Clinical, Immune, and Microbiome Traits of Gingivitis and Peri-implant Mucositis

Abstract

Tissues surrounding dental implants and teeth develop clinical inflammation in response to microbial stimuli. However, the literature suggests that differences exist in the microbial insult and inflammatory responses leading to gingivitis and peri-implant mucositis. In this pilot study, the authors use for the first time a systems biology approach to comprehensively evaluate clinical parameters, selected inflammatory markers, and the microbiome of subject-matched tooth and implant sites during native inflammation and in response to experimental plaque accumulation. Fifteen subjects with 2 posterior implants and corresponding contralateral teeth were examined at enrollment; at day 0, after reinstitution of gingival/mucosal health; at days 7, 14, and 21, during stent-mediated oral hygiene (OH) abstention; and at day 42, after resumption of OH. The subgingival microbiome was evaluated via 16S rRNA gene sequencing and 8 selected inflammatory markers measured in crevicular fluid. Comparison of teeth and implants via general linear models based on orthogonal polynomials showed similar responses in clinical parameters, inflammatory mediators, and proportions of individual microbial taxa during OH abstention. Implants, however, accumulated less plaque and underwent more heterogeneous shifts in microbiome structure. A multilevel, within-group, sparse partial least squares analysis of covariation of microbial, inflammatory, and clinical parameters throughout all study visits found inflammation around teeth and implants positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Selenomonas, Prevotella, and 5 species-level phylotypes. Gingivitis, however, showed a stronger positive correlation with lactoferrin and IL-1ra and a stronger negative correlation with Rothia. Peri-implant mucositis, on the contrary, correlated positively with certain microbial taxa not associated with gingivitis by a previous study or the current one. In summary, differences existed between implants and tooth sites in microbiome evolution during OH abstention and in the correlation of specific inflammatory mediators and microbial taxa with clinical inflammation. Common biological features, however, were also identified for gingivitis and mucositis.

Intra‐oral single‐site comparisons of periodontal and peri‐implant microbiota in health and disease

“…Furthermore, the nature of the anatomical niche (i.e., dental implant vs. natural tooth) was not a major factor. This observation is in line with other studies that have examined intra‐personal variations in microbiota present in periodontal and peri‐implant niches (Payne et al, ; Schincaglia et al, ; Schwarzberg et al, ). It is conceivable that the distinct differences among individuals could result from a combination of behavioral, environmental, and biological factors, such as dietary and oral hygiene habits, anatomical characteristics, amount and content of saliva and crevicular fluid secretion, hormonal, and immunological conditions (Marsh & Zaura, ; Mira et al, ).…”

“…The bacterial occurrence network analysis shown here (Figures and ) revealed a conserved pattern of dysbiosis within periodontitis and peri‐implantitis niches that commonly involved higher abundances of and/or positive co‐correlations between Prevotella spp . , Treponema , Porphyromonas, Tannerella, Filifactor, Parvimonas, Desulfobulbus, and Synergistetes taxa, consistent with findings from other microbiome studies (Apatzidou et al, ; Chen et al, ; Kröger et al, ; Lafaurie et al, ; Park et al, ; Schincaglia et al, ; Shi et al, ; Shiba et al, ). Several other taxa appear to play important etiological roles, including the as‐yet‐uncultivated Peptostreptococcaceae [XI] and Bacteroidetes [G‐5] phylotypes.…”

The effect of dental caries and restorative biomaterials on IL-1 β and TNF-α levels in the gingival crevicular fluid

“…Concentration of GCF IL-1β and TNF-α were extensively studied in local inflammatory conditions as periodontitis 35,36,37,38 and perimplantitis 39,40,41,42,43,44 or even as a systemic inflammatory condition like diabetes 45,46 or connective tissue disease 47,48,49,50 . Comparing to these inflammatory conditions, cytokines were infrequently investigated in dental caries, especially in GCF of caries teeth 51,52,53 .…”

The immune response to Prevotella bacteria in chronic inflammatory disease

“…). The role of Prevotella in driving Th17‐mediated immune responses in periodontitis is supported by studies linking IL‐1 α and IL‐1 β levels in crevicular fluid to Prevotella colonization …”