The Effect of Non-surgical Periodontal Treatment on Dickkoff-1 and Secreted Frizzled Related Protein-5 Levels

Overview

Periodontitis is a condition that is defined by microbial-associated, host-induced inflammation, which ultimately results in the loss of periodontal attachment.Periodontal clinical parameters are the most reliable indicators of periodontal disease; however, they provide information about past tissue destruction and are insufficient for predicting future periodontal disease activity. Therefore, evaluation of Dickkopf-1 (Dkk-1) and secreted Frizzled related protein 5 (sFRP5), which are Wnt signaling pathway antagonists, in periodontal inflammation may be a focus of interest. A total of 99 individuals, 44 male and 55 female, participated in our study and were divided into three groups as periodontally healthy, gingivitis and periodontitis. Non-surgical periodontal treatment was applied to the disease groups. Dkk-1 and sFRP5 were evaluated in gingival crevicular fluid (GCF) at the baseline and after periodontal treatment.

The participants were divided into three groups in accordance with their periodontal status according to the 2017 World Workshop on the classification of periodontal diseases : Periodontally healthy (group H, n = 33, probing depth (PD) ≤3 mm, fullmouth bleeding scores; bleeding on probing (BOP) % \<10, no clinical attachment levels (CAL) and radiologic bone loss), gingivitis (group G, n = 33 PD ≤3 mm, % BOP \>30, no CAL(due to periodontal disease) and radiologic bone loss), Stage 3 Grade B periodontitis (group P, n = 33, These individuals had a minimum of two non-adjacent teeth with sites with PD ≥6 mm, CAL ≥5 mm, BOP ≥30%, tooth loss due to periodontitis ≤4 teeth, the alveolar bone loss at radiographs extending to middle or apical third of the root, the presence of consistent amounts of plaque biofilm/calculus deposits commensurate with the severity of periodontal tissue breakdown, the proportion of percentage bone loss to age values were between 0.25 and 1). Panoromic and periapical radiographic examination was also performed for the diagnosis of periodontitis. Periodontal status of each individual included in the study was determined by measuring plaque index (PI), gingival index (GI), PD, clinical attachment level (CAL) and bleeding of probing (BOP). PD and CAL were measured on six sites (mesio-buccal/ facial, mid-buccal/facial, disto-buccal/facial, mesio-lingual/palatinal, mid-lingual/palatinal, disto-lingual/palatinal) of the teeth in baseline and after periodontal treatment. Bleeding was observed up to 10 sec after the examination of probing depth and BOP score was calculated as the number of BOP-positive sites was divided the number of total sites, after multiplied with 100. Panoramic and periapical radiographs were used to determine the alveolar bone loss. All clinical measurements were recorded using a standard Williams periodontal probe. Within 2 weeks from the screening visit, phase 1 periodontal treatment/scaling and root planing under local anesthesia using manual instruments and ultrasonic devices in a single appointment were performed and oral hygiene instructions were given to all participants with periodontitis by a single calibrated periodontist. In gingivitis and periodontally healthy groups, phase 1 periodontal treatment and oral hygiene education were given to each one. All periodontal clinical measurements recorded and gingival crevicular fluid (GCF) samples collection were at baseline and the 6-8 th week after the periodontal treatment in patients with G and P group and at one time point (baseline) in H group.