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Objectives:The antiplaque and antigingivitis effects of a gel containing 10% Punica granatum Linn extract were evaluated using a 21-day partial-mouth experimental model of gingivitis.Methods:23 volunteers participated in this cross-over, doubleblind study, carried out in 2 phases of 21 days each. For each period of the experiment, an acrylic toothshield was made for each volunteer to carry the test or placebo gel as well as to avoid brushing of the 4 experimental teeth (posterior teeth in the lower left quadrant). The subjects were randomly assigned to use either the placebo gel (control group) or the test gel (experimental group) and were instructed to brush the remaining teeth normally 3 times a day. On days 0 and 21, the visible plaque index (VPI) and gingival bleeding index (GBI) were recorded.Results:The results did not show statistically significant difference between control and experimental groups for either of the indices (VPI and GBI).Conclusion:The gel containing 10% Punica granatum Linn extract was not efficient in preventing supragingival dental plaque formation and gingivitis.

Visceral pain is the most common form of pain for which the patients often seek medical care. Ascending pathways in the spinal cord that relay nociceptive information from the periphery to supraspinal central nervous system sites has been studied as potential targets for disrupting pain processing and providing relief. Despite the considerable advances in knowledge regarding the basic mechanisms underlying visceral pain and visceral hyperalgesia, no new effective therapies for abdominal pain have been discovered. Tissue injury, inflammation, and algesic chemicals produce changes in the stimulus response, leading to either sensitisation or desensitization of peripheral sensory afferents. An enormous range of pharmacological agents and endogenous substances via numerous receptors influence the visceral afferents. These substances produce their effects on visceral afferents by sensitization, opening of ion channels or by altering the expression of mediators, channels, or receptors. 1) In recent years, a central importance is given to capsaicin (vanilloid) receptor 1 (VR1, also called transient receptor potential V1, TRPV1) in the regulation of the activity of sensory afferent nerves. TRPV1 gene knock out mice are analgesic to a wide range of painful inflammatory states, suggesting that TRPV1 receptor antagonists may be effective in those pain states associated with tissue injury, and chemical exposure.2,3) Currently, inflammatory hyperalgesia is managed by NSAIDs (cyclo-oxygenase inhibitors) and opioids, although very effective against inflammatory hyperalgesia, both of these therapeutic classes possess significant limitations. 4,5) Opioids induce constipation, and nausea, whereas NSAIDs possess significant side effects on the gastrointestinal, cardiovascular and renal systems.In the recent past, many novel structures derived from a number of natural sources have been examined for the development of drugs acting as agonists or antagonists at vanilloid receptors, which include compounds like polygodial, a full vanilloid agonist derived from marsh pepper; warburganal from the bark of warburgia trees; isovelleral with terpenoid structure isolated from fungi; scalaradial, an unsaturated dialdehyde isolated from sponges; and scutigeral, isolated from edible mushrooms.6) The natural triterpenic mixture a-and b-amyrin, isolated from Protium heptaphyllum has recently been shown to exert gastroprotective effect against ethanolinduced lesions and an antinociceptive effect in the visceral model of nociception induced by capsaicin, possibly involving the capsaicin-sensitive sensory afferents. 7,8) Chemically, the a-and b-amyrin is a mixture of two triterpenes belonging to the ursane (a-amyrin) and oleanane (b-amyrin) series. Oleanolic acid is a pentacyclic triterpene that pertains to oleanane (b-amyrin) series (Fig. 1) and previous studies established its gastro-and hepato-protective and anti-inflammatory effects.9,10) So far there have been no available reports that show the efficacy of oleanolic acid in animal models of noci...

The anti-inflammatory pentacyclic triterpene, oleanolic acid (OA) was examined on acute nociception induced by intraplantar injection of capsaicin in mice. OA administered orally to mice at 10, 30 and 100 mgkg(-1), significantly attenuated the paw-licking response to capsaicin (1.6 microg/paw) by 53%, 68.5% and 36.6%, respectively. Ruthenium red (3 mgkg(-1), s.c.), a non-competitive vanilloid receptor (V1, TRPV1)-antagonist also suppressed the capsaicin nociception by 38.6%. The maximal antinociception produced by 30 mgkg(-1) OA was significantly blocked in animals pre-treated with naloxone (2 mgkg(-1), i.p.), the opioid antagonist; l-arginine (600 mgkg(-1), i.p.), the substrate for nitric oxide synthase; or glibenclamide (2 mgkg(-1), i.p.), the K(ATP)-channel blocker, but was unaffected by yohimbine (2 mgkg(-1), i.p.), an alpha(2)-adrenoceptor antagonist. In open-field and rota-rod tests that detect motor deficits, mice received 30 mgkg(-1) OA did not manifest any effect per se, indicating that the observed antinociception is not a consequence of motor abnormality. These data suggest that OA inhibits capsaicin-evoked acute nociception due to mechanisms possibly involving endogenous opioids, nitric oxide, and K(ATP)-channel opening.

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