Fixation by a single screw is considered the current treatment of choice for a slipped capital femoral epiphysis. This approach promotes premature physeal closure. The use of a modified, standard, single, cannulated screw designed to maintain epiphyseal fixation without causing premature closure of the physis was reviewed in ten patients. The nine boys and one girl aged between 10.6 and 12.6 years with unilateral slipped capital femoral epiphysis (SCFE), were markedly skeletally immature (Tanner stage I, bone age 10 to 12.6 years).

Clinical and radiological review at a mean follow-up of 44.3 months (36 to 76) showed no difference in the time to physeal closure between the involved and uninvolved side. Measurement of epiphyseal and physeal development showed continued growth and remodelling in all patients.

Use of this device provided epiphyseal stability and maintained the capacity for physeal recovery and growth following treatment for both unstable and stable slipped capital femoral epiphysis.

We performed intra-articular reconstruction of the anterior cruciate ligament (ACL) with the semitendinosus tendon placed in 2 mm diameter tunnels in 21 skeletally immature rabbits. The operation caused 11% damage to the physis of the femur on the frontal plane and 3% of its cross-sectional area but no alteration of growth or axial deviation of the bone resulted. In the tibia, the operation caused 12% damage to the physis in the frontal plane and 4% of the cross-sectional area. Two tibiae developed valgus deformities and one was shortened. Histological examination showed no areas of epiphysiodesis. There was no abnormality of growth-plate thickness in the two cases of tibia valga. Osseous metaplasia in the grafted tendons did not occur. The results suggest the need for careful evaluation of the percentage of damage to the growth plate before using intra-articular methods for reconstruction of the anterior cruciate ligament in adolescents.

We obtained specimens of growth-plate cartilage from four patients with osteogenesis imperfecta. Light microscopy showed structural changes in the tissue and morphological changes in chondrocytes and matrix, particularly in the hypertrophic zone. There were changes in the process of calcification in the primary mineralisation zone of the cartilage. We also found histochemical changes in the matrix glycosaminoglycans (GAGs) in the zones where physiological mineralisation was disturbed and where the trabeculae were interrupted and poorly mineralised. In addition to the known molecular defects in collagen, changes in GAGs and non-collagenous proteins are important factors in the pathogenesis of the disease.