Page 1105 - Adams and Stashak's Lameness in Horses, 7th Edition

Lameness in the Young Horse 1071

OSTEOCHONDROSIS

VetBooks.ir c. Wayne McilWraiTh

INTRODUCTION
Osteochondritis dissecans (OCD) is arguably the
most important entity within the developmental
orthopedic disease (DOD) complex. It is a frequent
cause of lameness in young athletic horses and is the
most frequent condition of the complex requiring sur­
gical intervention. OCD has been classically consid­ Ossifying
ered as a manifestation of osteochondrosis. Rejno Epiphyseal epiphysis
10
22
and Stromberg described the first stages of osteo­ cartilage
chondrosis as a disturbance of cellular differentiation
in the growing cartilage and the second as involving
the process of basal forces within the joint, giving rise
to fissures in the damaged cartilage. The terms osteo­
chondrosis, osteochondritis dissecans, and osteochon­ Defect in
endochondral
drosis dissecans have been regularly used as synonyms, ossification
but this is misleading. Poulos distinguished them as
18
follows: osteochondrosis is the disease, osteochondri­
tis is the inflammatory response to the disease, and
OCD is the condition in which a flap can be demon­
strated. This is a simple but fairly appropriate
representation.
Subchondral bone cysts (SBC) or subchondral cystic
lesions (SCLs) were also proposed by Rejno and
Stromberg as a manifestation of osteochondrosis. The
26
author considers that SCLs showing up clinically in the
first 2 years of life are indeed manifestations of
osteochondrosis. However, they represent quite a
different disease than OCD. Examination of the lining Splitting of cartilage to give Retention of cartilage
of enucleated SCLs in the medial femoral condyle osteochondritis dissecans lesions and its necrosis leads to
showed that they produce increased levels of PGE , subchondral cystic lesion
2
neutral metalloproteinases, and nitric oxide (NO) and Figure 10.46. The proposed pathways of osteochondrosis
that there was enhanced osteoclastic resorption activity leading to both OCD and SCLs.
attributable to the tissue. In situ hybridization of
20
sections of fibrous tissue of SCLs showed that mRNA
of IL‐1β was upregulated at the periphery of the cystic
lesion and IL‐6 was upregulated in the fibrin tissue of OSTEOCHONDRITIS DISSECANS (OCD)
the center. Other work showed that SCLs could be Disease Manifestation
21
produced after 5‐mm‐diameter, 3‐mm deep defects
were created in the subchondral bone plate at the Three categories of OCD lesions are recognized:
central weight‐bearing of the medial femoral condyle, 1. Those showing clinical and radiographic signs.
19
leading to an alternative pathogenesis for clinical cases 2. Those showing clinical without radiographic (but
in older horses. arthroscopic) signs.
Other diseases in the DOD complex have sometimes 3. Those showing radiographic, but no clinical signs.
been referred to as osteochondrosis, but the important
clinical manifestations of osteochondrosis (and the pri­ Data from the first two categories of disease have
mary ones that fit this pathogenesis) are OCD and been tabulated from the most commonly selected joints
9
SCLs, and discussion will be limited to those condi­ from the author’s surgical case reports. The relative
tions. Osteochondrosis also can occur in the physis, but incidence of clinical signs vs. radiographic lesions also
it is uncommon and rare for it to cause a clinical prob­ has been documented in the femoropatellar joint by
15
lem. Figure 10.46 illustrates the proposed pathways of McIntosh and McIlwraith. The third category of radi­
osteochondrosis leading to both OCD and SCLs. More ographic lesions has become increasingly important
details on the osteochondrosis process can be found because of the common use of presale radiographs of
elsewhere. 28 yearlings. 6,7