Introduction: In the growth plate, chondrocyte swelling (hypertrophy) is a crucial event during endochondral ossification and bone lengthening, accounting for ~80% of the increase in bone length (1,3). The swelling is dramatic (~10x) and closely regulated. Failure of chondrocyte hypertrophy may underlie the chondrodysplasias of the vertebrate skeleton (1). However, the mechanisms which control cell swelling are poorly understood although there must be a key role for chondrocyte osmolyte transporters which are sensitive to an increase in cell volume. We have used confocal scanning laser microscopy (CLSM) to study volume regulation by living in situ growth plate chondrocytes at varying degrees of hypertrophy.

Methods: Bovine growth plates were taken from the ends of young (~12d) bovine ribs. In situ growth plate chondrocytes at the proliferative through to hypertrophic stages were fluorescently-labelled (calcein-AM; 5μM), imaged (Zeiss CLSM510) and volumes determined quantitatively as described (2). An acute osmotic challenge (280-140mOsm) was delivered by perfusion to determine volume-regulatory capacity by cells in the various zones.

Results: The resting volumes of proliferative and hypertrophic cells were 550±63μm³ and 5227±1974μm³ respectively. Reducing osmolarity resulted in a rapid (within ~1min) cell swelling, proliferative and hypertrophic chondrocytes increasing in volume by 126±2% and 146±5% (n=5) respectively. Chondrocytes within the proliferative zone then recovered in volume by ~60% over the following 20mins (p=0.04), whereas no volume recovery was detected in hypertrophic cells (p=0.94).

Conclusions: For the increase in growth plate chondrocyte volume to produce hypertrophy it is essential that the membrane transporters which normally prevent cell swelling are suppressed, otherwise the increase in volume will be compromised. These results suggest that chondrocyte hypertrophy is associated with reduced activity of the swelling-stimulated osmolyte transporter whereas the pathway is active in proliferating chondrocytes. Changes in the activity of this pathway are likely to be an important component in the control of chondrocyte hypertrophy. It is clear that the contributions of other membrane transporters in mediating chondrocyte swelling must be identified in order to understand the overall hypertrophic process.

The hip joints are commonly affected in Juvenile Idiopathic Arthritis (JIA) in childhood. Common features are pain, subluxation, femoral anteversion, coxa valga, significant fixed flexion deformity and a true arthritis, with loss of articular cartilage principally from the femoral head but also the acetabulum.

In children with JIA, it is accepted that a medial soft tissue release of the hips, dividing adductor longus, adductor brevis and the ilio-psoas, is a useful tool in the management of significant hip joint involvement. The principal indication for surgery is the relief of pain, but other benefits are correction of fixed flexion deformity, restoration of articular cartilage, increased abduction of the hips and, in those children who are unable to walk, frequently a transition to the potential to walk. The procedure is nearly always performed bilaterally.

Our study aimed to document the restoration of articular cartilage at the hips following soft tissue release. It has been noted in the literature that there is regrowth of articular cartilage in the hip but there has been no true documentation of this and x-ray studies are unreliable as the elimination of fixed flexion deformity can prejudice accurate analysis of femoral head geometry on 2 –dimensional views.

We therefore carried out MRI scanning of the hips, immediately prior to the soft tissue release and 12–18 months post-operatively. In 10 consecutive patients analysed, scans demonstrated true articular cartilage regrowth in 8 cases.

We thus conclude that soft tissue release of the hips in JIA is a useful management tool, and may to some extent reverse the severe articular cartilage loss seen in these children. The next stage of our study is to analyse the articular cartilage at the time of subsequent hip arthroplasty to determine whether true hyaline cartilage is reformed or whether the reconstitute represents fibrocartilage.

Perthes' disease is common in certain urban areas within Britain. It is one manifestation of a generalised growth disorder and nutritional causes are suspected. Orthopaedic surgeons throughout the Yorkshire region recorded all new patients with Perthes' disease over two years. There were large geographical differences in incidence which could not be explained by urban-rural or social class differences. No cases were recorded in a large area within the eastern part of the region, which is in high-grade farming land and has had a relatively low infant mortality throughout this century.

There is a high incidence of Perthes' disease among the children of unskilled manual workers in underprivileged urban areas in Britain. The skeletal measurements of 38 Liverpool children with Perthes' disease were compared with those of their siblings and of normal children from the inner and outer city. Children in families where Perthes' disease occurs have retarded growth of the trunk, with reduced sitting height and bi-acromial diameter. Among those who develop the disease there is also retarded limb growth, most evident as unusually small feet.