Application of Endotoxin Testing in Periodontal Disease

Adult tooth loss is primarily caused by periodontal disease, a major oral disease that threatens human health and teeth. Most of the conditions that cause periodontitis are caused by local factors, but the most important pathogenic factor is dental plaque. Gingivitis is mainly the chronic inflammation of the periodontal support tissue caused by local factors. Oral diseases, whether caries or periodontal disease, are caused by plaque biofilm, bacteria in plaque, and toxins produced by bacteria, and the key toxic substance is endotoxin. Endotoxin is a lipopolysaccharide (LPS), a component of Gram-negative bacteria's outer cell membrane. Many studies have confirmed that endotoxin is one of the main causes of periodontal damage. It binds to the Toll receptor of the body's immune system and causes the inflammatory response of the host cells, causing the host cells to uncontrollably produce a variety of inflammatory cytokines. The control of endotoxin can inhibit the number and types of periodontal bacteria, thereby protecting oral health.

Oral endotoxin has the potential to prime or tolerize the infiltrating neutrophil.Figure 1. Oral endotoxin has the potential to prime or tolerize the infiltrating neutrophil. (Zenobia C, et al., 2022)

Discussion

Periodontitis is a relatively common disease in the clinical oral cavity. It has a high incidence in my country and has become an important factor in tooth loss in adults. Endotoxin (LPS) promotes bacterial destruction by binding to Toll-like receptor 4 (TLR4) in the host innate immune system, activating nuclear factor κB (NFκB), triggering the production of pro-inflammatory cytokines. Clinical evaluations of LPS activity in healthy dental pockets from periodontal disease patients revealed that LPS is a TLR4 agonist, further demonstrating that it is one of the main virulence factors of periodontal pathogens. It destroys periodontal tissues by stimulating inflammatory cytokines to be synthesized and released. Long-term stimulation of endotoxin during periodontitis may weaken the body's tolerance to future stimulation. Due to the inhibition of endotoxin on wound healing and osteogenesis, clinicians must remove endotoxin while removing dental calculus and plaque during treatment. Therefore, the detection of endotoxin levels in oral saliva or blood is beneficial to the clinical diagnosis of periodontal disease and has positive significance for the prevention and treatment of patients.

Conclusions

Periodontal disease can even increase the risk of systemic diseases. Dental biofilms contain Gram-negative bacteria that produce endotoxins that activate the immune system, inducing periodontal disease. Currently, the assessment of the severity of human gingivitis and periodontitis is achieved clinically by observing gingival redness, gingival bleeding, or pocket depth. However, this method cannot be quantified and errors may occur. Therefore, it is of great significance to find a fast and accurate diagnostic method to improve the accuracy of early diagnosis of periodontal disease and provide a reliable basis for clinical treatment. It is possible to detect endotoxins using a variety of methods, including dynamic turbidity, endpoint chromogenic, endpoint turbidimetric, and dynamic chromogenic, which are easy to use and highly sensitive. In summary, the use of endotoxin detection has a high predictive value for periodontal disease, and it is worthy of clinical application.

Creative BioMart can provide a series of comprehensive and accurate endotoxin detection services and a variety of endotoxin removal kits, which are convenient for you to use in scientific research. If you are interested in our applications, please contact us for more details.

We provide multiple services but not limited to:

Our advantages

Reference

  1. Zenobia C, Darveau R P. (2022). Does Oral Endotoxin Contribute to Systemic Inflammation?[J]. Frontiers in Oral Health. 3: 911420.

Online Inquiry

Enter Your Email Here to Subscribe.
© Creative BioMart. All rights reserved.