Accumulation of fat mass in obesity may result from hypertrophy and/or hyperplasia and is frequently associated with adipose tissue (AT) dysfunction in adults. Here we assessed early alterations in AT biology and function by comprehensive experimental and clinical characterization of 171 AT samples from lean and obese children aged 0 to 18 years. We show an increase in adipocyte size and number in obese compared with lean children beginning in early childhood. These alterations in AT composition in obese children were accompanied by decreased basal lipolytic activity and significantly enhanced stromal vascular cell proliferation in vitro, potentially underlying the hypertrophy and hyperplasia seen in obese children, respectively. Furthermore, macrophage infiltration, including the formation of crownlike structures, was increased in AT of obese children from 6 years on and was associated with higher hs-CRP serum levels. Clinically, adipocyte hypertrophy was not only associated with leptin serum levels but was highly and independently correlated with HOMA-IR as a marker of insulin resistance in children. In summary, we show that adipocyte hypertrophy is linked to increased inflammation in AT in obese children, thereby providing evidence that obesity-associated AT dysfunction develops in early childhood and is related to insulin resistance.Obesity is characterized by the accumulation of fat mass and is often associated with adipose tissue (AT) dysfunction (1). Clinical data indicate that obesity already develops during early childhood between 2 and 6 years of age (2). Expansion of AT can be achieved by hyperplasia (increase in adipocyte number) or hypertrophy (increase in adipocyte size) or the combination of both (3). Early studies suggested that adipocyte number is determined in childhood and remains relatively constant during adulthood, implying that expansion of AT mass in (adult) obesity occurs via hypertrophy of adipocytes (4,5). On the other hand, the capability for cell renewal, achieved by differentiation of preadipocytes into mature adipocytes, persists throughout life (6). Whether AT expansion in the development of obesity occurs primarily by hyperplasia or hypertrophy and the time point when AT dysfunction emerges are still a matter of debate.In addition to the mere accumulation of fat mass, obesity is often associated with changes in AT biology and

Recent studies suggested the persistence of brown adipocytes in adult humans, as opposed to being exclusively present in infancy. In this study, we investigated the presence of brown-like adipocytes in adipose tissue (AT) samples of children and adolescents aged 0 to 18 years and evaluated the association with age, location, and obesity. For this, we analysed AT samples from 131 children and 23 adults by histological, immunohistochemical and expression analyses. We detected brown-like and UCP1 positive adipocytes in 10.3% of 87 lean children (aged 0.3 to 10.7 years) and in one overweight infant, whereas we did not find brown adipocytes in obese children or adults. In our samples, the brown-like adipocytes were interspersed within white AT of perirenal, visceral and also subcutaneous depots. Samples with brown-like adipocytes showed an increased expression of UCP1 (>200fold), PRDM16 (2.8fold), PGC1α and CIDEA while other brown/beige selective markers, such as PAT2, P2RX5, ZIC1, LHX8, TMEM26, HOXC9 and TBX1 were not significantly different between UCP1 positive and negative samples. We identified a positive correlation between UCP1 and PRDM16 within UCP1 positive samples, but not with any other brown/beige marker. In addition, we observed significantly increased PRDM16 and PAT2 expression in subcutaneous and visceral AT samples with high UCP1 expression in adults. Our data indicate that brown-like adipocytes are present well beyond infancy in subcutaneous depots of non-obese children. The presence was not restricted to typical perirenal locations, but they were also interspersed within WAT of visceral and subcutaneous depots.

Background: Idiopathic genu valgum is a frequently diagnosed growth disorder in adolescence. Whenever the possibilities of conservative therapy have been exhausted, leg straightening by means of hemiepiphysiodesis has become the standard form of treatment. Because of their flexible screw-plate connection, eight-Plates have been reported in the literature to lead to lower complications regarding implant loosening and fracture compared to other implants. The aim of this retrospective survey was to analyse our own patient population who were treated for genu valgum by means of temporary hemiepiphysiodesis near the knee using eight-Plates to modulate growth. Methods: Between July 2007 and July 2015, 198 eight-Plates were implanted near the knee in 132 children suffering from genu valgum to modulate growth. Depending on the deformity analysis, an eight-Plate was implanted on the distal medial femur and/or the proximal medial tibia. By December 2015, they had been removed from 105 patients. The etiology of genu valgum was mainly idiopathic or associated withobesity. Evaluation was carried out clinically and radiologically (whole-leg X-ray in standing) including determination of the joint angles. Results: The median follow-up period was about 46 months (12-102 months). The median age at implantation was 12.7 +/−6.76 years. Of the 105 patients, 45.7% (n = 48) were girls. The eight-Plates remained in place for a median period of 13 +/−1.76 months. Irrespective of the location of hemiepiphysiodesis, the intermalleolar distance was corrected to a median of 0 +/−2.1 cm while the anatomical femorotibial angle was corrected by on average 9 +/−2.7°M echanical lateral distal femoral angle changed an average 7 +/− 7.72 degrees. Medial proximal tibial angle changed an average 4 +/− 6.02 degrees. Complications necessitating surgery occurred in 2.8% of cases (1 wound infection, 3 corrective osteotomies following overcorrection). Conclusion: Temporary hemiepiphysiodesis using eight-Plates is a gentle, simple and effective procedure used to treat genu valgum by modulating growth. Slight overcorrection is desirable due to the rebound phenomenon, especially in young patients with high growth potential and risk groups such as obese children. In adolescents with only low growth potential (older than 14 years), owing to the low correction potential, the indication should be strictly reviewed and the possible failure of therapy should be discussed with the patient. No differences were observed regarding the location of the implanted eight-Plates (femoral or tibial).

In children with acute appendicitis, we identified several oral bacterial pathogens. Based on postprandial viability of selected species, a viable migration from the oral cavity through the stomach to the appendix seems possible. Thus, the oral cavity could be a relevant reservoir for acute appendicitis.

A retrospective analysis of 332 children with osteomyelitis (OM), managed from 1966 to 1996, was undertaken to evaluate etiology, clinical course and treatment results. In 64% of all patients positive bacterial cultures were obtained, Staphylococcus aureus, streptococci, pneumococci, and Haemophilus influenzae were the most frequently cultured pathogens. In two-thirds of the cases long bones (femur, tibia, humerus) were affected. Osteoarthritis or suppurative arthritis was evident in 27%; 32 of 170 (19%) re-evaluated patients had moderate or severe sequelae. Risk factors for an unfavorable course were the onset of disease in early infancy, suppurative arthritis, and an affected epiphysis. Suppurative arthritis, in particular, needs early evacuation to prevent sequelae. In recent years we observed an increasing number of patients presenting with atypical forms of OM. Since 1989 10 patients were considered to have chronic recurrent multifocal OM (CRMO). In 6 of them the clavicle was involved; their ages ranged from 3 to 14 years. The erythrocyte sedimentation rate was elevated (median 48, range 9-110 mm), while other inflammatory parameters like C-reactive protein (median 9, range <5-85 mg/l) or leucocyte count were slightly elevated or normal. Histopathology was stage-dependent, with a predominance of lymphoplasmacellular infiltration. A nonbacterial origin of CRMO is probable but not proven. Histopathology is not suitable for differentiation between bacterial and nonbacterial forms of bone inflammation.