ABSTRACT The advances made in the areas of genetics and nutrition during this century have resulted in improved growth rates for livestock. However, one drawback has been the increased prevalence of long bone growth problems, such as rickets, avian tibial dyschondroplasia, and osteochondrosis. Growth plate cartilage, which regulates long bone development, must maintain a tightly controlled balance between cartilage synthesis and degradation as well as chondrocyte proliferation and apoptosis. This paper will briefly review the various nutritional factors, cell signals, and proteins that help regulate growth plate chondrocytes. Some of the growth plate diseases will be discussed with an emphasis on how a breakdown in growth plate metabolism is related to the observed problems. The author's intention is that readers will gain an appreciation for the complexity of this relatively small tissue and for why a better understanding of its physiology will be important in the years to come for the prevention of skeletal problems related to long bone growth.
Implications in the Livestock Industry Proper development of a long bone requires that growth plate cartilage maintain a delicate balance of cartilage synthesis and degradation followed by bone formation. In the animal industry, the emphasis on maximizing the growth rate of livestock through genetics and nutrition has led to more abnormalities associated with the growth plate and long bone growth. As an example, within the past 30 yr the growth rate of birds reared for meat production has increased dramatically (Lilburn, 1994). A problem that developed because of the accelerated growth is tibial dyschondroplasia (TD), a disorder in which growth plate cartilage accumulates in the proximal region of the tibia and femur. It was an insignificant health concern over 30 yr ago, whereas currently it is found in 50% of broiler chickens (Leach, 1996). Problems associated with TD include lameness, increased fractures in the fibula, and an increased susceptibility to osteomyelitis. In turkeys, it increases the incidence of breast blisters. All of these problems can lead to significant economic losses at the processing plant, exceeding $200 million in a single year (Edwards, 1983). Some experimental conditions and compounds that have been found to induce TD include fusarochromanone, thiram, antabuse, excessive dietary levels of cysteine and homocysteine, Cu deficiency, metabolic acidosis, and some environmental conditions (Orth and Cook, 1994). However, the etiology of TD in the field has not been clarified. The problem is that growth plate cartilage in birds with TD is not properly degraded and accumulates at the expense of bone formation (Freedman et al., 1985; Orth et al., 1991). Chondrocyte differentiation and hypertrophy are interrupted before cell maturation is reached (Hargest et al., 1985; Bashey et al., 1989). A recent finding links impairment of apoptosis to TD. The researchers compared histological sections from normal and dyschondroplastic growth plates and found that relatively few apoptotic chondrocytes were present in dyschondroplastic cartilage (Ohyama et al., 1997). Thus, understanding the regulatory molecules in chondrocyte differentiation and apoptosis could be critical to alleviating or preventing this growth plate disorder. Also, birds reared for meat production can develop a rachitic growth plate very quickly if the proper ratio and amounts of Ca and P are not in the diet.
Osteochondrosis (OCD) is a developing cartilage disorder with similarities to TD that occurs in domesticated animals. It is characterized by a failure of endochondral ossification in the articular/epiphyseal and growth plate cartilage in the weight-bearing region of long bones. Osteochondrosis can be a significant economic problem (Hill, 1990; Jeffcott, 1991). In pigs, growth rate and hormonal imbalance have been implicated in the disease. The use of recombinant porcine somatotropin by either injection or a slow-release implant increased the incidence of OCD in Yorkshire pigs (He et al., 1994). Growth rate was not a factor in this experiment since pigs that received a slow-release implant grew at the same rate as control animals. Excessive levels of growth hormone, and possibly other growth factors such as IGF-1, might disrupt the balance between cartilage synthesis and degradation. Osteochondrotic cartilage contains decreased percentages of uronic acid (component of proteoglycans), collagen, and collagen cross-links when compared to unaffected age-matched cartilage (He et al., 1994; Wardale and Duance, 1994). Abnormal proteoglycans were found in osteochondrotic lesions isolated from horses (Lillich et al., 1997). Others have observed problems with the cartilage canal blood supply in both horses and pigs (Carlson et al., 1991, 1995). Necrotic chondrocytes were located around necrotic blood vessels and thus the cells could not fully differentiate. In another study, lesions contained small rounded chondrocytes that suggested a disruption in the progression from the proliferative to hypertrophic phase (Henson et al., 1997). Some causative factors of OCD in horses that have been reported include diets high in digestible energy, P, Zn, and a deficiency in Cu (Lillich et al., 1997).
Because of the susceptibility of developing cartilage to problems during growth, good skeletal structure should be considered when selecting livestock for production. Identification of biological markers that can be used to monitor long bone growth could facilitate the selection process. Unfortunately, selection for good bone growth or structure currently does not appear to correlate well with overall growth performance. Boars selected for both gait and growth performance had a 24% reduction in growth performance relative to boars selected only for growth performance (Steenbergen et al., 1990). Turkeys selected for walking ability had reduced breast widths relative to commercial lines (Ye et al., 1997). Thus, the challenge for geneticists and nutritionists will be to maintain and, in some cases, improve skeletal structure while improvements to lean tissue growth rates and feed conversion are being pursued.
Key Words: Growth, Reviews, Osteochondritis, Dyschondroplasia, Growth Factors
© 1999, by the American Society of Animal Science and the American Dairy Science Association. All rights reserved.
AM Symp. 183-189