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Periodontal tissue destruction in aggressive periodontitis: Determination of gene or environmental factors
AIM: This study observed the role of defective neutrophil function in aggressive periodontitis through FPR1 gene polymorphism and the level of Il-8 compared with the role of dental plaque presence towards periodontal tissue damage (Clinical Attachment Loss/CAL) in patients in Indonesia. METHODS: Cas...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445446/ https://www.ncbi.nlm.nih.gov/pubmed/30983842 http://dx.doi.org/10.1016/j.sdentj.2018.12.003 |
Sumario: | AIM: This study observed the role of defective neutrophil function in aggressive periodontitis through FPR1 gene polymorphism and the level of Il-8 compared with the role of dental plaque presence towards periodontal tissue damage (Clinical Attachment Loss/CAL) in patients in Indonesia. METHODS: Case-control study was used to detect differences in polymorphism expression of FPR1 gene, the level of Il-8, dental plaque, and Clinical Attachment Loss/CAL from 32 Aggressive Periodontitis (AP) and 29 Non-Aggressive Periodontitis (NAP) samples, selected with consecutive sampling method. Polymorphism was identified using polymerase chain reaction (PCR) technique, and the level of IL-8 in the gingival crevicular fluid was identified using the enzyme-linked immunosorbent assay (ELISA) test. The Clinical Attachment Loss was analysed by using William periodontal probe, and the oral environment analysis was performed by using the OHI-S plaque index. Statistical analysis was used to determine the significance of the polymorphism difference of FPR gene, Il-8, Plaque and CAL amongst all subjects and also the control and correlations among these factors. RESULTS: The results showed that in the Aggressive Periodontitis (AP), the presence of the polymorphism of c576 T > C > G of FPR1 gene caused as much as 5.04 times higher occurrence of aggressive periodontitis (p = 0.006; OR = 5.040 (1.51–16.74)). The low level of Il-8 (below 0.064 pg/μl), showed as much as 34.5 times higher occurrence of aggressive periodontitis (OR = 34.5 (6.76–176.08)). The oral hygiene of the AP samples were better significantly (p = 0.002), and on the Clinical Attachment Loss (CAL) sample was even more (p = 0.02). The polymorphism of c301 G > C of FPR1 gene correlated with the CAL (r = 0.37; p = 0.039). The polymorphism of c576 T > C > G correlated significantly with the Il-8 (r = 0.5; p = 0.0287). The polymorphism of c348 T > C correlated significantly with the dental plaque (r = 0.355; p = 0.049), whereas the dental plaque correlation with CAL was not significant. CONCLUSION: The research conclusion showed that in aggressive periodontitis, genetic and environmental factors were correlated with the cause of periodontal tissue injury, and the role of genetic factors was more prominent on the injury. |
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