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Am J Clin Pathol. 2014 April ; 141(4): 587–592. doi:10.1309/AJCPX81AUNFPOTLL.

Placental Histomorphometry in Gestational Diabetes Mellitus

Rhonda Bentley-Lewis, MD1, Deanna L. Dawson1, Julia B. Wenger, MPH2, Ravi I. Thadhani,
MD2, and Drucilla J. Roberts, MD3
1Medicine/Diabetes Unit, Massachusetts General Hospital, Boston, MA
2Medicine/Division of Nephrology, Massachusetts General Hospital, Boston, MA
3Pathology, Massachusetts General Hospital, Boston, MA.

Abstract
Objectives—We examined placental histomorphometry in gestational diabetes mellitus (GDM)
for factors associated with race/ethnicity and subsequent type 2 diabetes mellitus (T2DM).
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Methods—We identified 124 placentas from singleton, full-term live births whose mothers had
clinically defined GDM and self-reported race/ethnicity. Clinical and placental diagnoses were
abstracted from medical records.

Results—Forty-eight white and 76 nonwhite women were followed for 4.1 years (median, range
0.0-8.9 years). White women developed less T2DM (12.5% vs 35.5%; P = .005) but had higher
systolic (mean ± SD, 116 ± 13 vs 109 ± 11 mm Hg; P < .001) and diastolic (71 ± 9 vs 68 ± 7 mm
Hg; P = .02) blood pressure, more smoking (35.4% vs 10.5%; P = .004), and more chorangiosis
(52.1% vs 30.3%; P = .02) than nonwhite women.

Conclusions—Although more nonwhite women developed T2DM, more white women had
chorangiosis, possibly secondary to the higher percentage of smokers among them. Further study
is necessary to elucidate the relationship among chorangiosis, subsequent maternal T2DM, and
race.

Keywords
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Placental histomorphometry; Gestational diabetes mellitus; Type 2 diabetes mellitus; Race/

ethnicity

Gestational diabetes mellitus (GDM) affects approximately 7% of all pregnancies in the

United States, but prevalence estimates are as high as 18% among women of nonwhite race/
ethnicity.1 GDM increases the risk for type 2 diabetes mellitus (T2DM) and cardiovascular
disease subsequent to pregnancy2; therefore, early risk stratification of women with GDM is
critical to the development of appropriate primary prevention strategies. Although several
risk factors have been identified as associated with progression to T2DM in women with

© American Society for Clinical Pathology

Address reprint requests to Dr Bentley-Lewis, Massachusetts General Hospital, 55 Fruit St, Bulfinch 4-415, Boston, MA 02114;
Bentley-Lewis.Rhonda@mgh.harvard.edu..
These data were presented in part as an abstract poster presentation at the Endocrine Society’s 95th Annual Meeting; June 15, 2013;
San Francisco, CA.
 Bentley-Lewis et al. Page 2

GDM, including higher body mass index, older age, and higher frequency of GDM in past
pregnancies,3 these factors incompletely identify the risk. Because the placenta reflects the
maternal metabolic milieu during pregnancy, the use of placenta-derived data for subsequent
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maternal disease is another opportunity to inform risk stratification in this population.

The placenta is the critical organ responsible for fetal growth and development, as well as
the transfer of blood, oxygen, nutrients, and waste between the mother and the fetus.4
Normal placental anatomy comprises the lacuna, floating and anchoring villi, villous and
extravillous cytotrophoblasts, syncytiotrophoblasts, uterine blood vessels, and uterine
connective tissue.5 Pathologic changes in placental structure and function have been
observed in type 1 diabetes mellitus (T1DM)6 and T2DM.7 In addition, placental
abnormalities in GDM have been reported8 and have paralleled those associated with
pregestational diabetes, including increased fetal and placental weight, diameter, and
thickness9; cytotrophoblastic hyperplasia; villous edema and fibrin deposits; and
chorangiosis.8 However, placental abnormalities in GDM have not been associated with
subsequent maternal risk for T2DM. In addition, the role of race/ethnicity in GDM placental
pathology has not been fully elucidated.
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Therefore, we sought to compare placental histomorphometry from pregnancies complicated

