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Although numerous animal models for low back pain associated with intervertebral disk (IVD) degeneration have been proposed, insufficient data have been provided to make any conclusions regarding pain. Our aim in this study was to determine the reliability of complete Freund's adjuvant (CFA) injection into the rat spine as an animal model representing human discogenic pain.We studied IVD degenerative changes with pain development after a 10-microL CFA injection into the L5-6 IVD of adult rats using behavioral, histologic, and biochemical studies. Serial histologic changes were analyzed to detect degenerative changes. Expression of calcitonin gene-related peptide (CGRP), prostaglandin E (PGE), and inducible nitric oxide synthase (iNOS) were determined using immunohistochemistry or real-time polymerase chain reaction as support data for pain development. In addition, CGRP immunoreactivity (ir) at the IVD was considered indirect evidence of neural ingrowth into the IVD.There was a significant increase of the hindpaw withdrawal response in the CFA group until 7 wk postoperatively (P0.05). Histologic analyses revealed progressive degenerative changes of the disks without any damage in adjacent structures, including nerve roots. In the CGRP-ir staining study, the bilateral dorsal horns and IVD had positive ir after intradiscal CFA injection. CGRP mRNA expression was increased in the dorsal root ganglion (DRG) at 2 and 4 wk, whereas PGE and iNOS mRNAs were markedly increased at 2 wk. The increment of CGRP expression was higher in allodynic rats compared with nonallodynic rats.Intradiscal CFA injection led to chronic disk degeneration with allodynia, which was suggested by pain behavior and expression of pain-related mediators. The increment of CGRP, PGE, and iNOS also suggest pain-related signal processing between the IVD and the neural pathway in this animal model. This animal model may be useful for future research related to the pathophysiology and development of novel treatment for spine-related pain.

We report a follow-up of 35 children, on average 17 years after they had intervertebral discitis. 15 patients still complained of backache. Flexion of the low back was normal in 32 patients, while extension was markedly restricted in 30. 26 patients had a block vertebra, and 28 patients had narrowing of the vertebral canal. Mode of treatment did not appear to affect the outcome.

Pseudomonas pickettii, a nonfermenting, gram-negative rod, is rarely pathogenic. Previous reports of infection with P. pickettii have largely involved direct contamination of supplies presumed to be sterile. We describe a case of vertebral osteomyelitis and intervertebral discitis caused by P. pickettii in a debilitated patient. The aggressive nature of this infection demonstrates that P. pickettii may be a more invasive organism than previously noted, particularly in hosts with weakened immunity secondary to underlying disease.

Discitis (with intervertebral disc destruction), found pathologically in the thoracic region of 8 out of 114 rheumatoid patients, is shown to derive and spread from primary rheumatoid involvement of the costovertebral joints. Erosion and destruction of bone may occur, followed by healing, visible radiologically as disc narrowing and posterolateral bony sclerosis and sometimes with ankylosis. There are few clinical symptoms, since most of these patients have limited locomotor function.