Aims. To explore the of age of onset distribution for Perthes’ disease of the hip, with particular reference to gender, laterality and conformity to the lognormal distribution. Patients and Methods. A total of 1082 patients were identified from the Liverpool Perthes’ Disease Register between 1976 and 2010, of which 992 had the date of diagnosis recorded. In total, 682 patients came from the geographical area exclusively served by Alder Hey Hospital, of which 673 had a date of diagnosis. Age of onset curves were analysed, with respect to the predefined subgroups. Results. The age of onset demonstrated a positive skew with a median of 5.8 years (interquartile range 4.6 to 7.5). Disease onset was a mean five months earlier in girls (p = 0.01) and one year earlier in those who went on to develop bilateral disease (p < 0.001). There was no difference in the age of onset between geographical districts with differing incidence rates. The entire dataset (n = 992) conformed to a lognormal distribution graphically and with the chi-squared test of normality (p = 0.10), but not using the Shapiro-Wilk test (p = 0.01). The distribution for the predefined geographical subgroup (n = 673) conformed well to a lognormal distribution (chi-squared p = 0.16, Shapiro-Wilk p = 0.08). Given the observed lognormal distribution it was assumed that Perthes’ disease followed on incubation period consistent with a point-source disease exposure. The incubation period was further examined using Hirayama’s method, which suggested that the disease exposure may act in the prenatal period. Conclusion. The age of onset in Perthes’ disease conforms to a lognormal distribution, which allows comparisons with infectious disease epidemiology. Earlier onset in girls and those who develop bilateral disease may offer clues to understanding the aetiological determinants of the disease. The analysis suggests that an antenatal aetiological determinant may be responsible for disease. Take home message: Perthes’ disease age of onset conforms to a lognormal model, which is most typical of infectious diseases. The shape of the distribution suggests that an aetiological trigger in the pre-natal period may be an important determinant of disease. Cite this article: Bone Joint J 2016;98-B:710–14

Aims

The aim of this study was to determine the consensus best practice approach for the investigation and management of children (aged 0 to 15 years) in the UK with musculoskeletal infection (including septic arthritis, osteomyelitis, pyomyositis, tenosynovitis, fasciitis, and discitis). This consensus can then be used to ensure consistent, safe care for children in UK hospitals and those elsewhere with similar healthcare systems.

Aims

The aim of this study was to determine the extent to which patient demographics, clinical presentation, and blood parameters vary in Kingella kingae septic arthritis when compared with those of other organisms, and whether this difference needs to be considered when assessing children in whom a diagnosis of septic arthritis is suspected.

Aims

This multicentre, retrospective study aimed to improve our knowledge of primary pyogenic spinal infections in children by analyzing a large consecutive case series.

Perthes’ disease is an osteonecrosis of the juvenile hip, the aetiology of which is unknown. A number of comorbid associations have been suggested that may offer insights into aetiology, yet the strength and validity of these are unclear. This study explored such associations through a case control study using the United Kingdom General Practice Research database. Associations investigated were those previously suggested within the literature. A total of 619 cases of Perthes’ disease were included, as were 2544 controls. The risk of Perthes’ disease was significantly increased with the presence of congenital anomalies of the genitourinary and inguinal region, such as hypospadias (odds ratio (OR) 4.04 (95% confidence interval (CI) 1.41 to 11.58)), undescended testis (OR 1.83 (95% CI 1.12 to 3.00)) and inguinal herniae (OR 1.79 (95% CI 1.02 to 3.16)). Attention deficit hyperactivity disorder was not associated with Perthes’ disease (OR 1.01 (95% CI 0.48 to 2.12)), although a generalised behavioural disorder was (OR 1.55 (95% CI 1.10 to 2.17)). Asthma significantly increased the risk of Perthes’ disease (OR 1.44 (95% CI 1.17 to 1.76)), which remained after adjusting for oral/parenteral steroid use.

Perthes’ disease has a significant association with congenital genitourinary and inguinal anomalies, suggesting that intra-uterine factors may be critical to causation. Other comorbid associations may offer insight to support or refute theories of pathogenesis.

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.

Panton-Valentine leukocidin secreted by Staphylococcus aureus is known to cause severe skin, soft tissue and lung infections. However, until recently it has not been described as causing life-threatening musculoskeletal infection. We present four patients suffering from osteomyelitis, septic arthritis, widespread intravascular thrombosis and overwhelming sepsis from proven Panton-Valentine leukocidin-secreting Staphylococcus aureus. Aggressive, early and repeated surgical intervention is required in the treatment of these patients.

The Panton-Valentine leukocidin toxin not only destroys host neutrophils, immunocompromising the patient, but also increases the risk of intravascular coagulopathy. This combination leads to widespread involvement of bone with glutinous pus which is difficult to drain, and makes the delivery of antibiotics and eradication of infection very difficult without surgical intervention.