Placental changes in idiopathic intrauterine growth ...causes of IUGR, such as maternal . disorders like pre-eclampsia, foe-tal intrauterine infections, congeni-tal malformations,

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Placental changes in idiopathic intrauterine growth restriction

S Biswas*

AbstractIntroductionPlacenta is the maternal–foet-al contact zone. The placentas of ‘idiopathic’ intrauterine growth reta-rdation babies may hold the key to the aetiology of growth restricti-on. It was noted by most workers that in cases of intrauterine grow-th retardation placentas, there were some abnormal positions of insertion of umbilical cords, pla-cental weight and volume was signi-ficantly lower than the controls and they also had smaller diameters. The greater placental coefficient in intrauterine growth retardation indicates that though both place-ntas and babies in intrauterine gro-wth retardation had less weight, placental sizes were not relatively less. This article aims to review literature to identify any morphol-ogical and structural peculiarities of placenta that might contribute to development of idiopathic int-rauterine growth retardation.DiscussionLight microscopy suggested that syncytiotrophoblastic lining was more degenerated and a nu-mber of syncytial knots increased in intrauterine growth retardation placentas than that of the control placentas. X cells were present in both the cases, though more in int-rauterine growth retardation. Intra-villous and perivillous fibrin depo-sitions were markedly increased in intrauterine growth retardation; also there were more

hypovascular/avascular villi and large areas of infarction.ConclusionReview of the literature to estab-lish any relationship between pla-cental histomorphometric changes and intrauterine growth retardation suggests that intrauterine growth re-tardation pregnancies are associated with reductions in villous tree elabo-ration, particularly affecting the vol-ume and surface area of terminal and intermediate villi, thereby restrict-ing surface area over which foeto-maternal exchange may occur. Thus, placental oxygen transfer might be reduced, thereby restricting foetal growth and development.

IntroductionThe placenta is the vital organ for maintaining pregnancy and promot-ing normal foetal development. It is elaborated by both maternal and foe-tal tissues to serve as an instrument for transfer of essential elements.

The foetus and the placenta share the same genetic make-up, therefore, are expected to have parallel growth potentials. Maturation-associated increase in the placental nutrient transfer capacity improves placental efficiency, permitting an increase in the number of grams of foetal weight supported by every gram of placental mass. Not surprisingly, ‘placental in-sufficiency’ is invoked commonly in cases of impaired foetal growth.

The most important cause of neo-natal loss is the low birth weight. A low birth weight baby is defined by the ninth revision of International Classification of Diseases of World Health Organization (1977) as one whose birth weight is 2500 g or less, irrespective of gestational age. After

correlating both birth weight and gestational age they are classified into two groups: pre-term and intra-uterine growth retardation (IUGR) or small-for-date (SFD).

There are many well-established causes of IUGR, such as maternal disorders like pre-eclampsia, foe-tal intrauterine infections, congeni-tal malformations, chromosomal anomalies, etc., but in the cases of idiopathic IUGR, there is no obvious foetal or maternal cause. The placen-tas of these ‘idiopathic’ IUGR babies might hold the key to the aetiology of the growth retardation, though the contribution of placental changes re-mains controversial.

This paper reviews the significan-ce or importance of morpholog-ical, histological and quantitative histomorphometric changes of placentas associated with IUGR.

The methodical study of growth rate of normal foetuses and their placentas to ascertain the interrela-tionship through the stages of intra-uterine life was first undertaken by Hamilton and Girmes1, and Boyd and Hamilton2.

While correlating certain morpho-logical and histological findings of placenta with IUGR, the comments of Macpherson3 can be kept in mind that it is fanciful to assume that every adverse perinatal outcome is associ-ated with an abnormal placenta, and equally fanciful to expect that every abnormal placenta will result in a poor perinatal outcome.

Sinclair4 observed that placental weight increased linearly as gesta-tion progressed. He was unable to account for great microscopic vari-ability among placentas. Accord-ing to Little5, placental co-efficients

* Corresponding author Email: [email protected]

Department of Anatomy, N.R.S. Medical College, Kolkata, India

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(placental weight: foetal weight) between 0.10 and 0.18 were to be considered normal. Any value <0.08 were to be considered abnormally small and more than 0.2 abnormally large. Gruenwald and Minh6 had ob-served 1232 deliveries and opined that placental weight did not deter-mine the size of the baby, though the weight must be considered as one of the several factors affecting placental function and adequacy.

