Placental growth is continuous throughout the pregnancy to reach maturity at term [
1,
2]. The size and weight of the placenta are independent factors affecting the fetal growth and fetal wellbeing [
3,
4,
5,
6,
7]. Placenta in a large part demonstrates a lateral growth pattern due in part to the mechanical limit of the uterine cavity with continuous expansion of a number of cotyledons from the periphery [
1]. Like many other mammalian organs, there are regulatory mechanisms of size control and cell number control in the growth of placenta [
8,
9,
10]. Development of cotyledons laterally from the center involves the development of new anchoring villi, trophoblastic cell shell and column with corresponding spiral artery remodeling so that the fetal villous vessels are connected to the uteroplacental intervillous circulation [
1]. It is reasonable to believe that there is a time sequence (temporal sequence) in regard to spiral artery remodeling from the center where spiral artery remodeling occurs first and peripheral part of the placenta later (spatial sequence), although the spatiotemporal sequence of placental development is not frequently studied [
11,
12]. Spiral artery remodeling is a significant vascular transformation of maternal vessels to accommodate the embryonic and placental growth and to establish the utero-placental circulation [
13]. Spiral artery remodeling is a temporal but dynamic development process predominantly occurring in the first and second trimester [
1]. Based on previous studies, there is no morphologic evidence of spiral artery remodeling after the end of the second trimester [
14]. The size of the placenta increases to about 20 cm in diameter and 25–40 cotyledons at term from a blastocyst at the beginning of implantation, although the most significant placenta weight increase occurs in the third trimester [
1]. The questions remain if the spiral artery in the central portion of the placenta and those in the peripheral portion show synchronous morphologic changes of remodeling, and how this difference of spiral artery remodeling in the time between the central and peripheral portions of placenta affects the development of decidual vasculopathy at late gestation, and how this spatiotemporal spiral artery remodeling affects the interpretation of morphologic changes of placenta in normal pregnancy and complications. The spatiotemporal difference is typically not an issue for most placental pathologists when the placental surface is examined and decidual vasculopathy found, as the entire placenta can be easily accessed after delivery. However, the placental bed biopsy interpretation of maternal vessels will be affected significantly due to the tissue sections obtained from the biopsy sites at the placental bed [
15]. The central portion of the placental bed is emphasized for placental bed biopsy in order to achieve the expected results [
15]. Under these circumstances, the spatiotemporal sequence of maternal vascular changes makes a difference in interpretation of the material obtained for the procedure [
15]. Furthermore, the theory of “failure to invade” has been proposed as the key pathogenic mechanism of preeclampsia and hypertensive disorders of pregnancy, and the cardinal vascular change of “failure to invade” theory is the lack of trophoblastic invasion of vascular wall in the superficial myometrium. In this setting, an attempt was made to delineate the difference of morphologic features of the maternal vessels within the center and the peripheral areas of maternal surface in regards to the presence and absence of decidual vasculopathy and vascular regeneration/restoration. A slight modification of standard placental examination protocol for a period of this study was made in order to answer this question.