The Journal of Bone and Joint Surgery 83:53 (2001)
© 2001 The Journal of Bone and Joint Surgery, Inc.
Spontaneous Repair of Full-Thickness Defects of Articular Cartilage in a Goat Model
A Preliminary Study
Douglas W. Jackson, MD,
Peggy A. Lalor, PhD,
Harold M. Aberman, DVM and
Timothy M. Simon, PhD
Investigation performed at the Orthopaedic Research Institute,
Southern California Center for Sports Medicine, Long Beach, California
Douglas W. Jackson, MD
Harold M. Aberman, DVM
Timothy M. Simon, PhD
Orthopaedic Research Institute, Southern California Center for
Sports Medicine, 2760 Atlantic Avenue, Long Beach, CA 90806
Peggy A. Lalor, PhD
SkeleTech, 22002 26th Avenue S.E., Room 104, Bothell, WA 98021
Although none of the authors has received or will receive benefits
for personal or professional use from a commercial party related
directly or indirectly to the subject of this article, benefits
have been or will be directed to a research fund, foundation, educational
institution, or other nonprofit organization with which one or more
of the authors is associated. Funds were received in total or partial support
of the research or clinical study presented in this article. The
funding sources were the Douglas W. Jackson Orthopaedic Research
Trust and an unrestricted research grant from Howmedica.
Background: Full-thickness defects measuring
3 mm in diameter have been commonly used in studies of rabbits to evaluate
new procedures designed to improve the quality of articular cartilage
repair. These defects initially heal spontaneously. However, little
information is available on the characteristics of repair of larger
defects. The objective of the present study was to define the characteristics
of repair of 6-mm full-thickness osteochondral defects in the adult Spanish
goat.
Methods: Full-thickness osteochondral defects measuring
6 „ 6 mm were created in the medial femoral condyle of the knee
joint of adult female Spanish goats. The untreated defects were
allowed to heal spontaneously. The knee joints were removed, and
the defects were examined at ten time-intervals, ranging from time
zero (immediately after creation of the defect) to one year postoperatively.
The defects were examined grossly, microradiographically, histologically,
and with magnetic resonance imaging and computed tomography.
Results: The 6-mm osteochondral defects did not
heal. Moreover, heretofore undescribed progressive, deleterious
changes occurred in the osseous walls of the defect and the articular
cartilage surrounding the defect. These changes resulted in a progressive increase
in the size of the defect, the formation of a large cavitary lesion,
and the collapse of both the surrounding subchondral bone and the
articular cartilage into the periphery of the defect. Resorption
of the osseous walls of the defect was first noted by one week,
and it was associated with extensive osteoclastic activity in the
trabecular bone of the walls of the defect. Flattening and deformation
of the articular cartilage at the edges of the defect was also observed
at this time. By twelve weeks, bone resorption had transformed the
surgically created defect into a larger cavitary lesion, and the
articular cartilage and subchondral bone surrounding the defect
had collapsed into the periphery of the defect. By twenty-six weeks,
bone resorption had ceased and the osseous walls of the lesion had become
sclerotic. The cavitary lesion did not become filled in with fibrocartilage.
Instead, a cystic lesion was found in the center of most of the cavitary
lesions. Only a thin layer of fibrocartilage was present on the
sclerotic osseous walls of the defect. Specimens examined at one
year postoperatively showed similar characteristics.
Conclusions: Full-thickness osteochondral defects,
measuring 6 mm in both diameter and depth, that are created in the
medial femoral condyle of the knee joint of adult Spanish goats
do not heal spontaneously. Instead, they undergo progressive changes
resulting in resorption of the osseous walls of the defect, the formation
of a large cavitary lesion, and the collapse of the surrounding
articular cartilage and subchondral bone.
Clinical Relevance: As surgeons apply new reparative
procedures to larger areas of full-thickness articular cartilage
loss, we believe that it is important to consider the potential
deleterious effects of a "zone of influence" secondary to the creation
of a large defect in the subchondral bone. When biologic and synthetic matrices
with or without cells or bioactive factors are placed into surgically
created osseous defects, the osseous walls serve as shoulders to
protect and stabilize the preliminary repair process. It is important
to protect the repair process until biologic incorporation occurs
and the chondrogenic switch turns the cells on to synthesize an
articular-cartilage-like matrix. It takes a varying period of time
to fill a large, surgically created bone defect underlying a chondral
surface. The repair of such a defect requires bone synthesis and
the reestablishment of a subchondral plate with a tidemark transition
to the new overlying articular surface. The prevention of secondary
changes in the surrounding bone and articular cartilage and the
durability of the new reparative tissue making up the articulating
surface are issues that must be addressed in future studies.
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