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Journal of Drug Delivery and Therapeutics

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Open Access Full Text Article  Research Article

Histopathological Evaluation of Placental Changes in Women with Excessive Gestational Weight Gain

Özkan Yükselmiş, Murat Akkuş *, Fırat Aşır 

Department of Histology and Embryology, Medical Faculty, Dicle University, 21280, Sur, Diyarbakır, Turkey

Article Info:

_______________________________________________ Article History:

Received 26 Nov 2025  

Reviewed 12 Jan 2026  

Accepted 03 Feb 2026  

Published 15 Feb 2026  

_______________________________________________

Cite this article as: 

Yükselmiş Ö, Akkuş M, Aşır F, Histopathological Evaluation of Placental Changes in Women with Excessive Gestational Weight Gain, Journal of Drug Delivery and Therapeutics. 2026; 16(2):164-167  DOI: http://dx.doi.org/10.22270/jddt.v16i2.7574                                             _______________________________________________

For Correspondence:  

Murat Akkuş, Department of Histology and Embryology, Medical Faculty, Dicle University, 21280, Sur, Diyarbakır, Turkey

Abstract

_______________________________________________________________________________________________________________

Objective: Excessive weight gain during pregnancy has been associated with adverse maternal and fetal outcomes; however, its effects on placental histomorphology remain incompletely characterized. The present study aimed to evaluate placental histopathological alterations in women who gained excessive weight during pregnancy using Hematoxylin–Eosin (H&E) staining.

Materials and Methods: Placental tissues were obtained postpartum from 45 normal-weight pregnant women (BMI <30 kg/m²) and 45 women with excessive gestational weight gain/obesity (BMI ≥30 kg/m²). All samples underwent routine histological processing and were stained with H&E. Placental sections were examined under light microscopy for villous architecture, syncytiotrophoblast integrity, stromal changes, fibrin deposition, vascular congestion, and syncytial knot formation.

Results: Placentae from the control group exhibited preserved villous architecture, intact syncytiotrophoblast layers, and normal stromal and vascular morphology. In contrast, placentae from the high-BMI group demonstrated marked histopathological alterations, including villous structural disorganization, stromal degeneration, increased fibrin deposition, prominent vascular congestion, and an increased number of syncytial knots.

Conclusion: Excessive weight gain during pregnancy is associated with significant placental histomorphological alterations detectable by routine H&E staining. These structural changes may reflect impaired uteroplacental circulation and reduced placental functional capacity, potentially contributing to an adverse intrauterine environment.

Keywords: Gestational weight gain, placenta, hematoxylin–eosin, histopathology, villous degeneration

 


 

INTRODUCTION

Pregnancy is a dynamic physiological process requiring complex maternal adaptations to support fetal growth and development1. The placenta plays a central role in this process by mediating nutrient exchange, gas transfer, metabolic regulation, and immunological tolerance between the mother and fetus 2. Preservation of placental structural integrity is therefore essential for optimal pregnancy outcomes. In recent decades, excessive gestational weight gain and maternal obesity have emerged as major public health concerns3. These conditions have been linked to increased risks of gestational diabetes, hypertensive disorders, cesarean delivery, and long-term metabolic disease in offspring4. Growing evidence suggests that maternal metabolic stress adversely affects placental development, leading to morphological and functional abnormalities5.

Histopathological studies have reported that excessive maternal weight gain may be associated with villous immaturity, increased fibrin deposition, stromal edema, vascular congestion, and altered trophoblastic morphology6. Such changes can impair uteroplacental blood flow and compromise fetal oxygen and nutrient delivery7. However, detailed histomorphological evaluations focusing exclusively on routine H&E findings remain limited8.

Therefore, the present study aimed to investigate placental histopathological changes associated with excessive gestational weight gain using Hematoxylin–Eosin staining, providing a structural basis for understanding placental dysfunction in this population.

MATERIALS AND METHODS

Study Population and Tissue Collection

This study was conducted at Dicle University Faculty of Medicine, Department of Obstetrics and Gynecology. Placental tissues were collected from women aged 18–40 years following delivery. The control group consisted of 45 normal-weight pregnant women (BMI <30 kg/m²), while the study group included 45 women with excessive gestational weight gain/obesity (BMI ≥30 kg/m²). Pregnancies complicated by systemic diseases, gestational diabetes, preeclampsia, infection, or other obstetric complications were excluded.

Placental samples not required for routine pathological diagnosis were collected immediately after delivery for histological analysis.