by GDM and examine factors that distinguished women from racially/ethnically diverse
populations compared with white populations. We hypothesized that the placentas of women
from racially/ethnically diverse populations would have a higher prevalence of vascular
abnormalities given the higher prevalence of GDM and concomitant cardiovascular disease
risk among these populations.2 Second, because women with GDM have similar placental
pathology as women with T1DM and T2DM, we hypothesized that placental pathology
would provide insight regarding the risk of subsequent T2DM postpartum.

Materials and Methods

Population Selection
Participants for this study were selected from placental pathology specimens received in the
Massachusetts General Hospital (MGH) Pathology Department between January 1, 2001,
and December 31, 2009 (n = 765). We then cross-referenced this population with a
population of women who presented for prenatal care to the MGH Obstetrical Department
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between September 1998 and January 2007 and were participants in the MGH Obstetric
Maternal Study (MOMS).10 These women, initially followed during pregnancy for the
development of preeclampsia, were subsequently observed for a median of 11.1 years
postpartum and had data on the development of T2DM subsequent to pregnancy.

Of the population of women with pathology specimens who also had longitudinal clinical
data from the MOMS data set (n = 178), we selected those categorized as having a clinically
confirmed diagnosis of GDM by Carpenter-Coustan criteria.11 Women were diagnosed if
they had two or more venous plasma glucose values greater than or equal to the defined
threshold levels (fasting, ≥95 mg/dL; 1 hour, ≥180 mg/dL; 2 hours, ≥155 mg/dL; and 3
hours, ≥140 mg/dL) on a 100-g oral glucose tolerance test. Among the women who met the

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GDM criteria (n = 157), only those who delivered full-term, singleton live births were
selected for the study (n = 129).
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Race and ethnicity were self-reported, and the women identified themselves as black, white,
Asian, Hispanic, or “other.” Those who did not self-identify race/ethnicity were categorized
as “unknown” (n = 5) and were not included in the population of women examined by race/
ethnicity (n = 124). All participants completed informed written consent to encompass this
study, and the study protocol was approved by the Partners Human Research Committee
Institutional Review Board.

Placenta Specimen Examination

The pathologic specimens previously had been processed by gross and histologic
examinations. A standard gross template was followed, and at least three sections of
placenta were sampled for histology (cord, membranes, and parenchyma). One of four
perinatal pathology experts rotating on service (including D.J.R.) performed the initial
diagnostic examination and reported the findings. All placental specimens selected for our
database were reexamined by two authors (D.J.R. and D.L.D.), who were both blinded to
clinical history.
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The gross parameters examined included placental weight, cord weight, cord length, and
cord insertion site. Samples were also coded for villous maturation, categorized as mature,
slightly immature, or immature. Mature villi had at least a minimum of one vasculosyncytial
membrane and one syncytiotrophoblastic knot per two terminal villi. Slightly immature villi
were coded for villi bordering the two other classifications but not meeting criteria for
villous maturational arrest.12 Immature villi were coded when the villi were large without
vasculosyncytial membranes and with a prominent cytotrophoblastic layer.

On histologic examination, we scored and diagnosed villous maturational arrest; dysmorphic

villi, defined as villi with prominent trophoblastic layers without knots, irregular villous
contours, open villous stroma, and hypovascularization; and chorangiosis, defined as 20 or
more capillaries in a cluster of villi in three ×40 fields.13 We captured maternal
inflammation as an aggregate of the measures of villitis of unclear or unknown etiology14;
interface inflammation, confluent basal plate chronic villitis with deciduitis, and/or
confluent chronic inflammation on the fetal side of the chorionic plate; and plasma cell
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deciduitis. Maternal and fetal evidence of acute chorioamnionitis was classified using the
Redline nosology.15 Measures of fetal stress identified included the presence of an increased
number of circulating fetal nucleated RBCs and multifocal or diffuse acute villous edema.
Measures of placental perfusion pathologies included placental infarcts, distal villous
hypoplasia, and fetal thrombotic vasculopathy.16 Decidual vasculopathy was characterized
by fibrinoid necrosis with or without atherosis in the decidua capsularis, decidual necrosis
with atherosis in the decidua basalis, or the presence of small muscularized arterioles in the
decidua basalis. Meconium, fibrin deposition, intervillous thrombi, and calcification were
also evaluated.

