Holes in the cartilage-bearing surface of your joints were long thought to be not repairable. From the earliest descriptions of cartilage injuries in the Hippocratic era to the words of physician William Hunter in 1743, “cartilage is a troublesome thing, once injured never repaired.”
This was the dogma that all orthopaedic surgeons were taught. The holes, or divots, often enlarged over time, and arthritis of the joints — so it was believed — was the inevitable outcome. Yet isolated cartilage injuries did not always fall down this rabbit hole. Several investigators noted that these injuries sometimes healed on their own, and at other times, never caused a problem. But the path the injury took was unpredictable.
For most of the 20th century, methods for repairing cartilage injuries focused on bone marrow stimulation. Drill bits, or awls, were used to create passageways for the marrow cells to exit onto the fractured surface and create a “super clot.” This freed the pluripotential progenitor and marrow cells within the marrow to form healing tissue on the divot in the bone.
These liberated marrow cells were believed to have all the healing powers necessary to form new cartilage. When continuous motion was applied (using machines, pool exercises or stationary bikes) the newly formed tissue received mechanical signals, inducing the production of new cartilage, rather than bone or scar tissue. Unfortunately, this release of potent healing cells often fell short of forming true cartilage. The repair tissue usually looked like scar tissue and, in the joints of athletes, failed to provide the durability necessary for impact sports.
In the early 1990s, two major approaches were initiated to solve the problem of cartilage healing. The most popular — and most expensive — was an effort to grow cartilage cells called chondrocytes in the lab, squirt them onto the cartilage defect and cover them with a layer of fibrous tissue from the bone. This sequence required two surgical procedures and expensive laboratory work. It relied on the wishful thinking that the cells would actually stay in place and somehow make enough surrounding tissue to form cartilage before the patient’s activity squished it out of the knee. Tens of millions of dollars were spent on this effort. It was eventually abandoned in favor of preloading cells onto matrices of resorbable material. A version of this technique, called MACI, was recently approved by the Food and Drug Administration — though the results from studies in Europe have been decidedly mixed.
A second approach used plugs of intact cartilage and bone from other parts of the knee or from donors, which were placed like hair transplants into the defects. These plugs sometimes worked but rarely fused with the surrounding cartilage. The donor surfaces never quite matched the patient’s own geometry, and when they failed, they left large holes in the knee.
In 1991, I pioneered a third approach: It’s called articular cartilage paste grafting. This technique relied on turning the dead divot or arthritic area of the joint into a full, fresh fracture, then pasting on a mixture of the patient’s own articular cartilage, bone and underlying cells. A core of cartilage and bone was taken from the intercondylar notch of the knee (where it is not needed and grows back on its own anyhow). This core was mashed into a paste in the operating room and immediately packed into the defect. This mashing was shown to activate the cartilage cells to release growth factors, while the matrix of cartilage was shown to stimulate more normal healing when motion was applied.
This “paste graft” technique has been validated independently in multiple animal models and has shown to be superior to marrow stimulation alone. It requires nothing more than routine operating room tools. The absence of commercial support has caused it to be ignored by much of the orthopaedic industry. Yet now, 26 years later, the results of articular cartilage paste grafting in humans and animals match or exceed that of any other technique.
Our goal is to expand and improve the efficacy of this cartilage repair technique, with the goal of achieving full biologic joint replacements for people with severe sports injuries and arthritis. The addition of stem cells and growth factors will also be tested, to determine if these factors alone are enough to improve the outcomes for cartilage repair.
More compelling data awaits to be compiled to push this adoption. Meanwhile we strongly believe, based on current research, that isolated divots in the cartilage can be repaired with simple, inexpensive outpatient techniques—but only if doctors will use them.
Dr. Kevin R. Stone is an orthopedic surgeon at The Stone Clinic and chairman of the Stone Research Foundation in San Francisco.