Why Seek Alternatives to Microfracture

Microfracture—the puncturing of holes to release marrow blood in joint surfaces with cartilage injuries—is reported to be failing in most cases after a few years. Multiple studies, reported this year at the international cartilage meetings, provide the reason and offer solutions.

Here’s how microfracture works. Holes created in the joint bone release marrow cells and blood that form a clot on the surface of the fractured bone. This clot contains healing factors that lead to formation of collagen repair tissue. Similar to a clot on the skin, the collagen that forms is scar tissue: disorganized fibers of protein that, over time, remodel into fairly good-looking tissue.  

But microfracturing the bone alone, especially in the setting of arthritis, fails to heal normally at multiple levels. First, the bone cavities created by the fracture process sometimes fail to heal, leading to cysts in the bone. These cysts eventually lead to pain and deformity of the bone. Second, the structure of the bone above the cysts fails to form a rigid base. This base is comparable to the subflooring in your house—it’s required so the protective layer of tissue that forms above it can absorb force and wear properly. Third, the collagen formed is usually in a scar pattern that sometimes—but not always—forms into the normal cartilage structure required for lasting durability.

For athletes, the temporary repair provided by the microfracture process often breaks down after a few years of playing on the joints. No amount of subsequent injections will bring back a complete, healthy structure of bone and cartilage.

There are several solutions. In one procedure we developed called the paste graft technique, the bone is repaired by providing a viable bone matrix that the new cells can use as a template or stimulus for complete healing. This is accomplished by expanding the microfracture to stimulate a true, fresh fracture. This larger fresh injury brings in all the repair cells, blood vessels, and stem-cell-derived self-repair cells necessary to form normal bone and cartilage. The cells that migrate to the surface encounter the stimulating factors and cells found in a normal articular cartilage matrix. This way they will form cartilage—and not scar tissue—when motion is applied to that surface region. Lastly, electrical and mechanical stimulation must be applied in a manner that promotes healing while not damaging the repairing tissue. This is accomplished with continuous passive motion machines, bone stimulators, and exercise.

The success of these and other therapies are now being reported by multiple authors. We just published our 10 - 23 year outcome study of patients who underwent a “paste grafting” procedure, which combines all of the above features. The paste graft was also used to salvage failed microfracture procedures in a large number of cases. Other surgeons and investigators are reporting good long-term outcomes using intact donor tissues and plugs (which provide pre-formed bone and cartilage to the damaged areas) to achieve their results.

The lesson is clear. In injuries, and especially arthritis, the entire complex of the injury must be addressed in a way similar to how the body heals itself. Nature has a funny way of reminding us how she works.