Elevated Baseline Salivary Protease Activity May Predict the Steadiness of Gingival Inflammation During Periodontal Healing: A 12-Week Follow-Up Study on Adults.

Ulvi Kahraman Gürsoy,Daniel Belstrøm,Eija Könönen,Dareen Fteita,Kamran Nazmi,Maria Anastasia Grande,Mervi Gürsoy,Floris J Bikker

doi:10.3390/pathogens9090751

Abstract

Aim was to profile salivary total protease, Porphyromonas gingivalis gingipain, and neutrophil elastase activities in relation to the resolution of periodontal inflammation, salivary macrophage-derived chemokine (MDC), and macrophage inflammatory protein-1α concentrations. Nonsurgical periodontal treatment was performed in 24 periodontitis patients in a prospective interventional study design. Periodontal clinical parameters were recorded, and stimulated saliva samples were collected at baseline and 2, 6, and 12 weeks after treatment. Salivary total protease and gingipain activities were determined using fluorogenic substrates, elastase activity by chromogenic substrates, and cytokine concentrations by Luminex immunoassay. For statistical analyses, generalized linear mixed models for repeated measures were used. Salivary total protease activity elevated, while gingival inflammation and plaque accumulation decreased 2 and 6 weeks after periodontal therapy. Salivary MDC concentration was elevated 12 weeks after periodontal treatment. Patients with elevated protease activities at baseline in comparison to patients with low baseline total protease activities, had higher levels of gingival inflammation before and after periodontal treatment. In conclusion, elevations in salivary total protease activity seem to be part of periodontal healing at its early phases. Higher levels of salivary total protease activities before periodontal treatment may predict the severity and steadiness of unresolved gingival inflammation.

Highlights

Periodontitis is characterized by a complex cascade of inflammatory interactions between the periodontal pathogenic bacteria residing in the subgingival biofilm and the host immune system.Periodontal pathogens produce proteolytic enzymes that impair the host response and epithelial integrity, which, in turn, facilitate microbial invasion into the surrounding tissues [1,2]
The aim of this study was to profile the total protease, gingipain, and elastase activities in saliva of periodontitis patients before and after treatment and to examine whether their levels are related to clinical periodontal indices, salivary macrophage-derived chemokine (MDC), and macrophage inflammatory protein (MIP)-1α concentrations
The following clinical measurement scores were recorded during the baseline and periodontal healing: plaque index (PI): 84.2%, 41%, 43%, and 41.8%; bleeding on probing (BOP): 56%, 27.1%, 34.6%, 41.3%; and probing depth (PD): 3.4 mm, 3.0 mm

Summary

Introduction

Periodontitis is characterized by a complex cascade of inflammatory interactions between the periodontal pathogenic bacteria residing in the subgingival biofilm and the host immune system.Periodontal pathogens produce proteolytic enzymes that impair the host response and epithelial integrity, which, in turn, facilitate microbial invasion into the surrounding tissues [1,2]. The subsequent recruitment and migration of neutrophils to the site of infection require the activation of a chemotactic. Pathogens 2020, 9, 751 inflammatory network [3,4] Besides their antimicrobial activity, neutrophils constitute a main source of host proteolytic enzymes, including neutrophil elastase, matrix metalloproteinases, cathepsins, and serine proteases, which collectively contribute to the degradation of periodontal tissues [5]. The migration of inflammatory cells towards the wound site is dominated by the mesenchymal cell differentiation of the phagocytic neutrophils, monocytes, and lymphocytes, which engulf invading microbes and secrete proteolytic enzymes to digest necrotic tissues. Macrophages and lymphocytes orchestrate the formation of granulation tissue through the secretion of growth factors and cytokines, which, subsequently, recruit resident cells to establish a cell-rich remodeling tissue [6]

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