Measurement of atherosclerosis markers in individuals with periodontitis.

PURPOSE: The inflammatory response due to inflammatory cytokines, bacterial pathogens, and the altered lipoprotein metabolism in patients with periodontitis indicates that infection with periodontal anaerobic bacteria may influence atherogenesis in vitro and in vivo. We aimed to explore the effect of periodontitis concerning clinical and ultrasound markers of early atherosclerosis. METHODS: In this case-control study, a total of 30 systemically healthy adults (15 with periodontitis and 15 without periodontitis) over 40 years of age were studied. Periodontitis was determined by measuring the clinical attachment level (CAL) and radiographic bone loss (RBL). Conventional cardiovascular risk factors, including body mass index, serum levels of total cholesterol (TCH), triglycerides (TG), and high-density and low-density lipoprotein (HDL and LDL, respectively) cholesterol were evaluated. Carotid artery intima-media thickness (IMT) was measured using ultrasonography. RESULTS: The mean values of the CAL and carotid IMT were 5.02±0.9 mm and 0.084±0.01 cm vs. 1.6±0.61 mm and 0.072±0.02 cm in the periodontitis and healthy groups, respectively, reflecting statistically significant differences (P=0.001 and P=0.037, respectively). There were statistically significant differences in the serum levels of TCH, TG, and LDL between the 2 groups (P=0.017). The CAL and RBL were positively associated with carotid IMT and serum cholesterol levels, except for HDL, whereas tooth loss was not associated with any markers (P<0.05). Compared to the healthy group, participants with periodontitis exhibited 2.09 times higher odds (95% confidence interval, 1.22-3.59) of having subclinical atherosclerosis. CONCLUSIONS: The presence of periodontitis increased the risk of atherosclerosis.

[Changes in the innervation of the taste buds in diabetic rats]. / Ízlelobimbók beidegzésének változása diabetes mellitusban patkányban.

INTRODUCTION: Abnormal sensations such as pain and impairment of taste are symptoms of approximately 10% of patients having diabetes mellitus. AIM: The aim of the study was to investigate and quantify the different neuropeptide containing nerve fibres in the vallate papilla of the diabetic rat. METHODS: Immunohistochemical methods were used to study the changes of the number of different neuropeptide containing nerve terminals located in the vallate papillae in diabetic rats. Diabetes was induced in the rats with streptozotocin. RESULTS: Two weeks after streptozotocin treatment the number of the substance P, galanin, vasoactive intestinal polypeptide and neuropeptide Y immunoreactive nerve terminals was significantly increased (p<0.05) in the tunica mucosa of the tongue. The number of the lymphocytes and mast cells was also increased significantly. Some of the immunoreactive nerve terminals were located in the lingual epithelium both intragemmally and extragemmally and were seen to comprise dense bundles in the lamina propria just beneath the epithelium. No taste cells were immunoreactive for any of the investigated peptides. Vasoactive intestinal polypeptide and neuropeptide Y immunoreactive nerve fibres were not detected in the taste buds. For weeks after streptozotocin administration the number of the substance P, calcitonin gene related peptide and galanin immunoreactive nerve terminals was decreased both intragemmally and intergemmally. In case of immediate insulin treatment, the number of the immunoreactive nerve terminals was similar to that of the controls, however, insulin treatment given 1 week later to diabetic rats produced a decreased number of nerve fibers. Morphometry revealed no significant difference in papilla size between the control and diabetic groups, but there were fewer taste buds (per papilla). CONCLUSIONS: Increased number of immunoreactive nerve terminals and mast cells 2 weeks after the development of diabetes was the consequence of neurogenic inflammation which might cause vasoconstriction and lesions of the oral mucosa. Taste impairment, which developed 4 weeks after streptozotocin treatment could be caused by neuropathic defects and degeneration or morphological changes in the taste buds and nerve fibres.

Changes of the different neuropeptide-containing nerve fibers and immunocells in the diabetic rat's alimentary tract.

Peripheral neuropathy is a common complication of diabetes mellitus, where neuropeptides and immunocells might play important roles in the pathogenesis of the disease. In this article we have quantified the different neuropeptide-containing nerve fibers and immunocells in the streptozotocin-induced diabetic rat's alimentary tract (tongue, duodenum, colon) using immunohistochemical and immunocytochemical methods. The immunoreactive (IR) nerve fibers were found in all layers of the alimentary tract and their distribution pattern was similar in both control and diabetic groups. Mast cell-nerve fiber contacts were rarely found in the controls. However, after 4 weeks duration of diabetes the number of IR nerve fibers and the immunocompetent cells increased significantly (P < 0.05), and the number of mast cell-nerve fiber contacts was even more significantly increased (P < 0.001). The distance between nerve fibers and immunocells was about 1 mum or even less. Some of the mast cells were degranulated in the vicinity of nerve fibers. No immunocompetent cells were IR for any antisera in the control. However, after the streptozotocin treatment, a large number of the immunocompetent cells showed immunoreactivity for SP and NPY. Counting all immunocompetent cells in whole sections showed that 12.3% of them were IR for SP and 25.4% were IR for NPY. Increased number of SP-containing nerve fibers and immunocells in diabetes mellitus might be the reason for painful neuropathy and might amplify the inflammatory reaction in an axon reflex manner; the released histamine and leukotrienes, cytokines, and chemokines might cause inflammations and lesions of the mucosa.

Morphological evidence of sensory neurons in the root of the rat tongue.

