Objective:The aim of this study was to determine alterations in microhardness of crown dentin and enamel, after 2 and 12-month storage in de-ionized water, 0.2% glutaraldehyde, Hanks’ Balanced Salt Solution (HBSS), 0.1% sodium hypochlorite (NaOCl) or 0.1% thymol.Materials and Methods:Freshly extracted, nonsterile 60 intact human premolars were distributed to five groups. Six teeth from each group were evaluated after two, and other six teeth were evaluated after 12 months storage. After grinding and polishing of teeth, Vickers hardness was evaluated with making indentations on enamel and dentin, using a pyramid diamond indenter tip exerting 100 g load for 15 s.Results:After 2 months storage in solutions, range of the hardness values (HV) of enamel and dentin were in between 315–357 and 64–67, respectively. However, 12 months storage of the teeth resulted in a statistically significant decrease in microhardness when compared to microhardness of teeth stored for 2 months (P = 0.001). Although the differences were not significant regarding solutions, all solutions decreased the microhardness both in enamel and dentin (P > 0.05). However, decrease in microhardness was relatively less in de-ionized water and thymol solutions while glutaraldehyde decreased microhardness the most: 63% for enamel and 53% for dentin.Conclusions:Microhardness of enamel and dentin was in an acceptable range when teeth were stored for 2 months in de-ionized water, glutaraldehyde, HBSS, NaOCl or in thymol; thus, teeth kept up to 2 months in these solutions can be used for mechanical in vitro tests. However, 12 months storage significantly decreased the microhardness of enamel and dentin.
Introduction. Sarcoidosis is a chronic granulomatous disease, which can involve different organs and systems. Coexistence of sarcoidosis and spondyloarthritis has been reported in numerous case reports. Purpose. To determine the prevalence of sacroiliitis and spondyloarthritis in patients previously diagnosed with sarcoidosis and to investigate any possible relation with clinical findings. Materials and Methods. Forty-two patients with sarcoidosis were enrolled in the study. Any signs and symptoms in regard to spondyloarthritis (i.e., existence of inflammatory back pain, gluteal pain, uveitis, enthesitis, dactylitis, inflammatory bowel disease, and psoriasis) were questioned in detail and biochemical tests were evaluated. Sacroiliac joint imaging and lateral heel imaging were performed in all patients. Results. Sacroiliitis was found in 6 of the 42 (14.3%) sarcoidosis patients and all of these patients were female. Common features of the disease in these six patients were inflammatory back pain as the major clinical complaint, stage 2 sacroiliitis as revealed by radiological staging, and the negativity of HLA B-27 test. These six patients with sacroiliitis were diagnosed with spondyloarthritis according to the criteria of ASAS and of ESSG. Conclusion. We found spondyloarthritis in patients with sarcoidosis at a higher percentage rate than in the general population (1–1.9%). Controlled trials involving large series of patients are required for the confirmation of the data.
Calprotectin is one of the major antimicrobial S100 leucocyte proteins. Serum calprotectin levels are associated with certain inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus and inflammatory bowel disease. The aim of this study was to investigate serum and fecal calprotectin levels in patients with ankylosing spondylitis (AS) and show their potential relations to the clinical findings of the disease. Fifty-one patients fulfilling the New York criteria of AS and 43 healthy age-and gender-matched volunteers were included in the study. Physical and locomotor system examinations were performed and history data were obtained for all patients. Disease activity parameters were assessed together with anthropometric parameters. Routine laboratory examinations and genetic testing (HLA-B27) were performed. Serum calprotectin levels and fecal calprotectin levels were measured by an enzyme-linked immunosorbent assay. The mean age of the patients was 41.5 years, the mean duration of the disease was 8.6 years, and the delay in diagnosis was 4.2 years. Serum calprotectin levels were similar in both AS patients and in the control group (p=0.233). Serum calprotectin level was correlated with Bath AS disease activity index (BASDAI) and Bath AS functional index (BASFI) (p=0.001, p=0.002, respectively). A higher level of fecal calprotectin was detected in AS patients when compared with the control group. A statistically significant correlation between fecal calprotectin level and BASDAI, BASFI, C-reactive protein and Erythrocyte sedimentation rate were detected (p=0.002, p=0.005, p=0.001, p=0.002, respectively). The results indicated that fecal calprotectin levels were associated with AS disease findings and activity parameters. Calprotectin is a vital disease activity biomarker for AS and may have an important role in the pathogenesis of the disease. Multi-centered prospective studies are needed in order to provide further insight.
Main finding of our study was the presence of increased oxidative DNA damage in lean normoglycemic offspring of Type 2 diabetic patients. There is a need for further clinical studies in order to explain whether oxidative stress is present in genetically predisposed subjects and induces the insulin resistance.
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