Rat anti Rhesus Macaque TNF monoclonal antibody, clone 293423

The inflammatory diseases rheumatoid arthritis (RA) and periodontitis show similarities in misbalances of cytokine levels, such as tumor necrosis factor-alpha (TNF-alpha). RA has been treated for two decades with TNF inhibitors which are effective by blocking TNF's destructive action. Since RA and periodontitis show similarities in high levels of TNF, the periodontal status of RA patients may improve with the use of anti-TNF therapy. To assess this, a systematic review with special emphasis on duration of therapy was performed to evaluate the effect of anti-TNF-alpha treatment on the periodontal status of RA patients. Overall, studies showed an improvement in periodontal health with anti-TNF therapy. When analyzed over time (6 weeks to 9 months), it became apparent that initial improvements concerned bleeding on probing (BOP) and gingival index (GI) after therapy duration of 6 weeks. Periodontitis parameters that improved after prolonged treatment were: probing pocket depth (PPD) after 3 months and clinical attachment level (CAL) after 6 months. In conclusion, this systematic review reveals that anti-TNF treatment is therefore not only beneficial for rheumatic joints but also for the gums of rheumatoid arthritis patients. We propose that the sequential tissue recovery due to anti-TNF therapy progresses as follows: 1. block of diapedesis by lowering vessel permeability, 2 fewer leukocytes in the inflamed tissue, and 3. reduced proteolytic activity and subsequent repair of collagen fiber functionality and normalization of osteoclast activity. Clinically, this could lead to a decrease in bleeding on probing and ultimately in an improved clinical attachment level.

Male fetal sex associates with higher rates of materno-fetal complications. Inflammation and inadequate vasoactive responses are mechanisms implicated in obstetric complications, and alterations in maternal plasma cytokine profile and nitric oxide (NO) metabolites are potential predictive biomarkers. We aimed to assess if these parameters are influenced by fetal sex. A prospective, observational study was carried out in 85 healthy pregnant women with singleton pregnancies in the first trimester of gestation. A blood sample was extracted at the tenth week of gestation. In plasma, we assessed: 1) cytokines (micro-array): pro-inflammatory (IL1 alpha, IL1 beta, IL6, TNF alpha), anti-inflammatory (IL4, IL10, IL13), and chemoattractant (IL8, MCP1, IFN gamma), and 2) NO metabolites (liquid chromatography-tandem mass spectrometry and Griess reaction): L-arginine, ADMA, SDMA, nitrates (NOx). Women with a male fetus (n = 50) exhibited, compared with those with a female (n = 35): higher IL1 beta (OR = 1.09 with 95% CI: 0.97-1.28), and lower IL13 (OR = 0.93 with 95% CI: 0.87-0.99), and higher plasma NOx (OR = 1.14 with 95% CI: 1.03-1.31). Our data suggest that fetal sex influences maternal plasma cytokine profile and NO in early pregnancy. Women with a male fetus may have a worse capacity to counteract an inflammatory response. They may have better vasodilator capacity, but in the presence of an oxidative environment, a higher nitrosative damage may occur. These data reinforce the need to include sex as variable in predictive models.