Cartilage

What it is and where it lives

Cartilage is a family of dense, low-friction tissues your body builds for very specific mechanical jobs. It’s made of specialized cells (chondrocytes) embedded in a protein scaffold of collagen and water-binding molecules called proteoglycans. That mix is what gives cartilage its slipperiness and its springiness.

There are three kinds. Orthopedics deals primarily with the first two:

• Hyaline (articular) cartilage — the polished, glistening surface coating the ends of bones inside every joint. It’s thinnest at the ankle (about 1 mm), thickest at the kneecap (4–6 mm) — and that difference partly explains why the ankle, despite carrying your body weight, develops osteoarthritis far less often than the knee.
• Fibrocartilage — denser and tougher, designed to absorb and distribute load. The meniscus of the knee, the labrum of the shoulder and hip, and the intervertebral discs of the spine are all fibrocartilage.
• Elastic cartilage — lives in the ear and at the tip of the nose. Outside our wheelhouse.

When patients say “I tore my cartilage,” they almost always mean either the meniscus (fibrocartilage) or the articular surface (hyaline). The distinction matters — the two have different healing capacities and different surgical menus.

Why cartilage doesn’t heal like bone does

Hyaline cartilage has almost no blood supply and no nerves. Instead of blood vessels feeding it directly, it gets its nutrition by soaking up nutrients from the fluid inside the joint (synovial fluid) every time you move — a slow, indirect delivery system that's part of the trade-off for being smooth and slippery. The lack of blood vessels is what makes it slick enough to glide; the lack of nerves is why a chondral defect can sit silent for years before it announces itself. The result is a tissue with a very limited capacity for self-repair — there’s no inflammatory cascade to recruit repair cells the way a fracture or a muscle tear does.

When the body does manage a healing response — usually only when a defect goes all the way down to bone marrow — it fills the hole with fibrocartilage, not the original hyaline. Fibrocartilage carries load, but it’s mechanically inferior: less stiff, less durable, and prone to breaking down years sooner than the surface it replaced. So when surgeons say cartilage “doesn’t heal,” what they really mean is: it doesn’t heal back to its original tissue on its own. That’s the problem cartilage restoration surgery exists to address.

Two different problems — focal defects vs diffuse osteoarthritis

A surgeon’s first job when they hear “cartilage damage” is to figure out which of two very different problems you have. The treatment paths barely overlap.

Focal chondral defects — a discrete spot of cartilage damage with surrounding cartilage that’s still intact. Common in younger patients after a sports injury, an ACL tear, an OCD lesion, or a single hard impact. Imaging shows a crater on a healthy joint surface. These patients are candidates for cartilage restoration, because the surrounding healthy cartilage gives the repair somewhere to integrate.

Diffuse osteoarthritis — generalized cartilage thinning across an entire joint surface (or multiple compartments), usually in older patients, usually with the bone changes that come with it: subchondral sclerosis, cysts, and bone spurs (osteophytes). There’s no isolated defect to fix because the wear is everywhere. Restoration techniques don’t apply; management is symptomatic until joint replacement.

The patient who walks in with knee pain at 28 after an ACL injury and the patient who walks in with knee pain at 68 after decades of activity have the same complaint and almost completely different treatment menus. Telling them apart is the most consequential decision in the visit.

Imaging — what we look at

For diffuse osteoarthritis, weight-bearing X-rays are the workhorse. Joint-space narrowing, subchondral sclerosis, osteophytes, and cysts tell the story without an MRI. We add MRI when something doesn’t fit or when we’re planning surgery.

For focal defects, MRI is the primary tool. Modern cartilage-specific MRI sequences map the depth and area of a defect, look at the underlying bone, and help grade severity before any procedure. Diagnostic arthroscopy — looking inside the joint with a small camera — remains the gold standard when the MRI is uncertain or when treatment will happen in the same setting.

Treatment — matching the procedure to the problem

There is no single “cartilage treatment.” The right approach depends on whether you have a focal defect or diffuse arthritis, how big and deep the damage is, your age and activity demands, and the alignment and stability of the surrounding joint.

For symptomatic osteoarthritis

The goal is managing symptoms while protecting what cartilage remains.

