Prior research studies have shown that the endocannabinoid system, influenced by CBD and THC, plays a role in bone remodeling. As both the research on cannabis and use of cannabis continue to grow, novel medicinal uses of both its constituents as well as the whole plant are being discovered. This review examines the role of cannabinoids on osteoporosis, more specifically, the endocannabinoid system and its role in bone remodeling and the involvement of the cannabinoid receptors 1 and 2 in bone health, as well as the effects of Δ9-tetrahydrocannabinol (THC), cannabidiol (CBD), and synthetic cannabinoids on bone.
A comprehensive literature search of online databases including PUBMED was utilized.
A total of 29 studies investigating the effects of cannabis and/or its constituents as well as the activation or inactivation of cannabinoid receptors 1 and 2 were included and discussed.
While many of the mechanisms are still not yet fully understood, both preclinical and clinical studies show that the effects of cannabis mediated through the endocannabinoid system may prove to be an effective treatment option for individuals with osteoporosis.

Introduction: Cannabinoids have long been known for their ability to treat nausea and vomiting. Recent reports, however, have highlighted the paradoxical proemetic effects of cannabinoids. Cannabinoid hyperemesis syndrome (CHS) is characterized by cyclical episodes of nausea and vomiting, accompanied by abdominal pain following prolonged, high-dose cannabis use, which is alleviated by hot baths and showers. Little is known about the cause of this syndrome. Discussion: Cannabinoids produce a biphasic effect on nausea and vomiting, with low doses having an antiemetic effect and high doses producing emesis. Presentation and treatment of CHS are similar to cyclical vomiting syndrome as well as chemotherapy-related anticipatory nausea and vomiting, suggesting that these phenomena may share mechanisms. The prevalence of CHS is not known because of the symptomatic overlap with other disorders and the lack of knowledge of the syndrome by the public and physicians. Treatment with typical antiemetic drugs is ineffective for CHS, but anxiolytic and sedative drugs, along with hot showers, seem to be consistently effective at reducing symptoms. The only known way to permanently end CHS, however, is abstinence from cannabinoids. Case studies and limited pre-clinical data on CHS indicate that prolonged high doses of the main psychotropic compound in cannabis, Δ9-tetrahydrocannabinol (THC), result in changes to the endocannabinoid system by acting on the cannabinoid 1 (CB1) receptor. These endocannabinoid system changes can dysregulate stress and anxiety responses, thermoregulation, the transient receptor potential vanilloid system, and several neurotransmitters systems, and are thus potential candidates for mediating the pathophysiology of CHS. Conclusions: Excessive cannabinoid administration disrupts the normal functioning of the endocannabinoid system, which may cause CHS. More clinical and pre-clinical research is needed to fully understand the underlying pathophysiology of this disorder and the negative consequences of prolonged high-dose cannabis use.