Injectable Simvastatin in Periodontal Defects and Alveolar Ridges : Pilot Studies
Identifieur interne : 000357 ( PascalFrancis/Curation ); précédent : 000356; suivant : 000358Injectable Simvastatin in Periodontal Defects and Alveolar Ridges : Pilot Studies
Auteurs : Melissa S. Morris [États-Unis] ; Yeonju Lee [États-Unis] ; Mark T. Lavin [États-Unis] ; