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Review
. 2021 Jun 11:35:117-127.
doi: 10.1016/j.jare.2021.06.006. eCollection 2022 Jan.

Neurophysiological mechanisms of cancer-induced bone pain

Affiliations
Review

Neurophysiological mechanisms of cancer-induced bone pain

Xuan-Qi Zheng et al. J Adv Res. .

Abstract

Background: Cancer-induced Bone Pain (CIBP) is an important factor affecting their quality of life of cancer survivors. In addition, current clinical practice and scientific research suggest that neuropathic pain is a representative component of CIBP. However, given the variability of cancer conditions and the complexity of neuropathic pain, related mechanisms have been continuously supplemented but have not been perfected.

Aim of review: Therefore, the current review highlights the latest progress in basic research on the field and proposes potential therapeutic targets, representative drugs and upcoming therapies.

Key scientific concepts of review: Notably, factors such as central sensitization, neuroinflammation, glial cell activation and an acidic environment are considered to be related to neuropathic pain in CIBP. Nonetheless, further research is needed to ascertain the mechanism of CIBP in order to develop highly effective drugs. Moreover, more attention needs to be paid to the care of patients with advanced cancer.

Keywords: Acidic environment; Cancer-induced bone pain; Central sensitization; Neuroinflammation; P2X Family; TRPV.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

None
Graphical abstract
Fig. 1
Fig. 1
Schematic diagram showing the mechanism of cancer-induced bone pain. The cell body of the primary afferent neurons innervating the body is in the dorsal root ganglia and it transports sensory information from the periphery to the spinal cord and brain. Unmyelinated C fibers are involved in the detection of a variety of harmful stimuli. When bone tumors occur, or when bone destruction occurs, sensory neurons will behave as sprout and produce toxic irritants. Besides, DRG activation, microglia activation, acidic environment production, inflammatory factor expression, ion channel changes and many other factors participate in the generation and maintenance of cancer pain.
Fig. 2
Fig. 2
Schematic representation of the roles of the acidic environment and inflammatory response related pathway in the mechanism of cancer-induced bone pain.

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References

    1. Lechner B., Chow S., Chow R., Zhang L., Tsao M., Danjoux C., et al. The incidence of neuropathic pain in bone metastases patients referred for palliative radiotherapy. Radiother Oncol. 2016;118(3):557–561. - PubMed
    1. Smith B.H., Raja S.N. NeuPSIG: investing in solutions to the growing global challenge of neuropathic pain. Br J Anaesth. 2017;119(4):705–708. - PubMed
    1. Treede R.D., Jensen T.S., Campbell J.N., Cruccu G., Dostrovsky J.O., Griffin J.W., et al. Neuropathic pain: redefinition and a grading system for clinical and research purposes. Neurology. 2008;70(18):1630–1635. - PubMed
    1. Finnerup N.B., Haroutounian S., Kamerman P., Baron R., Bennett D.L., Bouhassira D., et al. Neuropathic pain: an updated grading system for research and clinical practice. Pain. 2016;157(8):1599–1606. - PMC - PubMed
    1. Jung C., Ichesco E., Ratai E., Gonzalez R., Burdo T., Loggia M., et al. Magnetic resonance imaging of neuroinflammation in chronic pain: a role for astrogliosis? Pain. 2020;161(7):1555–1564. - PMC - PubMed