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Inflammatory process begins around root apex as a result of bacterial infection of pulp cavity in chronic apical periodontitis. Bone destruction can begin in apical region after immunological reactions at the end of inflammatory process, and radiolucent periapical lesion seems in this way. If bone destruction around apical region is in the rate of 30%, we can notice this difference eventually. Histological manifestations of periapical inflammation can be observed in the result of pulp necrosis and inflammation around apical region. Mocelular methods can determine the type of therapy in various diseases. Each region and tissue reserve specific host factors. Vast majority of pulpal inflammation was trigerred by microorganisms. Certain bacterial virulence factors may damage host tissue directly, other virulence factors can stimulate prolonged non-specific immune response causing tissue damage. In the last phase of infection, immunopathological destruction of pulp tissue is observed due to humoral response. IL-17 is an important inflammatory cytokine released from T cells of the immune system. TNF-alpha and RANKL are also mediators responsible for bone destruction metabolism. TNF is a cytokine mediating immunologic changes during periodontal disease. TNF induction stimulate secondary mediators taking part as chemotactic cytokines. TNF has two different types; TNF-alpha and TNF-beta. TNF-alpha is a polypeptide cytokine produced by macrophages and monocytes. TNF-alpha stimulates bone resorption . There has been limited researches analyzing GCF, blood and tissue of pulp, dentin-derived fluid and periapical fluid for molecular diagnosis so far. GCF is a fluid derived from gingival groove. This fluid contains a lot of host factors such as anticor, bacterial antigen, protein and cytokines. GCF sampling is a non-invasive method, it can be used to provide diagnostic information in all clinical cases. In this study, we will evaluate the levels of IL-17, TNF-alpha and RANKL in the gingival crevicular fluid of teeth with periapical lesion diagnosed with chronic apical periodontitis. Thus, it will be evaluated whether these markers can be used for diagnosis and follow-up of the disease in teeth with periapical lesions.
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It is planned to include volunteer patients who came to Van YYU Faculty of Dentistry, Oral and Maxillofacial Radiology Department between February and March 2022 for routine examination. Patients who applied to Yüzüncü Yıl University Faculty of Dentistry for treatment and met the study criteria will be included in the study by signing an informed consent form. 40 patients diagnosed with chronic apical periodontitis and having teeth with radiographic periapical lesions will be included in the study. Patients with periodontitis will not be included in the study.
GCF samples will be taken from the teeth diagnosed with chronic apical periodontitis and the contralateral teeth (from healthy teeth). The tooth which is resource of GCF will be isolated with cotton pellets. After the supragingival plaque is carefully removed with a curette, the tooth will be air-dried for 10 seconds, and periopaper strips will be placed in the gingival sulcus until resistance is felt. Periopaper strips will be removed from the gilgival sulcus after 1 minute. The levels of IL-17, TNF-alpha and RANKL from the samples in the gingival crevicular fluid will be evaluated.
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40 participants in 2 patient groups
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Hacer Aydınyurt, PhD; Murat Tunca, PhD
Data sourced from clinicaltrials.gov
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