LEG WEAKNESS AND OSTEOCHONDROSIS IN SWINE: A REVIEW

Abstract

Leg weakness (lameness) in swine is a problem resulting in economic loss. Osteochondrosis, a noninfectious condition manifested as a failure of endochondral bone formation, is thought to be a principal predisposing cause of leg weakness. Frequent sites of osteochondrotic lesions include the medial condyles of the femur and humerus, semilunar notch of the ulna and the distal ulnar physis. Osteochondrosis results in focal thickening of cartilage with the affected portion of cartilage, which fails to ossify, retained in the subchondral bone. The retained cartilage is frequently associated with chondrocyte death and loss of extracellular matrix proteoglycans. An advanced degree of the condition is observed as osteochondrosis dissecans or secondary osteoarthrosis, and frequently causes lameness of animals. Changes in proteoglycan structure are noted in severely affected porcine joint cartilage. Causes of leg weakness and osteochondrosis remain unclear. Many researchers suggest that mechanical overloading is responsible for the relatively high frequency of osteochondrotic lesions on the weight-bearing surfaces of affected bones. Leg weakness and joint lesions have been studied in relation to various factors associated with animal feeding and management practices (e.g., growth rate, exercise and floor types). Rapid weight gain has often been suggested to be related to the incidence of osteochondrosis, but results are not consistent among experiments reported. The incidence of osteochondrosis is very high (> 90% in one study) even in genetically selected slow-growing pigs, and most attempts to prevent or reduce the incidence of osteochondrosis are unsuccessful. A certain amount of exercise is essential for normal growth of bone and cartilage, but data are lacking concerning whether pigs under normal confinement systems need additional exercise. Experiments with enforced exercise on treadmill or brisk walking suggest that the treatments have little effect on soundness of limb joints of swine. It is unlikely that the incidence of joint lesions could be reduced by changing type of floors studied so far. It has been reported that dietary supplementation of various minerals and vitamins within wide limits has little effect on the incidence or severity of osteochondrosis, suggesting that prevention of joint lesions by nutritional means is also difficult. Genetic studies suggest that the heritabilities of leg weakness and osteochondrosis are low to moderate (0.1 – 0.3), and therefore the problem will be difficult to solve by selection alone. Other factors including carcass characteristics, sex or breed are also discussed in realtion to leg abnormalities. It is possible that pathogenesis of or susceptibility to joint abnormality differs among animals studied, even in the same experiment, resulting in a failure to observe a correlation between a certain factor and the occurrence of leg abnormalities. The last part of this review covers studies examining recovery of pigs from lameness or osteochondrosis including therapeutic means. Treatment of osteochondrotic lame boars by intramuscular administration of glycosaminogiycan polysulfate (GAGPS) improves their locomotory ability. Key words: Leg weakness, osteochondrosis, joint cartilage, bone, growth, pig