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Statistical Analysis
The placental pathologic and clinical parameters were compared and used to evaluate the
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differences in placental pathology and vasculature between the two populations. Continuous
variables were summarized using means and standard deviations, while frequency
distributions accounting for missing values were used for categorical variables. Summary
characteristics of white vs nonwhite subjects were compared using Mann-Whitney tests and
χ2 tests where appropriate. To complete our analysis of the placenta, clinical and pathologic
data were analyzed and compared to examine the differences in placental vasculature in
women from the nonwhite population to the white population. The statistical analyses were
performed using the SAS for Windows version 9.1 statistical software package (SAS
Institute, Cary, NC). A P value less than .05 was considered statistically significant.

Results
Clinical Findings
From the initial 765 specimens available, we identified the 129 women with biochemically
defined GDM who had full-term, singleton live births. Among these 129 women, 5 women
did not identify their race/ethnicity and were excluded from the analysis population (n =
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124). Maternal and neonatal baseline characteristics for the study population are listed in
Table 1. Of the 124 women who provided information regarding their race, 48 were white,
four were black, 14 were Asian, 51 were Hispanic, one was Native American, and six were
“other” nonwhite but unspecified race/ethnicity. The women were followed for a median of
4.1 (range, 0.0-8.9) years from delivery to last MGH encounter, and we observed that the
development of T2DM after pregnancy among the nonwhite population was nearly three
times more frequent compared with the white population (35.5% vs 12.5%; P = .005). White
women also had higher systolic (mean ± SD, 116 ± 13 vs 109 ± 11 mm Hg; P < .001) and
diastolic (71 ± 9 vs 68 ± 7 mm Hg; P = .02) blood pressure compared with nonwhite
women. Notably, the number of past or current smokers was significantly higher among the
white compared with the nonwhite women (35.4% vs 10.5%; P = .004). Otherwise, both the
white and nonwhite populations had similar clinical, prenatal, and perinatal parameters.

Pathologic Findings
Gross and histomorphometric examinations were performed on all 129 placentas in the
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study cohort, and the findings are listed in Table 2. Placental weight (mean ± SD, 532 ± 108
vs 540 ± 148 g; P = .88) and gestational age at delivery (39.4 ± 1.1 vs 39.4 ± 3.3 weeks; P
= .53) were similar between the white and nonwhite populations. We observed a larger
number of slightly immature placentas in the white population compared with the nonwhite
population (91.7% vs 89.5%), but this difference did not achieve statistical significance in
the overall maturation category. Chorangiosis was significantly higher in placentas from the
white population compared with the nonwhite population (52.1% vs 30.3%, P = .02) Image
1. Excluding chorangiosis, the placental pathology parameters were not statistically
significantly different between the white and nonwhite populations (Table 2).

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Discussion
In our study, we analyzed the placental histomorphometry of GDM among women from
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white and nonwhite populations. To our knowledge, this is the first study that has examined
racial/ethnic differences in the placental pathology of women with GDM with a
consideration of the clinical implications during and subsequent to pregnancy. Clinically, we
observed that white women had higher blood pressure, were more likely to be smokers, and
were less likely to develop subsequent T2DM than the nonwhite women. From a pathology
perspective, we observed that placental pathology was largely similar between the white and
nonwhite populations. However, we did observe that white women with GDM had a greater
percentage of chorangiosis than was evident among nonwhite women with GDM, a finding
worthy of further consideration.

