Abstract
BackgroundLegg-Calve-Perthes Disease (LCPD) is an idiopathic osteonecrosis of the developing femoral head complicated by pain and disability of the hip joint. To date, the pathological mechanisms of LCPD are not well-known. This study screened the changes in serum protein expression in patients with LCPD.MethodsAge- and sex-matched serum samples from 10 control subjects and 10 patients with LCPD were compared using the isobaric tags for relative and absolute quantification (iTRAQ) technique. Gene ontology analyses, KEGG pathway and functional network analyses were performed. Proteins of interest with large differences in expression, S100-A8, alpha-1-acid glycoprotein 1, haptoglobin and apolipoprotein E, were compared by western blotting.ResultsThe disease/control ratios showed 26 proteins were significantly differentially expressed (all p < 0.05). Including higher abundances of complement factor H (1.44), complement C4-B (1.45), isocitrate dehydrogenase [NAD] subunit alpha (2.7) alpha-1-acid glycoprotein 1 (1.87), heptoglobin (1.53) and Ig lambda-2 chain C regions (1.46), and lower levels of apolipoprotein E (0.50), apolipoprotein F (0.60), apolipoprotein C-III (0.69), S100-A8 (0.73), S100-A9 (0.75) and prothrombin (0.77) in LCPD than in controls. The alpha-1-acid glycoprotein 1 and haptoglobin increases, and apolipoprotein E and S100-A8 decreases were confirmed by western blot. KEGG pathway analysis revealed these proteins were related to the complement and coagulation cascades, Staphylococcus aureus infection, PPAR signaling, fat digestion and absorption, and vitamin digestion and absorption. Functional network analysis suggested that the proteins were involved in lipid regulation.ConclusionsThe complement and coagulation cascades, and abnormal lipid metabolism may be involved in the pathogenesis of LCPD.
Highlights
Legg-Calve-Perthes disease (LCPD) is an idiopathic osteonecrosis of the developing femoral head complicated by pain and disability of the hip joint
The cartilage metabolism related protein S100A8/S100-A9 was reduced in the disease group
We found that the immune response related protein, Ig kappa chain C region and Ig lambda-2 chain C region, had significant increased expression in Legg-Calve-Perthes Disease (LCPD)
Summary
Legg-Calve-Perthes Disease (LCPD) is an idiopathic osteonecrosis of the developing femoral head complicated by pain and disability of the hip joint. The estimated annual incidence ranges from 0.2 to 19.1 per 100,000 among children under 15 years [1]. It occurs 5 times more often in boys than in girls [2]. The main long-term problem with this disease is a permanent deformity of the femoral head, which increases the risk of Coagulation abnormalities [4,5,6], vascular interruptions of the blood supply to the proximal femur [7] and abnormal immunological reactivity [8] are all linked to the pathogenesis of LCPD. Another study showed abnormalities in the vascular structure and function in children with LCPD disease [10]. Acute bone morphogenic protein 2 (BMP2) upregulation [11], increased vascular endothelial growth factor (VEGF) expression
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