CHAPTER 114 Osteochondrosis
Osteochondrosis is one of the most important joint diseases affecting young growing horses. The reported incidence varies, but there seems to be a trend toward an increase over the past few decades. Early work reports an incidence of 10% to 15%, but more recent publications mention figures up to 32%. All major studbooks and breeders regard the disease as a substantial problem. The mean incidence is estimated at 25%, and in northwestern Europe alone, 25,000 foals annually develop osteochondrosis. The impact of osteochondrosis on the equine industry, both in terms of economic loss and in impairment of animal welfare, cannot be overemphasized.
The published literature contains inconsistencies pertaining to nearly every characteristic of the disease. The terms osteochondrosis, osteochondritis, osteochondritis dissecans (OCD), and dyschondroplasia are used regularly as synonyms. To avoid further confusion and because the term osteochondrosis (OC) is well established in the literature, this term alone will be used in this chapter.
In 1558, the French surgeon Ambroise Paré was the first to remove free bone fragments, attributed to OC, from human joints. Centuries passed before König published the first clear statements on the disease in 1887. Further expansion of the definition of OC to include disorderly bone or cartilage growth resulted in an ever-growing list of human orthopedic conditions with different eponymous names. This has introduced a confusing array of distantly related heterogeneous conditions. In equine OC, many dissimilar lesions have been included under the heading, creating considerable confusion. Osteochondral fractures, developmental orthopedic diseases such as subchondral cysts, physitis, angular limb deformities, and cervical vertebral malformation have all been included in the encompassing term osteochondrosis. A narrower classification of equine OC is important because it contributes to a better understanding of the disease, a more accurate account of its true impact, and better management practices leading to reduction in its incidence. The previously mentioned developmental orthopedic diseases and osteochondral fractures (including dorsal and palmar or plantar fragments of the proximal phalanx) will not be discussed here.
Endochondral ossification is the process of bone formation over a cartilage template; the process results in simultaneous growth and transformation of the initially cartilaginous primordial skeleton into bone. There is little doubt that endochondral ossification plays a role in OC. Although ossification at birth in precocial species like foals is advanced, large cartilaginous sections remain at the transition between diaphysis and epiphysis (the physis) and near the joint surfaces (the articular-epiphyseal cartilage complex), allowing for continued growth in the juvenile animal. Nutrition of these cartilaginous sections is provided through vessels passing through the so-called cartilage canals. During endochondral ossification of the articular-epiphyseal cartilage complex, the cartilage layer on the articular side becomes thinner and is converted into epiphyseal bone and the final articular cartilage layer of the mature animal.
The classic hypothesis of equine OC is that there is disturbance of the physiologic process of endochondral ossification that leads to locally thickened cartilage plugs (Figure 114-1). At the same time, cartilage canals disappear in a physiologic process called chondrification. From that moment, nutrition of the articular cartilage depends exclusively on diffusion of nutrients from the synovial fluid. Excessive thickening of the cartilage layer leads to malnutrition of certain areas and hence to focal necrosis and weakening of the tissue. Together with biomechanical influences, this may result in the formation of fissures, cartilage flaps, and eventually loose fragments or joint mice.
(Courtesy PR van Weeren, Utrecht University)
This hypothesis seems straightforward, but many concerns, including the fact that thickened cartilage or necrosis is not always seen with typical OC lesions, have been expressed that call into question the accuracy of the single hypothesis for OC. Recent investigations of the molecular mechanisms of OC indicate that the collagen component of the cartilage extracellular matrix is primarily affected. It is hypothesized that a defective collagen network results in disturbed calcification of cartilage, as has been shown in bone, causing delayed endochondral ossification, which is the hallmark of OC. Furthermore, a defective collagen network likely reduces the tensile strength of the cartilage and may, together with or without local cartilage thickening and biomechanical forces, result in the development of characteristic cartilage flaps or fragments. Osteochondrosis is a complex disease of multifactorial origin, and how these factors interrelate to produce the disease remains poorly understood.
It seems logical to expect that chondrification of cartilage canals may contribute to reduced cartilage nutrition and possible necrosis when nutrition is impeded by increased cartilage thickness. Both persistence and early regression of cartilage canals have been proposed as causative mechanisms of OC. Most likely, persisting cartilage canals affect the endochondral ossification process and indirectly play a role in the development of OC lesions. The time of the normal chondrification process is the window of susceptibility for development of OC lesions.
A strong indication of the influence of loading is the fact that lesions have been reported in foals within weeks of birth, but no lesions have been found in stillborn foals or fetuses. The consistent location of OC lesions within joints also suggests that loading plays a role in development of lesions. Loading definitely plays a role in converting a clinically silent OC lesion into a dissecting clinical lesion, independent of primary weakening of cartilage resulting from increased thickness or structural deficits. Direct trauma and shearing of cartilage canals have also been related to loading conditions.
Conflicting evidence exists regarding the role of exercise in development of OC. In one study, increased exercise intensity and frequency in horses from 3 to 24 months of age reduced the incidence of OC lesions, from 20% to 6%. However, another more recent study in which the influence of exercise from 0 to11 months of age was investigated did not substantiate a decrease in OC incidence, although a tendency toward decreased severity of lesions was reported. Recent research confirms the importance of exercise for normal joint development and shows that exercise can be an asset in prevention of OC. However, specific exercise regimens that are beneficial in prevention of OC have yet to be determined.
Numerous investigations of the role of nutritional factors in the development of OC have been undertaken. Growth and average daily weight gain are positively correlated with OC in both the hock and stifle joints. However, it appears to be of no importance whether the high growth rate is caused by high food intake or by genetic predisposition. Overfeeding and high dietary energy intake has been shown to desynchronize several endocrine factors, including insulin, insulin-like growth factors 1 and 2 (IGF-1 and 2), and thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). High dietary energy intake may desynchronize the balances among these hormones, and alterations in their secretion and metabolism may result in abnormal cartilage development.
An association between copper deficiency or zinc-induced copper deficiency and equine OC-like lesions was proposed for many years. Copper deficiency has been traditionally related to inferior collagen quality as a result of reduced cross-linking. However, more recent studies in which foals were fed less than the recommended 10 ppm of copper did not result in an increased incidence of OC. Furthermore, increased liver copper content is not related to the number of lesions, but apparently there is a positive effect of copper on the repair of lesions. High calcium concentration in the diet does not affect the occurrence of OC lesions; however, very high phosphorus concentrations increase the number of lesions. More likely, these lesions are the result of increased osteoporosis and weakening of the subchondral plate, and not OC.
Early reports suggested that the incidence of OC in horses was substantially higher in males than in females; however, recent studies in which results were corrected for growth rate revealed no sex predisposition.
There is no doubt that OC is at least partially determined by genetics, but research on inherited factors has received less attention than research on environmental factors. Furthermore, reports on heritability are contradictory or inconclusive. Estimates of heritability vary widely, from 0 to 0.58, with mean values of 0.25 to 0.30. This means that on average 25% to 30% of OC is genetically fixed and that the remaining 70% to 75% is caused by environmental effects.