In-Vitro Assessment of the Corrosion Potential of an Oral Strain of Sulfate-Reducing Bacteria on Metallic Orthodontic Materials.

AIM: Orthodontic literature is scant when it comes to microbial corrosion. The oral prevalence of many bacteria which are capable of causing microbial corrosion is reported in the dental literature. The aim of this study is to experimentally determine the corrosive potential of an oral strain of Sulfate-reducing bacteria. MATERIALS AND METHODS: Stainless steel (SS) bracket, stainless steel archwire, NiTi archwire, Titanium molybdenum (TMA) archwire, and titanium miniscrew were immersed in five media which included Artificial saliva (group I), Sulfate rich artificial saliva (group II), API agar medium specific for SRB (group III), AS + API medium+ bacterial strain (group IV), SRAS+ API medium+ bacterial strain (group V). The materials were then subjected to Scanning electron microscopy and energy-dispersive X-ray analysis (EDX). RESULTS: Materials in groups I, II, and III did not show any surface changes whereas materials in groups IV and V which contained the bacteria showed surface changes which were erosive patches suggestive of corrosion. EDX analyses were in line with similar findings. CONCLUSION: This in vitro study suggested that the oral strain of Sulfate-reducing bacteria was able to induce corrosive changes in the experimental setup.

Assessing the In Vitro Antioxidant and Anti-inflammatory Activity of Moringa oleifera Crude Extract.

BACKGROUND: Chronic inflammation and oxidative stress play a vital role in the pathogenesis of various diseases of the oral cavity including periodontal disease. Phytochemicals present in plants with antioxidant (AO) and anti-inflammatory properties could aid as a therapeutic adjunct in the management of these diseases. AIM: To assess the antioxidant and anti-inflammatory effects of aqueous and ethanolic extracts of Moringa oleifera Lam. (MOL) in an in vitro environment. MATERIALS AND METHODS: Aqueous and ethanolic extracts of M. oleifera Lam. were prepared by maceration. Antioxidant activity was assessed by FRAP, hydroxyl radical scavenging activity, and DPPH radical scavenging assay. Anti-inflammatory activity was assessed by Albumin Denaturation Assay. Experiments were repeated thrice, and mean and standard deviation were calculated. RESULTS: Both the test substances exhibited significant antioxidant and anti-inflammatory activity, and aqueous extracts exhibited higher activity than ethanolic extract. SUMMARY AND CONCLUSION: The anti-inflammatory and antioxidant activity of M. oleifera Lam. could be further explored for the management of periodontal disease as a local drug delivery system with the extract could be developed.

Activation of the nuclear factor-κB pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2.

A significant portion of lung development is completed postnatally during alveolarization, rendering the immature lung vulnerable to inflammatory stimuli that can disrupt lung structure and function. Although the NF-κB pathway has well-recognized pro-inflammatory functions, novel anti-inflammatory and developmental roles for NF-κB have recently been described. Thus, to determine how NF-κB modulates alveolarization during inflammation, we exposed postnatal day 6 mice to vehicle (PBS), systemic lipopolysaccharide (LPS), or the combination of LPS and the global NF-κB pathway inhibitor BAY 11-7082 (LPS + BAY). LPS impaired alveolarization, decreased lung cell proliferation, and reduced epithelial growth factor expression. BAY exaggerated these detrimental effects of LPS, further suppressing proliferation and disrupting pulmonary angiogenesis, an essential component of alveolarization. The more severe pathology induced by LPS + BAY was associated with marked increases in lung and plasma levels of macrophage inflammatory protein-2 (MIP-2). Experiments using primary neonatal pulmonary endothelial cells (PEC) demonstrated that MIP-2 directly impaired neonatal PEC migration in vitro; and neutralization of MIP-2 in vivo preserved lung cell proliferation and pulmonary angiogenesis and prevented the more severe alveolar disruption induced by the combined treatment of LPS + BAY. Taken together, these studies demonstrate a key anti-inflammatory function of the NF-κB pathway in the early alveolar lung that functions to mitigate the detrimental effects of inflammation on pulmonary angiogenesis and alveolarization. Furthermore, these data suggest that neutralization of MIP-2 may represent a novel therapeutic target that could be beneficial in preserving lung growth in premature infants exposed to inflammatory stress.