Wigglesworth7 demonstrated that placental infarct of more than 5% area had been a key factor in causing low birth weight. Histological exami-nation revealed considerable regional variations in villous structures from both normal and abnormal pregnan-cies. Changes like increased fibrin deposition both within and between the villi, thinning of syncytium and increased syncytial knots and prolif-eration of Langhans cells were noted in placentas having insufficiency. In normal placentas (Figure 1), syncy-tiotrophoblastic lining of the villi are thinned out and aggregated as syncyt-ial knots in most areas of all placentas. At places, there were no tropho-blastic lining. Plenty of intravillous cytotrophoblasts were seen within villous stroma. Intravillous fibrin depositions were present at places. At some places, mostly in the marginal and subchorionic areas, perivillous fibrin depositions were noted. Many villi were completely entrapped in the perivillous fibrin. These villi had incomplete syncytiotrophoblastic lin-ing. Few large extravillous cytotroph-oblasts, also termed as X cells, were entrapped in the fibrin deposits.

In mature placenta, typical layer-ing of basal plate is not expected. Chorionic plates are observed to have multi-layered structure, consisting of amniotic epithelium, compact layer, spongy layer, followed by a compact layer of chorionic mesoderm that is separated from the Langhans fibrinoid stria by a basement membrane (Fig-ure 2). Chorionic plates were lined by Langhan’s layer of fibrinoid, which in

Figure 2: Microphotograph showing chorionic plate with all the layers in normal term placenta. A, amnionic epithelium, AM, amnionic mesenchyme; S, spongy layer; CM, chorionic mesenchyme; L, Langhan’s layer of fibrinoid. Stain used: H&E. Magnification ×100.

Figure 1: Microphotograph of normal term placenta. Villi (v) are seen with syncytial knots (arrow) and capillaries are present within villi. Stain used: H&E. Magnification ×100.

turn was lined by syncytiotrophoblast towards the intervillous spaces. Many villi were entrapped in this layer, and few extravillous cytotrophoblast cells (X cells) were also seen.

Aherne and Dunnill8 dealt with quantitative aspects of placental structure. They worked out vol-ume proportions of villi and total surface areas using point counting

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and linear intercept methods. They observed that at term, abnormally small infants’ placentas had reduced mean volumes. There was a signifi-cant deficit of parenchyma; the mean values for villous surface area and foetal capillary surface area in the placentas of abnormally small in-fants were significantly lower than normal. They suggested that stunt-ing might occur due to primary placental hypoplasia.

Thomson et al.9 remarked that pla-cental weight was a poor indicator of placental adequacy. SFD babies did not have relatively small placentas. The observation was based on re-cords of 52,004 singleton births over a period of 18 years.

Increased villous fibrosis and syncytial knotting was reported by Mehrota et al.10 in placentas of mothers having anaemia and subse-quently low birth weight babies. In another observation by Agboola11, presence of low haematocrit was associated with higher placental weight and lower foetal weight. Histologically, more villous fibrosis was seen as compared with nor-mal control group. After studying undernourished pregnant Indian women, Mirchandani et al.12 ob-served that placentas were sig-nificantly smaller in mature IUGR babies. Syncytial knotting (Figure 3), trophoblastic basement mem-brane thickening, villous stromal fibrosis, fibrinoid necrosis, severe degree of intervillous fibrin deposi-tion completely or partially filling up the intervillous spaces (Figure 4) were noted by them in the placentas of IUGR foetuses.

Benrischke and Driscoll13 observed that the histological findings of pla-centa included marked increase in fibrin deposits in the decidual floor with encasement of many villous tips (Figure 5). There was an increase of extravillous trophoblasts (X cells). Ermocila and Altshuler14 also found increased proliferation of X cells in IUGR.

Figure 4: Microphotograph showing that perivillous fibrin deposition (arrow), red in colour, has partially replaced trophoblastic lining of villi (v) in an IUGR placenta. Few villi (v) are seen to be entrapped in the fibrinoid. Stain used: Masson’s trichrome. Magnification ×100.

Figure 3: Chorionic villi showing a faintly positive PAS stain in the villous core and basement membrane of the trophoblasts. Cytotrophoblast cells (arrowhead) seen within the villous stroma. Syncytial lining is present at places. Syncytial knots (arrows) are plenty. Stain used: PAS. Magnification ×400.

According to Bjoro15, velamentous in-sertion of cord, single umbilical artery and placental infarct occurred more frequently in placentas with IUGR.

In a study by van der Veen and Fox16, placentas of idiopathic IUGR revealed excess of villous cyto-trophoblastic cells and endarteritis

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in umbilical arteries, these changes were frequently seen.

