Abstract Aim Interleukin‐1β ( IL ‐1β) and prostaglandin E 2 ( PGE 2 ) are key inflammatory mediators involved in periodontitis. The purpose was to compare their salivary concentrations in relation to periodontal status and their changes after periodontal treatment, to determine their use as non‐invasive diagnostic tools. Materials and Methods In this study, 74 subjects grouped in periodontally healthy, mild, moderate and severe periodontitis, according to clinical attachment level ( CAL ) and probing pocket depth ( PPD ) served as participants. IL ‐1β and PGE 2 were determined in unstimulated whole saliva by enzyme‐linked‐immunosorbent assay (ELISA). Results Interleukin ‐1β increased with the severity of periodontitis with a large effect size in prediction of CAL ( η 2 = 0.35, p = 0.0001). PGE 2 showed an increment in mild periodontitis and another in moderate. A significant effect size was also found between PGE 2 and PPD ( η 2 = 0.12, p = 0.003). Both mediators decreased after periodontal treatment. With a selected threshold of 212 pg/ml, salivary IL 1‐β predicted periodontitis with 78% sensitivity and 100% specificity. With a selected threshold of 121 pg/ml, salivary PGE 2 predicted periodontitis with 78% sensitivity and 91% specificity. Conclusion The high sensitivity and specificity of salivary IL ‐1β and PGE 2 in identifying periodontitis suggest a potential use as biomarkers for diagnosis of periodontitis presence and severity.
The mechanism and receptor subtypes involved in carbachol‐stimulated amylase release and its changes after castration were studied in parotid slices from male rats. Carbachol induced both amylase release and inositol phosphate (IP) accumulation in parotid slices from control and castrated rats, but castration induced a decrease of carbachol maximal effect. The effect of castration was reverted by testosterone replacement. The selective M 1 and M 3 muscarinic receptor antagonists, pirenzepine and 4‐diphenylacetoxy‐ N ‐methylpiperidine methiodide, respectively, inhibited carbachol‐stimulated amylase release and IP accumulation in a dose‐dependent manner in parotid slices from control and castrated rats. A diminution of binding sites of muscarinic receptor in parotid membrane from castrated rats was observed. Competition binding assays showed that both, M 1 and M 3 muscarinic receptor subtypes are expressed in membranes of parotid glands from control and castrated rats, M 3 being the greater population. These results suggest that amylase release induced by carbachol in parotid slices is mediated by phosphoinositide accumulation. This mechanism appears to be triggered by the activation of M 1 and M 3 muscarinic receptor subtypes. Castration induced a decrease of the maximal effect of carbachol evoked amylase release and IP accumulation followed by a diminution in the number of parotid gland muscarinic acetylcholine receptors. British Journal of Pharmacology (2003) 139 , 399–407. doi: 10.1038/sj.bjp.0705260
Evans blue extravasation in rat skin was used to study the effects of calcium, lanthanum, L-type calcium channel blockers and trifluoperazine on histamine-induced leakage. Histamine effect was inhibited by calcium 1-2.5 mM, lanthanum 1-10 mM, nifedipine 0.1 and 1 microM and trifluoperazine 30 and 100 microM. The effects of calcium decreased progressively as its concentrations rose up to 10 mM. The association of nifedipine 0,1 microM or trifluoperazine 30 microM with calcium 3 microM increased the inhibitory effects. Calcium 10mM reversed the effect of nifedipine 0.1 microM but not that of lanthanum 1 mM or trifluoperazine 30 microM. It is proposed that the effect of calcium on histamine-induced leakage is the expression of a balance between an extracellular inhibitory effect and an intracellular enhancing effect.
The parotid gland participates in the digestive process by providing fluid, electrolytes and enzymes that facilitate the onset of digestion. Neurotransmitters, hormones and biologically active peptides regulate its activity. The autonomic system is the main regulatory mechanism of the gland. Sympathetic stimulation induces amylase release through beta(1)-receptor activation and few fluid secretion by alpha(1)-receptor activation. The parasympathetic system controls basal activity of the gland acting on M(1) and M(3) muscarinic acetylcholine receptors and induces the secretion of fluid saliva rich in electrolytes through the modulation of ion channels and the Na(+)-K(+)-ATPase activity. In addition, its activation induces amylase release. The mechanisms involved in amylase secretion by isoproterenol and carbachol, as well as the mechanism of the cholinergic regulation of Na(+)-K(+)-ATPase activity and the changes observed after orchiectomy, are the scope of this review.
Here we determine the relationship between salivary levels of mucin and amylase and the clinical parameters of periodontal disease before and after periodontal treatment.Ninety two subjects were clinically examined and distributed into four groups namely clinically healthy, mild, moderate and severe periodontitis, according to the periodontal status, classified according the values of clinical attachment level (CAL) and probing pocket depth (PPD). Unstimulated saliva was collected for 5 min. Salivary proteins, amylase and mucin were determined by colorimetric methods.A significant positive correlation (P < 0.0001) was observed between salivary mucin, amylase or protein and PPD or CAL before periodontal treatment while flow rate showed a negative correlation. Mucin and amylase output also showed a positive correlation with PPD or CAL. After treatment, the improvement of clinical parameters was accompanied by a diminution of salivary mucin, amylase or protein concentration and output in moderate and severe group.The increment of mucin and amylase output in relation to periodontal status indicates that salivary glands respond to the disease by increasing the protective potential of saliva when necessary and return to the normal rate of secretion after the resolution of the inflammatory process.