Method

The anteroposterior pelvic radiographs of 84 children (87 hips with developmental dysplasia) seen between 1995 and 2004 were reviewed retrospectively. Each radiograph was photographed digitally and converted to the negative using Microsoft Photo Editor. Arthrograms were also assessed at the time of femoral head reduction. The acetabular index (AI) and femoral head deformity were assessed. Acetabular response was measured using the AI at 6 and 12 months post-reduction.

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.

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.

The aim of this study was to correlate two outcome measurements of clubfoot surgery. A modified, partially subjective, clinical scoring system was compared with an objective biomechanical assessment, using the optical Dynamic Pedobarograph foot pressure system. The outcomes of the latter method were developed into a classification system for future prospective studies and to complement clinical evaluation of patients, especially those with relapse.

Many different functional outcome measures have been designed. Differing number of points are allocated to various subjective and objective items of relevance. The weighting given to each item in the overall score depends entirely on the importance the surgeon believes that particular item has on what he believes constitutes a good corrected clubfoot. This makes the scoring systems arbitrary and therefore results of clubfoot surgery between various centres impossible to compare. Sixteen patients [21 feet] were randomly selected from a poll of patients that had undergone clubfoot surgery. The operations were carried out by a single surgeon and consisted of a lateral-posteromedial peritalar release utilising the Cincinnati incision. Post-operatively, all feet were independently classified using a modified scoring system, based on the ones designed by Laaveg and Ponseti and the one by McKay, which scores both objective and subjective findings. This system has a good interobserver reproducibility. After finalisation of treatment, patients were referred to the Foot Pressure Analysis Clinic in Dundee where a novel method has been developed for the evaluation of clubfeet, using a static and dynamic foot pressure analysis system which provides both a graphical and analytical model for comparison. A pedobarographic classification system was developed. An excellent result entails that the patient does not require further treatment. A good result has been achieved if a near normal posture and pressure distribution is recorded. However, this means that there are still functional problems, which, as the foot matures, may lead to future relapse. These feet may therefore require long-term treatment with an orthotic support to let the foot develop its normal shape. A fair result requires major orthotic support of shoe adaptation, or further surgical releases. The correlation between clinical and biomechanical outcomes in the 21 feet was calculated using Kendall’s tau rank test for non-parametric data. The r value was 0.3524, which was significant [p< 0.05]

There is a significant correlation between the above mentioned outcome measurements. Biomechanical assessment cannot replace clinical evaluation, but can complement it and perhaps give a more subtle and earlier prediction of the need for further additional treatment. This technique has not only proven to be objective but also clinically valuable and cost effective. A prospective study to refine this biomechanical classification system into a reliable predictor of relapse in surgically corrected clubfeet is currently being considered.

Over the last 30 years 215 Chiari medial displacement pelvic osteotomies have been carried out, principally for dysplasia of the hip, presenting after adolescence or following previous surgical treatment. Substantial pain relief was achieved initially in 93 per cent of the patients, particularly when the osteotomy was undertaken before stiffness and arthritic change had developed. Survivor-ship analysis, using revision of the hip as the index of failure, revealed that there was a progressive deterioration of the result with time, but that almost 4 out of every 5 hip joints were functioning acceptably at 25–30 years.

The radiographic characteristics of 110 osteotomies in 89 patients were evaluated 5-30 (mean 18) years after surgery which was performed at the age of 15.9+-9.5 years. Revision was significantly (p < 0.05) more likely in those patients operated upon after the age of 25 years. The centre-edge (CE) angle increased from 2.5+-13.9 degrees preoperatively to 41.8+- 15.0 degrees immediately after operation; the increase in the CE angle was maintained at long-term review (39.5+-16.5 degrees), and even with severe dysplasia (CE angle less than zero) a substantial improvement in femoral head cover was achieved, usually by the medial shift of the lower pelvic fragment. However, the femoral head was not invariably medialised by the osteotomy and lateral movement of the ilium was noted when the preoperative position of the joint was relatively medial, or when the hip was arthritic. In the longer term pelvic remodelling did not reverse the medialisation produced by the osteotomy, and femoral head cover was maintained. The osteotomy is at its most effective between the ages of 10–35 years and is not recommended above the age of 40 years.

Congenital Dislocation of the Hip (CDH) has been routinely screened for at birth using clinical tests since the early 60’s. In Edinburgh Macnicol (1) assessed the screening programme between 1962 to 1986. It particularly focussed on the change in incidence of late diagnosis when screening was undertaken by experienced staff in comparison to junior staff. The treatment of Orthopaedic conditions in children within the Edinburgh area was combined at the Royal Hospital for Sick Children in 1995. Therefore this paper aims to reassess the screening programme for CDH between 1995–1999 and compare it with the previously achieved results in the same population.

From 1 Jan 1995 to 31 Dec 1999 there were 34,597 live births at Edinburgh’s Maternity hospitals. An orthopaedic clinical assistant examined all infants within the first 24 hours with considerable experience in this field. In addition to the Ortolani and Barlow tests, skeletal and skin fold asymmetry, limitation of abduction and loss of the physiological flexion deformity present in the normal neonate were observed. FH, delivery and circumstances of the pregnancy were noted. Hips found to be clinically unstable were referred on to the CDH clinic where further assessment and ultrasound were performed in order to decide upon the further management of each child.

In 1995 there were 7179 live births, 2.93 of which were harnessed (incidence per 1000 births), 1.11 late diagnosis, (incidence per 1000 births) and 1.39 were operated upon (incidence per 1000 births).

In 1996 there were 7144 live births, 3.64 of which were harnessed (incidence per 1000 births), 1.40 late diagnosis, (incidence per 1000 births) and 1.82 were operated upon (incidence per 1000 births).

In 1997 there were 7065 live births, 2.12 of which were harnessed (incidence per 1000 births), 0.57 late diagnosis, (incidence per 1000 births) and 0.71 were operated upon (incidence per 1000 births).

In 1998 there were 6763 live births, 4.14 of which were harnessed (incidence per 1000 births), 0.59 late diagnosis, (incidence per 1000 births) and 0.30 were operated upon (incidence per 1000 births).

In 1999 there were 6446 live births, 6.12 of which were harnessed (incidence per 1000 births), 0.78 late diagnosis, (incidence per 1000 births) and 0.62 were operated upon (incidence per 1000 births).

Overall there were 34597 live births, 3.76 of which were harnessed (incidence pre 1000 births), 0.89 late diagnosis, (incidence per 1000 births) and 0.98 were operated upon (incidence per 1000 births).

The incidence of late diagnosis of CDH in Midlothian has increased from 0.5 per 1000 as reported by Macnicol between 1962–1986 to 0.89 per 1000 over the last 5 years. These results are clearly disappointing. Although Catford et al (2) has proposed that the incidence of CDH has been increasing this does not explain the size of the increase in late diagnosis seen. Further investigation is required in order to reduce this late presentation rate to that previously achieved.