The periodontal status of 77 diabetic children and adolescents, and 77 paired, systemically-healthy, sex- and age-matched control subjects, was clinical examined. Fasting blood glucose, fructosamine and glycosylated haemoglobin (HbA1) values were determined. The mean periodontal pocket depths, clinical attachment levels and the parameters to assess diabetes mellitus from the diabetic group were significantly higher than those of the controls. We found a positive correlation between the duration of diabetes and clinical attachment loss, but not with periodontal probing depth, plaque index and gingival index in the diabetic group. A positive correlation was also assessed between the present serum fructosamine and gingival index in the diabetic group, but not in controls.

Cyclosporin A is an endecapeptide that has been used clinically since 1978 as an immunosuppressant agent. Although cyclosporine appears to be uniformly beneficial in the treatment of a wide variety of disorders, its use may result in a number of side effects. One of the most important adverse effects is gingival overgrowth. This report relates a case of severe gingival overgrowth in a 31‐year‐old female who had received cyclosporine therapy in conjunction with a kidney transplant. Because of the severe gingival overgrowth, we analyzed a biopsy, which was positive for human papillomavirus. The case was treated and followed for 18 months. J Periodontol 1996;67:528–531.

The facultative intracellular pathogen Brucella abortus interacts with several organelles of the host cell to reach its replicative niche inside the endoplasmic reticulum. However, little is known about the interplay between the intracellular bacteria and the host cell mitochondria. Here, we showed that B. abortus triggers substantive mitochondrial network fragmentation, accompanied by mitophagy and the formation of mitochondrial Brucellacontaining vacuoles during the late steps of cellular infection. Brucella-induced expression of the mitophagy receptor BNIP3L is essential for these events and relies on the iron-dependent stabilisation of the hypoxia-inducible factor 1α. Functionally, BNIP3Lmediated mitophagy appears to be advantageous for bacterial exit from the host cell as BNIP3L depletion drastically reduces the number of reinfection events. Altogether, these findings highlight the intricate link between Brucella trafficking and the mitochondria during host cell infection.

24 adult patients suffering from Adult periodontitis were assigned to 4 groups: the 1st rinsed for 1 min with 0.2% chlorhexidine gluconate (CHX); the 2nd group were irrigated for 15 s with 0.2% CHX in a pulsed oral irrigator; the 3rd group rinsed for 1 min with saline and the 4th group were irrigated for 15 s with saline. Plaque vitality was measured after the 4 experimental procedures, using the method described by Netuschil et al. and scored using the method described by Rundegren et al. The results showed that a single rinse or irrigation with 0.2% CHX solution decreased the % of viable micro‐organisms, but the vitality of the bacteria remained unchanged in saline groups. Statistical analysis indicated that irrigation with CHX was more effective at reducing plaque vitality than rinsing with CHX.

The facultative intracellular pathogen Brucella abortus interacts with several organelles of the host cell to reach its replicative niche inside the endoplasmic reticulum. However, little is known about the interplay between the bacteria and the host cell mitochondria. Here, we showed that B. abortus triggers a strong mitochondrial network fragmentation accompanied by mitophagy and the formation of mitochondrial Brucella-containing vacuoles in the late steps of cellular infection. The expression of the mitophagy receptor BNIP3L induced by B. abortus is essential for these events and relies on the iron-dependent stabilization of the hypoxia-inducible factor 1 alpha. Functionally, BNIP3L-mediated mitophagy appears to be advantageous for bacterial exit of the host cell as BNIP3L depletion drastically reduced the number of reinfection events. Altogether, these findings highlight the intricate link between Brucella trafficking and the mitochondria during host cell infection.