Chorangiosis refers to the presence of excess blood vessels in the placental villi. Ogino and
Redline13 observed that chorangiosis is significantly associated with having enlarged
placenta, immature villi, and maternal diabetes. In addition, they observed in the literature
that chorangiosis is also associated with maternal anemia, smoking, twin gestations, and
delivery at high altitudes. In our study, all women were healthy, and none were reported to
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have anemia or cardiovascular disease. In addition, all pregnancies in our study cohort were
singleton and delivered at MGH, so ambient altitude was not a factor. However, a
significantly greater number, 35.4%, of the white women identified as past or current
smokers compared with 10.5% of the nonwhite population (P = .004). Therefore, it is
possible that the relatively high proportion of past or current smokers in the white
population contributed to the greater degree of chorangiosis in that population, although
both populations’ insulin dependence during pregnancy should also be considered.

Several studies have considered glycemic control during pregnancy when investigating
placental pathology associated with diabetes. Calderon et al17 found that abnormal glycemic
levels could contribute to morphometric abnormalities observed in the GDM placenta.
Gauster et al8 supported these findings, concluding that poorly controlled GDM could result
in villous edema and increased fibrin in the placenta. While GDM has numerous
implications for the vasculature and gross characteristics of the placenta, it has also been
shown to contribute to impaired placental function, including reduced glucose metabolism
and the ability to metabolize other substrates.18,19
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Alternatively, good glycemic control during pregnancy reduces adverse clinical pregnancy
outcomes associated with GDM,20 but normoglycemia does not mediate all the pathologic
characteristics associated with GDM.21-23 In our population, the only pathologic difference
was that chorangiosis was significantly more prevalent among the white compared with the
nonwhite women with GDM. Because we do not know the degree of insulin use or glycemic
control of these women, we do not know if the greater incidence of chorangiosis among
white women resulted from greater intrapartum insulin use, presumably leading to improved
intrapartum glycemic control and consequently less T2DM development subsequent to
pregnancy. Conversely, more intrapartum insulin use among nonwhite women with GDM
would be consistent with data suggesting an increased rate of subsequent development of

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T2DM in this setting.24 Nonetheless, we require the data regarding insulin use and glycemic
control to clarify this relationship.
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Accordingly, one limitation of our study is the lack of information on glucose control or
insulin use during pregnancy. These data would facilitate the elucidation of the etiology of
chorangiosis in our population. In addition, to elucidate the observed racial difference in the
degree of chorangiosis, it would be beneficial to examine a population of white women
without GDM to distinguish this association with chorangiosis as race mediated or GDM
associated. Furthermore, we had limited racial/ethnic diversity within our nonwhite
population. This could have limited the differences between the white and nonwhite
populations.

In summary, we identified that chorangiosis was more prevalent among white compared
with nonwhite women with GDM. Excluding chorangiosis, we found that the placental
pathology of the white and nonwhite women did not differ significantly. This finding is
clinically relevant for at least two reasons. First, the placentas of women with GDM may not
undergo routine pathologic examination depending on institutional practice. However, our
findings suggest that placental pathologic examination may demonstrate changes with
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implications for maternal postpartum cardiometabolic disease risk surveillance. Second, the
identification of placental pathology may serve as an indicator of underlying maternal
disease. For example, in our study, we identified a racial/ethnic difference in the presence of
chorangiosis, which has been directly linked to clinical parameters such as maternal
dysglycemia and anemia.13 Consequently, this may be correlated with the prenatal
measurements of these parameters and potentially lead to the consideration of additional
prenatal intervention in certain populations.

