Retracted: Methotrexate in the treatment of symptomatic knee osteoarthritis: randomised placebo-controlled trial.

This article has been retracted.

Rheumatoid arthritis, periodontal disease and coronary artery disease.

Rheumatoid arthritis (RA), periodontal disease (PD), and coronary artery disease (CAD) are common chronic inflammatory diseases. RA is associated with accelerated vascular risk resulting in an increased prevalence of CAD with attendant early mortality and excess morbidity. RA and PD have a common pathobiology. Accordingly, the aim of this study was to evaluate the association between RA, PD, and CAD and the influence of systemic inflammatory factors. A total of 100 active RA patients of which 50 had established CAD and 50 had no CAD were assessed for PD. All subjects underwent a clinical, cardiac, dental, laboratory, and radiological evaluation. Blood samples were obtained, and the level of high sensitivity C-reactive protein (hs-CRP), total white blood counts (WBC), erythrocyte sedimentation rate (ESR), fibrinogen and tumor necrosis factor (TNF) alpha, total cholesterol (TC), and high density lipoprotein (HDL) were assayed. The findings of this study demonstrated an association between RA, PD, and CAD. The RA patients with CAD had significantly more PD than RA patients without CAD. The inflammatory markers, hsCRP, ESR, WBC, fibrinogen, and TNF-alpha, were raised in all patients but were significantly higher in RA patients with CAD who also had PD. HDL levels were lower in RA patients with CAD when compared to RA patients without CAD. Evidence from this study shows an association between RA, PD, CAD, and systemic levels of the inflammatory mediators. The implication is that inflammation may be the central link between the chronic inflammatory, autoimmune disorders, and atherosclerosis.

Chronic inflammatory autoimmune disorders and atherosclerosis.

Rheumatoid arthritis (RA), periodontal disease (PD), and coronary artery disease (CAD) are common chronic inflammatory diseases. RA is associated with accelerated vascular risk resulting in an increased prevalence of CAD with attendant early mortality and excess morbidity. RA and PD have a common pathobiology. Accordingly, the aim of this study was to evaluate the association between RA, PD, and CAD and the influence of systemic inflammatory factors. A total of 100 active RA patients of which 50 had established CAD and 50 had no CAD were assessed for PD. All subjects underwent a clinical, cardiac, dental, laboratory, and radiological evaluation. Blood samples were obtained and the level of high-sensitivity C-reactive protein (hs-CRP), total white blood counts (WBC), erythrocyte sedimentation rate (ESR), fibrinogen and tumor necrosis alpha (TNF-alpha), total cholesterol (TC), and high-density lipoprotein (HDL) were assayed. The findings of this study demonstrated an association between RA, PD, and CAD. The RA patients with CAD had significantly more PD than RA patients without CAD, P < 0.001. The inflammatory markers hs-CRP, ESR, WBC, fibrinogen, and TNF-alpha were raised in all patients but were significantly higher in RA patients with CAD who also had PD, that is, in those with more inflammatory disease burden. HDL levels were lower in RA patients with CAD when compared to RA patients without CAD, P < 0.005. Evidence from this study shows an association between RA, PD, CAD, and systemic levels of the inflammatory mediators. The implication is that inflammation may be the central link between the chronic inflammatory autoimmune disorders and atherosclerosis.

Spinal tuberculosis: overlooked?

OBJECTIVE: The aim of the present study was to ascertain the degree of occurrence of tuberculous infection in patients presenting with low back pain (LBP). METHODS: Forty consecutive patients seeking primary medical attention for the main symptom of LBP and presenting to the Rheumatology Outpatient Clinic of our institution from January 2004 to June 2005, were recruited in this cohort study. All patients were thoroughly interrogated (occupational, trauma, infection, diabetes mellitus and medication history), subjected to a rigorous clinical examination and a battery of investigations RESULTS: Twelve of the 40 patients (33%) proved to have spinal TB as the cause of backache. Eight of these patients were above the age of 65. Five of the 12 patients with spinal TB also had concomitant osteoarthritic changes of the spine and two patients had concomitant disc prolapse. Eleven of the 12 patients with spinal TB had a completely normal chest X-ray and in 10 of these patients the plain X-ray of the lumbosacral region failed to show any significant lesion. In all 12 patients, sputum analysis failed to reveal acid-fast bacilli. CONCLUSIONS: The findings of this study indicate that TB is a common cause of LBP that is liable to be overlooked in the differential diagnosis of LBP. Furthermore, evidence of concurrent active intrathoracic TB may be lacking and consequently a high level of suspicion is required. The need for prompt diagnosis and treatment of skeletal TB is of utmost importance to prevent serious bone and joint destruction and severe neurological sequelae. A reliable imaging modality for diagnosing spinal TB seems to be magnetic resonance imaging.

Embryopathy in experimental diabetic gestation: assessment of PGE2 level, gene expression of cyclooxygenases and apoptosis.

The causes of, and predisposing conditions for, increased congenital anomalies in embryos of experimental diabetic gestation are not fully identified. In the present study, some possible factors involved in diabetes-induced embryopathy are explored. The concentration of PGE2, the gene expression of cyclooxygenases (COX-1 and COX-2) and level of apoptosis (measured by caspase-3 activity) are assessed during organogenesis in the embryos of streptozotocin-induced diabetic rats. The concentrations of PGE2 in the embryos of diabetic rats were lower than controls, with the lowest values in malformed embryos and their associated membranes (yolk sacs). The pattern of change in PGE2 was similar in the embryos of the control and diabetic groups, which showed a steady decline between days 9 and 11 of gestation. These changes in PGE2 were accompanied by a small decrease in COX-1 expression in all embryos and associated membranes during the same gestational period. Expression of COX-2, which was below normal in diabetic embryos, decreased between days 9 and 11 of gestation in all groups. In the membranes of non-malformed embryos, COX-2 expression peaked on day 10 of gestation. It was found that there was little or no detectable COX-2 expression in the membranes of malformed embryos on day 9 of gestation and although its expression was detectable on the following days it was much lower than in the other groups. Caspase-3 activity increased substantially between days 9 and 11 of gestation. Embryos from the experimentally diabetic group showed higher activity than did controls, with the largest increases in the malformed embryos. It would appear that COX-2 expression and PGE2 concentration (in both embryo and associated membranes) play a significant role in organ formation. The data presented here suggest that an unhealthy placenta may be instrumental in the development of malformed embryos.