Osteogenezis imperfekta: bir olgu sunumu

Osteogenezis İmperfekta Oİ , diğer adıylakırılgan kemik hastalığı, oldukça yaygın görülenkalıtımsal geçiş gösteren kemiklerde deformite,fraktür ve frajilite ile seyreden konnektif dokuhastalığıdır. Moleküler çalışmalar, bu bozukluğunsebebinin, çoğu vakada tip 1 kollajenin yapımındansorumlu olan genin mutasyonu olduğunu göstermiştir. Kemiklerin dışında kollajeni yapısındabulunduran tendon, ligament, deri, sklera, dişler,orta ve iç kulak etkilenebilir. Hastalarda sıkgörülen dental anomaliler, dentinogenezis imperfekta Dİ ve maloklüzyondu

A 5 year retrospective study of biopsied jaw lesions with the assessment of concordance between clinical and histopathological diagnoses.

The jaw can be affected by several lesions that manifest in the oral cavity, but little is known about their distribution patterns in various populations

Molecular Profiling of Odontogenic Tumors - Pilot Study

Background/Aim: In the pathogenesis of odontogenic tumors which arise from the rests of the dental apparatus in the jaw, several molecular pathways have been shown to play critical roles such as genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor. Next generation genomic sequencing has identified gene mutations in many different tumors. Materials and Methods: Here we report four types of odontogenic tumor including six cases in which five had mutation according to next generation sequencing analysis from archival paraffin blocks that diagnosed previously as ameloblastoma (solid), amloblastoma (unicystic-mural), ameloblastic fibroma, squamous odontogenic tumor, and adenomatoid odontogenic tumor. Results: All ameloblastomatic tumors were shown BRAF mutation and adenomatoid odontogenic tumors were KRAS mutation. Conclusion: This evidence may highlight the poorly understood pathogenesis of odontogenic tumors. Further comparisons need to be made with other benign and malignant odontogenic tumors so that unique odontogenic features may be found

Efficiency of B-RAF-/MEK-inhibitors in B-RAF mutated Ameloblastoma: Case report and review of literature

Background: Ameloblastoma is a benign but locally invasive and aggressive odontogenic tumor harboring activating BRAF V600E mutations in about two thirds of the cases. Case presentation: Neoadjuvant therapy with Dabrafenib and Trametinib was given to a 42-year-old male patient with recurrent ameloblastoma of the right mandible with a BRAF V600E mutation for 18 months. The patient manifested an excellent response to the therapy with remarkable reduction in tumor size from 72.6 mm to 55.9 mm. Histopathologically, the tumor underwent significant degenerative changes with only a few sparse vital residuals revealing 0 % Ki67 proliferative index. Conclusions: Neoadjuvant therapy with BRAF-inhibitors or BRAF-MEK-inhibitors is an effective means to reduce the size of mandibulary ameloblastomas. We propose the consideration of neoadjuvant therapy in future treatment modalities to minimize post-surgical morbidity and facial deformations

Elevated Interleukin‐17A expression in amlodipine‐induced gingival overgrowth

WOS:000563549300001PubMed: 32173874Background and objectives Amlodipine, a calcium channel blocker derivative, is frequently used by patients with high blood pressure. Studies reported that it can induce gingival overgrowth. However, the underlying mechanism is not fully described yet. Interleukin-17A (IL-17A) is known as a proinflammatory cytokine, but current studies indicate that it has a role in fibrotic disorders and epithelial-mesenchymal transition (EMT). The aim of this study was to figure out the possible role of IL-17A in amlodipine-induced gingival overgrowth. Materials and methods Twenty-nine (29) individuals participated in the study, and they were assigned into 3 groups based on medical status and clinical periodontal examination; 9 patients with amlodipine-induced gingival overgrowth, 11 patients with inflammatory gingival overgrowth, and 9 healthy individuals as a control group. Clinical periodontal parameters including plaque index (PI), gingival index (GI), and gingival overgrowth index (GOI) were recorded. Blood and gingival crevicular fluid (GCF) samples were obtained. Gingival tissues were taken by appropriate periodontal surgery following initial periodontal therapy. To detect IL-17A on tissue samples, immunohistochemistry (IHC) was performed. Quantitative analysis was done, and the expression level of IL-17A was given as the percent positively stained cells. Enzyme-linked immunosorbent assay (ELISA) kits were used to analyze IL-17A in serum and GCF samples. Results All recorded clinical parameters were significantly higher in gingival overgrowth groups compared with control. Evaluation of inflammation on tissue sections did not show any significant change within the groups. Immunohistochemistry findings showed that IL-17A expression was increased in amlodipine samples (81.90%) compared with control samples (42.35%) (P < .001). There was an increase in the inflammatory group (66.08%) which is significantly less than the amlodipine group (P < .05). IL-17A levels in serum and GCF samples were not different within the study groups. Conclusion In this study, elevated IL-17A expression regardless of inflammation shows that amlodipine might cause an increase of IL-17A in gingival tissues. This increase might induce fibrotic changes and EMT in gingival overgrowth tissues. The association of IL-17A with fibrosis and EMT in gingival tissues requires further investigation.Scientific and Technological Research Council of Turkey (TUBITAK), Ankara, TurkeyTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK)The Scientific and Technological Research Council of Turkey (TUBITAK), Ankara, Turkey