It was postulated by Xu23 that the development of IUGR was related to smaller functional areas of the placenta. In their histomorphomet-ric study of placentas in IUGR, they noted that the ratio of parenchymal tissue, absolute villi components and surface area values and villous capil-laries were significantly smaller in IUGR placentas than the control ones.

Markedly increased number of X cells (Figure 6) were found to be associated with placentas of IUGR by Vernof et al.24. These X cells were found in close proximity of affected villi. Histological evidence of placen-tal infarction, characterized by large conglomeration of necrotic villi, was found by Laurini et al.25 to be signifi-cantly associated with IUGR.

In a study of placentas from pre-term IUGR infants, Salafia et al.26 concluded that placentas of asym-metric IUGR infants were character-ized by decreased foeto-placental weight ratio, decreased placental weight, increased number of infarcts located throughout the placental area as compared with that of the placentas of AGA infants. Histological evidence of abruptio placentae, in-creased proliferations of extravillous cytotrophoblast (X cells) and avas-cular terminal villi were found. Ex-tensive perivillous fibrin deposition, villous stromal fibrosis, syncytial knotting and increased incidence of chronic villitis were noted in cases of symmetric IUGR. They opined that though single placental infarct was more common at term, presence of many placental infarcts was signifi-cantly related to IUGR.

Beebe et al.27 studied 1252 placen-tas of different categories, and con-cluded that histological evidence of placental ischaemic changes and in-farction were significantly increased in cases of IUGR as compared with normal babies.

The study conducted by Dawson et al.28 revealed that main microscopic

Figure 5: Microphotograph of IUGR placenta showing massive perivillous fibrin deposit (arrow), red in colour, near the basal plate (B). The villi (V) are green in colour, avascular and sclerosed. Stain used: Masson’s trichrome. Magnification ×100.

of large stem villous arteries. They suggested that these changes were due to uteroplacental ischaemia, and pathogenesis of IUGR was due to restriction of nutrition supply to the foetus because of inadequate physi-ological changes of spiral arteries.

Davies et al.17 observed that IUGR placentas were smaller in weight, volume and area. Marginal insertion of cord was a significant finding. In-creased numbers of villi with fibri-noid necrosis were also noted.

Teasdale18 did quantitative analy-sis of placentas in IUGR. He ob-served that these placentas were 45% smaller than controls and had significantly less surface area of ex-change between mother and foetus. Mainly, the peripheral capillary area, villous surface area and intervillous space volume were found to be less. Total numbers of cells were also seen to be markedly decreased, placental membrane showed 51% decrease in trophoblastic mass or cellular con-tent. These findings suggested that, in idiopathic IUGR, the placental

morphological changes were bound to produce placental insufficiency and foetal growth retardation. It was revealed by him that microvilli were often distorted and reduced in num-ber in idiopathic IUGR.

In another quantitative struc-tural study of placenta by Boyd and Scott19, lower total placental volumes in IUGR were revealed. With light mi-croscopic study, they observed lower volume of parenchyma, reduced vil-lous surface area and increased vol-ume proportion occupied by foetal capillaries in these placentas in com-parison to control groups.

Terminal villi deficiency has been interpreted as a result of reduced foetal capillary growth in the villous periphery (Kaufmann et al.)20. They suggested that due to the lack of ter-minal villi, there might be reduction of exchange surface and increase in materno-foetal diffusion distance. Hypercapillarization was suggested by Bacon et al.21 and Scheffen et al.22 to be induced by hypoxia. In IUGR with preserved end-diastolic flow

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Biswas et al.37 had similar observa-tions and commented that since the surface area of the villi presents the interface between maternal and foe-tal circulation, its reduction might be the cause of idiopathic intrauterine growth restriction of the foetus.

DiscussionThe author has referenced some of its own studies in this paper. These referenced studies have been conducted in accordance with the Declaration of Helsinki (1964), and the protocols of these studies have been approved by the relevant ethics committees related to the institution in which they were performed. All human subjects, in these referenced studies, gave informed consent to participate in these studies. Contradictory histolo-gical and morphological findings were recorded by various authors.

Velamentous insertion and mar-ginal insertion of cord was a signifi-cant finding in the placentas of IUGR fetuses15,17. Biswas and Ghosh38 found that in the majority of IUGR cases, positions of insertions of umbilical cords were eccentric whereas in the control group, the majority was cen-tral.

