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    Boric acid inhibits alveolar bone loss in rats by affecting RANKL and osteoprotegerin expression
    (Wiley, 2014) Saglam, M.; Hatipoglu, M.; Koseoglu, S.; Esen, H. H.; Kelebek, S.
    Background and Objective: The goal of the present study was to evaluate the effects of systemic boric acid on the levels of expression of RANKL and osteoprotegerin (OPG) and on histopathologic and histometric changes in a rat periodontitis model. Material and Methods: Twenty-four Wistar rats were divided into three groups of eight animals each: nonligated (NL); ligature only (LO); and ligature plus treatment with boric acid (BA) (3 mg/kg per day for 11 d). A 4/0 silk suture was placed in a subgingival position around the mandibular right first molars; after 11 d the rats were killed, and alveolar bone loss in the first molars was histometrically determined. Periodontal tissues were examined histopathologically to assess the differences among the study groups. RANKL and OPG were detected immunohistochemically. Results: Alveolar bone loss was significantly higher in the LO group than in the BA and NL groups (p < 0.05). The number of inflammatory infiltrate and osteoclasts in the LO group was significantly higher than that in the NL and BA groups (p < 0.05). The numbers of osteoblasts in LO and BA groups were significantly higher compared with NL group (p < 0.05). There were significantly more RANKL-positive cells in the LO group than in the BA and NL groups (p < 0.05). There was a higher number of OPG-positive cells in the BA group than in the LO and NL groups (p < 0.05). Conclusion: The present study shows that systemic administration of boric acid may reduce alveolar bone loss by affecting the RANKL/OPG balance in periodontal disease in rats.
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    Could immune cells be associated with nephropathy in Fabry disease patients?
    (Springer, 2023) Turkmen, K.; Karaselek, M. A.; Celik, S. C.; Esen, H. H.; Ozer, H.; Baloglu, I.; Ozturk, Y.
    BackgroundIn Fabry Disease (FD), although the primary factor initiating kidney damage is glycosphingolipid accumulation, secondary conditions such as increased inflammation and fibrosis may cause this damage to progress. These processes may be induced by immune cells. Therefore, we aimed to investigate the peripheral lymphocyte subgroup analysis of the patients with FD and compare these results with healthy individuals. In addition, we performed T, B, NK, and plasma cell analyses in kidney biopsy materials and compared these kidney biopsy results with the biopsy results of patients whose kidney functions were impaired after 4 years of regular ERT.Materials and methods18 FD and 16 healthy individuals were included in the study. T-B lymphocyte and NK-cell populations were determined. We performed kidney biopsies (KBx) on 13 patients with FD prior to ERT. Of these, 4 patients had rebiopsy after 4 years of regular ERT. Immunohistochemical staining was performed to define immune cell infiltration.ResultsThere was no statistically significant difference in terms of total, helper and cytotoxic T-lymphocyte and CD3(-)CD16(+)CD56(+) natural killer (NK)-cell count (p = 0.20; p = 0.12; p = 0.76; p = 0.75, respectively).According to KBx findings prior to ERT, all patients had interstitial fibrosis (IF), podocyte vacuoles (PV), and podocyte inclusion (PI), CD3, CD4, CD8, CD16, and CD56 positivity at different levels. None of the patients had CD19, CD20, and CD138 positivity at the first biopsies. When we compared the first and the second KBx results of the two progressors, we also demonstrated that CD3(+)4(+)T-cells infiltration remained the same, whereas CD8(+)T cells, CD16(+) and 56(+)NK-cells infiltration were significantly decreased. In contrast, CD20(+)B cells and CD138(+)plasma cell infiltration were significantly increased despite 4 years of ERT (15 fold and sixfold, respectively). The CD20(+)B and CD138(+) plasma cells and IF were positively correlated with proteinuria.ConclusionsThe progression of FD nephropathy and proteinuria is increased despite a long-term ERT. Immune cells, primarily B and plasma cells, might cause these unwanted consequences.
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    Interleukin-33 could play an important role in the pathogenesis of periodontitis
    (Wiley, 2015) Koseoglu, S.; Hatipoglu, M.; Saglam, M.; Enhos, S.; Esen, H. H.
    Background and ObjectiveInterleukin-33 (IL-33) controls T-helper type 2 (Th2) cytokines and the development of mast cells. This study aimed to investigate the expression of IL-33 and its association with RANKL and osteoprotegerin (OPG) in periodontal health and experimental periodontitis. Material and MethodsEighteen Wistar rats were assigned to two study groups of nine animals each: ligature only (LO) and nonligated (NL). Silk sutures were placed subgingivally, surrounding the right lower first molars. The animals were killed on day 11 after ligature placement, and the alveolar bone loss at the first molars was determined histometrically. Periodontal tissues were examined histopathologically to evaluate the differences between the groups. The expression of IL-33, RANKL and OPG was detected immunohistochemically. ResultsThe LO group showed significantly greater alveolar bone loss compared with the NL group (p<0.05). The numbers of osteoclasts, osteoblasts and inflammatory cells were significantly higher in the LO group compared with the NL group (p<0.05). Osteoblastic activity was significantly lower in the LO group than in the NL group (p<0.05). There was significantly higher expression of IL-33 and RANKL and a greater number of OPG-positive cells in the LO group (p<0.05). IL-33 expression showed a positive correlation with RANKL expression and with the number of mast cells (p<0.05). ConclusionThe experimental periodontitis group exhibited increased expression of IL-33 and RANKL compared with the healthy group. Additionally, there was a positive correlation between these expressions. According to these results, IL-33 could be associated with the pathogenesis of periodontal disease.
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    Prevalence of sicca symptoms and Sjogren's syndrome in coeliac patients and healthy controls
    (Taylor & Francis Ltd, 2020) Ayar, K.; Tunc, R.; Pekel, H.; Esen, H. H.; Kucuk, A.; Cifci, S.; Ataseven, H.
    Objective: There has been no previous study comparing the frequency of sicca symptoms and Sjogren's syndrome (SS) in coeliac patients (CPs) and healthy controls (HCs) using a tight screening method. The aim of this study was to compare the frequency of sicca symptoms and SS in HCs and CPs. Method: The study included 80 CPs and 100 HCs. This study was designed as a case-control study with four phases. The frequency of SS in CPs and HCs was defined according to the 2002 American-European Consensus Group (AECG) and 2012 American College of Rheumatology (ACR) classification criteria. The frequency of sicca symptoms and SS was compared between CPs and HCs. Results: Ocular and oral symptoms occurred in 22% and 26% of CPs, respectively, compared to 13% and 10% of HCs, respectively. Proportions with oral symptoms were statistically significantly different between CPs and HCs (p = 0.005), whereas there was no significant difference for ocular symptoms (p = 0.113). According to ACR and AECG criteria, the prevalence of SS was 3.8% and 5.0% in CPs and 3.0% and 2.0% in HCs, respectively. Conclusion: Although oral symptoms were more frequent in CPs than in HCs, the frequency of SS was not different between the groups. The increased frequency of oral symptoms may be related to reasons other than autoimmunity.