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Patients showed the greatest improvement in abductor strength within the first 6 months after THA, especially during the first 3 months. Abductor strength was consistently greater in patients with mild dysplasia than in patients with severe dysplasia. The extent of preoperative LLD and the increase in abductor length were related with post-THA abductor strength recovery in patients with DDH.

BackgroundSciatic nerve injury is a disastrous adverse complication of surgery and can cause debilitating pain, functional impairment and poor quality of life. Patients with developmental dysplasia of the hip (DDH) have a high incidence of sciatic nerve injury after total hip arthroplasty (THA). A better understanding of the course of the sciatic nerve in patients with DDH may help minimise the risk of sciatic nerve injury after THA.MethodsA total of 35 adult patients with unilateral DDH were enrolled in this retrospective study. We reviewed the patients’ computed tomography (CT) scans, which included the area from the iliac crest to below the lesser trochanter. The distance between the sciatic nerve and regional anatomic landmarks in four different sections on CT scans was measured to identify the course of the sciatic nerve.ResultsThe distance from the sciatic nerve to the spine’s midline was shorter on the affected side than on the healthy side (p < 0.05); the same difference was also detected in the distance to the ilium/ischium outside the true pelvis (p < 0.05). The distance to the greater trochanter was longer on the affected side (p < 0.05). However, the two sides showed no significant difference in the distance from the sciatic nerve to the lesser trochanter (p > 0.05).ConclusionsFor patients with unilateral DDH, the sciatic nerve was located near the ischium and ilium but relatively far from the femur of the affected hip joint, compared to its location on the healthy side. These findings reveal that sciatic nerve becomes shorter in the affected low-limb and is relatively unlikely to be directly injuried using the posterolateral approach in patients with unilateral DDH.

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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.