Obesity is thought to be an aetiological factor for slipped capital femoral epiphysis (SCFE). We analysed changes in the incidence of SCFE in Scotland over the last two decades. During this period rates of childhood obesity have risen substantially and evidence for a relationship between these changes and the incidence of SCFE was sought.

We found that the incidence of SCFE increased from 3.78 per 100 000 children in 1981 to 9.66 per 100 000 in 2000 (R² = 0.715): a two and a half times increase over two decades. It was seen at a younger age, with a fall in the mean age at diagnosis from 13.4 to 12.6 years for boys (p = 0.007) and 12.2 to 11.6 for girls (p = 0.047). More children under eight years old were seen with SCFE in Scotland in the decade to 2000 than in the previous decade (p = 0.002, R² = 0.346).

A close correlation was observed between rising childhood obesity over the last 20 years in Scotland and an increasing incidence of SCFE.

A nationwide study of Perthes’ disease in Norway was undertaken over a five-year period from January 1996. There were 425 patients registered, which represents a mean annual incidence of 9.2 per 100 000 in subjects under 15 years of age, and an occurrence rate of 1:714 for the country as a whole. There were marked regional variations. The lowest incidence was found in the northern region (5.4 per 100 000 per year) and the highest in the central and western regions (10.8 and 11.3 per 100 000 per year, respectively). There was a trend towards a higher incidence in urban (9.5 per 100 000 per year) compared with rural areas (8.9 per 100 000 per year). The mean age at onset was 5.8 years (1.3 to 15.2) and the male:female ratio was 3.3:1.

We compared 402 patients with a matched control group of non-affected children (n = 1 025 952) from the Norwegian Medical Birth Registry and analysed maternal data (age at delivery, parity, duration of pregnancy), birth length and weight, birth presentation, head circumference, ponderal index and the presence of congenital anomalies. Children with Perthes’ disease were significantly shorter at birth and had an increased frequency of congenital anomalies.

Applying Sartwell’s log-normal model of incubation periods to the distribution of age at onset of Perthes’ disease showed a good fit to the log-normal curve. Our findings point toward a single cause, either genetic or environmental, acting prenatally in the aetiology of Perthes’ disease.