Children's Orthopaedics

For most of the years that I have been in orthopaedic practice, Perthes' disease has been somewhat stagnant; cause unknown, treatment heterogeneous,  outcome uncertain.  Although predictive classifications existed through the work of Catterall and Herring, these were most effectively applied in the middle of the disease process when it appeared that the best chance for intervention had gone.  Add in the observation that 50% of cases did well at least for 30 years and it’s easy to see how the doctrines of supervised neglect and masterly inactivity became attractive.  Herring summarised the situation by quoting Dorothy Parker  “everyone keeps asking what the answer is. Truth is there ain’t no answer, there ain’t never been no answer, and there ain’t going to be no answer, and that’s the answer”

Presentations at the recent meeting of the British society for children’s orthopaedic surgery suggest that the Perthes' pond is being stirred.

Dan Perry from Liverpool, in a huge piece of work for his PhD, has updated and extended the Merseyside epidemiology studies published over 30 years ago.  He also studied the incidence in the GP research database, and did a systematic review of the international Perthes' epidemiological literature. 

The UK headlines were:

• The UK incidence of Perthes' has halved in a 20 year period
• The current incidence is 5.7/100,000 children
• The incidence in Scotland is double that in London
• Perthes' is associated with deprivation
• The declining incidence is much more marked in deprived areas

Worldwide the incidence was determined firstly by race with whites affected eight times more frequently than East Asians.  Latitude was an independent predictor after adjusting for race (not vitamin D again….)

 The overseas guest lecturer was Harry Kim from Dallas, USA.  For a number of years he’s been conducting experimental studies on the pig model originally developed by Salter.   His group have convincingly demonstrated that bisphosphonates used prior to, or immediately after, the surgical insult that precipitates experimental Perthes' can prevent femoral head collapse and extensive resorption that we recognise as the fragmentation stage.  This could also be achieved with biological inhibitors of osteoclast activity.  Applying this is difficult as in the natural history the head undergoes revascularisation and repair with new bone formation.  His group have attempted to stimulate the repair phase using BMP-2, initially with excessive heterotopic bone. 

He also reported to us the accuracy of perfusion MRI for prognosis.  The prospects for early assessment of severity and effective biological treatment appeared to be very real.

Mr James Hunter, Consultant Trauma and Paediatric Orthopaedic Surgeon, Queen's Medical Centre, Nottingham, UK