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Legg-Calvé-Perthes Disease. 100 years of research.
Nuno Craveiro Lopes M.D.
Orthopedic Department, Garcia de Orta Hospital
Almada, Portugal
Legg-Calvé-Perthes disease (LCPD), was described as a individual nosological entity for nearly
100 years ago, successively in North America by Arthur Legg (1), in France by Jacques Calvé (2)
and in Germany by Georg Perthes (3). Until that time, several other authors had described the
disease as a form of benign infection (4), or joint tuberculosis (5) as a result of a "crushing" of the
epiphysis due to its vulnerability (6), as secondary to a dystrophy or congenital dislocation of the hip
(7) or as a kind of vascular necrosis by micro-embolisation of unknown cause (8). After the
communications of Legg, Calvé and Perthes, the disease have progressively loosed its aura of
mystery, in particular with the anatomic work of Zemansky (9) and the radiographic study of
Waldenstrom (10), that characterized it as an avascular necrosis and described his evolutive stages
of condensation, fragmentation and reconstruction, although some authors continued to doubt on the
autonomy of the described lesions (11).
It is still accepted the finding that Phemister made in 1921 (12): the initial event that triggers
LCPD is a necrosis by ischemic events, still not perfectly understood, reaching the proximal
epiphyseal nucleus, the growth plate and the metaphyseal portion of the femoral head. In fact, this
region of the osteo-articular structure presents during the growth period, particularly between 3 and
11 years of age, a very poor vascular supply at the expense of cervical arteries and veins with intra-
articular trajectory and terminal type distribution (13). This would facilitate its collapse in case of
intra-articular effusion, traumatic or inflammatory and vicious joint positions (14). It is thought
however, that children affected by the disease, have a predisposition that facilitates this type of
necrosis and that genetic or metabolic factors may be involved and predispose to the existence of a
lower stature (15), delayed bone age (16, 17) and bilateral lesions (18, 19).
Over the past few decades, research have been developed trying to highlight the existence of
these factors in the genesis of the disease, including genetic (20, 21), haematological (22, 23, 24) and
metabolic (25,26), without convincing results. On the other hand, several authors have documented
the existence of histological signs of bone necrosis and repair, repeated over time (27, 28, 29, 30, 31,
32, 33, 34), which suggests the possibility of repeated ischemic events in the aetiology of DLCP,
with abundant documentation pointing to the existence of mechanical factors that lead to a repeated
interruption of the vascular supply, such as vicious prolonged lower limb positions and repeated
intra-articular effusion (35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47).
Thus, according to the current concepts (32), after an initial silent period where intermittent
ischemic events were produced in a variable part of the femoral epiphysis, a decrease in mechanical
resistance of the epiphyseal structure lead to a subchondral pathological fracture due to microtrauma
and trauma of gait and load. It is from this pathological fracture which LCPD starts and the sequence
of stages that characterize the disease begins: Collapse with formation of a sequestrum
(condensation), bone resorption of the sequestrum and its replacement by granulation tissue and
fibro-cartilaginous matrix (fragmentation) and reossification of fibro-cartilaginous matrix
(reconstruction). During the fragmentation stage, due to bone resorption and the proliferation of
granulation tissue, a pronounced deformation can be produced with extrusion out of the acetabulum
of the "softened" antero-lateral area of femoral head, which was identified radiologically by Lloyd-
Roberts and Catterall (49) as a "head at risk" sign.
More recently importance as a factor of better prognosis was given to the maintenance of more
than 50% of the lateral height of the femoral epiphysis, the so-called "lateral column" (50, 51). In
addition to the "head at risk" signs, it is known that several other factors influence a poor prognosis,
especially female sex, the older age at the beginning of the disease and the extent of the lesions (52).
