From Konig to the present: What have we learned?
Cathy Carlson
In 1887, König proposed the term “osteochondritis dissecans” for an underlying lesion in the
joint cartilage facilitating formation of loose bodies in the absence of significant trauma.11
Subsequent histological studies have not supported a primary inflammatory etiology for the
condition, making “osteochondrosis” (OC) the more accurate term, as suggested by Howa1d in
1942.4,6However, the original phrase has persisted, and in fact, “osteochondrosis” and
“osteochondritis” are often used interchangeably. In the human clinical literature, when a fissure
or fracture in the overlying articular cartilage is present, the condition is nearly universally
referred to as osteochondritis dissecans (OCD), although osteochondrosis dissecans would be
more appropriate. In the veterinary medical field, focal abnormalities of endochondral
ossification involving the articular-epiphyseal cartilage complex (AECC) are referred to as
osteochondrosis (or osteochondrosis dissecans, as appropriate) regardless of anatomical location.
Conversely, in the human literature, manifestations of OC at various anatomical sites are given
different names.
In veterinary medicine, much progress in our understanding of the pathogenesis of OC has been
made over the past 30 years or so due to the fact that it is possible, in animals, to study
predilection sites of the disease prior to the age/time at which it is clinically evident. Studies of
preclinical disease in pigs, horses, dogs, and cattle have confirmed that the earliest recognizable
morphological lesion is a microscopic area of necrosis of epiphyseal cartilage that often is
centered on one or more necrotic cartilage canal blood vessels and involves neither the overlying
articular cartilage nor the subchondral bone.2,9 This finding was first pursued in pigs, through a
combination of vascular perfusion studies, histological comparisons, and experimental
interruption of blood supply to induce lesions in otherwise normal growth cartilage.3,12 In swine
these studies have focused primarily on the medial femoral condyle; however, subsequent studies
in horses included multiple predilection sites as well as experimental induction of lesions in the
lateral trochlear ridge of pony foals.8 The study of the association of these early lesions with a
similar failure in cartilage canal vasculature in various predilection sites and in two different
species (pigs and horses) has provided strong evidence that, although predilection sites among
species can and do vary, the pathogenesis of this condition is closely similar among species.
These insights were initially delayed due to a failure to recognize that, although an animal may
present with clinical signs of OCD relatively late in adolescence or early in adulthood, the
underlying lesions were formed in the first few weeks or months of life, at which time the
epiphyseal cartilage was dependent on a cartilage canal blood supply.
In human medicine, OCD is still considered by many to be a focal, idiopathic alteration of
subchondral bone.1,5 In human medicine, however, it is not possible, except in very unusual
circumstances, to obtain biopsy samples from predilection sites, except at the time of a surgery
that is done to repair end stage disease, often after the chondro-osseous flap has been present for
years. This, combined with 1) the inability of imaging modalities to identify vascular structures
in epiphyseal cartilage with diagnostic clarify, 2) the differences in clinical presentation among
the different predilection sites in humans, and 3) the lower tendency for physicians to seek
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insights from naturally occurring disease in animals, have lead to a conclusion held by many that
osteochondrosis has a different pathogenesis not only among species but among predilection
sites within a species (human). The recent development of MRI techniques to visualize cartilage
canal vessels in vivo are likely to change this perception, as these will allow characterization of
the cartilage canal vasculature in humans and the identification of subclinical disease well before
it manifests clinically.7,10 Although OC is the first orthopaedic disease to be definitely linked to
a failure in cartilage canal blood supply, it is likely that, once it is possible to visualize
epiphyseal vasculature in vivo, other developmental orthopaedic diseases in both animals and
humans (e.g., hip dysplasia, acetabular impingement, orthopaedic complications secondary to
sickle cell anemia, etc.) will follow.
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2 Carlson CS, Hilley HD, Meuten DJ: Degeneration of cartilage canal vessels associated
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and experimental lesions of osteochondrosis. Journal of orthopaedic research :
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12 Ytrehus B, Andreas Haga H, Mellum CN, Mathisen L, Carlson CS, Ekman S, et al.:
Experimental ischemia of porcine growth cartilage produces lesions of
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Orthopaedic Research Society 2004:22(6):1201-1209.
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