cyclic-gmp and Periodontitis

Several studies have suggested an increase of cardiovascular disease (CVD) risk on periodontitis patients. An enhancement has been demonstrated on both platelet activation and oxidative stress on periodontitis patients, which may contribute for this association. Therefore, the aim of this study was to evaluate the effects of non-surgical periodontal treatment on the l-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway and oxidative status in platelets. A total of eight periodontitis patients and eight controls were included in this study. Clinical, laboratory and experimental evaluations were performed on baseline and 90 days after periodontal treatment (except for western blot analysis). The clinical periodontal evaluation included measurements of probing pocket depth (PPD), clinical attachment loss (CAL), % of sites with plaque and % of sites with bleeding on probing. We evaluated: l-[(3)H]arginine influx; nitric oxide synthase (NOS) and arginase enzymes activity and expression; expression of guanylate cyclase and phosphodiesterase-5 enzymes; cGMP levels; platelet aggregation; oxidative status through superoxide dismutase (SOD) and catalase activities, and measurement of reactive oxygen species (ROS) levels and C-reactive protein (CRP) levels. The initial results showed an activation of both l-arginine influx and via system y (+ )L associated with reduced intraplatelet cGMP levels in periodontitis patients and increased systemic levels of CRP. After periodontal treatment, there was a significant reduction of the % of sites with PPD 4-5mm, % of sites with CAL 4-5 mm, and an enhancement in cGMP levels and SOD activity. Moreover, CRP levels were reduced after treatment. Therefore, alterations in the intraplatelet l-arginine-NO-cGMP pathway and oxidant-antioxidant balance associated with a systemic inflammatory response may lead to platelet dysfunction, which may contribute to a higher risk of CVD in periodontitis.

Topics: Adult; Arginine; Blood Platelets; C-Reactive Protein; Cardiovascular Diseases; Cyclic GMP; Humans; Middle Aged; Nitric Oxide; Nitric Oxide Synthase; Oxidative Stress; Periodontitis; Platelet Activation; Platelet Aggregation; Signal Transduction

Periodontitis is one of the important risk factors resulting in cardiovascular diseases. Erectile dysfunction (ED) is strongly correlated with cardiovascular diseases. The expression of endothelial nitric oxide synthase (eNOS) in penile tissue has an important role in the mechanism of erection.. To investigate the effect of periodontitis on erectile function and the possible mechanism.. After induction of periodontitis in rat, the ratio of maximum intracavernosal pressure/mean arterial pressure (ICPmax /MAP)×100, the expression of eNOS in penile tissue, the level of serum C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α), and the ultrastructural changes of the cavernous tissue were examined and compared between periodontitis rats (group A) and control rats (group B).. Periodontitis significantly decrease not only the ICPmax/MAP×100 and the expression of eNOS but also the activity of NOS and the level of cyclic guanosine monophosphate (cGMP) in cavernous tissue of rat.. After electrostimulation by 3 and 5 voltage, the ratio of ICPmax /MAP×100 in group A was significantly less than that in group B (19.54±6.16 vs. 30.45±3.12; 30.91±5.61 vs. 50.52±9.52, respectively; P<0.05).The level of serum CRP and TNF-α in group A is significantly higher in group B (P<0.05).The quantitative real-time reverse transcription polymerase chain reaction study demonstrated no statistically significant difference in the expression of mRNA of eNOS in cavernous tissue between the two groups (P>0.05). But there was significant decrease in eNOS protein of the cavernous tissue in group A than in group B (P<0.05). Total NOS activity and cGMP level in cavernosal tissue were significantly lower in group A than in group B (P<0.05). There was no significant alternation occurred in the ultrastructures of penile cavernous tissue.. The function of penile erection is impaired by periodontitis. The decreased in the expression of eNOS and NOS activity in penile cavernous tissue caused by mild systemic inflammatory status in periodontitis may be one of the important risk factors of ED.

Topics: Animals; Blood Pressure; Blotting, Western; C-Reactive Protein; Cyclic GMP; Erectile Dysfunction; Male; Microscopy, Electron, Transmission; Nitric Oxide Synthase; Nitric Oxide Synthase Type III; Penis; Periodontitis; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Tumor Necrosis Factor-alpha

Experimental findings suggest a protective role for cyclic nucleotides against induction of oxidative stress in saliva. Oxidative stress is a major contributor to the pathogenesis of inflammatory diseases. This study was conducted to evaluate salivary oxidative stress along with cGMP and cAMP levels in periodontitis subjects. cAMP and cGMP are second messengers that have important roles in salivary gland functions. Unstimulated whole saliva samples were obtained from periodontitis patients and age- and sex-matched healthy individuals. Saliva samples were analyzed for thiobarbituric reactive substances (TBARS) as a marker of lipid peroxidation, ferric reducing ability (total antioxidant power, TAP), and levels of cAMP and cGMP. Concentrations of cAMP and cGMP were reduced in the saliva of patients with moderate and severe periodontitis. Saliva of patients with severe periodontitis had higher TBARS and lower TAP than control subjects. The presence of oxidative stress and lower levels of salivary cGMP and cAMP in periodontitis are in association with disease severity.

Topics: Adult; Analysis of Variance; Antioxidants; Case-Control Studies; Cyclic AMP; Cyclic GMP; Female; Humans; Immunoenzyme Techniques; Lipid Peroxidation; Male; Middle Aged; Nitric Oxide; Oxidative Stress; Periodontitis; Phosphodiesterase Inhibitors; Saliva; Statistics, Nonparametric

To investigate the mechanism by which polymorphonuclear leukocytes (PMNLs) contribute to tissue injury in periodontitis, NO-activity was bioassayed by measuring its ability to increase cGMP accumulation in cultured fibroblasts in the absence or presence of PMNLs isolated from blood and gingival fluid in healthy volunteers and patients with periodontitis. Non-activated PMNLs do not NO-induced stimulation of cGMP accumulation in the detector cells. However, activated PMNLs inhibited NO-induced cGMP accumulation whereas the effects of sodium nitroprusside was unaffected. Peripheral PMNLs periodontitis impaired NO-dependent cGMP accumulation more markedly than from healthy volunteers. PMNLs from periodontal pockets in periodontal patients destroyed NO significantly higher than in venous blood of the same patients without additional activation. It is assumed that the deactivation of NO by activated PMNLs is a one of the pathomechanisms of disorders in periodontitis.

Topics: Adult; Cell Line; Cells, Cultured; Chronic Disease; Cyclic GMP; Fibroblasts; Gingival Crevicular Fluid; Humans; Middle Aged; Neutrophils; Nitric Oxide; Periodontitis

Topics: Adult; Cyclic AMP; Cyclic GMP; Estradiol; Female; Humans; Hydrocortisone; Kidney Diseases; Male; Middle Aged; Periodontitis; Radioimmunoassay; Testosterone; Yang Deficiency; Yin Deficiency