Peripheral Neuropathic FacialTrigeminal Pain and RANTESCCL5 in Jawbone Cavitation

Abstract EN

Introduction.

In this study, we elucidate the possible causative role of chronic subclinical inflammation in jawbone of patients with atypical facial pain (AFP) and trigeminal neuralgia (TRN) in the local overexpression of the chemokine regulated on activation and normal T-cell expressed and secreted (RANTES/C-C motif ligand 5 CCL5).

Neurons contain opioid receptors that transmit antipain reactions in the peripheral and central nervous system.

Proinflammatory chemokines like RANTES/CCL5 desensitize μ-opioid receptors in the periphery sensory neurons and it has been suggested that RANTES modifies the nociceptive reaction.

Materials and Methods.

In 15 patients with AFP/TRN, we examined fatty degenerated jawbone (FDOJ) samples for the expression of seven cytokines by multiplex analysis and compared these results with healthy jawbones.

Results.

Each of these medullary jawbone samples exhibited RANTES as the only highly overexpressed cytokine.

The FDOJ cohort with AFP/TRN showed a mean 30-fold overexpression of RANTES compared to healthy jawbones.

Conclusions.

To the best of our knowledge, no other research has identified RANTES overexpression in silent inflamed jawbones as a possible cause for AFP/TRN.

Thus, we hypothesize that the surgical clearing of FDOJ might diminish RANTES signaling pathways in neurons and contribute to resolving chronic neurological pain in AFP/TRN patients.