Local IL‐10 level as a predictive factor in generalized aggressive periodontitis treatment response

Abstract

Generalized aggressive periodontitis (GAgP) presents a reduced response to non‐surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty‐four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL‐1β and IL‐10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post‐treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P > .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P < .05). In the SRP group, IL‐10 showed a predictive value for clinical response. The higher the IL‐10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P > .05). It can be concluded that the IL‐10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

Evaluation of Microcirculation, Cytokine Profile, and Local Antioxidant Protection Indices in Periodontal Health, and Stage II, Stage III Periodontitis

“…Moreover, IL-10 has a key function in the osteoclastic bone resorption and the regulation of osteoblastic bone formation [57]. Taiete et al (2019) demonstrated that in generalized aggressive periodontitis patients treated with scaling and root planning, a higher IL-10 concentration at baseline was associated with a higher reduction in probing pocket depth at 6 months [58]. One recent study has demonstrated, in an animal model, which IL-10 can modulate local host immune responses and prevent inflammatory damage of alveolar bone by reducing pro-inflammatory cytokine expression and decreasing local proliferation of Th17 cells [59].…”

IL10 promoter rs6667202 polymorphism is functional in health but not in grade c periodontitis patients: A pilot study

“…This is important when some microbiological assays have shown a more specific microbial community in Perio4C, 33,34 along with altered cytokines in gingival fluid, as IL-10. 35 IL-10 is a cytokine that can be produced by multiple immune cell types, including the T regulatory (Treg) cells, as is a more relevant representant for the Treg response. These cells are known for producing cytokines that suppress the inflammatory response against specific pathogens, restricting the host tissue damage during chronic infection.…”

Cross‐sectional comparisons of subgingival microbiome and gingival fluid inflammatory cytokines in periodontally healthy vegetarians versus non‐vegetarians

“…12 These include the pro-inflammatory cytokines IL-1β, 13,14 TNFα, 13,15 IL-8, 15,16 and IL-6 16 and the anti-inflammatory cytokine IL-10. [17][18][19] These biomarkers initiate the gingival inflammatory response to microbial plaque, mobilize immune cells to the gingival tissues, and advance the inflammatory front closer to the alveolar bone leading to periodontal tissue damage. 20 Vegetarian dietary patterns have been associated with lower levels of blood inflammatory markers.…”

“…Plaque‐related inflammatory periodontal disease is associated with increased levels of several inflammatory biomarkers in the gingival tissues 12 . These include the pro‐inflammatory cytokines IL‐1β, 13,14 TNF‐α, 13,15 IL‐8, 15,16 and IL‐6 16 and the anti‐inflammatory cytokine IL‐10 17–19 . These biomarkers initiate the gingival inflammatory response to microbial plaque, mobilize immune cells to the gingival tissues, and advance the inflammatory front closer to the alveolar bone leading to periodontal tissue damage 20 …”