Background: Miscarriage occurs when a pregnancy ends spontaneously before the fetus is viable outside the uterus. Early miscarriage, sometimes referred to as first-trimester miscarriage, happens before 12 weeks. Vascular endothelial growth factor (VEGF), an angiogenic protein essential for blood vessel formation, and cluster of differentiation 68 (CD68), a marker of macrophages, are vital to the immune response.
Objective: This research aimed to evaluate VEGF and CD68 expression patterns in placental tissues and decidua from first-trimester miscarriage, to ascertain their potential roles in immune response and angiogenesis in miscarriage.
Methods: The study included 60 women who experienced spontaneous abortion during the first trimester, 30 with missed abortion, and 30 with incomplete abortion. Using immunohistochemical staining, the expression of CD68 and VEGF in decidua and placental tissues was investigated. Expression levels were scored semi-quantitatively by averaging data from five fields per slide and subjected to statistical analysis.
Results: Building on these methods, immunohistochemical staining confirmed significantly elevated CD68 expression in both placental and decidua tissues from missed and incomplete abortions, indicating enhanced macrophage infiltration. Widespread staining (>50%) was seen in 50% of incomplete abortion decidua and 30% of missed abortion tissues. In contrast, VEGF expression was predominantly negative across all samples, with no case showing positive staining, indicating impaired angiogenesis.
Conclusion: The findings highlight a dual pathological mechanism in early miscarriage characterized by enhanced inflammatory macrophage infiltration and deficient angiogenic support. This imbalance may contribute to placental dysfunction and pregnancy failure. These results underscore the potential diagnostic and therapeutic relevance of immune–angiogenic pathways in early miscarriage