Our aim was to investigate the relationship between urinary excretion of deoxypyridinoline (DPD) as a marker of bone resorption, and Perthes’ disease. There were 39 children with Perthes’ disease in the florid stage who collected first-morning urine samples at regular intervals of at least three months. The level of urinary DPD was analysed by chemiluminescence immunoassay and was correlated with the radiological stage of the disease as classified by Waldenström, and the severity of epiphyseal involvement according to the classification systems of Catterall and Herring. The urinary DPD levels of a group of 44 healthy children were used as a control. The median urinary DPD/creatinine (CREA) ratio was significantly reduced (p <
0.0001) in the condensation stage and increased to slightly elevated values at the final stage (p = 0.05) when compared with that of the control group. Herring-C patients showed significantly lower median DPD/CREA ratios than Herring-B patients (p = 0.03). The significantly decreased median DPD/CREA ratio in early Perthes’ disease indicated a reduced bone turnover and supports the theory of a systemic aetiology. Urinary levels of DPD may therefore be used to monitor the course of Perthes’ disease.
We compared the dynamic instability of 25 dysplastic hips in 25 patients using triaxial accelerometry before and one year after periacetabular osteotomy. We also evaluated the hips clinically using the Harris hip score and assessed acetabular orientation by radiography before surgery and after one year. The mean overall magnitude of acceleration was significantly reduced from 2.30 m/s This study suggests that periacetabular osteotomy provides pain relief, improves acetabular cover and reduces the dynamic instability in patients with dysplastic hips.
Between January 1998 and December 1998, 82 consecutive patients (86 hips) underwent total hip arthroplasty using a trabecular metal monoblock acetabular component. All patients had a clinical and radiological follow-up evaluation at six, 12 and 24 weeks, 12 months, and then annually thereafter. On the initial post-operative radiograph 25 hips had a gap between the outer surface of the component and the acetabular host bed which ranged from 1 to 5 mm. All patients were followed up clinically and radiologically for a mean of 7.3 years (7 to 7.5). The 25 hips with the 1 to 5 mm gaps were studied for component migration at two years using the Einzel-Bild-Roentgen-Analyse (EBRA) digital measurement method. At 24 weeks all the post-operative gaps were filled with bone and no acetabular component had migrated. The radiographic outcome of all 86 components showed no radiolucent lines and no evidence of lysis. No acetabular implant was revised. There were no dislocations or other complications. The bridging of the interface gaps (up to 5 mm) by the trabecular metal monoblock acetabular component indicates the strong osteoconductive, and possibly osteoinductive, properties of trabecular metal.
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.
