The study published in the journal Science and Technology of Advanced Materials, by Shinichi Arakawa and colleagues at Tokyo Medical and Dental University and Japan’s National Institute of Advanced Industrial Science and Technology, evaluated the bactericidal activities of ozone nano-bubble water – also known as NBW3 – against the two main bacterial agents that cause periodontitis as well as its toxicity to human oral tissue cells.
Their results showed that NBW3 can kill periodontal pathogens within 30 seconds of exposure, yet has only a minor impact on the viability of oral tissue cells after 24 hours of exposure.
Based on their in vitro results, the researchers conclude that NBW3 could become a valuable tool for treating periodontitis. However, since in vitro models cannot be directly compared to real-life clinical situations in which oral antiseptics are diluted with saliva, the authors recommend further research to determine the extent to which NBW3′s potency may be reduced by the saliva of dental patients.
Periodontitis is an inflammation of the oral tissues that surround and support our teeth – it is caused by bacteria residing in “biofilms” or dental plaque.
The traditional first step of periodontal treatment involves “mechanical debridement” (i.e. scraping away the dental plaque and dental calculus). Various antiseptics and antibiotics have been used to supplement mechanical debridement.
But antibiotic therapies have several significant drawbacks, such as the selectivity of antimicrobial action, possible development of resistant bacteria, and risk for adverse host reactions. For these reasons, the topical use of a low-cost, broad-spectrum antiseptic agent with low potential for adverse reactions is preferable.
One possible alternative is ozone (O3), which has strong antimicrobial activity against bacteria, fungi, protozoa and viruses, and does not induce microbial resistance. Aqueous ozone is highly biocompatible with oral tissue cells. However, ozonated water must be used within the first 5 to 10 minutes after production to assure its potency.
Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results.
We measured serum pepsinogen I (PGI) and pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs).
After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl−1) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl−1). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76).
Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.
Source: British journal of oncology