does that actually mean for treatment? The answer hinges on two measurements your surgeon will want to establish before anything else — how deep the lesion goes, and how large an area it covers.

Articular cartilage lines both surfaces of the hip joint: the rounded femoral head and the cup-shaped acetabulum. Unlike bone or muscle, this tissue has no direct blood supply, so it cannot recruit the repair cells that would normally patch an injury. Left alone, a cartilage defect does not fill in; it either stays stable or widens over time under the repetitive loads the hip absorbs with every step.

Depth and area work together to define the clinical problem. Depth is graded on a 1–4 scale: Grade 1 is surface softening; Grade 4 means full-thickness loss reaching the underlying bone. Area is measured in square centimetres and separates a small, contained focal lesion from the diffuse cartilage thinning seen across the whole joint in osteoarthritis. These are fundamentally different problems — and they call for fundamentally different responses, ranging from a targeted restorative procedure to symptom management or, at the far end of the spectrum, joint replacement.

Grading hip cartilage damage: depth, area, and what they mean

Lesion area is where the grade system alone stops being sufficient. Once depth has been established, the question shifts to how many square centimetres are affected — and two thresholds recur throughout the clinical literature. Defects smaller than roughly 2 cm² sit within the range where a single-stage marrow-stimulation or autograft technique may be appropriate. Beyond approximately 4 cm², the biology of those simpler techniques becomes less reliable and cell-based or scaffold-based repair tends to be preferred. The 2–4 cm² band is a transitional zone where the choice depends on containment, the condition of the surrounding cartilage, and the patient's age and activity demands.

A Grade 4 lesion — full-thickness loss reaching the subchondral bone — does not automatically place a defect beyond repair. A small, well-contained Grade 4 hole in an otherwise healthy joint is a very different clinical problem from Grade 4 change spread across a wide arc of the femoral head or acetabulum. Containment and area matter as much as depth in determining whether restoration is realistic.

Focal damage versus diffuse osteoarthritis

Femoroacetabular impingement (FAI) — abnormal cam or pincer bony morphology at the hip — is one of the more common causes of focal cartilage damage in younger, active patients. The irregular bone contact abrades cartilage and stresses the labrum over time. Hip arthroscopy can address both the bone deformity and the cartilage lesion in the same procedure, which is why FAI context is central to surgical planning rather than a separate concern.

Where cartilage loss is focal and contained, restorative treatment is in scope. Where thinning is diffuse — affecting the joint broadly in the pattern of hip osteoarthritis — the clinical pathway shifts towards symptom management and, in advanced cases, joint replacement. That distinction is the pivot around which every technique described in this article turns.

Small focal defects: single-stage and injectable options

For a confirmed focal hip cartilage defect, the minimally invasive starting point in many cases is now an injectable scaffold rather than an operation.

ChondroFiller injection is delivered under ultrasound guidance as an outpatient procedure. The acellular collagen scaffold gels in situ within the defect and recruits the patient's own progenitor cells through matrix-induced chondrogenesis — a regenerative mechanism that requires no cell harvesting or laboratory culture. Ultrasound guidance achieves a reported 100% accurate intra-articular placement, compared with 72% for landmark-guided injection. Published hip data show a mean improvement in the modified Harris Hip Score of approximately 30 points. The scaffold is described for defects up to roughly 3 cm², with some protocols extending to 6 cm² for well-contained lesions.

Where surgery is the appropriate route, hip arthroscopy provides the operative framework — allowing FAI correction and cartilage repair to be combined in one procedure. AMIC (autologous matrix-induced chondrogenesis) is a single-stage option that bridges marrow stimulation and cell-based repair: subchondral bone is perforated and the released marrow cells are stabilised within a collagen matrix, producing a more organised repair environment than microfracture alone.

OATS and mosaicplasty transplant cylindrical osteochondral plugs taken from a lower-load region of the patient's own joint into the defect. Mosaic configurations can address lesions up to roughly 4 cm², and long-term follow-up data support superior clinical scores over microfracture for appropriate focal defects. Donor-site morbidity — discomfort or minor surface change at the harvest site — is a meaningful consideration in any decision.

Microfracture carries a well-documented historical role but is no longer considered first-line. The repair tissue it stimulates is fibrocartilage rather than native hyaline cartilage: mechanically inferior under hip loading and prone to breakdown within two to three years. Damage to the subchondral bone plate may also narrow the options for any future repair procedure.

