Evaluation of vitamin C as an adjunct to periodontal therapy: Systematic review

Background: Periodontitis is an inflammatory disease that affects the periodontium, which is the protective apparatus that surrounds a tooth and includes the gingiva, alveolar bone, cementum, and periodontal ligament and is initiated by bacterial infection, subsequently progresses because of altered host response, and causes periodontal tissue destruction. These bacteria have the capacity to destroy the collagen fibres and ground substance directly by releasing virulence factors like enzymes - collagenase and toxins - gingipains. Indirectly act on various receptors like toll receptors and activate host immune response. Some immune cells like neutrophils, start producing reactive oxygen species (ROS). Vitamin C acts as an antioxidant, by acting as an electron donor Thereby preventing lipid peroxidation by ROS. Vit. C also controls collagen synthesis by directly activating collagen synthesis transcription and stabilizing procollagen mRNA. Along with other properties, Vitamin C is said to have anti-inflammatory and wound healing properties. Aim: This study aimed to systematically review to assess the effect of Vitamin C, as an adjunct to periodontal therapy

Gene regulators associating the T2DM and periodontitis contributing disease prognostic markers and therapeutic target

Periodontitis can be exacerbated by variety of systemic disorders including type 2 diabetes. T2DM patients exhibited a threefold increased risk of periodontitis. The mechanism through which T2DM induces periodontitis is uncertain. This study aims to identify co-regulatory molecules involved in T2DM periodontitis. Understanding the mechanisms could lead to new prognostic biomarkers and therapeutic targets. Methodology: Gene expression datasets (GSE156993)with experimental conditions: 1) healthy control 2) periodontitis, and 3). T2DM with periodontitis were assessed. The up-regulated genes in Group1 (healthy control vs periodontitis) and Group2 (healthy control vs T2DM with periodontitis)were identified. Protein interaction network were constructed from up-regulated genes and the topological characteristics network were determined. Each network's hubs containing the transcription factor that was up-regulated, as well as its coregulators were retrieved. Finally, the hubs were enriched based on the gene ontology and molecular pathways to recognize thehubs function. Results: 751 genes in Group1 and 762 in Group2 were noticed up-regulated. Two individual protein interaction network constructed from theseup-regulated genesthat showed complex interactions based on topological analysis. Theextracted hubs from each network displayed a variety of pathways relevant to the immune system, cell cycle, and signal processing. Analysis of hubs showed FOS transcription factor was common in both conditions containing diverse transcriptional coregulators such PKP2, RUNX2, TSC22D3, SUPT6H, and MAP3K7 in periodontitis and IDS, OPTN, PPP1R12A, BATF, and LMNA in T2DM with periodontitis. Conclusion: Our findings demonstrate FOS has a variety of regulatory patterns, providing evidence of T2M progression to periodontitis. Further experiments are still needed to confirm these transcriptional coregulators as prognostic biomarkers and therapeutic targets