Autologous chondrocyte implantation (ACI) is a promising treatment for articular cartilage degeneration and injury; however, it requires a large number of human hyaline chondrocytes, which often undergo dedifferentiation during in vitro expansion. This study aimed to investigate the effect of suramin on chondrocyte differentiation and its underlying mechanism. Porcine chondrocytes were treated with vehicle or various doses of suramin. The expression of collagen, type II, alpha 1 (COL2A1), aggrecan (ACAN); COL1A1; COL10A1; SRY-box transcription factor 9 (SOX9); nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX); interleukin (IL)-1β; tumour necrosis factor alpha (TNFα); IL-8; and matrix metallopeptidase 13 (MMP-13) in chondrocytes at both messenger RNA (mRNA) and protein levels was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot. In addition, the supplementation of suramin to redifferentiation medium for the culture of expanded chondrocytes in 3D pellets was evaluated. Glycosaminoglycan (GAG) and collagen production were evaluated by biochemical analyses and immunofluorescence, as well as by immunohistochemistry. The expression of reactive oxygen species (ROS) and NOX activity were assessed by luciferase reporter gene assay, immunofluorescence analysis, and flow cytometry. Mutagenesis analysis, Alcian blue staining, reverse transcriptase polymerase chain reaction (RT-PCR), and western blot assay were used to determine whether p67phox was involved in suramin-enhanced chondrocyte phenotype maintenance.Aims
Methods
Pathological fractures in children can occur
as a result of a variety of conditions, ranging from metabolic diseases and
infection to tumours. Fractures through benign and malignant bone
tumours should be recognised and managed appropriately by the treating
orthopaedic surgeon. The most common benign bone tumours that cause pathological
fractures in children are unicameral bone cysts, aneurysmal bone
cysts, non-ossifying fibromas and fibrous dysplasia. Although pathological
fractures through a primary bone malignancy are rare, these should
be recognised quickly in order to achieve better outcomes. A thorough
history, physical examination and review of plain radiographs are
crucial to determine the cause and guide treatment. In most benign
cases the fracture will heal and the lesion can be addressed at
the time of the fracture, or after the fracture is healed. A step-wise
and multidisciplinary approach is necessary in caring for paediatric
patients with malignancies. Pathological fractures do not have to
be treated by amputation; these fractures can heal and limb salvage
can be performed when indicated.