Placental weights and volumes of IUGR group were lower than those of the controls. It was observed that placental coefficient was significantly greater in IUGR than normal-weight babies29; though both placentas and babies in IUGR had less weight, pla-cental sizes were not relatively less. In fact, these placentas were func-tional, and even tried to compensate the abnormal morphology32.

On light microscopic study of the histological sections of the pla-centas of both control and IUGR group, marked regional variations of structures of chorionic villi, the intervillous spaces, basal and chori-onic plates were noted. In the chori-onic villi, syncytiotrophoblastic linings

findings of IUGR placentas included shrunken fibrosed villi with de-creased number of capillaries per villus, prominent cytotrophoblasts, increased fibrin and syncytial knots and increase in stromal fibrosis.

Oliveira et al.29 found that the placentas in IUGR had significantly greater incidence of chorioamnio-nitis, placental infarction and exten-sive perivillous fibrin deposition. They were lighter and had smaller diameters. Placental index (placen-tal weight: foetal weight) was also significantly greater, indicating that placental impairment was relatively less.

Katzman et al.30 found massive perivillous fibrin deposition strongly associated with IUGR. Similar views were given by Bane and Gillan31.

Fox (1976, 1981 and 2000)32 conducted several studies and ob-served that in the majority of cases of IUGR, the small foetus could not be explained by so-called ‘placental insufficiency,’ for which there was lit-tle morphological or other evidenc-es. In 2003, he also observed that

placentas from cases of idiopathic IUGR were considered to be smaller, but placental–foetal weight ratios were usually normal. Very extensive perivillous fibrin deposition, ma-ternal floor infarction, widespread thrombosis of foetal arteries might be associated with IUGR but such lesions were found on only a small minority of placentas from growth retarded foetuses. Histological exam-ination of placentas in IUGR revealed no constant or diagnostic findings.

In placental stereological studies by Mayhew et al.33,34, the exchange surface areas of peripheral (terminal and intermediate) villi and their foe-tal capillaries were estimated. They observed that IUGR (with or without PE) was associated with reduced sur-face areas and this was the principal factor leading to a smaller membrane diffusive conductance in these pla-centas.

Ansari et al.35 and Egbor et al.36 also observed that in idiopathic IUGR, the surface areas of terminal villi were significantly (p < 0.001) reduced, also their volumes were reduced.

Figure 6: Microphotograph of the basal plate of an IUGR placenta showing plenty of large extravillous trophoblastic cells (X cells) (x) embedded in fibrinoid. Cross section of a utero-placental blood vessel is seen (BV); its coats are replaced by fibrinoid (arrowhead).

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pathological changes of placenta. J Obstet Gynaecol Ind. 1979;29:1131–9.13. Benrischke K, Driscoll SG. The pathol-ogy of human placenta. Springer-Verlag: New York; 1967.14. Ermocilla R, Altshuler G. The ori-gin of X-cells of the human placenta and their possible relationship to intrauterine growth retardation: an enigma. Am J Ob-stet Gynaecol. 1973 Dec;117(8):1137–40.15. Bjoro K Jr. Gross pathology of pla-centa in intrauterine growth retardation. Ann Chir Gynaecol. 1981;70(6):316–22.16. van der Veen F, Fox H. The humanplacenta in idiopathic intrauterine growth retardation; a light and electron microscopic study. Placenta. 1983 Jan–Apr;4(1):65–77.17. Davies BR, Casaneuva E, Arroyo P. Pla-centas of small-for-date infants: a small controlled series from Mexico city. Am J Obstet Gynaecol. 1984 Aug;149(7):731–6.18. Teasdale F, Jean-Jaques G. Intrauterine growth retardation; morphometry of mi-crovillous membrane of human placenta. Placenta. 1988 Jan-Feb;9(1):47–55.19. Boyd PA, Scott A. Quantitative struc-tural studies of human placentas as-sociated with pre-ecclampsia, essential hypertension and intra-uterine growth retardation. Br J Obstet Gynaecol. 1985 Jul;92(7):714–21.20. Kaufmann P, Luckhdart M, Leiser R.Three dimensional representation of fetal vessel system in human placenta. Trophoblast Res. 1988;3:113–37.21. Bacon BJ, Gilbert RD, Kaufmann P, Smith AD, Trevino FT, Longo LD. Pla-cental anatomy and diffusing capac-ity of guinea-pigs following long-term maternal hypoxia. Placenta. 1984 Nov-Dec;5(6):475–88.22. Scheffen I, Kaufmann P, Phillipens L,Leiser R, Geisen C, Mottaghy K. Alteration of the fetal capillary bed in the guinea pig placenta following long-term hypoxia. In: Piiper J, Goldstick TK, Mayer D, editors. Oxygen transfer of tissue, XII. Plenum Press: New York; 779–90.23. Xu W. Histomorphometric study of placenta in intrauterine growth retar-dation. Zhonghua Fu Chan Ke Zhi. 1989 Nov:24(6):338–40.24. Vernof KK, Benrischke K, Kephart GM, Warmoen TL, Gleich GJ. Maternal floor infarction: relationship to X-cells, major basic proteins, and adverse perinatal outcome. Am J Obstet Gynaecol. 1992 Nov;167(5):1355–63.