Since the beginning of the nineteen century, specific therapeutic measures have been
recommended. Schwartz in 1914 (53), recommends casting. First Waldenstrom (54) and later
Danforth (55), pointed the importance of unloading in decubitus to alleviate the consequences of the
disease, especially when supplemented with traction and positioning in abduction (56). Latter, in an
attempt to decrease the time in decubitus, which usually extended for more than 1 year, various
authors suggested different types of walking callipers and braces (57, 58). In the recent decades,
several evidence based comparative studies have shown that the treatment with those callipers and
braces was not effective and it have been progressively abandoned in favour of surgical treatment
(59). Other means of treatment have been tried with inconsistent results, including electro-magnetic
waves (60), hyperbaric oxygenation (61), anticoagulants (62), diphosphonates (63) and botulinium
toxin (64).
The first attempts at surgical treatment begun around 1930, based on the idea that the drilling of
the necrotic bone could stimulate the vascular ingrowth, leading to a faster rebuilding process. For
this purpose, Bozsan (65) proposes drilling through the trochanter and Fergusson and Howorth (66)
advocate the same method by direct approach of the anterior cervical region, describing a shorter
course of the disease and better final results, particularly when the intervention was carried out early.
Other authors advocate curettage and graft of the neck (67) or of the epiphysis (68) with some results
described as promising. However, this type of interventions eventually were abandoned on the fifties,
after the introduction of recentering surgical techniques by femoral varus osteotomy, advised by
Soeur (69), Craig (70) and Axer (71), which although more aggressive, were more effective in the
treatment of the disease. From 1970, the publication by various authors of large series of
homogeneous treatments and the confrontation of long-term results, notably by Mose (72), Meyer
(73), Lauritzen (74), Loyd-Roberts, Catterall and Salomon (49) and Salter (32), allowed the
definition of the objectives and indications of surgical treatment, which included varus femoral
osteotomy and pelvic inonimate osteotomies: to prevent the subluxation and preserve as possible the
sphericity of femoral head in order to prevent secondary arthrosis; avoid leg length discrepancy and
Trendelenburg and to allow a normal gait.
Recently, multicentre studies coordinated by Herring (75), confirmed by other authors (76),
establish the groups of patients which have better results receiving surgical treatment by femoral or
inonimate osteotomy: patients with 8 or more years of age with B or B/C lesions. Patients with less
than 8 years would have good outcome with no treatment and group C with 8 or more years of age
would have bad result with any type of treatment. Research of several authors showed that in these
groups, the best results of surgical treatment with femoral varus osteotomy were obtained with an
early intervention in the necrotic or beginning of fragmentation stages, with a final neck-diaphyseal
angle no less than 110 degrees (77). The Group of older patients (8 or more years of age) that
developed lesions of worse prognosis (Herring C, in particular with hinge hip) in which surgical
treatment with femoral or pelvic osteotomy was done, had poor results. The surgical option on those
cases was limited to late rescue techniques, including at the level of the pelvis the Shelf and Chiary
osteotomies and at the femur, valgus osteotomy and cheilectomy. This has encouraged the search for
new treatment methods for this group of patients with worst prognosis, based on the principle of
arthrodiastasis with external fixators, technique that have shown encouraging results (78, 79, 80, 81,
82, 83, 84, 85, 86.87).
Following the ideas of Hungerford (88) and Ficat (89) about the early treatment of idiopathic
femoral head necrosis in adults and based on experimental research (90, 91, 92, 93), Craveiro Lopes
(94) have rehabilitated the early neck-head drilling technique for the treatment of Perthes disease,
with the intention of improving the conditions of arterial supply and venous drainage and promoting
the process reabsoption of necrotic bone tissue by the cutting cones and speedup of the
reconstruction of the epiphyseal femoral head. The Author noted that when used early in the stage of
necrosis, it leaded to a rapid reabsoption of the necrotic zone in 2 to 3 months, with a earlier onset of
the reconstruction stage, on average of 4 and a half months (3 to 10 months). The reconstruction
stage did not appear to be influenced by the drilling procedure.
The idea of prevention of Perthes disease came after a study (95) in which the authors detected
the existence of a morphotype of LCPD which includes a delay of height and weight, delayed bone
age and femoral anteversion, predominantly in a child between 4 and 12 years of age, which features
repeated coxalgia, aspects also referred in part by other authors (96, 97, 98, 99, 100, 101, 102).
