cannabidiol and Osteoporosis

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.

Topics: Cannabidiol; Cannabinoids; Cannabis; Dronabinol; Endocannabinoids; Humans; Osteoporosis; Receptors, Cannabinoid

Topics: Animals; Biomarkers; Bone Density; Bone Resorption; Humans; Osteoporosis

Cannabidiol (CBD), the non-psychoactive component of the Cannabis sativa plant, is marketed as a potential therapeutic agent and has been studied for its roles in reducing inflammation and managing neuropathic pain. Some studies have reported that CB1 and CB2 receptor activation can attenuate and reverse bone loss in experimental animal models. Despite this, little is known about the impact of CBD on fracture healing. We investigated the effects of CBD in vitro using human osteoprogenitor cells and in vivo via murine femur fracture and osteoporosis models. In vitro mesenchymal stem cells were treated with increasing concentrations of crystalized pharmaceutical grade CBD or vehicle solution. Cell viability and proliferation were significantly increased in cells treated with CBD compared to vehicle control. Osteocalcin expression was also significantly higher in the CBD-treated human stem cells compared to vehicle control. In vivo the effect of CBD on bone mineral density and fracture healing in mice was examined using a two-phase experimental approach. Fluoxetine was used for pharmacologic induction of osteoporosis and surgical oophorectomy (OVX) was used for hormonal induction of osteoporosis. X-ray and microCT analysis showed that CBD prevented both fluoxetine- and OVX-induced osteoporosis. We found that while OVX resulted in delayed bone healing in control mice, CBD-pretreated mice exhibited normal bone healing. Collectively these in vitro and in vivo findings suggest that CBD exerts cell-specific effects which can be exploited to enhance bone metabolism. These findings also indicate that CBD usage in an osteoporotic population may positively impact bone morphology, warranting further research.

Topics: Animals; Cannabidiol; Cell Proliferation; Cell Survival; Fluoxetine; Gene Expression; Humans; Mesenchymal Stem Cells; Mice; Models, Animal; Osteoporosis

Patients with spinal cord injury (SCI) undergo severe loss of bone mineral below the level of lesion, and data on available treatment options after SCI is scarce. The aim of this work was to investigate the therapeutic effect of cannabidiol (CBD), a non-psychoactive cannabis, on sublesional bone loss in a rat model of SCI. The adult male rats were exposed to surgical transection of the cord and treated with CBD for consecutive 14 days. It was found that CBD treatment elevated the serum levels of osteocalcin, reduced the serum levels of collagen type I cross-linked C-telopeptide, and enhanced bone mineral density of tibiae and femurs. Treatment of SCI rats with CBD enhanced bone volume, trabecular thickness, and trabecular number, and reduced trabecular separation in proximal tibiae, and increased ultimate compressive load, stiffness, and energy to max force of femoral diaphysis. Treatment of SCI rats with CBD upregulated mRNA expression of alkaline phosphatase and osteoprotegerin and downregulated mRNA expression of receptor activator of NF-κB ligand and tartrate-resistant acid phosphatase in femurs. Furthermore, treatment of SCI rats with CBD enhanced mRNA expression of wnt3a, Lrp5 and ctnnb1 in femurs. In conclusion, CBD administration attenuated SCI-induced sublesional cancellous bone loss.

Topics: Animals; Cancellous Bone; Cannabidiol; Gene Expression Regulation; Male; Osteoblasts; Osteoclasts; Osteoporosis; Rats; Rats, Wistar; RNA, Messenger; Spinal Cord Injuries; Tibia