Periodontal İnflamasyon Salya, Serum C-Reaktif Protein ve Fetuin-A Düzeylerini Etkiler mi?

Yıl 2022, , 70 - 79, 11.04.2022

Esra Sinem Kemer Dogan , Burak Doğan , Özlem Fentoğlu

https://doi.org/10.22312/sdusbed.1004879

Öz

Amaç: Periodontal hastalık konak savunma sistemini etkileyerek immün yanıtı harekete geçirmektedir. İnflamasyon sonucunda çoğunluğu karaciğer tarafından salgılanan pozitif ve negatif akut faz reaktanları açığa çıkmaktadır. Periodontitisin oluşturduğu inflamatuvar yükü ölçmek için periodontal inflame yüzey alanı (PİYA) son zamanlarda kullanılmaya başlanmıştır. Bu çalışmanın amacı PİYA’nın salya ve serumda pozitif, negatif akut faz reaktanları olan C-reaktif protein (CRP) ve fetuin-A seviyelerine etkilerini incelemektir.
Materyal-Metot: Çalışmaya 47 birey dahil edildi ve periodontal durumlarına göre periodontal olarak sağlıklı (n=15), gingivitis (n=15) ve periodontitis (n=17) olmak üzere 3 gruba ayrıldı. Hastaların sosyodemografik verileri anket aracılığıyla kaydedildi, periodontal kayıtları alındı, hastalardan salya ve serum örnekleri toplandı. PİYA, periodontal cep derinliği, klinik ataşman seviyesi ve sondalamada kanama yüzdesi kullanılarak hesaplandı. Salya ve serum örneklerinde CRP ve fetuin-A seviyeleri ELISA ile analiz edildi.
Bulgular: Periodontal parametreler ve PİYA periodontitisli grupta sağlıklı ve gingivitisli gruba göre daha yüksekti. Sağlıklı grupla kıyaslandığında periodontitis grubunda salya CRP daha yüksek, salya ve serum fetuin-A ise daha düşüktü. Periodontitis grubunda gingivitisli gruba kıyasla serum fetuin-A daha düşük, salya CRP daha yüksekti. Uyumlandırılmış çok değişkenli lineer regresyon analizi sonucunda PİYA ile salya ve serum fetuin-A’nın negatif, serum CRP’nin ise pozitif ilişkili olduğu belirlendi.
Sonuç: Fetuin-A ve CRP seviyelerinin periodontal hastalık patogenezinde biyobelirteç olarak kullanılabileceği öngörülmektedir. 

Anahtar Kelimeler

Alfa-2-HS-Glikoprotein, C-Reaktif Protein, Fetuinler, Periodontitis

Destekleyen Kurum

Hatay Mustafa Kemal Üniversitesi

Proje Numarası

18.M.094

Teşekkür

Biyokimyasal analizdeki katkılarından dolayı Prof. Dr. Nizami Duran’a teşekkürlerimizi sunarız.

Periodontal Inflammation Effect Salivary and Serum C-Reactive Protein and Fetuin-A Levels?

Öz

Objective: Periodontal disease triggers the immune response by affecting the host defence system. Positive and negative acute phase reactants, mostly secreted by liver, are released as a result of inflammation. Periodontal inflamed surface area (PISA) has recently been used to measure the inflammatory load caused by periodontitis. The purpose of this study is to examine the effects of PISA on the levels of positive, negative acute phase reactants C-reactive protein (CRP) and fetuin-A in saliva and serum.

Material-Method: Forty-seven individuals were included in the study and divided into 3 groups according to their periodontal status as periodontal healthy (n=15), gingivitis (n=15), or periodontitis (n=17). Sociodemographics were recorded through a questionnaire, periodontal indices were taken, and saliva and serum samples were collected from patients. PISA was calculated using periodontal probing depth, clinical attachment level, and percentage of bleeding on probing. CRP and fetuin-A levels in saliva and serum samples were analysed by ELISA.

Results: Periodontal parameters and PISA were higher in periodontitis group than healthy and gingivitis group. When compared to healthy group, salivary CRP was higher and salivary and serum fetuin-A was lower in periodontitis group. Serum fetuin-A was lower and salivary CRP was higher in periodontitis group compared to gingivitis group. As a result of the adjusted multivariate linear regression analysis, it was determined that PISA was negatively correlated with salivary and serum fetuin-A, and positively correlated with serum CRP.

Conclusions: Fetuin-A and CRP levels were suggested to be used as a biomarker in periodontal disease pathogenesis.

Anahtar Kelimeler

Alpha-2-HS-Glycoprotein, C-Reactive Protein, Fetuins, Periodontitis

Proje Numarası

18.M.094

Kaynakça

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