National University - Sudan (NUSU)
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Item NLRP3 Inflammasome in Autoinflammatory Diseases and Periodontitis Advance in the Management(Journal of Pharmacy and Bioallied Sciences, 2024) Hashim, Nada; Babiker, Rasha; Mohammed, Riham; Rehman, Mohammed Mustahsen; Chaitanya, Nallan CSK; Gobara, Bakrict Inflammatory chemicals are released by the immune system in response to any perceived danger, including irritants and pathogenic organisms. The caspase activation and the response of inflammation are governed by inflammasomes, which are sensors and transmitters of the innate immune system. They have always been linked to swelling and pain. Research has mainly concentrated on the NOD‑like protein transmitter 3 (NLRP3) inflammasome. Interleukin (IL)‑1 and IL‑18 are pro‑inflammatory cytokines that are activated by the NOD‑like antibody protein receptor 3 (NLRP3), which controls innate immune responses. The NLRP3 inflammasome has been associated with gum disease and other autoimmune inflammatory diseases in several studies. Scientists’ discovery of IL‑1’s central role in the pathophysiology of numerous autoimmune disorders has increased public awareness of these conditions. The first disease to be connected with aberrant inflammasome activation was the autoinflammatory cryopyrin‑associated periodic syndrome (CAPS). Targeted therapeutics against IL‑1 have been delayed in development because their underlying reasons are poorly understood. The NLRP3 inflammasome has recently been related to higher production and activation in periodontitis. Multiple periodontal cell types are controlled by the NLRP3 inflammasome. To promote osteoclast genesis, the NLRP3 inflammasome either increases receptor‑activator of nuclear factor kappa beta ligand (RANKL) synthesis or decreases osteoclast‑promoting gene (OPG) levels. By boosting cytokines that promote inflammation in the periodontal ligament fibroblasts and triggering apoptosis in osteoblasts, the NLRP3 inflammasome regulates immune cell activity. These findings support further investigation into the NLRP3 inflammasome as a therapeutic target for the medical treatment of periodontitis. This article provides a short overview of the NLRP3 inflammatory proteins and discusses their role in the onset of autoinflammatory disorders (AIDs) and periodontitis.Item Highlighting the Effect of Pro‑inflammatory Mediators in the Pathogenesis of Periodontal Diseases and Alzheimer’s Disease(Journal of Pharmacy and Bioallied Sciences, 2024) Hashim, Nada; Babiker, Rasha; Mohammed, Riham; Chaitanya, Nallan CSK; Rahman, Muhammed M.; Gismalla, BakriAlzheimer’s disease (AD) is a neurological condition that is much more common as people get older. It may start out early or late. Increased levels of pro‑inflammatory cytokines and microglial activation, both of which contribute to the central nervous system’s inflammatory state, are characteristics of AD. As opposed to this, periodontitis is a widespread oral infection brought on by Gram‑negative anaerobic bacteria. By releasing pro‑inflammatory cytokines into the systemic circulation, periodontitis can be classified as a “low‑grade systemic disease.” Periodontitis and AD are linked by inflammation, which is recognized to play a crucial part in both the disease processes. The current review sought to highlight the effects of pro‑inflammatory cytokines, which are released during periodontal and Alzheimer’s diseases in the pathophysiology of both conditions. It also addresses the puzzling relationship between AD and periodontitis, highlighting the etiology and potential ramifications.