ConclusionFrom this review, it can be said that though IUGR foetuses were more frequently associat-ed with morphologically and histologically abnormal placentas, it could not be conclusively decid-ed whether these abnormalities contributed to the intrauterine gro-wth restriction. Quantitative, rath-er than qualitative changes of plac-ental structure might be responsib-le for the phenomenon. Many more quantitative histomorphometric studies have to be undertaken by researchers to come to a definite conclusion regarding placental changes as cause of idiopathic IUGR.

References1. Hamilton WJ, Girmes D. A statistical analysis of the growth of human placenta correlated with the fetus. J Anat. 1962 Jul;105(Pt 1):204.2. Boyd JD, Hamilton WJ. The human pla-centa. Cambridge, England: Heffer; 1970.3. Macpherson T. Fact and Fancy—whatcan we really tell from the placenta? Arch Pathol Lab Med. 1991 Jul;115(7):672–81.4. Sinclair JG. Significance of placental and birth weight ratios. Anat Rec. 1948 Oct;102(2):245–58.5. Little W. The significance of placental/fetal weight ratios. Am J Obstet Gynaecol. 1960 Jan;79:134–7.6. Gruenwald P, Minh HN. Weight of body and placenta of surviving and autopsied infants. Am J Obstet Gynaecol. 1961 Aug;82:312.7. Wigglesworth JS. Morphological vari-ation in insufficient placenta. J Obstet Gynaecol Br Commonw. 1964 Dec;71: 871–84.8. Aherne W, Dunnill MS. Quantitative as-pects of placental structure. J Pathol Bac-teriol. 1966 Jan;91(1):123–39.9. Thomson AM, Billewicz WZ, Hytten FE. The weight of placenta in relation to birth weight. J Obstet Gynaecol Br Commw. 1969 Oct;26(10):865–72.10. Mehrota VG, Mukherjee J, Pandey N. JObstet Gynaecol Ind. 1972;22:248.11. Agboola A. Placental changes in pa-tients with low hematocrit. Br J Obstet Gynaecol. 1975;82:225–7.12. Mirchandani JJ, Malik GB, Chitra S.Correlation of fetal outcome with some

were thinned out in most of the areas of control placentas, whereas in IUGR placentas, the linings were thinned as well as disrupted. Villous cytotropho-blast cells were seen at places along the margins of villi in both the groups. In IUGR placentas, they were more numerous and even present within the villous stroma. Syncytial knottings were present in both groups, but they were more prominent and their numbers were increased in IUGR pla-centas. Though intravillous fibrinoid depositions were present at places in term control placentas, in IUGR cases they were more frequently observed. Few X cells were found entrapped in these intravillous fibrinoid. Replace-ment of degenerated trophoblastic linings of villi by perivillous fibrin depositions were positively corre-lated with IUGR. These perivillous fibrin depositions might be acting as a barrier between foetal and mater-nal circulation, thereby reducing the transfer of the essential nutrients to the foetus, thus causing IUGR7,27,31.

The number of X cells in basal plate markedly increased in the placentas of IUGR babies. Many workers like Brosens39 and Khong40 reported that the muscle and elastic coats of the placental bed arteries were replaced by fibrinoid.

The diffusion of different elements from mother to foetus or vice versa occurs at the presenting surface of villi containing foetal vessels and maternal blood present in the inter-villous space. The findings of lower surface area of villi in IUGR com-pared with control placentas suggest less oxygen and nutrients reaching foetuses of IUGR group.

The mean total volumes of villi (terminal and intermediate) of IUGR placentas were found to be signifi-cantly lower than that of control pla-centas by some workers36. But, both Aherne and Dunnilla8, and Biswas et al.41 observed that the volume pro-portions of chorionic villous tissue of IUGR did not differ significantly from those of normal pregnancies.

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