Small Joints Discogenic Low Back Pain, Pain Transmission Mode And Mechanism Of Experimental Research

ObjectivesTo investigated the neuron innervation and transmission of lower facet joint in the condition of inflammation in rats. MethodsThe retrograde neurotransport method and immunohistochemistry was used in this study. Fluoro-Gold crystals was applied to the L5-L6 facet joint in rats. Five days later, 50μl saline (control group, n=16) or complete Freund's adjuvant (inflammatory group, n=16) was injected into the facet joint. Twelve days after the first operation, bilateral T13-L5 DRG were resected and processed for SP or IB4 immunohistochemistry. The sections were observed with a fluorescent microscope. ResultF-G labeled neurons were found in the ipsilateral DRGs from L1-L5, the numbers of F-G labeled neurons in L3-L5 DRGs were more than those in L1 and L2DRGs, this difference is considered to be statistically significant, P<0. 05. Of the F-G-labeled neurons, the ratio of SP-ir neurons was higher in the inflammatory group (36±3%) (Mean±S.E.) than in the control group(21 ±2%), P<0.01. What's more, the cross-section area of F-G labeled SP-positive neurons in inflammatory group(900.1 ± 34. 8μm²) was larger than that in control group(738. 8 ± 30. 2μm²), P <0.01. No IB4-binding neuron was found in either group. And the ratio of SP-ir neurons in L1 and L2 DRGs was significantly lower than those in L3-5 DRGs (P<0.001). Conclusions1. The lumbar facet joint is innervated mainly by NGF-dependent neurons from the ipsilateral L1-L5 DRGs, multisegmentally. And these neurons mainly distribute inL3-L5 DRGs.2. The inflammation of the lumbar facet joint makes an increase in the number and the cross-section area of SP-positive neurons.3. Perhaps there are no GDNF-dependent neurons innervating the lumbar facet joint.4. It suggested that one of the possible mechanisms of the lower back pain of the lumbar facet joint origins was: the injury of the facet joint leads to the chronic inflammation. And then the inflammatory stimulation will transfer the SP or CGRP-negative NGF dependent neurons innervating the lumbar facet joint to SP or CGRP-positive neurons. These changes may upregulate the levels of SP and CGRP or other pain related NGF. The increase of trkA may occur. All of these leads to the lower back pain or generate hypersensitivity and hyperalgesia. In such circumstance, even the physiological loads will produce pain.