It has been suggested that third molars increase mandibular fragility because they do not contribute to its strength. For ethical reasons, a human study design that would permit the elucidation of this interference is not possible. This study evaluated the impact of the presence of erupted third molars on the mandibular angle of resistance when submitted to trauma. A three-dimensional (3D) mandibular model was obtained through finite element methodology using computed tomography (CT) with the geometry and mechanical properties to reproduce a normal mandibular structure. Human mandibles with no, one or two erupted third molars were evaluated. Whenever the third molar was present there was a greater concentration of tensions around the cervical part of its alveolus. Approximated Von Mises equivalent stress of the third molar region was 107.035 MPa in the mandible with teeth and 64.6948 MPa in the mandible without teeth. In the condylar region it was 151.65 MPa when the third molar was present and 184.496 MPa when it was absent. The digital models created proved that the mandibular angle becomes more fragile in the presence of third molars. When they are absent the energy concentrates on the lateral e posterior aspect of the condylar neck.

Pain after third molar extraction has been considered the most suitable pharmaceutical model to evaluate acute pain. This study aimed to evaluate the pre-emptive analgesic/anti-inflammatory efficacy of etoricoxib 120 mg following mandibular third molar surgery. A split-mouth, randomized, triple-blind, placebo-controlled study was conducted with patients undergoing the surgical removal of mandibular third molars. All volunteers were allocated randomly to receive either etoricoxib 120 mg or placebo 1h preoperatively, and inflammatory events were evaluated. An estimated sample of 18 surgical units per group was required based on a pilot study (95% confidence level and 80% statistical power). Rescue medication was analyzed by Kaplan-Meier method through log-rank Mantel-Cox test and Pearson linear correlation (P<0.05). Pre-emptive etoricoxib reduced postoperative pain scores significantly in comparison to placebo (P<0.001), with a pain score peak at 6h after surgery (P<0.001). The mean rescue medication consumption was lower in the etoricoxib group compared to the placebo group over the study period (P<0.05). There was no statistically significant difference between groups related to swelling and trismus. The pre-emptive administration of etoricoxib 120 mg significantly reduced the postoperative pain intensity and the need for rescue medication, but did not reduce swelling or trismus.

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1 The eects of ni¯umic acid (NFA), an inhibitor of calcium-activated chloride currents I Cl(Ca) , were compared with the actions of the voltage-dependent calcium channel (VDCC) blocker nifedipine on 5-hydroxtryptamine (5-HT)-and acetylcholine (ACh)-induced contractions of the rat isolated fundus. 2 NFA (1 ± 30 mM) elicited a concentration-dependent inhibition of contractions induced by 5-HT (10 mM) with a reduction to 15.5+6.0% of the control value at 30 mM. 1 mM nifedipine reduced 5-HT-induced contraction to 15.2+4.9% of the control, an eect not greater in the additional presence of 30 mM NFA. 3 In contrast, the contractile response to ACh (10 mM) was not inhibited by NFA in concentrations 4100 mM, although this response was partly inhibited by nifedipine (1 mM) to 67.6+11.8% of the control value. 4 NFA (1 ± 30 mM) did not aect contraction induced by either 20 mM or 60 mM KCl, suggesting that this drug was not acting via blockade of VDCCs or activation of potassium channels. In contrast, 3,5-dichlorophenylamine-2-carboxylic acid and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid were less selective in their inhibitory eects, inducing reductions of 60 mM KCl-induced contraction at concentrations 510 mM. 5 Our results show that NFA can exert selective inhibitory eects on the chloride-dependent 5-HTinduced contractions of the rat fundus. The data support the hypothesis that activation of Cl (Ca) channels leading to calcium entry via VDCCs is a mechanism utilized by 5-HT, but not by ACh, to elicit contraction of the rat fundus.

Novel derivatives of 2-[3-(trifluoromethyl)-analino]nicotinic acid (niflumic acid) were synthesized. The compounds were compared for their inhibitory effects on 5-hydroxytryptamine (5-HT)- and KCI-induced contraction of the rat fundus. The aim was to assess structure-activity relationships regarding the selectivity and potency of these compounds. Niflumic acid (1-100 microM) concentration-dependently inhibited 5-HT-induced tonic contractions with an IC50 value (concentration reducing the control contractile response by 50%, calculated from semi-log graphs) of 0.24 x 10(4) M (n = 9). In contrast, it was significantly less potent at inhibiting KCl-induced responses (IC50 = 1.49 x 10(4) M, n = 9). The methyl ester (NFAme) and amido (NFAm) analogues showed no selectivity between 5-HT- and KCl-induced contractions with IC50 values of 1.64 x 10(-4) M (n = 8) and 1.87 x 10(-4) M (n = 9) for 5-HT responses, and 2.61 x 10(-4) M (n = 8) and 2.55 x 10(-4) M (n = 7) for KCl-induced responses, respectively. Our results suggest that alteration of the carboxylic acid moiety of niflumic acid reduces the selectivity and potency of its inhibitory action on 5-HT-induced contractile responses of the rat fundus, possibly via a reduced interaction with calcium-activated chloride channels.

1 We have investigated the inhibitory effects of blockers of volume-activated (Cl vol ) and calciumactivated (Cl Ca ) chloride channels on hypotonic solution (HS)-induced contractions of rat trachea, comparing their effects with those of the voltage-dependent calcium channel (VDCC) blocker nifedpine. 2 HS elicited large, stable contractions that were partially dependent on the cellular chloride gradient; a reduction to 41.4577.71% of the control response was obtained when extracellular chloride was removed. In addition, HS-induced responses were reduced to 26.875.6% of the control by 1 mM nifedipine, and abolished under calcium-free conditions, indicating a substantial requirement for extracellular calcium entry, principally via VDCCs. 3 The established Cl vol blockers tamoxifen (p10 mM) and 4,4 0 -diisothiocyanatostilbene-2,2 0 -disulphonic acid (1-100 mM), at concentrations previously reported to inhibit Cl vol in smooth muscle, did not significantly inhibit HS-induced contractions. 4 In contrast, the recognized Cl Ca blocker niflumic acid (NFA; 1-100 mM) produced a reversible, concentration-dependent inhibition of HS responses, with a reduction to 36.676.4% of control contractions at the highest concentration. The mixed Cl vol and Cl Ca blocker, 5-nitro 2-(3-phenylpropylamine) benzoic acid (NPPB; 10-100 mM) also elicited concentration-related inhibition of HS-induced contractions, producing a decrease to 35.9711.3% of the control at 100 mM. 5 Our results show that HS induces reversible, chloride-dependent contractions of rat isolated trachea that were inhibited by NFA and NPPB, while exhibiting little sensitivity to recognized blockers of Cl vol . The data support the possibility that opening of calcium-activated chloride channels under hypotonic conditions in respiratory smooth muscle may ultimately lead to VDCC-mediated calcium entry and contraction.

Blood pressure did not present significant alterations after a local injection of 54 or 108 µg of epinephrine during surgery to remove 2 or 4 third molars. Although without significance, HR was more elevated in the 108-µg dose of epinephrine during the removal of 4 third molars.

Toxic levels of mepivacaine are possible, even when a submaximal dose is used. A twofold increase in the dose of mepivacaine caused the mean peak plasma concentration to increase proportionally, indicating that they may be predicted based on the relation of dose per bodyweight.