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. Methods. A prospective case series was undertaken at a single UK paediatric institution between October 2012 and November 2018 of all patients referred with suspected septic arthritis. We recorded the clinical, biochemical, and microbiological findings in all patients. Results. A total of 160 patients underwent arthrotomy for a presumed septic arthritis. Of these, no organism was identified in 61 and only 25 of these were both culture- and
Aims. We aimed to describe the epidemiological, biological, and bacteriological characteristics of osteoarticular infections (OAIs) caused by Kingella kingae. Methods. The medical charts of all children presenting with OAIs to our institution over a 13-year period (January 2007 to December 2019) were reviewed. Among these patients, we extracted those which presented an OAI caused by K. kingae and their epidemiological data, biological results, and bacteriological aetiologies were assessed. Results. K. kingae was the main reported microorganism in our paediatric population, being responsible for 48.7% of OAIs confirmed bacteriologically. K. kingae affects primarily children aged between six months and 48 months. The highest prevalence of OAI caused by K. kingae was between seven months and 24 months old. After the patients were 27 months old, its incidence decreased significantly. The incidence though of infection throughout the year showed no significant differences. Three-quarters of patients with an OAI caused by K. kingae were afebrile at hospital admission, 11% had elevated WBCs, and 61.2% had abnormal CRPs, whereas the ESR was increased in 75%, constituting the most significant predictor of an OAI. On MRI, we noted 53% of arthritis affecting mostly the knee and 31% of osteomyelitis located primarily in the foot. Conclusion. K. kingae should be recognized currently as the primary pathogen causing OAI in children younger than 48 months old. Diagnosis of an OAI caused by K. kingae is not always obvious, since this infection may occur with a mild-to-moderate clinical and biological inflammatory response. Extensive use of nucleic acid amplification assays improved the detection of fastidious pathogens and has increased the observed incidence of OAI, especially in children aged between six months and 48 months. We propose the incorporation of
This multicentre, retrospective study aimed to improve our knowledge
of primary pyogenic spinal infections in children by analyzing a
large consecutive case series. The medical records of children with such an infection, treated
at four tertiary institutions between 2004 and 2014, were analyzed
retrospectively. Epidemiological, clinical, paraclinical, radiological,
and microbiological data were evaluated. There were 103 children,
of whom 79 (76.7%) were aged between six months and four years.Aims
Patients and Methods
Matrix metalloproteinases (MMPs), responsible
for extracellular matrix remodelling and angiogenesis, might play
a major role in the response of the growth plate to detrimental
loads that lead to overuse injuries in young athletes. In order
to test this hypothesis, human growth plate chondrocytes were subjected
to mechanical forces equal to either physiological loads, near detrimental
or detrimental loads for two hours. In addition, these cells were
exposed to physiological loads for up to 24 hours. Changes in the
expression of MMPs -2, -3 and -13 were investigated. We found that expression of MMPs in cultured human growth plate
chondrocytes increases in a linear manner with increased duration
and intensity of loading. We also showed for the first time that
physiological loads have the same effect on growth plate chondrocytes
over a long period of time as detrimental loads applied for a short
period. These findings confirm the involvement of MMPs in overuse injuries
in children. We suggest that training programmes for immature athletes
should be reconsidered in order to avoid detrimental stresses and
over-expression of MMPs in the growth plate, and especially to avoid
physiological loads becoming detrimental. Cite this article:
A delay in the diagnosis of paediatric acute
and subacute haematogenous osteomyelitis can lead to potentially devastating
morbidity. There are no definitive guidelines for diagnosis, and
recommendations in the literature are generally based on expert
opinions, case series and cohort studies. All articles in the English literature on paediatric osteomyelitis
were searched using MEDLINE, CINAHL, EMBASE, Google Scholar, the
Cochrane Library and reference lists. A total of 1854 papers were
identified, 132 of which were examined in detail. All aspects of
osteomyelitis were investigated in order to formulate recommendations. On admission 40% of children are afebrile. The tibia and femur
are the most commonly affected long bones. Clinical examination,
blood and radiological tests are only reliable for diagnosis in
combination. Most studies were retrospective and there is a need for large,
multicentre, randomised, controlled trials to define protocols for
diagnosis and treatment. Meanwhile, evidence-based algorithms are
suggested for accurate and early diagnosis and effective treatment.
The role of heritable thrombophilic risk factors in the pathogenesis of the Perthes’ disease is controversial. The clinical and radiological findings of Perthes’ disease may be indistinguishable from those of Gaucher’s disease, and the most common Jewish N370S Gaucher mutation is threefold greater in patients with Perthes’ disease. Familial osteonecrosis of the femoral head is associated with variant mutations of collagen type II (COL2A1 mutations). We therefore studied the potential role of genetic thrombophilia and the Gaucher and COL2A1 mutations in children with Perthes’ disease. Genomic DNA of 119 children with radiologically-confirmed Perthes’ disease diagnosed between 1986 and 2005 was analysed for the thrombophilic polymorphisms Factor V Leiden, 677T-MTHFR and FIIG20210A. The results were compared with those of a group of 276 children without Perthes’ disease. DNA was also analysed for the Gaucher mutations N370S, G insertion (84GG), L444P, Intron 2 (IVS2+1G>
A) and R496H. Enzymic assays confirmed the Gaucher disease status. Collagen (COL2A1) mutations of the 12q13 gene were also analysed. The prevalence of thrombophilic markers was similar among the 119 patients with Perthes’ disease and the 276 control subjects. The prevalence of the Gaucher mutation was consistent with Israeli population carriership data and did not confirm an earlier-claimed association with Perthes’ disease. All 199 patients were negative for the studied COL2A1 mutations. We found no genetic association between Perthes’ disease and either Gaucher’s disease or COL2A1 mutations or increased genetic thrombophilia among our patients compared with the control group. A systematic review of case-control studies suggested that there was a positive association between Perthes’ disease and Factor V Leiden. The impact of this association upon the disease, although not consistent across the studies, remains unclear.