Effectiveness of non-surgical treatment to reduce il-18 levels in the gingival crevicular fluid of patients with periodontal disease

Abstract

The aim of this study was to evaluate the effectiveness of the non-surgical periodontal treatment in reducing the gingival crevicular fluid (GCF) levels of IL-18 from inflamed periodontal sites. Fourteen patients with periodontal disease were included, being 9 patients with chronic periodontitis (mean age: 48.8 SD ± 7.4 years) and 5 patients with gingivitis (mean age: 43.6 SD ± 11.8). The patients were divided in the following groups: gingivitis sites from periodontitis patients (sites GP), periodontitis sites from periodontitis patients (sites PP), and gingivitis sites from gingivitis patients (sites GG). Probing pocket depth (PPD), probing attachment level (AL), plaque index (PI) and gingival index (GI) were recorded, and gingival fluid samples were collected. The subjects received non-surgical treatment and were re-evaluated 30 days after treatment (day 30 AT). There was a significant reduction in PI in GG (1.0 ± 0.4 to 0.5 ± 0.2), GP (1.2 ± 0.3 to 0.5 ± 0.3), and in PP (1.3 ± 0.4 to 0.7 ± 0.3) 30 AT. There was also a significant reduction in the GI in GG (1.3 ± 0.3 to 0.7 ± 0.4). PPD reduced significantly in GG (2.4 ± 0.6 to 1.9 ± 0.1), and PP (6.7 ± 1.1 to 5.2 ± 0.9) 30 AT. When all the samples were analyzed together, there was a significant reduction in IL-18 (12.9 ± 7.2 to 10.0 ± 3.1). This study showed that non-surgical treatment was effective in reducing GCF levels of IL-18 from inflamed periodontal sites.

CD24 activates the NLRP3 inflammasome through c‐Src kinase activity in a model of the lining epithelium of inflamed periodontal tissues

“…It is reported that IL-18 levels in gingival crevicular fluid are elevated in sites of periodontal disease [48]. This is compatible with downregulation of the NLRP3 inflammasome in affected epithelia as reported in the present study.…”

History of Chronic Periodontitis Is a High Risk Indicator for Peri-Implant Disease

“…In periodontitis, the local inflammatory reaction to bacterial infection activates the innate immune system, resulting in the release of an array of cytokines and other mediators and propagation of inflammation through the gingival tissues (10,11). The failure to encapsulate this "inflammation front" within gingival tissue results in the expansion of the response to adjacent alveolar bone (10).…”

“…The failure to encapsulate this "inflammation front" within gingival tissue results in the expansion of the response to adjacent alveolar bone (10). Moreover, the host response is influenced by several possible risk factors including genetic factors.…”

Clinico-Pathogenetic Value of Some Cytokines in Periodontitis

“…Учитывая, что патогенез пародонтита большинство авторов связывают с нарушением микробиоты ротовой полости и механизмов местного иммунитета, можно полагать, что успехи в развитии концепции патогенеза, диагностики и лечения заболевания могут быть связаны с иммунологическими исследованиями иммунологии полости рта и оценкой свойств ротовой жидкости (РЖ) [6,9]. Это связано с тем, что по мере прогрессирования пародонтита происходит разрушение мягких тканей, деструкция костной ткани и высвобождение биологически активных веществ, которые могут быть определены в РЖ и затем рассматриваться как кандидаты на роль биомаркеров этого заболевания.…”

“…При воспалении тканей пародонта уровень факторов иммунной защиты в РЖ повышается, например, лактоферрина, секреторного иммуноглобулина А [2, 3]. Огромное число исследований посвящено изучению цитокинового статуса, играющего ключевую роль в патогенезе пародонтита, но их результаты отличаются крайней противоречивостью [7,8,9,12], что затрудняет применение полученных результатов в дальнейших изысканиях и их внедрение в клиническую практику. Это определило цель данного исследования -дать характеристику цитокинового статуса ротовой жидкости у больных хроническим пародонтитом.…”