Studies show that systemic diseases such as diabetes, hyperthyroidism, osteoporosis, and dyslipidemia may influence periodontal inflammation. However, few studies relate the influence of arterial hypertension on periodontitis. The present study was undertaken to assess the severity of the experimental ligature-induced periodontitis in an experimental model of genetic arterial hypertension. The experimental periodontitis model was induced in 6 spontaneously hypertensive rats (SHR) and 6 Wistar normotensive rats (NT) by cotton ligature, which was placed subgingivaly around the neck of the first left inferior molar tooth. In the same animal, the first right molar tooth was sham-ligated and used as a control. After 7 days, the mean arterial pressure (MAP) and heart rate (HR) were recorded in conscious animals. As expected, MAP was significantly higher in SHR (151 +/- 6 mmHg) than in NT (105 +/- 3 mmHg), without significant differences in HR. The histopathologic examination of the periodontal structure showed alveolar integrity and lack of neutrophils and osteoclasts in the control side of both SHR and NT. In contrast, examination of the ligated side in all animals showed collagen degradation in the alveolar process from a moderate (50%) to severe (50%) level in SHR and mild in NT (100%). These data show that experimental periodontitis, characterized by the spreading of the inflammatory process from the gingiva deep into periodontium tissues, is greatly exacerbated in SHR.

Both the presence of receptors for gonadal steroids in the pineal gland and in vitro observations of direct action of melatonin upon Leydig cells, inhibiting testosterone secretion, indicate a direct connection between pineal gland and gonadal function. In the present study, we used a transmission electron microscope to analyze the morphologic parameters of Leydig cells from adult Swiss outbred white mice treated with daily subcutaneous injections of 100 micrograms of melatonin (N-acetyl, 5-methoxytryptamine), during 22 consecutive days, compared with sham-control animals which had only received the melatonin vehicle. The melatonin group of mice showed a decrease in nuclear volume and fractional nuclear volume; smooth and rough endoplasmic reticulum; mitochondria; and Golgi complex. Our data also showed an increase in cytoplasmic volume, fractional cytoplasmic volume, and lysosomes in these same animals. The results suggest that melatonin, directly or indirectly, alters the ultrastructure of mouse Leydig cells and possibly influences their secretory activity by inhibiting their capacity to secrete steroids.

In order to evaluate melatonin implication in the regulating of its own secretory process by pinealocytes, we used morphometric techniques for transmission electron microscopy. In mice treated with 100 mg of melatonin (N-acetyl-5-methoxy-tryptamine) by daily subcutaneous injection, we observed a decrease in number and volumetric density of lysosomes. Our results showed that melatonin influences the secretory activity of pinealocytes and participates in a complex secretory regulating mechanism.

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