• Activity modificationsPhysical therapy and weight management. Strong muscles around the joint and lower body weight do more for OA pain than any single injection. The single most cost-effective intervention.
• Unloader bracing for one-compartment knee OA — shifts load away from the worn side.
• Corticosteroid injection for painful flares. Calms inflammation for weeks to a few months at a time. For patients who aren’t ready for — or aren’t candidates for — joint replacement, repeat injections every few months are a routine, reliable part of long-term arthritis care. There is some evidence that frequent steroid injections may contribute to cartilage loss over time, which is why your provider tracks spacing and total exposure, but for many patients the trade-off is well worth the relief.
• Hyaluronic acid (viscosupplementation) — modest benefit in selected patients, mostly for knee OA. The evidence is mixed and recent guidelines have softened the recommendation, but it remains a reasonable option for patients who can’t take NSAIDs or want to delay other interventions.
• Platelet-rich plasma (PRP) — growing evidence of pain benefit in mild-to-moderate knee OA, often outperforming hyaluronic acid in head-to-head trials. Not a regrowth treatment — it modulates the joint environment, it doesn’t rebuild cartilage.
• Bone marrow aspirate concentrate (BMAC) — uses concentrated cells from your own iliac crest. Evidence is evolving; we use it in selected cases.

For focal cartilage defects — the actual restoration menu

This is where the old line that “we can’t regrow cartilage” gets it wrong. In selected focal defects with healthy surrounding cartilage and correct alignment, modern restoration techniques can produce tissue that approaches or matches native hyaline. The candidate criteria are strict and the recoveries are long, but for the right patient these procedures preserve a joint that would otherwise be on a path to replacement.

• Microfracture — small holes drilled into the bone under the defect to recruit marrow cells. Fills the defect with fibrocartilage. Best for small lesions in lower-demand patients; results plateau and often decline over years.
• Osteochondral autograft (OATS / mosaicplasty) — cylindrical plugs of cartilage and bone harvested from a non-weight-bearing area of your own joint and transplanted into the defect. The transplanted plug carries real hyaline cartilage. Best for small to medium defects.
• Osteochondral allograft (OCA) — a size-matched donor plug containing real hyaline cartilage. The workhorse for larger defects, especially on the femoral condyle in younger patients.
• MACI (matrix-induced autologous chondrocyte implantation) — a two-stage procedure: your own cartilage cells are harvested arthroscopically, expanded in a lab over several weeks, then implanted on a collagen scaffold sized to your defect. Produces hyaline-like cartilage. Best for medium to large defects in active patients.
• Particulated juvenile cartilage allograft (DeNovo NT) — minced juvenile donor cartilage placed in the defect with fibrin glue. Single-stage, growing evidence base, and a useful option when MACI staging or graft size isn’t ideal.

For early-stage osteoarthritis with malalignment — joint preservation

Between the focal-defect and end-stage-arthritis worlds is a third group: younger patients with isolated wear in one part of the joint, often driven by alignment.

• High tibial osteotomy — re-cut and re-align the shin bone to shift load off the worn compartment. Buys decades for the right young patient with isolated medial knee OA.
• Partial (unicompartmental) knee replacement — resurface only the worn compartment, preserving the rest of your native joint.

For end-stage osteoarthritis — why replacement is the right answer

Restoration techniques work because the surrounding cartilage is healthy enough to anchor the repair. When wear is diffuse — the entire joint surface thinned, the bone underneath remodeled, alignment shifted — there’s no healthy edge for a repair to grow into. You’d be patching a single tile in a roof where every tile is failing.

That’s where joint replacement earns its place. Modern total knee and total hip replacement resurface the entire joint with metal and durable plastic in a single operation — a one-time, definitive fix that reliably eliminates arthritis pain and restores function for the vast majority of patients. It isn’t a last-resort consolation prize. For diffuse, end-stage cartilage loss, it’s the highest-evidence operation in all of orthopedics.

Protecting cartilage

Because cartilage repair is hard and incomplete, the most reliable strategy is preventing damage in the first place — and slowing the progression of damage that’s already there.

• Treat the index injury early. An untreated ACL tear or unstable meniscus tear changes how the joint loads and accelerates cartilage wear. Quick, decisive treatment of the original injury is itself a cartilage-preservation move.
• Maintain healthy body weight. Each pound of body weight translates to roughly 3–4 pounds of joint load during walking and 6–7 pounds during stair-climbing. Even modest weight loss has a measurable effect on knee OA pain.
• Build and keep strong muscles around the joint. Strong quadriceps and hip abductors don’t just feel good — they reduce the peak loads cartilage has to absorb during everyday movement.
• Stay active across activities. The “running ruins your knees” idea is largely myth at recreational doses; sedentary living is worse for cartilage health than measured running. The risk profile changes for elite-level distance running and for athletes with prior joint injuries — those are individual conversations.
• Address malalignment when it matters. Bowleg or knock-knee anatomy concentrates load on one side of the knee. In selected younger patients, a corrective osteotomy redistributes load and buys decades.

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