Delayed delivery interval between twins: a viable option? A case report.
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Adult↗
Biomedical subjects
Swapnil Shah
Publications and source records attributed to Swapnil Shah.
Infected fractures of the distal tibial metaphysis and plafond: achievement of limb salvage with free muscle flaps, bone grafting, and ankle fusion.
Infection after fractures of the tibial plafond is a challenging problem that may even result in amputation. The current study evaluates a limb salvage protocol and the associated long term functional outcome in 6 patients (mean age 46 years) who were treated for infection after a fracture of the distal tibial metaphysis and plafond. Our limb salvage protocol included 3 stages: 1) radical debridement and stabilization of the ankle with a bridging external fixator, 2) soft tissue coverage with free muscle flaps, and 3) ankle fusion using iliac crest bone graft for filling the existing defects measuring 4.2 cm on average. At a mean followup of 5.5 years (range, 2-10.5 years), limb-salvage and eradication of infection was accomplished in all extremities. Fusion of the ankle joint was achieved in all patients, with one patient requiring a supplemental bone grafting procedure for delayed healing of the fusion site. All patients are able to walk without assistive devices and five of six patients are pain free. Limb salvage with free muscle flaps, bone grafting, and ankle fusion is a viable option for the treatment of infected tibial metaphysis and plafond fractures.
Adult↗
Role of apoptosis in glucocorticoid-induced osteoporosis and osteonecrosis.
Bone disease is a side effect of concern regarding chronic glucocorticoid (GC) administration. Most GC-treated patients exhibit a process of bone loss, frequently leading to osteoporosis, with increased fracture risk, especially in spinal vertebrae. Some GC-treated patients will develop osteonecrosis, a disease with distinct clinical and histopathological features, most often occurring underneath the articular surface of the femoral head. Remarkably, both of these GC-induced bone diseases are associated with osteoblast and osteocyte apoptosis, which is emerging as a potential primary pathogenic mechanism. Here, we review the evidence for osteoblast and osteocyte apoptosis in GC-induced bone disease and highlight current debates: (1) With recent reports describing the antiapoptotic effect of GCs in some in vitro osteoblast models, and with the known adverse effects of GCs on osteoblast cell cycle and differentiation, could the in vivo osteoblast apoptosis be an indirect rather than a direct effect of GCs? (2) What is the pathogenic relationship between GC-induced osteoporosis and osteonecrosis? Could the latter be a mere manifestation of the former? and (3) How does apoptosis fit into the traditional concept of ischemia as a key etiology in osteonecrosis? Regardless of the answers, recent studies with cells, animals, and humans point out bone cell apoptosis as a potential target in the design of treatment for GC-induced bone disease.
Animals↗