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Dynamic Chiropractic – August 24, 1998, Vol. 16, Issue 18

Can Articular Cartilage Be Repaired?

By Warren Hammer, MS, DC, DABCO
Two important factors are necessary for tissue to heal: local or distant cells must be present to synthesize new tissue and clean up necrotic material, and a vascular supply must be available. The vascular supply can supply some of the above cells and also carry to the area bioactive molecules, such as growth factors, chemotactic, mitogenic and cytotactic factors.1 Unfortunately, cartilage is avascular, and the necessary inflammatory and repair products that healing depends upon are not readily available.

Mankin2 states that articular cartilage matrix may contain substances that inhibit vascular and macrophage invasion and clot formation which are necessary for healing. Chondrocytes, the basic cell of cartilage which maintains and synthesizes the matrix, are unable to migrate to the injury site from adjacent healthy cartilage because they are "literally imprisoned in a mesh of collagen and proteoglycan, unable to migrate to the injury site from adjacent healthy cartilage."1

It was thought that if the cartilage injury penetrated the subchondral plate there would be a vascular supply from the bone. While this is true and a fibrin clot forms allowing a healing response with the appearance of chondrocytes and the type II collagen (which makes up to 95% of the collagen in hyaline cartilage), the new collagen formation over time does not properly combine with the residual cartilage.3

It is known that many people injure the articular surface of their cartilage, and that the joint returns to an asymptomatic state after the transient synovitis subsides. Whether a cartilage lesion degenerates further or not depends on "the size and depth of the lesion, the integrity of the surrounding articular surface, the age and weight of the patient, associated meniscal and ligamentous lesions, and a variety of other mechanical and biomechanical factors."1

It is known that certain factors definitely influence cartilage healing. In a horse model, small defects (<3 mm) completely healed.4 Continuous passive motion increased the ability of fullþthickness defects to heal, producing a tissue that closely resembled hyaline cartilage5 and cartilage chondrocytes from skeletally immature animal donors show a greater ability to proliferate and synthesize larger proteoglycan molecules.6

Scientists have attempted to repair cartilage by adding cells capable of chondrogenesis and by increasing access to the vascular system. Cells have been transplanted from other animals (allografts) and from the individual (autografts). Tissues other than articular cartilage such as rib perichondrial cells and periosteal grafts capable of chondrogenesis have been attempted. Harvested mesenchymal stem cells have been attempted with some success, although they are in short supply in the older patient.

A relatively new method of transplantation is a tissue engineering method where synthetic materials are filled with the local cell population, grown in vitro and implanted into the patient. In 1994, Brittberg et al.7 used carbon fiber pads in patients with early osteoarthrosis of the knee and reported good to excellent results after a four-year followup. Brittberg8 stated that "whether a defect filled with repair tissue is able to protect the surrounding joint surface from degeneration remains to be proven."

While progress has been shown, Newman1 states that while there are early reports of good results with new techniques, later reports of failures occur after longer investigation. Unfortunately, surgeons are often premature in adopting a new surgical technique and later realize that "nothing ruins good results like followup."9


  1. Newman AP. Articular cartilage repair. Amer J Sports Med 1998;26(2):309-324.
  2. Mankin HJ. The response of articular cartilage to mechanical injury. J Bone Joint Surg 1982;64A:460-466.
  3. Shapiro G, Koide S, Glimcher MJ. Cell origin and differentiation in the repair of full-thickness defects of articular cartilage. J Bone Joint Surg 193;75A:532-553.
  4. Convery FR, Meyers MH, Akeson WH. The repair of large osteochondral defects. An experimental study in horses. Clin Orthop 1972;82:253-262.
  5. Moran ME, Kin HK, Salter RB. Biological resurfacing of fullþthickness defects in patellar articular cartilage of the rabbit. Investigation of autogenous periosteal grafts subjected to continuous passive motion. J Bone Joint Surg 1992;74B:659-667.
  6. Kreder JH, Moran M, Kelley FW, et al. Biologic resurfacing of a minor joint defect with cryopreserved allogenic periosteum under the influence of continuous passive motion in a rabbit model. Clin Orthop 1994;300:288-296.
  7. Brittberg M, Faxen E, Peterson L. Carbon fiver scaffolds in the treatment of early knee osteoarthritis. A prospective four-year followup of 37 patients. Clin Orthop 1994;307:155-164.
  8. Brittberg M, Nilsson A, Lindahl A, et al. Rabbit articular cartilage defects treated with autologous cultured chondrocytes. Clin Orthop 1996;326:270-283.
  9. Gross M. Innovations in surgery. A proposal for phased clinical trials. J Bone Joint Surg 1993;75B:351-354.

Warren I. Hammer, MS, DC, DABCO
Norwalk, Connecticut

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