Bone loss is pretty much inevitable with age and can be characterized by weak limbs. People are now looking for answers to reverse the deteriorating effects of bone loss and aging. Cannabinoids have been said to be able to treat chronic pain through their neuroprotective and anti inflammatory abilities. Cannabinoids are naturally occuring in the cannabis plant (cannabis sativa). Cannabinoids consist of tetrahydrocannabinol (THC) and cannabinol (CBD).
Here is the full scientific article if you wish to download it.
THC is the psychoactive part of marijuana and gives you the high feeling when smoked. CBD is the medicinal side of marijuana and this gives you the feeling of being relaxed. The endocannabinoid system holds two cannabinoid receptors, 1 and 2, that allow cannabinoids to bind and work throughout the body.
This paper will look at how cannabinoids can work in the body to reverse bone loss.
The active part of cannabis, THC, triggers the cannabinoid receptors 1 and 2, thus relaying the function of endogenous cannabinoids. Cannabinoid receptor 1 is predominantly neuronal and controls the cannabinoid psychoactive impacts. Cannabinoids receptor 2 is broadly communicated in peripheral tissues, majorly in pathological disorders. So far the major endocannabinoids, anandamide and 2-arachidonoylglycerol, have been discovered in bone at ‘neuronal’ levels.
The cannabinoid receptor 1 is in existence majorly in skeletal sympathetic nerve sections, thus mediating the adrenergic tonic restrain of bone manufacturing. Cannabinoid receptor 2 is communicated in osteoblasts and osteoclasts, triggers bone manufacturing, and induces bone suction.
As small bone matter is the only impulsive phenotype so far displayed in cannabinoid receptor 2 mutant mice, it seems that the primary physiologic involvement of cannabinoid receptor 2 is related with upholding bone remodeling at equilibrium, thus securing the skeleton versus age-related bone deterioration. Indeed, in animals, polymorphisms in CNR2, the gene encoding cannabinoid receptor 2, are massively related to postmenopausal bone loss. Preclinical experiments have illustrated that a synthetic cannabinoid 2-selective agonist saves ovariectomy-inhibited bone loss.
Recent experiments in rodents and humans indicate a detrimental position for the endocannabinoid network in the mediation of skeletal redesigning and the sequential problems on bone matter and biomechanical mechanism. Although the cannabinoid receptor 1 has been seen in sympathetic sections innervating the skeleton, its position in regulating bone turnover remains to be clarified.
The cannabinoid receptor 2 is communicated in bone tissues. Its bone anabolic ability, consisting of some of the actions involved, has been portrayed in minor descriptions, and is also implicated from human genetic experiments. These experiments illustrate polymorphisms in CNR2, the gene encoding cannabinoid receptor 2, as detrimental genetic danger factors for bone loss.
Taken together, the publications on cannabinoid receptors in mice and humans pave the path for the advancement of diagnostic measures to single out bone loss-susceptible polymorphisms in CNR2, and cannabinoid agents to fight bone loss.