Articular cartilage, specifically hyaline cartilage, makes the smooth, near-frictionless movement of joints like the knee and ankle possible. This durable tissue acts as a cushion, absorbing shock and protecting the ends of bones from grinding against each other. However, unlike bone or muscle, this tissue has an extremely limited capacity to heal once damaged. This slow timeline for repair is why cartilage injuries often necessitate medical intervention.
Why Natural Cartilage Repair Is Limited
The poor regenerative ability of hyaline cartilage stems directly from its biological composition and structure. Cartilage is an avascular tissue, meaning it contains no blood vessels to deliver the necessary building blocks for repair, such as oxygen, nutrients, or immune cells. Because there is no direct blood supply, the healing process cannot be triggered in the same robust way as it is in vascularized tissues.
The specialized cells responsible for maintaining the tissue, called chondrocytes, are sparsely distributed within the cartilage matrix. These cells have a very low metabolic rate and do not migrate easily to the site of an injury. When damage occurs, the remaining chondrocytes are often incapable of producing enough new matrix material to fill a significant defect.
If damage extends all the way to the underlying bone, a limited healing response may be initiated because the bone is vascularized. The resulting bleeding forms a clot rich in reparative cells. However, the body typically fills the defect with mechanically inferior fibrocartilage, a type of scar tissue, instead of new hyaline cartilage. This dense, fibrous patch lacks the smooth, elastic qualities of the original tissue, causing the repair to break down over time.
Non-Surgical Approaches to Cartilage Preservation
No non-surgical method can regrow significant amounts of true hyaline cartilage; treatments instead focus on pain management and slowing degradation. Physical therapy is a primary approach, strengthening surrounding muscles to improve stability and reduce stress on the damaged area. Weight management is also effective, as reduced body mass translates to a lower mechanical load on the articular surfaces.
Medications like non-steroidal anti-inflammatory drugs (NSAIDs) are used to reduce joint inflammation and pain. Injections can provide temporary relief and improved function. Corticosteroid injections diminish inflammation quickly, while hyaluronic acid injections supplement the joint’s natural lubricating fluid. These conservative strategies preserve remaining healthy tissue and manage symptoms, but they do not repair missing material.
Surgical Techniques Designed to Promote Regeneration
For localized defects, surgeons employ several techniques to stimulate new growth or replace the damaged area.
Microfracture
Microfracture is the most traditional method, a marrow-stimulation procedure where small holes are drilled into the subchondral bone beneath the defect. This creates a pathway for bone marrow elements, including stem cells and growth factors, to leak into the injury site. The resulting blood clot organizes into a repair tissue, though it is typically the less durable fibrocartilage.
Osteochondral Autograft Transplantation (OATS)
More advanced techniques focus on transplanting better quality tissue. OATS, also known as mosaicplasty, is a single-stage procedure. Small plugs of healthy bone and overlying hyaline cartilage are harvested from a less weight-bearing area of the joint and transferred to fill the defect. This provides a structural repair using native hyaline cartilage and is best suited for smaller, well-defined lesions.
Autologous Chondrocyte Implantation (ACI/MACI)
Autologous Chondrocyte Implantation (ACI) and Matrix-Induced Autologous Chondrocyte Implantation (MACI) aim to regenerate hyaline-like tissue. In the first stage, a small biopsy of the patient’s healthy chondrocytes is taken and expanded in a lab over several weeks. In the second stage, the millions of new cells are implanted into the defect. MACI delivers these cultured cells on a bioresorbable scaffold, which is secured into the defect to promote the growth of tissue that closely mimics the original hyaline cartilage.
Expected Recovery Timelines After Surgical Repair
The time required for cartilage to grow back or integrate after surgery is measured in months, reflecting the slow biological processes involved.
Microfracture Recovery
Following microfracture, patients are kept non-weight bearing for six to eight weeks to protect the fragile clot and allow the repair tissue to begin forming. The new fibrocartilage takes approximately six to twelve months to fully mature and withstand normal activity.
OATS Recovery
Procedures involving transplanted or cultured cells, such as OATS, ACI, and MACI, demand a longer, multi-phase rehabilitation process. For OATS, patients may begin partial weight-bearing sooner than with microfracture. However, the time before returning to full, unrestricted activity often spans five to seven months as the transplanted bone and cartilage plugs integrate.
ACI/MACI Recovery
Recovery for ACI and MACI is the longest because the implanted cells need time to produce a new, stable matrix. Rehabilitation is often structured over nine to twelve months before a return to high-impact activities is permitted. The initial phase involves restricted range of motion and non-weight-bearing to allow the newly implanted cells to adhere and establish themselves within the defect. This slow, gradual maturation of the hyaline-like repair tissue dictates the extended timeline, ensuring the new material is durable enough to handle the forces of daily life and sport.