Role of Reactive Oxidative Species in Periodontitis: A Review Article
Nanda Rachmad Putra Gofur, Aisyah Rachmadani Putri Gofur, Soesilaningtyas, Rizki Nur Rachman Putra Gofur, Mega Kahdina and Hernalia Martadila Putri
Published: December 28, 2021
Abstract
Introduction: Common periodontitis that attacks the human population is periodontitis induced by plaque. Periodontitis begins with the ordering of plaque that adheres to the tooth surface. Dental plaque is a thin layer of multi-species biofilm containing colonization of bacteria, bacterial products, and food debrish. The dental plaque that causes periodontitis is usually located in the subgingival area, then extends apical to the tooth, causing inflammation of the periodontal tissue. The causes of periodontitis in general are bacterial species found in dental plaque, and about 10 species have been identified as pathogens in periodontal disease, especially gram-negative stem bacteria, including Porphyromonas gingivalis, Prevotella intermedia, Actinomyces viscosus, Bacteroides forsythus, Campylobacter rectus, Treponema denticola, and Fusobacterium nucleatum.Apart from plaque factors, periodontitis can also be caused by systemic factors, genetic disorders as well as environmental and risk factors. Studies show that people with diabetes mellitus and smokers suffer from periodontitis a lot. Whereas in patients with periodontitis due to genetic disorders caused by damage to the periodontal tissue by macrophages that respond to IL-1 excessively. ROS, also plays role in pathophysiology in periodontitis.
Discussion: Chronic periodontitis is a chronic infectious disease with a complex etiology. The main etiology is bacteria and is exacerbated by various other factors. In this case, excessive production of ROS and changes in state can lead to abnormal activation of apoptosis, approaches important factors involved in the production of periodontitis extensions and various clinical features of periodontitis. Several studies have demonstrated a role for ROS in the deregulation of apoptosis. Between ROS and the body can produce neo-epitopes which then stimulate a broad spectrum associated with tissue damage and breakdown of the periodontium. Studies in periodontitis patients and involves oxidative stress in disease pathogenesis. Polymorphism genes coding for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and the gene encoding NADPH oxidase NCF2 have been identified in many ways with a risk of periodontitis. All biomolecules (lipids, proteins and DNA) can be damaged by the overproduction of ROS.
Conclusion: During infection, immune system produce reactive oxygen species (ROS) which are released into the extracellular environment. The ROS does not have a specific target that could damage tissue especially in periodontitis.
Keywords: ROS; Pathophysiology; Periodontitis