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| Main Authors: | , , , , , , |
|---|---|
| Format: | Recurso digital |
| Language: | English |
| Published: |
Zenodo
2025
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| Subjects: | |
| Online Access: | https://doi.org/10.5281/zenodo.15448223 |
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Table of Contents:
- <p><strong><em><span lang="EN-US">Abstract</span></em></strong></p> <p><strong><em><span lang="EN-US">Aim: </span></em></strong><em><span lang="EN-US">The study aimed to estimate and compare the levels of salivary hypoxia inducible factor-1 alpha (HIF-1α) in unstimulated saliva samples of periodontally & systemically healthy volunteers, generalized chronic gingivitis & periodontitis patients before and after non-surgical periodontal treatment (NSPT). <strong>Materials and Methods</strong>: A total of 24 subjects were categorized into 3 groups: Group I: 8 periodontally and systemically healthy volunteers; Group II: 8 generalized chronic gingivitis patients and Group III: 8 stage III grade B periodontitis patients. The periodontal parameters were recorded at 0 day in all three groups and reassessed following non-surgical periodontal treatment on 90th day in group II and group III. The saliva samples were collected on 0 day in all the three groups and on 30<sup>th</sup> day & 90<sup>th</sup> day in group II and group III. Molecular analysis was done for detection of HIF-1α using enzyme linked immunosorbent assay (ELISA). <strong>Results</strong>: On comparing the periodontal parameters at 0 day, the mean periodontal parameters were higher in both group II & III. Following the NSPT, both group II and III showed improved periodontal parameters with significant reduction at 90th day. Intra and intergroup comparison of the level of salivary HIF-1α was found be to be statistically significant in both group II & III compared to group I at 0, 30<sup>th</sup> and 90<sup>th</sup> days. <strong>Conclusion</strong>: The present study indicates that HIF- 1α can be used as potent biomarker to assess the effect of periodontal treatment and also signifies its possible interlink between hypoxia and periodontal disease pathogenesis.</span></em></p>