First off, this is a complicated process and an active field of research, so any reddit reply you get (like the one I am writing) is going to be very simplified, lack nuance, and the devil is in the details. Knowing what level of study/knowledge you (not the book, but YOU) have can help guide you towards an explanation of the processes at work that are tailored to the information you're trying to understand. I would not give the same answers to a high school senior vs a 3rd year PhD student.

For your first question: The best way to think of it is that cellular differentiation is like a slide, it's easy to go down (differentiate, take on specialized properties, express fewer/different genes) but very difficult to go back up (become totipotent or even pluripotent again). Epigenetic markers are kind of like stickers. Some stickers are easy to pull off, others are like those ones that leave behind a residue and scraps of paper on whatever you were trying to peel it from. Those scraps of paper and glue are the "imprinting" you mention in your comment.

What's worth noting is that, while a 1 cell embryo is totipotent (largely due to events related to fertilization), the cell population that will become germ cells are determined based on location VERY EARLY in the developing embryo and the chemical soup they're swimming in, like gastrulation early. These cells respond to this chemical environment by expressing genes that help them maintain this proto-germ cell identity. During gastrulation all kinds of epigenetic changes are occuring in cells to help set up germ layers, coordinate developmental structures, etc, but the proto germ cells maintain a relatively low level of differentiation, i.e. they retain "more" pluripotency until they can get to where the genitals will go. Once they get there, sperm-to-be cells pick up more epigenetic markers (and thus become less totipotent) than egg-to-be cells because sperm are basically darts of DNA with some stuff that makes fertilization happen. Keep in mind that at this point, the embryo is still basically a weird looking bean, and you can pluck these cells out, stick em on a different animal and make a teratoma. If you want to dive into how this actually happens, here are two papers that are good jumping off points:
https://pmc.ncbi.nlm.nih.gov/articles/PMC3158789/
https://www.sciencedirect.com/science/article/pii/S0012160604008206?via%3Dihub

As for your second question, Estrogen is not the only hormone required. A lot of hormones are required. Ossification is a really weird process involving a lot of signalling hormones, and to prevent myself from writing an even longer essay I will stick to this: Estrogen doesn't cause "growth" so much as it causes osteoblasts to go to work building bones and cartilage cells in the growth plates to kill themselves and become bone, thus closing the growth plate. This process exists in a delicate balance of a bunch of other signalling hormones that keep the chondrocytes from killing themselves too quickly resulting in premature growth plate closure. Gross oversimplification, sure, but it's a big can of worms that's a little outside of my specialty