In our previous studies, a large number of substance P (SP)-immunoreactive (IR) nerve fibers were detected in the rat tongue and their number increased after inflammation, suggesting that these fibers might be involved in the axon reflex. Therefore, in this study, we have examined the different neuropeptide-containing nerve elements by light, electron, and confocal laser microscopy. SP, vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY) IR varicose fibers were numerous compared with other ones. Small groups of ganglia with perikarya IR for SP, VIP, NPY, galanin, and somatostatin were observed. The SP-IR nerve cell bodies were mainly located in the tunica propria just below the epithelial lining. Double-labeling immunohistochemistry showed that the intrinsic SP-IR neurons did not colocalize VIP. The SP containing nerve terminals were observed in and below the epithelium as well as in very close contact to or making real synapses with other neurons in the intralingual ganglion. Our data confirmed the possibility of intrinsic sensory neurons, which might be the afferent branch of the intralingual reflex arch, while the VIP- and NPY-IR neurons located in the salivary glands, around the blood vessels, and in the muscle layer might constitute the efferent site of this reflex.

Plasticity of the different neuropeptide-containing nerve fibres in the tongue of the diabetic rat.

Common oral complications of diabetes mellitus are xerostomia, impairment of taste, atrophic lesions of the tongue, leukoplakia, lichen oris planus, and tumours, which might be the consequence of chronic inflammation and changes in innervation. In this work, we examined the density of different neuropeptide-containing nerve fibres immunohisto- and immunocytochemically in the root of the control and diabetic rat's tongue. Quantitative analysis showed that the number of immunoreactive (IR) nerve fibres was decreased after 1 week of the streptozotocin treatment, which was prevented by immediate insulin treatment. However, after 4 weeks duration of diabetes, the number of all investigated IR nerve fibres increased significantly (p<0.05), which was further enhanced by the delayed insulin treatment. The numbers of substance P (SP) and vasoactive intestinal polypeptide IR perikarya were also increased by insulin treatment. The electron-microscopic investigations showed that some of the nerve terminals from diabetic animals were found in degeneration. After 4 weeks duration of diabetes, the number of inflammatory cells as well as the mast cell/nerve fibre contacts was also increased. The immunocells also showed IR for SP and neuropeptide Y in the diabetic rats. The insulin treatment decreased both the number and the immunoreactivity of these cells. The increased synthesis and/or regeneration of neuropeptide-containing nerves might indicate the plasticity of nerve fibres in diabetes mellitus, which might happen as a consequence of the changes in the level of neurotrophic factors released by increased number of inflammatory cells or as an effect of insulin.

Immunohistochemical analysis of substance P containing nerve fibres and their contacts with mast cells in the diabetic rat's tongue.

Sensory neuropathy is common symptom of the diabetes mellitus and the prevalence of oral lesions is higher in diabetic patients. The distribution of substance P was studied immunohistochemically in streptozotocin induced diabetic rat's tongue. The morphological association of sensory nerves (substance P immunoreactive) with mast cells (nerve fibre-mast cell contact) was monitored. The substance P nerve fibre mast cell contacts were very scanty in control tongue. The number of substance P nerve terminals and mast cells was significantly increased (p < 0.05) in diabetes mellitus after 4 weeks of the treatment compared with the control tongue. The number of mast cell nerve contacts was even more significantly increased (p < 0.001) in diabetes. The distance between nerve fibres and mast cells was about 1 mm and very often less than 200 nm. In some instances, the mast cells were degranulated in the vicinity to nerve fibres. Increased number of mast cell nerve contacts in neurogenic inflammation might cause vasoconstriction and lesions of the oral mucosa, so some disorders such lichen planus, leukoplakia and cancer might frequently develop in diabetes mellitus.

[Changes of the nerve fibers innervating the minor salivary glands in Sjögren syndrome]. / A kis nyálmirigyek beidegzésében résztvevó idegelemek változása Sjögren-szindrómában.

INTRODUCTION: A large number of nerve fibres containing different neuropeptides/transmitters are also found in the salivary glands. The number and the distribution of nerve fibres is altered in many diseases, including in Sjögren's syndrome. AIM: Therefore in the present study the distribution and precise localisation of the nerve fibres containing the frequently observed neuropeptides were studied in the minor salivary glands. METHODS: Vasoactive intestinal polypeptide, neuropeptide Y, substance P, calcitonin gene-related peptide, somatostatin, nitric oxide synthase and tyrosine beta-hydroxylase antibodies were used as primary antisera, and then by the aid of avidin-biotin-peroxidase complex method the immunoreactive fibers in human labial glands (control and with Sjögren's syndrome) and in minor glands of the root of the rat's tongue were detected. RESULTS: Large number of vasoactive intestinal polypeptide and nitric oxide synthase immunoreactive nerve fibres were seen around the acini. The neuropeptide Y and tyrosine beta-hydroxylase positive nerve fibres were mainly found around the blood vessels. Some of the IR fibers were also found around the excretory ducts. In the biopsy of patients with Sjögren's syndrome, the acini were destroyed and only few excretory ducts were seen. The number of the nerve fibres was significantly decreased and many degenerated fibres were also observed among the acini. The electron-microscopic examinations showed that the immunoreactive nerve fibres were in close association to the secretory cells, to the smooth muscle cells of blood vessels and to the immunocells. The synaptic gap between the nerve fibres and the target cells were 40-200 nm. CONCLUSIONS: On the bases of the distribution of the different transmitters containing nerve fibres and their relationship to effector cells, the authors suppose that these transmitters control the function of the gland and regulate the blood flow. The close association to immunocells and decreasing the nerve fibres in Sjögren's syndrome imply that they may have also a role in the neuroimmunologic processes.