Spinal cannabinoid receptor-2 activation reduces hypersensitivity associated with bone cancer pain and improves the integrity of the blood–spinal cord barrier
In Summary:
Bone cancer pain (BCP) is a severe but common complication of metastatic and advanced cancer stages. Through a recent research study, scientists demonstrated that damage to the blood-spinal cord barrier (BSCB) is a cause of BCP. More specifically, in the mouse model of BCP, tight junctions proteins that serve to limit the entry of pathogens and other neurotoxic substances from the blood into the brain or spinal cord were found to be deficient. Such loss led to BSCB breakdown, which allowed cells of the immune system such as microglia and astrocytes to enter the spine. These activated immune cells produced pro-inflammatory chemicals that in turn further damage the BSCB and also increase chemotherapy-induced pain in cancer patients.
The study, however, also found that activation of the cannabinoid receptor type 2 (CB2) helped to partially restore tight junctions proteins and thus preserve the BSCB integrity. This, as a result, decreased the level of proinflammatory chemicals and activated immune cells.
With their research, the authors have contributed to both basic science and medicine. From a basic science standpoint, these findings illustrate a pathway that regulates pain associated with advanced-stage cancer. From a medical application standpoint, they demonstrate that pharmaceutical compounds activating CB2 can ameliorate bone cancer pain, serving as potential therapies for this condition.