Clinical Trial Details
— Status: Active, not recruiting
Administrative data
| NCT number |
NCT06075680 |
| Other study ID # |
TDK-2022-10763 |
| Secondary ID |
|
| Status |
Active, not recruiting |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
March 4, 2022 |
| Est. completion date |
November 2023 |
Study information
| Verified date |
October 2023 |
| Source |
Marmara University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
The present study aimed to assess the effect of non-surgical periodontal treatment on serum
and salivary IL-1beta, IL-18, NLRP3, ASC and Caspase-1 levels in gingivitis and Stage III
Grade C periodontitis. 15 periodontally healthy, 15 gingivitis and 15 Stage III Grade C
periodontitis patients were enrolled. At baseline, serum and saliva samples were collected
and the whole mouth clinical periodontal parameters were recorded. Periodontitis and
gingivitis patients received non-surgical periodontal treatment. Clinical parameters were
re-measured and samples were re-collected at 1 and 3 months after treatment. Serum and
salivary protein levels were analyzed by ELISA. Data were analyzed using appropriate
statistical tests.
Description:
New insights into the first line of immune response to infection and stress signals at the
cellular level have reported the participation of cytoplasmic nucleotide-binding domain-like
receptors containing multi-protein complexes named inflammasomes. The inflammasomes play a
key role in innate immunity by regulating maturation of proinflammatory cytokines of the
interleukin 1beta and 18. The inflammasome depends on assembly of a sensor, for instance
nod-like receptor family pyrin domaincontaining protein (NLRP), with an
adaptor,apoptosis-associated speck-like protein containing a caspase recruitment domain
(ASC), allowing recruitment and activation of an inflammatory caspase-1. Although different
inflammasomes have been described, the NLRP3/ASC/caspase-1 multi-protein complex, known as
NLRP3 inflammasome, has been most intensively studied.
Sample size was calculated based on a previous study concerning levels of inflammasome
complex proteins in periodontal diseases.To maintain estimates at an optimal level of
precision,minimize impact of exclusions and dropouts, and establish significant differences
in results at a 95% confidence level, alfa value=0.05, and 83% power.Therefore, the study
sample included a total of 45 patients( 15 periodontally healthy, 15 gingivitis, 15 sStage
III Grade C Periodontitis). The whole mouth clinical periodontal examination included
measurement of probing depth (PPD), clinical attachment level (CAL), presence of bleeding on
probing (BOP), gingival index (GI), and plaque index (PI) at 6 sites per tooth, except the
third molars. The presence and type of the alveolar bone loss were assessed on the digital
panoramic radiograph in each participant, which was supplemented with periapical radiographs
if necessary. Periodontal status of each patient was evaluated by a single calibrated
periodontists with a manual probe. The diagnosis of periodontitis or periodontally health was
determined according to the 2017 World Workshop on Classification of Periodontal and
Peri-Implant Diseases and Conditions. Periodontally healthy individuals (n=15) in the control
group had no sites with PD >3 mm and CAL >2 mm and also no radiographic evidence of alveolar
bone loss. BOP was <10% in the whole mouth. Healthy group also exhibited no history of
periodontitis. Gingivitis patients had PD≤3 mm, intact periodontium, no destruction in
alveolar bone radiographically and BOP>10%. Stage III grade C patient had clinical attachment
loss (CAL)≥ 5, radiographic bone loss (RBL) extending to the middle third of root and beyond,
≤ 4 tooth loss due to periodontitis, percentage of bone loss by age is >1.
Treatment The recruited periodontitis and gingivitis patients received conventional quadrant
scaling and root planning (SRP). SRP was performed by the same clinician using ultrasonic
inserts and manual periodontal curettes. Re-evaluations were performed at 1 and 3 months
following the completion of the SRP. No periodontal intervention was carried out in the
periodontally healthy controls.
Saliva and Serum Sampling A total of 5 mL of unstimulated whole saliva was collected by
passive drool method between 9:00 and 10:00 am. The participants were advised to avoid food
consumption for three hours before sample collection. The participants were seated upright
and saliva was collected over a period of 5 minutes with instructions to pool saliva in the
floor of the mouth and passively drool it into a sterile glass beaker. The saliva samples
were centrifuged at 5000 rpm for 10 minutes at room temperature, and supernatants were
collected and stored at -80°C. A total of 5 mL of blood was collected from the antecubital
fossa by venepuncture method. Serum was isolated from the blood by centrifuging at 3000 rpm
for 20 minutes followed by its rapid transfer to a sterile polypropylene tube and storage at
-80°C.
Biomarker Immunoassays: Serum and salivary samples of IL-1beta, IL-18, NLRP3, ASC and
Caspase-1 were measured by ELISA using commercial kits.
Statistical Analysis All statistical analyses were carried out with the standard statistical
software package. For the intra-group comparisons, if the data were not normally disturbed,
Friedman test and the Dunn test with the Bonferroni correction were used to analyze the
change between baseline and 1 month and 3 months after treatment. For inter-group
comparisons, Mann-Whitney U test for normally and non-normally disturbed data. The Spearman's
rank correlation test was used to detect the correlations of biochemical parameters with
clinical parameters and each others in diseased group before and after treatment. All tests
were performed at significance level of P <0.05.
