Editorial LEGG - CALVÉ - PERTHES DISEASE : 100 YEARS

Legg-Calvé-Perthes disease (LCPD) started to be studied 100 years ago (1910), thanks to the advent of the possibility of conducting clinical studies by means of radiographic images (1895). However, many questions remain open, both in relation to the etiology of this orthopedic condition and in relation to which therapeutic measures are valid. Thus, great controversy has been generated. In 1910, three studies were published, respectively by A. Legg, J. Calvé and G. Perthes. These studies described a new condition affecting children’s hips that differed from joint tuberculosis, which was the commonest disease found at that time. Calvé (1875-1954) worked at the “Berck Sur Mer” hospital, which was the biggest specialized tuberculosis service in France. In 1898, he acquired an X-ray machine and, using this, he identified 10 patients with the new disease, which he named pseudo-coxalgia. In turn, working in Leipzig, Germany, Perthes (1869-1927) was one of the first surgeons to use radiographs in his country, and he defined six clinical cases of a condition that he named “juvenile deforming arthritis”, which differed from tuberculosis of the hip. In the same year, in Boston, United States, the Harvard graduate Legg (1874-1939) described a new condition in a study on “an obscure hip condition”. Since then, over all the intervening years, around 2000 studies on this topic have been published. Some techniques and concepts have been described both for conservative treatment and for surgical treatment. The incidence of LCPD is around 15 cases per 100,000 individuals, and it is more common in boys than in girls, with a ratio of 5:1. The disease is very rare among Afrodescendent and Chinese individuals. It is interesting to note that its incidence is greater among individuals of poorer social class: 26 per 100,000 in class 5 versus 4 per 100,000 in class 1. What is known in relation to its etiology? The etiology continues to be obscure, with occurrences of disorders of the arterial circulation or the venous drainage of the growing femoral head, or both of these. Trueta (1949) attributed the cause of the necrosis to closure of the epiphyseal vessels located in the posterosuperior region of the hip, thus demonstrating that in children aged four to seven years, the only source of blood supply to the proximal femoral epiphysis is the lateral epiphyseal vessels. Trauma or inflammatory processes affecting these vessels, with consequent obstruction, may lead to LCPD. Camargo et al (1984) and Godoy Jr. (1988) demonstrated through selective angiographic studies on deep arteries that patients with LCPD present partial or total occlusion of the medial circumflex artery of the affected hips, which may make the proximal femoral epiphysis susceptible to ischemia within the age group from four to eight years. Dr. Robert Salter made an especially large contribution towards the anatomopathology of this condition through an experimental model in pigs. However, there is no reason to question the hypothesis that LCPD is caused by ischemia of the epiphysis. A deficit in the venous drainage of the hip may also occur. Hence, the etiopathology of this disease may be explained thus: 1) at birth, the child carries vascular abnormalities that are probably of genetic origin; 2) with the passage of time, the child develops abnormalities of skeletal growth and bone maturation; and 3) within the age group from four to eight years, when the epiphysis is most susceptible to ischemia, because of the vascular pattern in this age group, the process could be triggered by a factor capable of breaking down the precarious circulatory equilibrium that had been maintained until that