Larger contained defects: when cell-based repair becomes the priority

Beyond roughly 3 cm², the biology underpinning single-stage repair becomes less reliable, and cell-based techniques move to the foreground. MACI (matrix-induced autologous chondrocyte implantation) is the most established of these: cartilage cells are harvested from the patient during an initial arthroscopic procedure, cultured in a laboratory for several weeks, and then seeded onto a Type I/III collagen membrane before being implanted into the defect in a second procedure. The resulting repair tissue is hyaline-like rather than fibrocartilage — structurally closer to native cartilage and better suited to the repetitive loading demands of the hip joint.

The two-stage commitment carries real practical weight. There is a gap of weeks between procedures, a more intensive rehabilitation course, and greater demands on both the clinical team and the patient. Careful case selection is essential: MACI is not appropriate for every patient, and the presence of diffuse background osteoarthritis substantially reduces the likelihood of a successful outcome.

Particulated juvenile allograft cartilage (PJAC) offers an alternative for well-contained defects of approximately 1–6 cm², derived from donor cartilage rather than the patient's own cells. Where the opposing joint surface is also damaged (bipolar lesions) or significant subchondral bone loss is present, PJAC is relatively contraindicated and other approaches need to be considered.

Before treating published thresholds as settled, it is worth being clear about their evidential basis: the size criteria used to guide cell-based repair in the hip are largely extrapolated from studies conducted in other joints. Hip-specific randomised trial data for MACI remain limited, and the precise point at which cell-based repair outperforms simpler options — within the hip specifically — has not been definitively established in the clinical literature.

Diffuse OA: when the goal shifts from repair to management

Not every hip cartilage problem is a repair problem. When damage is diffuse — spreading across the joint surface rather than confined to one area — the clinical picture is consistent with osteoarthritis, and the treatment goal shifts from rebuilding cartilage to managing symptoms and preserving function for as long as possible.

The transition does not always follow a clean line. As the previous section noted, significant background OA raises failure risk for any repair technique, but the precise point at which that context tips a case from preservation to management is not sharply defined in the hip literature. Clinical assessment must weigh both the defect and the condition of the surrounding joint.

For symptomatic diffuse hip OA, intra-articular corticosteroid and hyaluronic acid (viscosupplementation) injections represent a legitimate and well-evidenced bridging strategy — not a lesser option than surgery, but an appropriate one at the right stage of the condition. They can deliver meaningful reductions in pain and improvements in day-to-day function, buying time before the joint reaches the point where surgical intervention is genuinely necessary. For patients with early degeneration who fall between repair and replacement, biologic adjuncts such as bone marrow aspirate concentrate (BMAC) or fat-derived stromal vascular fraction may offer additional support to the joint environment.

When those options are genuinely exhausted and OA is end-stage, total hip replacement is the appropriate and well-evidenced endpoint. Published data suggest approximately 58% of hip replacements are still functioning at 25 years — a durability record that reflects how reliably this procedure restores what diffuse cartilage loss has taken away, and a figure that puts the decision to proceed in its proper perspective.

The stepped pathway: how Lincolnshire Hip approaches the decision

Knowing which tier applies requires more than a scan report. A structured assessment brings together defect grade and area, MRI findings, the presence of FAI or background OA, and patient age and activity demands — the combination that determines whether the right starting point is an injectable scaffold, a surgical repair, a biologic strategy, or preparation for replacement.

The four tiers form a logical sequence:

• Preserve — intra-articular injections for symptomatic management in diffuse OA or early-stage disease
• Repair — focal cartilage restoration via ChondroFiller injection, AMIC, OATS, or MACI, matched to defect size and grade
• Rebuild — biologic approaches where early degeneration makes mechanical repair insufficient
• Replace — total hip arthroplasty once diffuse OA has exhausted joint-preservation options

The framework does not push patients toward replacement prematurely. A contained Grade 3 defect with no significant background OA belongs at the repair tier; attempting scaffold repair in a joint already affected by diffuse OA is unlikely to succeed. Accurate staging — both the lesion itself and the condition of the surrounding joint — is where the routing decision is made.

A practical question to bring to any consultation: has the defect been measured and graded, and has background OA been formally excluded? If imaging has not yet characterised both depth and area, that step should precede any treatment discussion.

Prof Paul Y.F. Lee's clinical scope — spanning hip preservation through to hip replacement — means patients at Lincolnshire Hip are assessed along the full spectrum rather than within a single subspecialty. Clinics are accessible in Sleaford and Grantham.

Lincolnshire Hip is part of the MSK Doctors group and accepts patients without referral for hip assessment.