Thomas J. Gill, M.D.
Visiting Assistant Professor
Harvard Medical School
Department of Orthopedic Surgery
Massachusetts General Hospital
15 Parkman Street
Boston, MA
02114
617-726-7797
617-726-3438 (FAX)
The microfracture technique is used for the treatment of full-thickness articular cartilage defects in the knee. It is classified as a “marrow-stimulation” technique, as opposed to cellular-based therapies such as autologous chondrocyte transplantation. The microfracture technique accesses the pluripotential mesenchymal cells in the underlying bone marrow, and relies on the stereotyped vascular response to injury. If the subchondral bone is not exposed following injury to the articular cartilage, the body is unable to heal the defect on its own.
The body’s response to
injury can be divided into three distinct phases - necrosis, inflammation and
repair (8). Necrosis begins immediately after injury and is most obvious at the
margins of chondral defects. Inflammation is produced by the local blood
supply. There is an increase in blood flow and capillary permeability which
results in a transudation and cellular exudation. This egress of cells is able
to form a dense fibrin mass at the site of injury (8). These cells have the
potential for cell division and modulation to repair cells, and forms a
primitive glue at the site of injury. As new blood vessels invade the fibrinous
clot, the repair phase is able to begin. Some of the cells differentiate into fibroblasts
which produce a loose granulation tissue, then a fibrous repair matrix, and
finally a scar. In tissue such as bone callus and tendon, the repair phase is
associated with replication of the damaged tissue type, rather than simply
collagen scar. A remodeling process then ensues in an attempt to approximate
normal anatomy.
Cartilage
undergoes the same necrotic phase as any other body tissue, but the
inflammatory phase is almost completely absent (8). Since there is no fibrin
clot which forms following a chondral injury, a repair process can not begin
unless the underlying subchondral bone is penetrated. Without cells from the
marrow, the existing chondrocytes are incapable of producing the required
repair products. Microfracture thus permits all three phases of repair, since
the underlying bone is able to provide primitive cells for differentiation and
modulation to fibroblasts or chondroblasts.
Immediately after penetrating
the subchondral bone, the base of the chondral defect fills with blood and organizes
into a fibrous clot. Blood cells, undifferentiated bone-marrow elements and
platelets become trapped in the defect (7). The undifferentiated mesenchymal
cells are capable of differentiation into fibrous tissue, bone, and synovial
membrane (3). The fibroblasts produce a reparative granulation tissue. With
progressive fibrosis, the defect forms a scar at ten days, which becomes less
vascular and more sclerotized. The fibrous tissue undergoes a progressive
hyalinization and chondrification to produce a fibrocartilaginous mass that
“heals” the defect, which is permanently marked by a pit or dimpled
scar (7).
The ability of undifferentiated
cells to transform into cartilage has been documented (2,4,6). Throughout the
body, the response to injury differs depending on the tissue which is injured.
Skin, liver and kidney repair with collagen scar, while bone, tendon and
synovium repair with like-tissue (8). The timing of the repair sequence has
been studied in a rabbit model (5). Deep chondral lesions fill with granulation
tissue. The fibroblasts then differentiate into chondrocytes by seven to ten
days after injury. The main collagen in the repair tissue after three weeks is
Type I. By six to eight weeks, Type II predominates by radiochemical analysis.
It is interesting to note that the quality of the cartilage continued to
improve up to one year. Type I still persisted, so the repair tissue never
fully resembled normal articular cartilage.
The effect of the local
environment on the line of differentiation of periosteal cells has been
established (1,10,12,13). High oxygen tension has been shown to result in bone
formation, while low oxygen pressure results in cartilage formation (12). Thus,
removal of too much cancellous bone in a chondral defect may promote increased
vascularization giving a higher oxygen tension, resulting in enchondral
ossification. A strong osteogenic stimulus from the cancellous bone may also
favor ossification (12). Thus, the subchondral bone is generally not abraded
during microfracture.
The beneficial effect of motion
in the post-operative period on the healing of articular injuries is
well-documented (1,9,11,14,15). Continuous passive motion improves the
nutrition and metabolic activity of articular cartilage, stimulates
pluripotential mesenchymal cells to differentiate into articular cartilage
rather than fibrous tissue or bone, and accelerates the healing of both
articular cartilage and periarticular tissues.
1. Amiel D, Coutts RD, Abel M, Stewart W, Harwood F, Akeson WH: Rib perichondrial grafts for the repair of full-thickness articular cartilage defects. A morphological and biochemical study in rabbits. J Bone Joint Surg 67-A: 911-920, 1985
2. Bennett GA, Bauer W: A study of the
repair of articular cartilage and the reaction of normal joints of adult dogs
to surgically created defects of articular cartilage, joint mice and patellar
displacement. Amer J Path 8:
499-523, 1932
3. Campbell CJ: The healing of cartilage
defects. Clin Orthop 64: 45-63,
1969
4. DePalma AF, McKeever CD, Subin DK:
Process of repair of articular cartilage demonstrated by histology and
autoradiogaphy with tritiated thymidine.
Clin Orthop 48: 229-242, 1966
5. Furukawa T, Eyre DR, Koide S, Glimcher
MJ: Biochemical studies on repair cartilage resurfacing experimental defects in
the rabbit knee. J Bone Joint Surg
62-A: 7989, 1980
6. Kettunen KO: Skin arthroplasty in the
light of animal experiments with special reference to functional metaplasia of
connective tissue. Acta Orthop
Scand, Suppl 29, 1958
7. Mankin HJ: The reaction of articular
cartilage to injury and osteoarthritis.
New Eng J Med 291: 1285-1292, 1974
8. Mankin HJ: The response of articular
cartilage to mechanical injury. J
Bone Joint Surg 64-A: 460-465, 1982
9. O'Driscoll SW, Salter RB: The induction
of neochondrogenesis in free intra-articular periosteal autografts under the
influence of continuous passive motion.
An experimental investigation in the rabbit. J Bone Joint Surg 66-A: 1248-1257, 1984
10. Ritsila VA, Santavirta S, Alhopuro S, et al. Periosteal and perichondrial grafting in reconstructive surgery. Clin Orthop 1994; 302:259-265
11. Rodrigo J, Steadman JR. Improvement of full-thickness chondral
defect healing in the human knee after debridement and microfracture using
continuous passive motion. Am J Knee Surg 1994; 7:109-116.
12. Rubak JM: Reconstruction of articular
cartilage defects with free periosteal grafts. Acta Orthop Scand 53: 175-180,
1982
13. Rubak JM, Poussa M, Ritsila V:
Chondrogenesis in repair of articular cartilage defects by free periosteal
grafts in rabbits. Acta Orthop
Scand 53: 181-186, 1982
14. Salter RB: The biologic concept of
continuous passive motion of synovial joints. The first 18 years of basic research and its clinical
application. Clin Orthop 242:
12-25, 1989
15. Salter RB, Simmonds DF, Malcolm BW,
Rumble EJ, MacMichael D, Clements ND: The biological effect of continuous
passive motion on the healing of full-thickness defects in articular
cartilage. J Bone Joint Surg 62-A:
1232-1250, 1980