Human variation in gingival inflammation

Abstract

Oral commensal bacteria actively participate with gingival tissue to maintain healthy neutrophil surveillance and normal tissue and bone turnover processes. Disruption of this homeostatic host–bacteria relationship occurs during experimental gingivitis studies where it has been clearly established that increases in the bacterial burden increase gingival inflammation. Here, we show that experimental gingivitis resulted in three unique clinical inflammatory phenotypes (high, low, and slow) and reveal that interleukin-1β, a reported major gingivitis-associated inflammatory mediator, was not associated with clinical gingival inflammation in the slow response group. In addition, significantly higher levels of Streptococcus spp. were also unique to this group. The low clinical response group was characterized by low concentrations of host mediators, despite similar bacterial accumulation and compositional characteristics as the high clinical response group. Neutrophil and bone activation modulators were down-regulated in all response groups, revealing novel tissue and bone protective responses during gingival inflammation. These alterations in chemokine and microbial composition responses during experimental gingivitis reveal a previously uncharacterized variation in the human host response to a disruption in gingival homeostasis. Understanding this human variation in gingival inflammation may facilitate the identification of periodontitis-susceptible individuals. Overall, this study underscores the variability in host responses in the human population arising from variations in host immune profiles (low responders) and microbial community maturation (slow responders) that may impact clinical outcomes in terms of destructive inflammation.

Association of oral bacteria with oral hygiene habits and self‐reported gingival bleeding

“…We found the highest bacterial community diversity in gingival fluid for those reporting often or always to bleed from the gums when they brushed their teeth. This is in line with studies on experimental gingivitis showing an increase in community diversity during transition from periodontal health to periodontitis (Kistler et al, 2013; Bamashmous et al, 2021). We found that those who reported the highest frequency of gingival bleeding had a lower abundance of the bacteria within the Firmicutes and Actinobacteria phyla.…”

“…We found that those who reported the highest frequency of gingival bleeding had a lower abundance of the bacteria within the Firmicutes and Actinobacteria phyla. These are typically gram‐positive phyla, which are also found to decrease in relative abundance during the onset of experimental gingivitis (Bamashmous et al, 2021). Although we cannot confirm the presence of gingivitis among our study participants, a recent study found that self‐reported questions regarding bleeding gums performed quite well in sensitivity towards gingival inflammation, as confirmed with bleeding on probing assessed by trained staff (Goulão et al, 2021).…”

“…Perturbation of microbial communities may occur before the full clinical symptoms of the disease become apparent (Liu et al, 2012). To understand the aetiology underlying the microbial shift from the healthy to the diseased state, studies on experimental gingivitis are useful for describing this shift (Kistler et al, 2013; Bamashmous et al, 2021). However, there is a lack of literature describing the composition of the oral bacterial community associated with self‐reported crude markers of periodontal health status, such as gingival bleeding.…”

SARS-CoV-2: Overview and Its Impact on Oral Health

“…Three different clinical responses in the periodontium to bacterial burden may shed light on COVID clinical responses to SARS-CoV-2 virus challenges. These host inflammatory clinical responses to oral bacteria were designated as "high", "low", and "slow" [22]. The high clinical response group to similar bacterial concentrations resulted in high IL-1β levels in inflamed tissues.…”

“…The high clinical response group to similar bacterial concentrations resulted in high IL-1β levels in inflamed tissues. Applying this model to COVID-19 infected individuals, the varying levels of inflammatory response may be a plausible explanation for non-vaccinated individuals being at varying levels of risk for pulmonary "cytokine storms", resulting in outcomes from hospitalizations to possible death [22]. The clinical presentation of SARS-CoV-2 infections are often asymptomatic or have mild to moderate symptoms; 5% or less develop multi-organ failure or acute respiratory distress syndrome.…”