Histological Processing and Hematoxylin–Eosin Staining

Placental tissue samples were fixed in 10% neutral buffered formalin for 24 hours, followed by routine dehydration, clearing, and paraffin embedding. Serial sections of 4 µm thickness were cut using a microtome and mounted on glass slides. Standard Hematoxylin–Eosin staining was performed according to established protocols.

RESULTS

Hematoxylin–Eosin Findings

Control Group (Figure 1): Placental sections from the control group demonstrated well-preserved chorionic villi with regular contours and uniform size. The syncytiotrophoblast layer was continuous and morphologically intact. The villous stroma appeared compact, with no evidence of degeneration, edema, or excessive fibrin deposition. Vascular structures were patent and evenly distributed, and intervillous spaces were well defined. Syncytial knot formation was minimal and within physiological limits.


 

 

image

Figure 1: Placental histology of the control group. Arrow: chorionic villus; arrowhead: syncytial knot; st: stroma; asterisk: villous capillary; f: fibrin deposition; star: intervillous space. Scale bar: 50 µm; Magnification: ×20.


 

High BMI Group (Figure 2): Placentae obtained from women with excessive gestational weight gain exhibited pronounced histopathological alterations. Chorionic villi appeared irregular, enlarged, and structurally disorganized. Stromal degeneration, including vacuolization and loss of normal connective tissue architecture, was frequently observed. Marked vascular congestion with erythrocyte accumulation was evident within villous capillaries and intervillous spaces. Fibrin deposition was increased in both villous and intervillous regions. Additionally, syncytial knots were more numerous and prominent compared with the control group.


 

 

image

Figure 2: Placental histopathological alterations in the high-BMI group. Arrow: chorionic villus; arrowhead: syncytial knot; st: stroma; asterisk: villous capillary; f: fibrin deposition; star: intervillous space. Scale bar: 50 µm; Magnification: ×20.


 

DISCUSSION

The present study demonstrates that excessive weight gain during pregnancy is associated with distinct placental histopathological alterations identifiable using routine Hematoxylin–Eosin staining. Compared with normal-weight pregnancies, placentae from women with high BMI exhibited significant villous structural disruption, stromal degeneration, vascular congestion, increased fibrin deposition, and enhanced syncytial knot formation. These findings are consistent with previous reports indicating that maternal metabolic stress adversely affects placental development9-12. Villous disorganization and stromal degeneration may reduce the effective surface area available for maternal–fetal exchange, while vascular congestion suggests impaired uteroplacental blood flow 13. Increased fibrin deposition is commonly interpreted as a marker of placental injury and hypoxic stress and has been associated with reduced placental efficiency 14.

The observed increase in syncytial knots may reflect accelerated trophoblastic turnover or chronic placental stress 15. Although syncytial knot formation can be a physiological feature of term placentae, excessive accumulation is often associated with placental hypoxia and impaired perfusion 16,17. Taken together, these histopathological changes suggest that excessive gestational weight gain creates a suboptimal intrauterine environment by compromising placental structure 18. Such alterations may contribute to adverse fetal outcomes and support the concept that maternal metabolic status plays a critical role in shaping placental morphology.

In conclusion, routine H&E staining provides valuable insight into placental structural changes associated with excessive maternal weight gain. Recognition of these alterations may enhance understanding of placental dysfunction in high-risk pregnancies and underscores the importance of optimal weight management during gestation.

CONCLUSION

Excessive gestational weight gain is associated with distinct histopathological alterations in the placenta. Routine Hematoxylin–Eosin examination revealed disruption of chorionic villous architecture, stromal degeneration, increased fibrin deposition, vascular congestion, and enhanced syncytial knot formation in placentae from the high-BMI group compared with controls. These structural changes suggest compromised placental integrity and may reflect an adverse intrauterine environment, underscoring the importance of appropriate maternal weight management during pregnancy.

Acknowledgements: This study was part of doctoral thesis of Dr. Özkan Yükselmiş at department of Histology and Embryology, Dicle University. 

Ethical Approval: This study was approved by the Dicle University Faculty of Medicine Non-Interventional Clinical Research Ethics Committee (Approval date: 16 April 2025; Approval number: 2025/150). All procedures were conducted in accordance with the ethical standards of the institutional and national research committees and with the principles of the Declaration of Helsinki.

Informed Consent: Informed consent was obtained from all participants prior to inclusion in the study.

Conflict of Interest: The author declares that there is no conflict of interest regarding the publication of this thesis.

Funding: This research was funded by Dicle University Scientific Research Platform (DÜBAP) by project number: TIP.25.029.

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