Longus colli has a postural function on cervical curvature.

To determine the postural role of longus colli (LC) and dorsal neck muscles, we have studied the relationship between their cross-sectional areas related to their force of contraction and the lordosis and the length of the cervical spine. This study was carried out in 36 healthy subjects. Muscle cross-sectional areas were measured by computerized tomography. The index of lordosis and the length of the cervical spine were measured on an X-ray profile. The cross-sectional area of LC was correlated to the lordosis index (R = -0.432, p < 0.02) whereas all the other parameters were not correlated. The authors conclude that LC counteracts the lordosis increment related to the weight of the head and to the contraction of the dorsal neck muscles. Postural functions of LC and postcervical muscles are complementary. They form a sleeve which encloses and stabilizes the cervical spine in all positions of the head.

Effects of repetitive strains on vertebral end plates in young rats.

A histologic study of vertebral end plates was performed on young rats' tails subjected to intensive passive motion. Seven six-week-old rats had two-hour motion cycles daily, for two months. Histologic changes of proximal caudal vertebrae in the experimental group were compared with those of a control group of seven rats of the same litter which were allowed to grow freely without mechanical stress. The main findings were three striking protrusions of disk tissue into end plates, not observed in the control animals. End plate axial bulges lacking spindle-shaped cells and an increase in chondrocytes in the adjacent articular cartilage were observed. The growth-plate thickness was uneven and was absent in some areas, with disorganization of chondrocyte columns. All of these findings were present to a lesser degree in the control group and appeared to be similar to histologic changes observed in Scheuermann's disease.

[Reflections on 25 failures during the immunologic treatment of 247 cases of spondylarthritis]. / Réflexions sur vingt-cinq échecs survenus au cours du traitement immunologique de 247 spondylarthrites.

Ten per cent of 247 patients suffering from Bechterew's disease failed to respond as expected to "classic" immunological treatment. Amongst those treated, there was a distribution of H.L.A. DR groups which deviated from the central group, similar to the incidence observed in psoriatic arthropathy.

[Induction of flare-ups of chronic progressive polyarthritis in mice after injection of type II homologous collagen]. / Induction d'une polyarthrite chronique évoluant par poussées chez la souris après injection de collagène de type II homologue.

Immunization by heterologous type II collagen induces in mice a sudden onset of subacute polyarthritis. In order to form a model of auto-immune pathology, we immunized DBA/1 mice with homologous type II collagen extracted from mice xiphoid process; the induced disease corresponds to a progressive chronic polyarthritis with bouts interspersed with remissions, and predominates especially in males. Type II anti-collagen auto-antibodies are found in the serum, with no correlation between the level of mice type II anti-collagen immunoglobulins G and the clinical manifestations of the disease. The histological study demonstrates signs of hyperplastic villous synovitis, with a discrete and infrequent infiltration with mononuclear cells. The model that is obtained is similar to rheumatoid polyarthritis, but also to spondylo-arthropathies.

Experimental autoimmune arthritis in mice. I. Homologous type II collagen is responsible for self-perpetuating chronic polyarthritis.

Immunisation with heterologous type II collagen (CII) induces arthritis in mice of the DBA/1 strain, which is genetically susceptible to this disease. To develop an experimental model of autoimmunity more adequate for the study of human rheumatoid arthritis (RA), DBA/1 mice were injected with 100 micrograms of native CII that had been purified from mouse xiphoid cartilage. About six weeks later the animals developed a chronic progressive polyarthritis involving the four paws but mainly confined to interphalangeal and metatarsophalangeal joints. The evolution of the disease fluctuated between remissions and exacerbations. The initial lesions assessed by clinical observations were more severe when the disease occurred early than in the case of late onset. Interestingly, the incidence of arthritis was clearly preponderant in males, and, moreover, the few female mice which developed arthritis had mild disease states with lower arthritic scores than the males. Varying levels of autoantibodies against mouse CII were found in the sera of immunised animals, regardless of the development of arthritis. These data indicate that the injection of homologous CII into mice caused a polyarthritis that is clinically closer to the human RA than the disease induced with heterologous CII and therefore will represent a useful tool for the study of the self-perpetuating mechanisms that characterise RA.

[Induction of arthritis in mice by injection of homologous type II collagen]. / Induction d'une arthrite chez la souris par injection de collagène de type II homologue.

Immunization with heterologous type II collagen (CII) induces arthritis in DBA/1 mice, a strain genetically susceptible to this disease. In order to develop an experimental model of autoimmunity more adequate for the study of human Rheumatoid Arthritis, DBA/1 mice were injected with homologous native CII. About 6 weeks later, the animals developed a chronic progressive polyarthritis assessed by clinical observations and histologic examination. The incidence of arthritis as well as the severity of the disease are clearly higher in males. Conversely, the secretion of autoantibodies raised against mouse CII is correlated neither with sex nor with activity score of the arthritis.

[Effect of imidazole on the trabecular bone volume of rats with calcium deficiency]. / Action de l'imidazole sur le volume trabéculaire osseux du rat carencé en calcium.

Low-calcium diet induces bone rarefaction in young rats by decreasing trabecular bone volume without any mineralization's defect. Given alone, calcium or imidazol increases, significantly but incompletely, trabecular bone volume. Given together, calcium and imidazol increase trabecular bone volume as well as normal diet does. These results indicate that imidazol acts likely by activating metabolic effects of calcium.