Researchers Identify New Clinical Response to Inflammation
Researchers at the University of Washington School of Dentistry have identified a third type of oral inflammatory phenotype that exhibits a delayed response to bacterial accumulation.
Researchers at the University of Washington (UW) School of Dentistry have identified a third type of oral inflammatory phenotype that exhibits a delayed response to bacterial accumulation. The study, “Human Variation in Gingival Inflammation,” is available in Proceedings of the National Academy of Sciences, PNAS.
The team, which includes Richard Darveau, PhD, and Jeffrey McLean, PhD, of the UW School of Dentistry, studied individual responses to bioburden associated with periodontal disease. The study revealed a new oral inflammatory phenotype.
Prior to this discovery, there were two known oral inflammatory phenotypes: high (or strong) clinical response, and low clinical response. This newly identified ”slow” phenotype displays a delayed strong inflammatory response to accumulated dental plaque. An individual’s inflammatory phenotype indicates how a person reacts to accumulated plaque, thereby identifying if he or she is at greater risk of chronic periodontal inflammation.
“This type of analysis offers the ability to predict those individuals who are more susceptible to developing gingivitis and potentially those who may progress to periodontitis,” explains Darveau, a professor in the Department of Periodontics and Oral Health Sciences at UW School of Dentistry.
Investigators found the microbial community in individuals with the slow phenotype differs from those with either high and low phenotypes in that they contain a higher amount of healthy commensal Streptococcus species, which may influence the low pathogenic biofilm accumulation and transition to more gram-negative species. “Our study may help identify individuals early on that have a higher risk of developing gingivitis and may require more frequent prophylaxis,” says Darveau. “This is a step toward personalized treatment.”
Additional findings revealed how host protective mechanisms use neutrophils to protect against tissue and bone damage during gingival inflammation. This mechanism was apparent in all three phenotypes.