Impairment of two types of circulating endothelial progenitor cells in patients with glucocorticoid-induced avascular osteonecrosis of the femoral head

ObjectivesThis study examined whether abnormalities of early EPCs and endothelial colony forming cells (ECFCs) are present and compared their functions in glucocorticoid (GC)-induced avascular osteonecrosis of the femoral head (ANFH).MethodsEarly EPCs and endothelial colony forming cells (ECFCs) were obtained from 33 patients with glucocorticoid-induced ANFH and 33 age- and sex-matched control subjects. Cells were isolated, in vitro cultured and studied by Flow Cytometry and Immunofluorescence. Colony-forming unit counts were observed from 33 patients and 33 healthy controls. Growth kinetics, migratory capacity to multiple chemo-attractants, in vitro tube formation capacity and cytokine (vascular endothelial growth factor and stromal cell-derived factor-1) levels in supernatants of two types of EPCs were assayed in ANFH patients and matched controls (n = 4).ResultsMean numbers of colonies formed by both types of EPCs were decreased in ANFH patients (Early EPCs: 2.42 ± 1.46 versus 4.52 ± 2.00, p < 0.05; ECFCs: 0.62 ± 0.55 versus 1.12 ± 0.82, p < 0.05,). Early EPCs from ANFH patients showed impaired migratory capacity (63.8 ± 11.7 versus 152.3 ± 12.4, p < 0.001) and VEGF secretion (50.8 ± 7.2 pg/ml versus 62.8 ± 10.1 pg/ml, p < 0.05). ECFCs from ANFH patients showed decreased tube formation capacity (7.1 ± 2.7 versus 23.8 ± 4.3, p < 0.001) and proliferation.DiscussionEarly EPCs and ECFCs were impaired in number and function in GC-induced ANFH, and their distinct reduced capacity profiles might reflect different roles they played in endothelial dysfunction of GC-induced ANFH.