Further study is warranted to determine the cause of greater chorangiosis in our white
population and examine whether this observation is related to smoking, insulin use,
glycemic control, or specifically race. We also found that more nonwhite women developed
T2DM after pregnancy than white women in our GDM population. However, further
research is necessary to determine if the higher rate of subsequent T2DM in nonwhite
populations is associated with differences in placental pathology. This may provide another
opportunity for risk stratification in GDM populations to inform evidence-based
interventions to alleviate racial/ethnic disparities in GDM and T2DM.
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Acknowledgments
We thank Kaitlyn Barnes, Stella St. Hubert, Grace Xiong, Melissa Ong, Annie Yang, and Jennifer Huynh of the
MGH Diabetes Research Center for their assistance with data compilation and manuscript preparation.

This study was supported by grant 1R03DK096152 from the National Institutes of Health (NIH) and the Robert
Wood Johnson Foundation Harold Amos Medical Faculty Development Program (R.B.-L.); Harvard Catalyst
Summer Clinical and Translational Research Program (D.L.D.); K24 DK094872 from the NIH (R.I.T.); and the
Massachusetts General Hospital (MGH) Pathology Department (D.J.R.).

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in women with mild hyperglycemia or gestational or overt diabetes. Diabetes Res Clin Pract. 2007;
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23. al-Okail MS, al-Attas OS. Histological changes in placental syncytiotrophoblasts of poorly
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Image 1.
Mature placentas at ×20. A, Chorangiosis. Multiple capillaries are in all villi with villous
expansion (H&E). B, Normal nonchorangiotic placenta showing normal number of
capillaries in villi (H&E).
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Table 1

Clinical Characteristics of the Study Population With Gestational Diabetes Mellitusa

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Characteristic All White Nonwhiteb P Value

No. of patients 129 48 76

Age, y 32.4 ± 5.8 32.7 ± 5.6 32.0 ± 6.0 .71
Body mass index, kg/m2 30.0 ± 6.7 30.5 ± 7.2 29.8 ± 6.4 .71

Systolic blood pressure, mm Hg 112 ± 12 116 ± 13 109 ± 11 .001c

Diastolic blood pressure, mm Hg 69 ± 8 71 ± 9 68 ± 7 .02c

Total cholesterol, mg/dL 195 ± 38 189 ± 41 199 ± 37 .52
High-density lipoprotein, mg/dL 53 ± 13 55 ± 14 51 ± 13 .44
Low-density lipoprotein, mg/dL 114 ± 28 109 ± 28 116 ± 29 .49
Triglycerides, mg/dL 172 ±128 188 ± 174 163 ± 90 .75
Gestational age at prenatal visit, wk 12.1 ± 6.0 11.5 ± 5.2 12.2 ± 6.3 .88
No. of total pregnancies 2.7 ± 1.7 2.4 ± 1.4 2.7 ± 1.6 .44
No. of live births 1.0 ± 1.3 0.7 ± 0.8 1.1 ± 1.3 .19
Weight gain, lb 21.3 ± 12.7 21.9 ± 13.8 20.7 ± 12.1 .85
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Preeclampsia 2 (1.6) 1 (2.1) 1 (1.3) .74

Gestational age at delivery, wk 39.5 ± 1.1 39.4 ± 1.1 39.4 ± 3.3 .53
Baby weight, g 3,670 ± 618 3,667 ± 505 3,676 ± 699 .66
Birth weight for gestational age percentile, % 62.9 ± 30.0 64.2 ± 29.0 61.7 ± 31.3 .64
Time from MGH delivery to follow-up, median (range), y 4.1 (0-8.9) 3.7 (0-8.5) 4.1 (0-8.9) .96

Essential hypertensiond 17 (13.2) 6 (12.5) 11 (14.5) .53

Diabetes mellitusd 34 (26.4) 6 (12.5) 27 (35.5) .005c

Smoking status .004c

Never 56 (43.4) 18 (37.5) 36 (47.4)

Past 18 (14.0) 17 (35.4)e 8 (10.5)e

Current 8 (6.2)
Race
White 48 (37.2)
Black 4 (3.1)
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Asian 14 (10.9)
Hispanic 51 (39.5)
Native American 1 (0.8)
Other nonwhite 6 (4.7)
Unknown 5 (3.9)

