الفهرس 
Nayroz Abdel Fattah Mohamed Tarrad
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Abstract
Oral lichen planus (OLP) is a long-standing inflammatory disorder associated with cell-mediated immunological dysfunction. Due to the anatomic, physiological, and functional characteristics of the oral cavity, OLP needs unique diagnostic and treatment assessments.
Numerous studies are currently focusing on inflammatory cytokines. Assuming that they might be triggered by unstable molecular alterations, leading to the development of OLP. At the moment, there is no solid evidence about the action of several cytokines in OLP.
Long non-coding RNAs (lncRNAs) are a class of RNA copies with a dimension longer than 200 nucleotides that regulate gene expression and function at the transcriptional, translational, and post-translational stages. The dysregulated lncRNA profile has been implicated in the development of several diseases, including cancer, metabolic disorders, and cardiovascular diseases. In particular, lncRNAs seem to be involved in tumor development and metastasis. Many lncRNAs have been shown to be hypothetical biomarkers and goals for the diagnosis and cure of cancers.
One of the promising markers for OLP diagnosis is IL-17 as may have a contribution in its pathophysiology by increasing T-cell-mediated reactions and encouraging chemokine and other cytokine production, which may in turn contribute to the disease.
The current study aimed to assess the salivary expression of lncRNA DQ786243 and IL-17 in OLP, to better understand the pathogenesis of OLP and provide effective targets for OLP therapy.
This study was conducted at Cairo University’s Faculty of Dentistry’s Out-Patient hospital’s clinic of Oral Medicine and Periodontology. It contained fifty-two patients, twenty-nine of whom had symptomatic OLP and were recruited in a sequential manner to eliminate bias, and were separated into three groups: Thirteen patients with reticular lichen planus (group A), thirteen patients with atrophic lichen planus (group B), thirteen patients with erosive lichen planus (group C), and thirteen patients in the control group (group D) were chosen to match OLP patients in terms of age and gender.
The outcome measures were evaluating the salivary expression of lncRNA DQ786243 and IL-17 using qRT-PCR.
The results of the current study have shown increase in the salivary expression level of both the LncRNA and the IL17 among patients with OLP than healthy patients. In addition to, there was a statistically significant difference in the expression of LncRNA DQ786243 and IL-17 between each type of OLP. This points out that the LncRNA DQ786243 might play a clear role in the severity of the disease as well so, as a conclusion, DQ786243 dysregulation is implicated in OLP pathogenesis and may have a role in the severity of the disease, indicating a possible treatment approach for OLP.
Secondly, our data imply that IL-17 is a key mediator in OLP pathogenesis and can help in differentiating between subtypes of OLP. More research is required to determine the precise function and origin of IL-17 in OLP