The expending incidence and the financial cost of osteoporosis make this pathology a major public-health issue. The brutal disruption of 17β-estradiol (E2) production by the ovaries wich occurs at menopause is responsible for a dramatic increase of osteoporosis incidence. This bone pathology is characterized by a global bone tissue demineralization leading to a weakening of the entire skeleton and a high risk of fracture. Far from being inert, bone is a highly dynamic tissue which undergoes a perpetual remodeling throughout life. Bone remodeling is a unique feature that allows bone to accommodate mechanical strength and repair microfractures. This process is essentially ensured by two cell types, bone-resorbing osteoclasts and bone-forming osteoblasts, the differentiation and the activity of which beinghighly regulated by E2 through estrogen receptor ERα. As the other member of the nuclear receptor family, ERα harbors two independent activating functions, (AF)-1 localized at the N-terminal extremity and AF2 at the C-terminal one of the receptor, both involved in transcriptional effects. Moreover, a fraction of ERα is located at the plasma membrane after cysteine 447 in human (or 451 in mice) palmitoylation. where it activates membrane initiated steroid signals” (MISS) effects. The aim of this thesis has been first to gain insight ER subfunctions involved in estrogen bone sparing effects. Thus, by combining the use of knock-out mice models targeting MISS (ERα –C451A) and AF1 (ERα-AF10) of ER with pharmacological tools, our results have contributed to highlight the role of these ERα sufunctions in different bone compartments (i.e. cortical versus trabecular) and cell types (osteoclasts versus osteoblasts). In addition, we extended previous work regarding beneficial estrogens effects on vertebrae and on the appendicular skeleton to the jaws. Indeed, increasing evidence support an association between osteoporosis and jaw bone demineralization in postmenopausal women. To this aim, impact of bilateral ovariectomy on mice mandibular bone was first evaluated in a time-depend matter. Then, exogenous E2 effect on mice mandibular bone from different knock-out mice models targeting ERα or ER (ERα-/-, ERβ-/-, ERαAF2°, ERαAF1°, ERα-C451A) was evaluated. In addition to their beneficial role to prevent osteoporosis, estrogens also decrease climacteric symptom, atheroma and type 2 diabetes incidences. However, estrogens also favor the promotion of uterus and breast cancer growth. Thus, the major challenge consists in uncoupling some beneficial actions from other deleterious ones, that is, selective ER modulation. Results obtained during this thesis provide a better understanding of the ERα signaling pathways involved in bone sparing effect and thus may contribute to the design of new, bone-specific treatment strategies or menopause treatment with minimal adverse effects.