Preeclampsia is a cardiovascular disorder of the second half of pregnancy that is characterised by the new onset of hypertension in conjunction with end-organ damage including placental dysfunction. There are three main phenotypes of preeclampsia: i) early-onset and ii) late-onset preeclampsia diagnosed before 34 weeks or from 34 weeks of gestation, respectively, and iii) post-partum preeclampsia. Despite preeclampsia being the leading cause of morbidity and mortality in pregnancy, still there is no cure. The pathogenesis of preeclampsia is associated with abnormal placentation occurring in the early stages of pregnancy where spiral uterine artery (SUA) remodelling is impaired, which often occurs due to inappropriate function of trophoblast cells (differentiation, migration, invasion) or underlying endothelial dysfunction. Limited knowledge of the molecular and cellular regulation of these aberrant processes has impeded the development of effective treatments for preeclampsia. This is further complicated by the fact that there are differences in the pathogenesis and features between three phenotypes of preeclampsia. Moreover, there is the lack of reliable and specific model systems of human pregnancy. Collecting first trimester placentae or primary trophoblasts is challenging, and it cannot be done routinely. To address this gap, we have developed a low-cost, relevant and reproducible 3D bioprinted model of trophoblast organoids that recapitulates three major trophoblast lineages of human placenta (E-cadherin+ villous cytotrophoblasts, β-hCG+ syncytiotrophoblasts and HLA-G+ extravillous trophoblasts (EVTs)). This 3D model of early placenta can be used as a tool to study early placental development and function. Live cell imaging revealed spontaneous organoid formation from single cells within a few days. Trophoblast organoids also demonstrated invasive capabilities of the matrix. In addition, we established a multicellular placenta-on-a-chip model representative of first trimester trophoblast cell migration and invasion of the endothelial-cell vascular networks as well as the heightened inflammatory environment of preeclampsia, within a microfluidics chip. We have utilised these models to elucidate the role of new angiogenesis- and inflammation-related signalling mechanisms on placental development and growth, in the context of preeclampsia. Similarly, the 3D placental platforms can be used for high-throughput screening of clinically available and emerging treatments for preeclampsia by investigating the effects/mechanisms on trophoblast differentiation, migration, invasion and remodelling of the vasculature or vascular dysfunction.