MGH, Massachusetts General Hospital,

a
Values are presented as mean ± SD or number (%) unless otherwise indicated, Percentages that do not add up to 100% denote missing or
unknown data,
b
Nonwhite group includes all categories except white and “unknown,”
c
Significant at P < .05,

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d
Percentage denotes development of disease following delivery,
e
Numbers include past and current smokers.
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Table 2

Placental Pathology Characteristics in the Study Population With Gestational Diabetes Mellitusa
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Characteristic All White Nonwhiteb P Value

Placental weight, g 536 ±132 532 ±108 540 ± 148 .88

Placental weight .95
percentile
<10 24 (18.6) 9 (18.8) 14 (18.4)
10-90 72 (55.8) 27 (56.3) 41 (54.0)
>90 33 (25.6) 12 (25.0) 21 (27.6)
Cord length, cm 36.1 ± 13.8 33.7 ±14.8 37.2 ± 13.2 .19
Cord insertion 5.0 ± 2.4 4.7 ± 2.5 5.2 ± 2.3 .25
Cord insertion location .26
Membranous 2 (1.6) 0 2 (2.6)
Maturation .92
Mature 9 (7.0) 3 (6.3) 6 (7.9)
Slightly immature 117 (90.7) 44 (91.7) 68 (89.5)
Immature 3 (2.3) 1 (2.1) 2 (2.6)
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Chorangiosis 49 (38.0) 25 (52.1) 23 (30.3) .02c

Chorangiosis— 7 (5.4) 4 (8.3) 3 (4.0) .30
focal diffuse
Dysmorphic 16 (12.4) 5 (10.4) 11 (14.5) .51
Maturation arrest 0 0 0 NA
Inflammation 51 (39.5) 19 (39.6) 30 (39.5) .99
Acute chorioamnionitis 22 (17.1) 6 (12.5) 14 (18.4) .38
Villitis of unclear/ 26 (20.2) 11 (22.9) 14 (18.4) .54
unknown etiology
Interface inflammation 4 (3.1) 2 (4.2) 2 (2.6) .64
Deciduitis 2 (1.6) 2 (4.2) 0 .07
Fetal acute 2 (1.6) 1 (2.1) 1 (1.3) .74
chorioamnionitis
Vasculitis 6 (4.7) 2 (4.2) 3 (4.0) .74
Nucleated RBCs 6 (4.7) 3 (6.3) 3 (4.0) .54
Acute villous edema 14 (10.9) 5 (10.4) 9 (11.8) .81
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Placental infarcts 20 (15.5) 8 (16.7) 12 (15.8) .90

Intervillous thrombi 26 (20.2) 9 (18.8) 16 (21.1) .76
Fetal thrombotic 9 (7.0) 1 (2.1) 8 (10.5) .07
vasculopathy
Avascular villi 5 (3.9) 1 (2.1) 4 (5.3) .38
Edema 1 (0.8) 1 (2.1) 0 .21
Meconium 39 (30.2) 11 (22.9) 27 (35.5) .14
Extensive meconium 2 (1.6) 0 2 (2.6) .26
Decidual vasculopathy 2 (1.6) 1 (2.1) 1 (1.3) NA
Calcification 14 (10.9) 4 (8.3) 9 (11.8) .53
Fibrin 11 (8.5) 2 (4.2) 8 (10.5) .21

Am J Clin Pathol. Author manuscript; available in PMC 2015 April 01.

 Bentley-Lewis et al. Page 13

Characteristic All White Nonwhiteb P Value

Atherosis 1 (0.8) 0 1 (1.3) .42

NIH-PA Author Manuscript

NA, not applicable.

a
Values are presented as mean ± SD or number (%). Percentages that do not add up to 100% denote missing or unknown data.
b
Nonwhite group includes all categories except white and “unknown.”
c
Significant at P < .05.
NIH-PA Author Manuscript
NIH-PA Author Manuscript

Am J Clin Pathol. Author manuscript; available in PMC 2015 April 01.