Objectives: (1) To establish whether the acute phase of Perthes’ disease is associated with abnormalities of growth or bone/collagen turnover. (2) To investigate subsequent changes during treatment and healing.

Methods: In a longitudinal study of 9 children (7 boys), mean age 6.5years (range 3.0 -9.8 years), we serially monitored insulin-like growth factor (IGF)-I, IGF binding protein (BP)-3, bone alkaline phosphatase (ALP, osteoblast activity), C-terminal propeptide of type I collagen (PICP, bone collagen synthesis), C-terminal telopeptide of type I collagen (ICTP, bone collagen degradation), and N-terminal propeptide of type III collagen (P3NP, soft tissue collagen synthesis) in weeks 1,2 and 12 following acute presentation with a limp and again (in 7/9 patients) 1-2 years after presentation. We measured lengths of both lower legs by knemometry at weeks 1,2,6 and 12. Height and weight were measured at baseline and at year 2 follow-up.

Results: Stature was normal at presentation but height SD score subsequently declined (P: 0;06). In week 1, patients already had low circulating IGF-I (P < 0.05), PICP and P3NP (P < 0.0001) and increased ICTP (P:0.001) compared with age ang sex-matched reference groups, indicating low rates of collagen synthesis and enhanced rates of collagen breakdown. Normal or high body mass index ruled out under-nutrition as a cause for the low IGF-I. IGF-I, ICTP and P3NP showed little further change over the next 2 years. Increases in bone ALP and PICP during follow-up (P < 0.06) may have reflected healing of infarcted epiphysis or increased bone turnover associated with reduced physical activity. Year 2 height SD scores correlated with IGF-I (r +0.83, P < 0.05), suggesting that persistently low IGF-I may have contributed to declining height SD scores. Asymmetrical lower leg growth observed during the acute phase may reflect differential weight-bearing on affected and unaffected limbs. Subsequent cessation, then resumption of symmetrical lower leg growth probably reflected our treatment of immobilisation followed by gentle remobilisation.

Conclusions: This study provides insights into the patho-physiology of the growth abnormalities associated with the fragmentation and healing phases of Perthes’ disease.