ObjectivesPelvic Organ Prolapse (POP) is a multifactorial disease with ageing as a most notable risk factor. Advanced Glycation End products (AGEs), biochemical markers of ageing are increased in prolapsed tissues. It is however unclear if AGEs are a cause or outcome of prolapse. By combining analysis of clinically relevant parameters in women with prolapse and POP tissues biochemically, this study aims to bridge the gap between existing clinical and biochemical research on the cause of POP. MethodsFollowing national and local ethical approval, a case study of 49 POP and 16 control tissues was carried out. The AGEs’ marker, pentosidine, was quantified via High Performance Liquid Chromatography. Oestrogen (ER-α) and glyoxalase I (GLO-I) expression of the tissues were studied. Age, obstetric factors and co-morbidities (hypertension, smoking, diabetes mellitus) were recorded and compared with biochemical findings. ResultsLower expressions of ER-α and GLO-I were observed in POP tissues in the comparison to the control, which also had significantly higher pentosidine content. Prolapsed tissue population had more notable age-dependent increase in pentosidine with significant differences between the 6th and 7th decade. Hypertension and smoking, which were more prevalent amongst women with POP, were associated with higher amounts of pentosidine in the vaginal tissues. ConclusionIn the light of recent research regarding the relationship between POP and glycation, the present study shows that age-related oestrogen decline is a key player in glycation accumulation in prolapsed vaginal tissues and that glycation is a cause rather than an effect of prolapse. Hypertension is a significant POP association which is linked to high glycation level.