- Residual osteochondral debris represents a clinical problem associated
with arthroscopic debridement and curettage of joint surfaces. At the Oregon
State University Veterinary Teaching Hospital (OSU-VTH), during a period
from January, 1983 to August, 1986, incidence of radiographically recognizable
osteochondral debris in the carpal joints of postarthroscopic equine patients was
excessive. Uncertainty exists regarding the fate and effects of this debris on the
normal equine joint. Reports in human medical literature implicate
osteochondral debris as both an inflammatory stimulus and a mechanical
abrasive in the pathogenesis of osteoarthrosis. This study was designed to
evaluate the fate and effects of surgically implanted autogenous osteochondral
fragments, intended to mimic remaining operative debris, on various physical
and biochemical parameters of normal equine middle carpal joints over a six
month time period.
Four autogenous osteochondral fragments, removed from the lateral
trochlear ridge of the talus, were arthroscopically placed as loose bodies into a
randomly selected middle carpal joint in each of 10 young horses (2 to 4 years
old). The contralateral middle carpal joint, subjected to a sham procedure,
served as control. Postoperative therapy was consistent with usual treatment of
clinical arthroscopic patients. Lameness evaluation, radiographic examination,
carpal circumference measurement, and synovial fluid analysis were performed
preoperatively and at scheduled intervals postoperatively. After two months of
confinement, the horses were subjected to an increasing level of exercise,
intended to mimic a four month conditioning program. Animals were
euthanatized at 1 month (1), 2 months (2), 4 months (1), and 6 months (6).
Gross and microscopic examination of remaining fragments, articular cartilage,
and synovial membrane of each middle carpal joint was performed.
Clinically, increased joint circumference, effusion, lameness, and
radiographic appearance of degenerative joint disease distinguished implanted
from control joints over the six month period. Implanted joints were grossly
characterized by grooved, excoriated cartilage surfaces and synovium which was
thickened, erythematous, and irregular. Loose bodies became adhered to
synovium at their subchondral bone surface within four weeks after placement
into the joint. At four weeks, bone within fragments was undergoing necrosis,
while cartilage was preserved. At eight weeks, fragments were radiographically
inapparent, grossly evident as pale plaques on the synovial surface, and
composed of dense fibrous connective tissue.
Histologically, synovial membrane specimens from implanted joints
demonstrated significant (P < 0.05) inflammatory change two months after
implantation. Mononuclear cells infiltrated the synovial layers. Significant
physical damage (P < 0.05) was apparent within the articular cartilage two and
six months after surgery. Chondrocyte degenerative change was significant
(P < 0.05) six months after surgery. Generalized reduction in Safranin-O uptake
was not apparent within each level of cartilage samples, but focal reduction in
staining was readily apparent in cartilage layers adjacent to physical defects.
Synovitis, physical articular damage, and focal chondrocyte degenerative
change resulted from a combination of 1) direct mechnical abrasion by the
implants or implant-derived debris, 2) an induced effect of osteochondral debris
on the synovium, 3) synovitis-induced cartilage degeneration, and
4) supraphysiologic loading associated with exercise.
In this study, osteochondral loose bodies of a defined size and shape
were resorbed by the synovium within two months after joint implantation.
These fragments directly and indirectly induced synovitis and significant articular
cartilage degeneration. Methods to prevent and reduce residual postoperative
debris and damage associated with its presence are discussed. Implementation
of this methodology should reduce the potential for subsequent articular