[Diabetic disease and periodontal disease. Diabetes and periodontopathy]. / Malattia diabetica e malattia parodontale. Diabete e parodontopatia.

Diabetic patients have been reported to be more susceptible to gingivitis and periodontitis than healthy subjects, and these diseases are commonly considered to be oral complications of diabetes. The influence of diabetes on the onset and development of periodontal disease has been studied for many years but clear agreement is still lacking on the nature of the relationship between diabetes and these oral disorders. In fact recent observational epidemiological studies suggest that diabetes should not be considered as the direct cause of periodontal disease but rather as a systemic promoting factor, able to produce conditions suitable for local agents producing gingivitis and periodontitis. The overriding oral problem in diabetes is infection, like with any of the dermal lesions in the diabetic. In fact periodontal disease is caused by specific bacteria (Bacteroides Gingivalis, Actinobacillus actinomycetemcomitans) growing in the periodontal pocket so that the bacterial products such as histolytic enzymes, endotoxins or exotoxins may exert a direct effect. Particular attention has been directed to the neutrophils and to their role in antibacterial defense. In fact a reduced phagocytosis, leukotaxis and leucocyte index have been reported in neutrophils from diabetics. The careful metabolic control was reported by most of the Authors to lower the incidence and to reduce the severity of periodontal disease. This may be related both to the improvement in leukocyte function and to a change in gingival fluid rendering it less suitable for bacterial growth. In diabetics also local factors, such as decreased pH of salivary fluid and a reduced salivary flow, seem to play an important role.(ABSTRACT TRUNCATED AT 250 WORDS)

Forskolin perturbs cGMP as well as cAMP levels in human thyroid cells.

Forskolin, at 10(-11) M, stimulates guanylate cyclase activity in primary human thyroid cell cultures, but does not modify cAMP accumulation. At a 10-fold higher concentration it still stimulates guanylate cyclase activity and becomes an inhibitor of cAMP production. Above 10(-9) M, forskolin stimulation of cGMP decreases, while it also becomes a stimulator of cAMP production. There is an additive effect of TSH and forskolin on cAMP production at concentrations of the diterpene which are stimulatory. Concentrations of forskolin which are inhibitory for cAMP, but stimulatory for cGMP, are inhibitory for TSH stimulation of cAMP. The addition of 8-bromo-cGMP duplicates the forskolin effect at low concentrations.