What is periodontitis?

Periodontitis is a serious gum infection that damages the soft tissue and destroys the bone that supports your teeth. It is a progressive condition that, if left untreated, can lead to tooth loss. Periodontitis is a type of periodontal disease, which is a group of inflammatory conditions affecting the tissues surrounding the teeth.


Periodontitis typically develops from untreated gingivitis, which is the inflammation of the gums caused by plaque buildup on teeth. Plaque is a sticky film of bacteria that forms on the teeth and gums, and if not removed through proper oral hygiene practices like brushing and flossing, it can harden into tartar or calculus. Tartar buildup can irritate the gums and lead to gingivitis.


If gingivitis is not treated promptly, it can progress to periodontitis. In periodontitis, the bacteria in plaque and tartar trigger an immune response that leads to inflammation and damage to the gums and bone supporting the teeth. Over time, the gums may recede from the teeth, forming pockets that become infected. As the infection spreads, it can cause further destruction of the bone and connective tissues, leading to loosening and eventually loss of teeth.


What is the relationship between periodontitis and oxidative stress?

The relationship between periodontitis and oxidative stress is multifaceted and plays a significant role in the pathogenesis and progression of the disease. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage and inflammation. Several key mechanisms link oxidative stress to periodontitis:


  • Inflammatory Response: Periodontitis is characterized by chronic inflammation of the gums and surrounding tissues in response to bacterial infection. Inflammation is associated with the production of ROS and reactive nitrogen species (RNS) by immune cells such as neutrophils and macrophages as part of the body’s defense mechanism against pathogens. However, excessive production of ROS/RNS and insufficient antioxidant defenses can lead to oxidative stress, amplifying tissue damage and inflammation in periodontal tissues.


  • Tissue Damage: ROS generated during the inflammatory response can directly damage periodontal tissues, including the gums (gingiva), periodontal ligament, and alveolar bone. ROS/RNS can oxidize lipids, proteins, and DNA, leading to cellular dysfunction, apoptosis (cell death), and degradation of extracellular matrix components. This oxidative damage contributes to the breakdown of periodontal tissues and the progression of periodontitis.


  • Matrix Metalloproteinases (MMPs) Activation: Oxidative stress can upregulate the activity of matrix metalloproteinases (MMPs), a family of enzymes involved in tissue remodeling and degradation of extracellular matrix proteins. Excessive MMP activity in periodontitis can lead to destruction of periodontal tissues, including collagen fibers in the gingiva and periodontal ligament, further exacerbating tissue breakdown and tooth mobility.


  • Antioxidant Defenses: In healthy periodontal tissues, antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase help neutralize ROS and protect cells from oxidative damage. However, in periodontitis, there is evidence of impaired antioxidant defenses and decreased antioxidant enzyme activity, leading to increased susceptibility to oxidative stress and tissue damage.


  • Systemic Effects: Periodontitis has been linked to systemic conditions such as cardiovascular disease, diabetes, and rheumatoid arthritis, which are associated with oxidative stress and inflammation. The systemic spread of inflammatory mediators and oxidative stress from periodontal tissues to other organs and tissues may contribute to the pathogenesis of these systemic diseases.


Overall, oxidative stress is intimately involved in the pathogenesis of periodontitis, contributing to tissue damage, inflammation, and the progression of the disease.