Bisphenols exposure induces bone loss and osteoporosis by binding to and activating the endocannabin

However, the exact mechanism of action, and the pathways involved with inhibiting bone growth, have not been identified. Bone growth has been found to be connected to the endocannabinoid system through cannabinoid receptor 1 (CB1) and 2 (CB2). Our findings demonstrate that there is an additive effect between bisphenols A (BPA), S (BPS), or tetrabromobisphenol A (TBBA) and the cannabinoid pathway that reduces osteoblast number and bone calcification.

Since the endocannabinoid pathway is known to regulate tissues, organs and systems throughout the body, this interaction demonstrates a greater need to study the effects of these safer alternatives on embryonic development in relation to the endocannabinoid system. Additionally, we found that activation of trpv1 occurred, but the negative impact on bone formation is linked to downregulation of apoa1b, apoa2, and ucp-1 as well as, dysregulated collagen synthesis, and ribosomal protein changes.

Downregulation of apoa1 causes decreased expression of ucp-1 and subsequent inflammation in bone tissues, and dysregulated collagen synthesis Furthermore, RNA-seq demonstrated increased expression of over 30 genes linked to increased osteoclastogenesis, and bone resorption.