The role of Toll-like receptor 2 and 4 in gingival tissues of chronic periodontitis subjects with type 2 diabetes.

BACKGROUND AND OBJECTIVE: Diabetes is one important risk factor of chronic periodontitis. However, the roles of toll-like receptor (TLR) 2 and TLR4, which are implicated in the inflammatory process in both chronic periodontitis and diabetes, have not been studied. This study aimed to determine whether TLR2 and TLR4 might be involved in the relationship between chronic periodontitis and diabetes by examining TLR2 and TLR4 expression in gingival tissues from subjects with chronic periodontitis without diabetes (CP) and with diabetes (CP+DM) and from periodontally healthy subjects without diabetes (PH) and with diabetes (PH+DM). MATERIAL AND METHODS: Gingival tissues were collected from 23 CP subjects, 21 CP+DM subjects, 22 PH subjects and 20 PH+DM subjects. The expression of TLR2 and TLR4 in gingival tissues was determined using an immunohistochemical method. In gingival epithelium, staining patterns and intensity levels of TLR2 and TLR4 expression were studied. In connective tissues, the percentages of TLR2- and TLR4-positive cells were calculated. The intensity levels and the percentages of positive cells were statistically analyzed. RESULTS: Chronic periodontitis or diabetes showed no significant effect on TLR2 expression in the oral epithelium. However, diabetes increased the expression of TLR2 in sulcular epithelium and changed the pattern of TLR2 expression in gingival epithelium. Chronic periodontitis decreased the expression of TLR4 in gingival epithelium. In connective tissue under sulcular epithelium, CP+DM subjects showed statistically significant higher percentages of TLR2- and TLR4-positive cells compared with PH and PH+DM subjects. CONCLUSION: Our results suggest that hyperglycemia and chronic periodontitis had effects on TLR2 and TLR4 expression in gingival tissue. The differences in TLR2 and TLR4 expression could contribute to a greater inflammatory response, leading to periodontal disease initiation and progression.

Serum transforming growth factor-beta1 and epidermal growth factor in biliary atresia.

BACKGROUND AND AIM: Biliary atresia (BA) is a serious liver disease in children. Since transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor (EGF) are involved in the hepatic reparative process, our objective was to investigate whether serum TGF-beta1 and serum EGF levels were associated with therapeutic outcomes in BA. METHODS: Serum levels of TGF-beta1 and EGF were determined with the ELISA method in 67 postoperative BA patients with a median age of 7 years and in 10 age-comparable healthy children. The BA patients were then divided into two groups depending on their therapeutic outcome: good outcome (jaundice-free) and poor outcome (persistent jaundice). Clinical data, serum TGF-beta1 and serum EGF levels were compared between the two groups of BA patients. Correlation analysis of serum TGF-beta1 with serum EGF was carried out. Data are expressed as mean +/- SD. RESULTS: Serum TGF-beta1 levels of BA patients were higher than those of controls (86.6 +/- 15.7 vs. 75.7 +/- 8.8 ng/ml, p = 0.0362). However, there was no difference in serum EGF between BA patients and controls (133.1 +/- 66.6 vs. 125.4 +/- 88.9 pg/ml, p = 0.744). Further subgroup analysis showed that patients with good outcomes (n = 40) had higher serum TGF-beta1 and serum EGF levels than patients with poor outcomes (TGF-beta1: 91.2 +/- 16.5 vs. 79.6 +/- 11.7 ng/ml, p = 0.002; EGF: 148.5 +/- 65.0 vs. 110.3 +/- 63.4 pg/ml, p = 0.02). In addition, serum TGF-beta1 was positively correlated with serum EGF (Pearson's r = 0.3418, p = 0.0046). CONCLUSION: Elevated serum TGF-beta1 and serum EGF levels were associated with a good outcome in BA patients. There was a positive correlation between serum TGF-beta1 and serum EGF. This suggests that the resultant TGF-beta1 and EGF pathways may be involved in the pathophysiological process in postoperative BA.

alpha v beta 6 Integrin upregulates matrix metalloproteinase 9 and promotes migration of normal oral keratinocytes.

The integrin alpha v beta 6 is a fibronectin receptor that is undetectable on normal keratinocytes in situ, but is increased significantly in wound healing and in culture-established keratinocytes, suggesting that it may promote changes associated with cell motility. Using normal human oral keratinocytes we have shown that cultured cells express relatively high levels of alpha v beta 6 and this integrin has a functional role in both cell adhesion and migration towards fibronectin. We provide experimental evidence that the increased expression of alpha v beta 6 by normal human oral keratinocytes results in coordinate changes, which promote a more migratory phenotype. Thus increased expression of alpha v beta 6 results in a fibronectin-dependent increase in pro-matrix metalloproteinase 9, matrix metalloproteinase 9 activity increases normal human oral keratinocyte migration, and this may be further dependent on plasmin activation. The results suggest a key role for alpha v beta 6 in these processes and indicate a coordinated link between alpha v beta 6 expression and upregulation of matrix metalloproteinase 9. It appears that alpha v beta 6 may function in normal human oral keratinocyte migration through matrix-metalloproteinase-9-dependent and -independent mechanisms.