Those children had a preferred sleeping position in ventral decubitus with forced medial rotation and
extension of the lower limbs, position that increases joint pressure with collapse of the cervical
retinacular arteries, a fact confirmed by other authors (103, 104). At the same time, numerous
authors have confirmed the hypothesis of the existence of symptomatic transient ischemic episodes
without evolution to Legg-Calvé-Perthes disease, what the authors called "abortive form of Perthes
disease" (99, 105, 106, 107, 108, 113, 109, 110, 111, 112, 114), suggesting the existence of a
possible independent pathological entity, which in certain circumstances can evolve to Legg-Calvé-
Perthes disease.
From the point of view of early diagnosis, it was demonstrated the possibility of identifying
through ultrasound study, the secondary synovitis to an ischemic episode of Legg-Calvé-Perthes
disease, based on the type of effusion/synovitis and articular cartilage thickness (42, 43, 115, 116).
By the other side, several authors have shown the specificity and sensitivity of the Tc 99m MDP
bone scan in the early diagnosis of a ischemic event of the femoral head (27, 44, 109, 117, 118, 119,
120), and later, of the superiority of nuclear magnetic resonance as regards to specificity, precocity
and ability to quantify this ischemic event compared with bone scan (121, 122, 123, 124, 125, 126,
127), allowing the confirmation of the initial epiphyseal ischemic episodes that characterize the
initial stage of the disease. On the basis of this data, Craveiro Lopes (92, 129) identified a new
clinical entity that develops in some susceptible children, characterized by successive ischemic
events in the proximal femoral epiphysis, which he called "Ischemic Disease of the Growing Hip"
(IDGH), that under certain circumstances, can progress to Legg-Calvé-Perthes disease. In this
context, a child with IDGH, at risk of developing Legg-Calvé-Perthes disease or with the disease in
its early stage, particularly if its age is more than 6 years, where the prognosis of the disease is worse,
Craveiro Lopes advocates the use of a Trans Neck-Head Drilling procedure (TNHD)(93, 129), in
order to increase the blood supply and venous drainage of the upper femoral epiphysis, thus avoiding
the repetition of ischemic episodes and preventing or aborting the appearance of Legg-Calvé-Perthes
disease.
CONCLUSION
Presently, there are scientific indications that Legg-Calvé-Perthes disease is multifactorial and
caused by a combination of congenital and environmental factors. Probably the pathologic situation
we know as LCPD have several aetiologies that originates a common evolution and similar
manifestations. The final deformation of the femoral head is the most important prognostic factor in
the long run. The worst his deformity, the greater the risk of developing osteoarthritis in the
adulthood.
The treatment of LCPD went through several stages. In the 1950 and 1960, the children were
admitted to hospitals and placed at rest in bed for months or years, as was the case with osteo-
articular tuberculosis. Between 1970 and 1980, several orthosis and braces were used, trying to
restrict load on the affected limb and to prevent the collapse and deformation of the femoral head.
After evidence that the results were not as expected, from 1990 surgical treatment based on
osteotomies became very popular. Recent prospective studies have shown that this type of surgery is
beneficial in some patients, but not in others. Evidence-based studies showed that in the group of
patients with less than 6 years old and in the one with more than 8 with pronounced femoral head
deformation, the surgery did not bring added value; in the first group the results are good and on the
second bad with or without surgical treatment by osteotomy. By the other side, in the last decade it
has become obvious that the osteotomy surgery has better result in the initial stages of the disease
without deformity, situation where the use of the prognostic value of Herring classification can not
be used. The controversy continues regarding the choice of the best treatment for the older group of
patients. Arthrodiastasis seems to be a promising way to deal with this group of patients with worse
prognosis, where the osteotomy surgery is not effective.
In the last years, it has been recognized that results of treatment may be improved with drugs. It
is necessary to invest in research to better understand the biological factors involved in the aetiology
and progression of the disease and develop biologically active treatments that could improve the
reconstruction of a spherical femoral head and shorten the course of the disease. Finally there is
evidence that the subchondral fracture that initiates the symptomatic stage of the disease, occurs in a
femoral head weakened by successive multi-factorial ischemic events. The understanding of this
initial stage of the disease is crucial to highlight the factors and direct the efforts to fight the disease
in its prevention.
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