BackgroundPeriodontal disease is thought to arise from the interaction of various factors, including the susceptibility of the host, the presence of pathogenic organisms, and the absence of beneficial species. The genetic factors may play a significant role in the risk of periodontal diseases. Cytokines initiate, mediate and control immune and inflammatory responses. The aim of this study is to compare genotypes and soluble protein of pro and anti-inflammatory cytokines (IL-1α, IL-1β, IL-6, IFN-γ, IL-10, TNF-α and IL-4) in subjects with or free of chronic periodontitis.MethodsA total of 1,290 Chinese subjects were recruited to this clinical trial: 850 periodontally healthy controls and 440 periodontal patients. All subjects were free of systemic diseases. Oral examinations were performed, and the following parameters were recorded for each subject: supragingival/subgingival calculus, gingival recession, bleeding on probing (BOP), probing depth (PD), clinical attachment loss (CAL), gingival recession and tooth mobility. The peripheral blood samples were collected for genetic and enzyme linked immunosorbent assay (ELISA) analysis. Restriction enzymes were used for digestion of amplified fragments of IL-1α, IL-1β, IL-6, IFN-γ, IL-10, TNF-α and IL-4.ResultsThe protein expressions of patient and control samples for IL-1α, IL-1β, IL-6, TNF-α, IFN-γ, IL-10, and IL-4 measured by ELISA confirmed a statistically significant difference (p < 0.001). The digestion of fragments of various genes showed that the pro-inflammatory cytokines IL-1α and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 demonstrated a correlation with chronic inflammation in patients (X2: p < 0.001). The remaining genes investigated in patients and healthy subjects (IL-1β, IL-6, IFN-γ and IL-10) did not show any significant difference.ConclusionsThe cytokine gene polymorphisms may be used as a marker for periodontitis susceptibility, clinical behaviour and severity. This detection offers early diagnosis and induction of prophylaxis to other family members against disease progression.

BackgroundFaecal calprotectin (FC), a cytosolic protein released by neutrophils (S100 family) in response to inflammation, is a simple, non-invasive test that can be used to differentiate irritable bowel syndrome (IBS) with inflammatory bowel disease (IBD), where there can be considerable symptom overlap.Aims and methodsThe aims of the study were (1) to be able to predict the ability of FC to exclude IBD and determine cut-offs when in remission, (2) to investigate the effects of time and temperature on stability of FC and (3) compare three ELISA kits to measure FC: Buhlmann, PhiCal v1 and PhiCal v2. A total of 311 patients with altered bowel habit were tested for FC; 144 with IBS, 148 with IBD and 19 with other organic causes.ResultsSensitivity and specificity of FC (with PhiCal v2 kit) to distinguish between functional disorder (IBS) and IBD using cut-off 50 μg/g were 88% and 78%, respectively, with a negative predictive value of 87%. Area under the receiver operating curve was 0.84 (CI 0.78 to 0.90). For those with IBD, FC values below 250 μg/g corresponded with remission of disease with a sensitivity and specificity of 90% and 76%, respectively. Area under the receiver operating curve was 0.93 (CI 0.89 to 0.97). FC was stable once extracted and frozen for up to 2.5 months. Pearson correlation was good between Buhlmann assay and PhiCal v2 (r2 = 0.95).ConclusionsFC has up to 87% negative predictive value to exclude IBD, and cut-offs less than 250 μg/g had 90% sensitivity to determine remission in IBD. Once frozen, FC is stable and the ELISA monoclonal plates were broadly comparable.

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BackgroundDNA methylation of certain genes frequently occurs in neoplastic cells. Although the cause remains unknown, many genes have been identified with such atypical methylation in neoplastic cells. The hypermethylation of E-Cadherin and Cyclooxygenase 2 (COX-2) in chronic inflammation such as chronic periodontitis may demonstrate mild lesion/mutation epigenetic level. This study compares the hypermethylation status of E-Cadherin and COX-2 genes which are often found in breast cancer patients with that in chronic periodontitis.MethodsTotal DNA was extracted from the blood samples of 108 systemically healthy non-periodontitis subjects, and the gingival tissues and blood samples of 110 chronic periodontitis patient as well as neoplastic tissues of 106 breast cancer patients. Methylation-specific PCR for E-Cadherin and COX-2 was performed on these samples and the PCR products were analyzed on 2% agarose gel.ResultsHypermethylation of E-Cadherin and COX-2 was observed in 38% and 35% of the breast cancer samples, respectively. In chronic periodontitis patients the detection rate was 25% and 19% respectively, and none was found in the systemically healthy non-periodontitis control subjects. The hypermethylation status was shown to be correlated among the three groups with statistical significance (p < 0.0001). The methylation of CpG islands in E-Cadherin and COX-2 genes in periodontitis patients occurs more frequently in periodontitis patients than in the control subjects, but occurs less frequently than in the breast cancer patients.ConclusionsThis set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis. The epigenetic changes presented in chronic inflammation patients might demonstrate an irreversible destruction in the tissues or organs similar to the effects of cancer. Chronic periodontitis to some extent might be associated with DNA hypermethylation which is related to cancer risk factors.

A prospective study was conducted to validate the retrospective finding that adolescents (11 to 15 years old) with skull fractures were prone to develop acute traumatic intracranial hematoma (ICH). Over a 4-year period, 1178 consecutive adolescents attended the emergency room directly, of whom 760 were discharged well and 418 were admitted. All underwent skull x-ray studies. Immediate computerized tomography (CT) scans were performed in patients with Glasgow Coma Scale (GCS) scores of less than 15, in those with radiological and/or clinical evidence of skull fracture, and whenever clinically indicated. Of the 418 admitted patients, only 26 had skull fractures; 13 of these developed ICH. Four patients without skull fracture developed diffuse brain swelling. The remaining 401 patients were discharged after observation periods of up to 48 hours. Of the 13 patients with ICH, 10 had admission GCS scores of 15; however, four deteriorated rapidly and required urgent operation, and four remained stable but were operated on due to their large ICH. Two required conservative treatment only and both made good recovery. Three patients were in coma (GCS score less than or equal to 8) on admission. One patient had an epidural hematoma and made good recovery after surgery. Two developed delayed ICH after operations for associated systemic injuries despite initial CT showing diffuse brain swelling only, and both died despite evacuation of the ICH. Multivariate analysis showed that skull fracture was the only independent significant risk factor in predicting ICH in adolescents (sensitivity of 100% and specificity of 97%). A routine skull x-ray study is therefore mandatory in all head-injured adolescents and, if a skull fracture is detected, immediate CT may be performed for early detection of ICH.

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Cytokine levels in GCF and saliva correlated well with clinical parameters and AP. Measurements of cytokines in saliva may be regarded as a noninvasive and quick method for monitoring periodontal disease activity.