Transposition of the apophysis of the greater trochanter for reconstruction of the femoral head after septic hip arthritis in children: 4 children followed for more than 15 years

Background and purpose Total necrosis of the femoral head after infection in children during their first months of life gives a dislocated hip with severe leg shortening. A new femoral head can be achieved with subtrochanteric osteotomy and transposition of the apophysis of the greater trochanter into the acetabulum. Previous reports have dealt with short-term results (up to 12 years). Here I present some results of this procedure 15–24 years after operation. Patients and methods 4 children aged 1–6 years with complete necrosis of the femoral head were operated on with transposition of the greater trochanter. Secondary shelf plasty was performed later in 1 child, distal femoral epiphysiodesis in another, and femoral bone lengthening in 1 child. The mean follow-up period was 19 (15–24) years. Results A new femoral head developed in all hips. 2 of them had a spherical head with a good acetabular cover, and without any osteoarthritis except for slight reduction of cartilage height. These hips were painless, with a mobility that allowed good walking function after 16 and 24 years, respectively. In the other 2 patients, in which there was a severe acetabular dysplasia at the primary operation, the new femoral head was somewhat flattened; painful osteoarthritis led to hip replacement 15 and 21 years after trochanter arthroplasty. Even these patients had a relatively good walking function until the last couple of years before hip replacement. Maximum leg length discrepancy was 7 cm. Interpretation Trochanter arthroplasty with subtrochanteric osteotomy in total femoral head necrosis after septic arthritis in children may give satisfactory long-term results provided adequate acetabular cover is obtained. Although the method cannot provide a normal hip, it can contribute to less length discrepancy, less pain, improved gait, and more favorable conditions for later hip replacement

Dimethyl fumarate attenuates reactive microglia and long-term memory deficits following systemic immune challenge

BACKGROUND: Systemic inflammation is associated with increased cognitive decline and risk for Alzheimer's disease. Microglia (MG) activated during systemic inflammation can cause exaggerated neuroinflammatory responses and trigger progressive neurodegeneration. Dimethyl fumarate (DMF) is a FDA-approved therapy for multiple sclerosis. The immunomodulatory and anti-oxidant properties of DMF prompted us to investigate whether DMF has translational potential for the treatment of cognitive impairment associated with systemic inflammation. METHODS: Primary murine MG cultures were stimulated with lipopolysaccharide (LPS) in the absence or presence of DMF. MG cultured from nuclear factor (erythroid-derived 2)-like 2-deficient (Nrf2 -/- ) mice were used to examine mechanisms of DMF actions. Conditioned media generated from LPS-primed MG were used to treat hippocampal neuron cultures. Adult C57BL/6 and Nrf2 -/- mice were subjected to peripheral LPS challenge. Acute neuroinflammation, long-term memory function, and reactive astrogliosis were examined to assess therapeutic effects of DMF. RESULTS: DMF suppressed inflammatory activation of MG induced by LPS. DMF suppressed NF-κB activity through Nrf2-depedent and Nrf2-independent mechanisms in MG. DMF treatment reduced MG-mediated toxicity towards neurons. DMF suppressed brain-derived inflammatory cytokines in mice following peripheral LPS challenge. The suppressive effect of DMF on neuroinflammation was blunted in Nrf2 -/- mice. Importantly, DMF treatment alleviated long-term memory deficits and sustained reactive astrogliosis induced by peripheral LPS challenge. DMF might mitigate neurotoxic astrocytes associated with neuroinflammation. CONCLUSIONS: DMF treatment might protect neurons against toxic microenvironments produced by reactive MG and astrocytes associated with systemic inflammation

Acetabular dysplasia and hip dislocation after selective premature fusion of the triradiate cartilage. An experimental study in rabbits

Premature fusion of the triradiate cartilage was obtained surgically in 10 three-week-old rabbits, and compared with isolated fusion of the ilio-ischial and of the ilio-pubic limbs of the triradiate cartilage in two further groups of 10 rabbits. Complete fusion caused acetabular dysplasia five weeks after operation in all animals and hip dislocation at nine weeks in half of them; ilio-ischial fusion had a comparable effect. Ilio-pubic fusion had only a minimal effect on acetabular development. The posterior position of the ilio-ischial limb in the acetabulum and its predominance in the formation of the triradiate cartilage in quadrupeds may have contributed to its decisive effect on acetabular development