Hyperlipidaemia and hyperglycaemia are major risk factors for cardiovascular disease. In recent years, some evidence has been presented that periodontal disease is associated with an increased risk of cardiovascular disease. To further elucidate this association, we have studied standard blood chemistry variables known as risk markers for cardiovascular disease in periodontally diseased and healthy subjects. We have measured levels of plasma lipids and fasting blood glucose in 39 subjects with moderate periodontal disease (age 50-60 years) and compared the results with those obtained in 40 age- and sex-matched controls. Both groups were systemically healthy according to their medical history. Total cholesterol, low density lipoprotein cholesterol and triglycerides were significantly higher in periodontally diseased subjects by about 8% (p<0.03), 13% (p<0.003) and 39% (p<0.001), respectively, when compared to controls. Although subjects with diabetes were excluded from the study, we found significantly higher blood glucose levels in the patient than in the control group (85 +/- 25 versus 73 +/- 17 mg/dl; p<0.02). There was also a significantly higher frequency of pathological plasma lipid profiles in the patient than in the control group. The results indicate that hyperlipaemia and pre-diabetes may be associated with periodontal disease in systemically healthy subjects. These data do not allow us to decide, whether periodontal disease causes an increase in hyperlipaemia and in a prediabetic state or whether periodontal disease and cardiovascular disease share hyperlipidaemia and the prediabetic state as common risk factors.

Chronic parasympathetic activation sensitizes the myocardium to cAMP-induced arrhythmia. These changes may be due to quantitative alterations in functional Gi alpha.

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[¹²⁵I]-cyanopindolol (ICYP) was used in a binding assay to compare the number and affinity of β₂-adrenoceptor binding sites on circulating polymorphonuclear leukocytes (PMN) of 21 children with atopic dermatitis (AD) and 23 age-matched controls. We found no correlation between the β₂-adrenoceptor density and the age of the children in either collective. Furthermore, the number and affinity of β₂-adrenoceptor binding sites on PMN was neither influenced by sex nor severity of disease, serum IgE level or percentage of eosinophils in the differential blood count. There was a tendency towards a lower number of β₂-adrenoceptors in AD subjects (1,429 ± 587 receptors/PMN) compared to controls (1,753 ± 596 receptors/PMN), but this difference was statistically not significant.

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