Utility of point-of-care vs reference laboratory testing for the evaluation of glucose levels.

AIMS: To assess the level of agreement between point-of-care and laboratory reference glucose values in defining glycaemic status. METHODS: We analysed 1292 overweight/obese, non-institutionalized participants, aged 40-65 years, in the San Juan Overweight Adults Longitudinal Study. Fasting venous blood glucose was determined using a point-of-care Bayer Contour Blood Glucose Meter and by Vitros System 250 instrument (laboratory). American Diabetes Association thresholds were used to classify participants into normoglycaemia (< 5.6 mmol/l), prediabetes (5.6 to 6.9 mmol/l), or diabetes groups (≥ 7 mmol/l). RESULTS: Bland-Altman plot analysis showed a slope of 0.04 (P=0.002) for the regression between the mean difference and the average of the two methods. The slopes were significantly different from zero among people with normoglycaemia (ß=-0.57, P<0.001), and prediabetes (ß=-0.75, P<0.001) but not among people with diabetes (ß=-0.02, P=0.68). When the prediabetes and diabetes groups were merged into one group, the slope was 0.01, and the glucose values remained similar using the two methods (P=0.76). CONCLUSION: Point-of-care blood glucose measurement may be useful to screen people with diabetes, and to assess glucose among individuals with diabetes where blood can be drawn, but laboratory tests are unavailable or untimely.

Gene expression dynamics during diabetic periodontitis.

Diabetes impairs the resolution of periodontal inflammation. We explored pathways altered by inflammation in the diabetic periodontium by using ligatures to induce periodontitis in type-2 diabetic Goto-Kakizaki rats. Ligatures were removed after 7 days, and rats were then treated with TNF inhibitor (pegsunercept) or vehicle alone and euthanized 4 days later. RNA was extracted from periodontal tissue, examined by mRNA profiling, and further analyzed by functional criteria. We found that 1,754 genes were significantly up-regulated and 1,243 were down-regulated by pegsunercept (p < 0.05). Functional analysis revealed up-regulation of neuron-associated and retina-associated gene clusters as well as those related to cell activity and signaling. Others were down-regulated by TNF inhibition and included genes associated with host defense, apoptosis, cell signaling and activity, and coagulation/hemostasis/complement. For selected genes, findings with microarray and rt-PCR agreed. PPAR-α was investigated further by immunohistochemistry due to its anti-inflammatory function and was found to be up-regulated in the gingiva during the resolution of periodontal inflammation and suppressed by diabetes. The results indicate that diabetes-enhanced inflammation both up- and down-regulates genes involved in cellular activity and cell signaling, while it predominantly up-regulates genes involved in the host response, apoptosis, and coagulation/homeostasis/complement and down-regulates mRNA levels of neuron, retina, and energy/metabolism-associated genes.

Association between metabolic syndrome and periodontal disease.

BACKGROUND: Metabolic syndrome has been suggested as a potential risk factor for periodontal disease. Data based on NHANES III, with 7431 subjects aged 20 years or older, were analysed to confirm the association between metabolic syndrome and periodontal disease, and identify which components of metabolic syndrome might play a role in this association. METHODS: Clinical criteria for metabolic syndrome included: (1) abdominal obesity; (2) increased triglycerides; (3) decreased HDL cholesterol; (4) hypertension or current use of hypertension medication; and (5) high fasting plasma glucose. Periodontal disease was evaluated by probing pocket depth (PPD) and was defined as mean PPD≥2.5 mm. RESULTS: Women with two or more metabolic components had significantly increased odds of having periodontal disease as compared to those with no component [(two components, OR=5.6 (95% CI: 2.2-14.4); three or more, OR=4.7 (2.0-11.2)]. Using the definition of metabolic syndrome as having three to five metabolic components (reference group with <3 components), the adjusted odds ratios were 1.0 (0.7-1.6) for men and 2.1 (1.2-3.7) for women. Abdominal obesity was the largest contributory factor in both genders. CONCLUSIONS: While the association between metabolic syndrome and periodontal disease was particularly significant for women, abdominal obesity appeared to be the contributing metabolic factor for both genders.

Levels of serum interleukin (IL)-6 and gingival crevicular fluid of IL-1beta and prostaglandin E(2) among non-smoking subjects with gingivitis and type 2 diabetes.

BACKGROUND: The goal of this study was to assess whether non-smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non-smoking patients without diabetes. METHODS: We used a cross-sectional database consisting of 725 self-reported lifelong non-smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)-1beta and prostaglandin E(2) (PGE(2)) and serum levels of IL-6 were measured using enzyme-linked immunosorbent assay. No participant had probing depth >3 mm. Participants with bleeding on probing (BOP) in <10% of sites were classified as healthy, whereas those with BOP in >or=10% of sites were defined as having biofilm-gingival interface (BGI) gingivitis. RESULTS: Approximately 53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2 diabetes, respectively. The mean age-adjusted level of GCF IL-1beta was significantly elevated in the diabetic group compared to the non-diabetic group (P = 0.048), but serum IL-6 (P = 0.14) and GCF PGE(2) were not (P = 0.98). The mean GCF IL-1beta and PGE(2) levels were significantly elevated in subjects with BGI gingivitis (136.2 +/- 112.9 ng/ml and 277.2 +/- 187.2 ng/ml, respectively) compared to subjects with gingival health (95.9 +/- 82.9 ng/ml and 205.7 +/- 149.6 ng/ml, respectively), regardless of diabetic status (P <0.001 for both). However, serum IL-6 was elevated in subjects with BGI gingivitis compared to subjects with gingival health only among subjects with diabetes (2.9 +/- 3.2 pg/ml versus 1.5 +/- 1.4 pg/ml; P = 0.008). With the exception of serum IL-6 in subjects without diabetes, an increase in the levels of proinflammatory mediators was associated with increased odds of having BGI gingivitis. The associations were stronger in the diabetic group. CONCLUSIONS: Type 2 diabetes may increase the host inflammatory response to oral biofilm, which, in turn, may exacerbate preconditions associated with gingivitis in susceptible individuals. Furthermore, systemic inflammation, as demonstrated by the increased level of serum IL-6, is associated with BGI gingivitis among non-smoking patients with diabetes.