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Table 2: Significant Observations in Host Modulation
Prostaglandins are found to be important mediators of bone resorption.
The mechanism of aspirin’s effect on the body is discovered to be through the inhibition of prostaglandins.
Prostaglandins are proposed to be major mediators of periodontal bone loss.
Inhibitors of prostaglandins (eg, aspirinlike drugs) are proposed to be studied as a way of blocking periodontal bone loss Indomethacin is found to inhibit ligature-induced bone loss in beagles.
Flurbiprofen is found to inhibit naturally occurring periodontal diseases in beagles.
Flurbiprofen significantly blocks the bone loss of human periodontal diseases.
Subantimicrobial dose doxycycline, which blocks matrix metalloproteinases, blocks human periodontal diseases.
Triclosan is found to be anti-inflammatory, as well as antimicrobial.
Host modulation strategies are viewed as an important treatment strategy for patients with periodontal diseases.
4 times daily) between 6 and 12 weeks.The findings of this study participated and applied randomized dentifrice formulations indicated that mechanical scaling plus acetylsalicylic acid result- (0.3%, 1%, or 3% ketoprofen vs placebo) twice daily. Although ed in synergistic reductions in gingival inflammation, probing intergroup differences in bone loss rates approached signifi- pocket depth, and clinical attachment loss.22 cance (P = .06) in the trial, significant strata-by-treatment In the mid-1990s, investigators began to examine the effect interactions were detected such that patients with advanced of topical NSAID formulations on periodontal diseases in hu- periodontitis dosing with 1% or 3% (S)-ketoprofen demon- man clinical trials. Heasman et al23,24 clinically and radiograph- strated comparatively greater improvements in disease progres- ically studied 49 adult periodontitis patients randomized for sion.25 In summary, a great deal of evidence gathered from adjunctive topical flurbiprofen or placebo gels. All patients preclinical and clinical studies since the late 1970s indicates that received conventional nonsurgical periodontal therapy at base- it is possible to inhibit periodontal disease progression via the line. Over the subsequent 12 months of topical dosing, no clin- local modulation of arachidonic acid metabolites with NSAIDs ical effects of flurbiprofen on plaque and bleeding scores, prob- (Table 2). Serhan et al26 described a novel series of oxygenated ing depths, and attachment levels were observed; however, arachidonic-acid derivatives called lipoxygenase interaction significantly more sites in the flurbiprofen-treated group ex- products or lipoxins. These derivatives (eg, lipoxin A4 and li- hibited bone gain when compared with the placebo group. In a poxin B4) arise via 15- or 5-lipoxygenase activities and by cell- 55-patient clinical trial, Jeffcoat and colleagues21 assessed the to-cell interactions, and appear to serve as endogenous anti- efficacy of a topical NSAID rinse, ketorolac tromethamine, for inflammatory mediators.26 Hasturk et al27 reported that these treating adult periodontitis. At baseline, patients were random- aspirin-induced lipoxins block ligature-induced bone loss in ized for 0.1% ketorolac rinse plus peroral placebo capsule, pla- cebo rinse plus peroral 50-mg flurbiprofen capsule, or placeborinse and placebo peroral capsule. Patients were monitored radiographically, clinically, and biochemically over a 6-month period during which they administered rinses and capsules Host cytokines are another group of inflammatory mediators twice daily. Although no significant differences among the highly implicated in periodontal disease pathogenesis and in- groups were detected for clinical parameters, patients treated tensely investigated as potential chemotherapeutic targets. Cy- with topical ketorolac or systemic flurbiprofen exhibited signif- tokines, literally “cell proteins” in etymology, transmit infor- icantly reduced alveolar bone loss rates and depressed pro- mation from one cell to another via autocrine or paracrine staglandin E2 levels in gingival crevicular fluid as compared mechanisms. Following specific binding to their complementary with patients treated with placebo. Paquette and colleagues25 receptors, proinflammatory cytokines like interleukin-1 (IL-1) conducted a 12-month clinical trial evaluating the clinical effi- and tumor necrosis factor (TNF) trigger intracellular signaling cacy of topical (S)-ketoprofen dentifrices. Ninety six patients events and catabolic cell behaviors.
DENTISTRY INDIA—NOVEMBER | DECEMBER 2008

Source: http://www.dentistryindia.net/content/DI/img/2008/11/table2.pdf

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