Spinal cord disorder due to spinal epidural abscess secondary to thoracic facet joint septic arthritis-a rare case with a surprising evolution.

INTRODUCTION: Septic arthritis of a facet joint (SAFJ) is a relatively rare medical entity and the lumbar segment is its most frequent location. Although unusual, a spinal epidural abscess (SEA) can occur as a complication of SAFJ and possibly damage the spinal cord. CASE PRESENTATION: A 53-year-old woman presented with acute right dorsal pain, fever, loss of sphincters control, and paraparesis without causal factor. Forty-eight hours after the symptoms started, imaging revealed a thoracic posterior epidural collection causing compression of the spinal cord and features suggestive of septic arthritis of right T5-T6 facet joint. She underwent an urgent laminectomy and drainage of the abscess. Both blood and abscess cultures isolated Staphylococcus aureus. A diagnosis of complete paraplegia grade A of the ASIA (American Spinal Injury Association) Impairment Scale (AIS) with neurologic level T10 was made 5 days after surgery. She took 3 months of an intensive rehabilitation program at our Physical and Rehabilitation Medicine ward. With an unexpected favorable evolution, both neurological and functional, she was discharged with an incomplete paraplegia AIS D and functionally independent in all tasks. DISCUSSION: This case reveals an infrequent medical condition on a rarely affected spinal segment. An early diagnosis and proper treatment of SAFJ and SEA are of major importance to avoid severe related consequences. Patients with spinal cord injury with severe neurological deficits due to these conditions greatly benefit from an interdisciplinary rehabilitation program to improve neuromotor and functional status.

Effects of stanozolol on normal and IL-1ß-stimulated equine chondrocytes in vitro.

BACKGROUND: Intra-articular administration of stanozolol has shown promising results by improving the clinical management of lameness associated with naturally-occurring osteoarthritis (OA) in horses, and by decreasing osteophyte formation and subchondral bone reaction in sheep following surgically induced OA. However, there is limited evidence on the anti-inflammatory and modulatory properties of stanozolol on articular tissues. The objective of the current study was to evaluate the effects of stanozolol on chondrocyte viability and gene expression in normal equine chondrocytes and an inflammatory in vitro system of OA (interleukin-1ß (IL-1ß) treated chondrocytes). RESULTS: Chondrocytes from normal metacarpophalangeal joints of skeletally mature horses were exposed to four treatment groups: (1) media only (2) media+IL-1ß (3) media+IL-1ß + stanozolol (4) media+stanozolol. Following exposure, chondrocyte viability and the expression of catabolic, anabolic and structural genes were determined. General linear models with Dunnet's comparisons with Bonferroni's adjustment were performed. Cell viability was similar in all groups. Stanozolol treatment reduced gene expression of MMP-13, MMP-1, IL-6 and COX-2 in both normal and IL-1ß treated chondrocytes. Stanozolol treatment reduced ADAMTS4 gene expression in normal chondrocytes. Stanozolol reduced the expression of COL2A1. CONCLUSIONS: The current study demonstrates stanozolol has chondroprotective effects through downregulation of genes for pro-inflammatory/catabolic cytokines and enzymes associated with OA. However, there is no evidence of increased cartilage stimulation through upregulation of the anabolic and structural genes tested.