Elevated serum IL-18 and interferon-gamma in medium-term survivors of biliary atresia.

INTRODUCTION: Biliary atresia (BA) is a fatal disease in children. Its main pathological feature is progressive immune-mediated cholangiopathy. Interleukin (IL)-12, IL-18, and interferon-gamma (IFN-gamma) play important roles in various immunological diseases. THE OBJECTIVE: was to investigate whether these serum markers were associated with clinical outcome in BA. METHODS: Serum levels of IL-12, IL-18, and IFN-gamma were determined using enzyme-linked immunosorbent assay from 46 BA patients (median age of 9 years) and 19 normal controls. The BA patients were then categorized into three groups according to their outcome: jaundice-free (29 cases), mild to moderate jaundice (10 cases), and marked jaundice (7 cases). The comparisons of serum IL-12, IL-18, and IFN-gamma levels among groups of the patients were performed using one-way analysis of variance with post-hoc tests. Data are expressed as mean + standard deviation. RESULTS: Serum IL-18 and IFN-gamma in BA patients were higher than the normal controls (IL-18: 113.3 + 82.6 vs. 80.5 + 9.9 pg/mL, p = 0.011 and IFN-gamma: 41.7 + 5.1 vs. 38.0 + 1.9 pg/mL, p < 0.001). There was no difference in serum IL-12 between BA and controls. Further analysis demonstrated that, in BA patients, only serum IL-18 levels significantly increased with the degree of jaundice (test for trend, p = 0.004). CONCLUSIONS: Serum IL-18 and IFN-gamma levels were increased in medium-term survivors of BA. The elevated serum IL-18 in BA patients was associated with worse clinical outcome. These results suggest that IL-18 and IFN-gamma play roles in the pathophysiology of BA. Additionally, IL-18 is likely to be involved in the disease progression.

Antiemetic effect of ondansetron 0.2 mg mL-1 in PCA morphine solution.

BACKGROUND AND OBJECTIVES: To study the effect of 0.2 mg mL-1 of ondansetron added to morphine patient-controlled analgesia solution after a 4 mg loading dose on the incidence and severity of postoperative nausea and vomiting. METHODS: One hundred and sixty patients scheduled for elective surgery, between 18 and 65 yr old, were studied. Patients who smoked, received antiemetics and hormonal therapy, had a history of motion sickness or gastrointestinal disease, a body mass index >35 or menstruation at the time of the study were excluded. Patients were assigned to the ondansetron and control groups by block randomization. At the end of anaesthesia, all patients received 4 mg of ondansetron intravenously and the same patient-controlled analgesia regimen of morphine. The ondansetron group (n = 80) received 0.2 mg of ondansetron per 1 mg of morphine. The nausea score, vomiting score and the requested ondansetron dose were evaluated at 1, 2, 6, 12 and 24 h. Patient-satisfaction for nausea/vomiting was recorded at the end of the study. RESULTS: Patient characteristics and cumulative morphine consumption were similar but ondansetron group had higher pain scores (P = 0.006). The ondansetron group had a lower nausea and vomiting scores, and more patients were free from nausea and vomiting than the control group (41 vs. 26, respectively, P = 0.025). The ondansetron group had fewer cumulative ondansetron doses than the control group and better patient satisfaction than the control group (P < 0.05). CONCLUSION(S): Ondansetron 4 mg plus 0.2 mg mL-1 given with PCA morphine can reduce nausea and vomiting thus improving patient satisfaction.

Expression of basement membrane components in odontogenic cysts.

OBJECTIVE: To compare the expression of basement membrane components (BMCs), including laminins 1 and 5, collagen type IV, and fibronectin in odontogenic keratocysts (OKCs) with dentigerous cysts (DCs) and radicular cysts (RCs). MATERIALS AND METHODS: Basement membrane components were analysed in 20 OKCs, 20 DCs and 20 RCs using an immunohistochemical technique. RESULTS: Odontogenic keratocysts, DCs and RCs showed positive reaction to all BMCs studied, with different distributions and intensity. OKCs showed continuous linear deposits for laminins 1 and 5 but two staining patterns (continuous and discontinuous) for collagen type IV and fibronectin. DCs exhibited continuous linear deposits for laminins 1 and 5 and collagen type IV but a discontinuous linear deposit for fibronectin. RCs displayed similar results to DCs for laminin 1, collagen type IV and fibronectin. Laminin 5 in RCs had two staining patterns. Constant results in all cysts were strong intensity for laminin 1 and moderate intensity for laminin 5. CONCLUSIONS: Substantial differences in the expression of BMCs among studied cysts were not observed, suggesting that the separation of the epithelial lining in OKCs is not associated with the existence of these proteins.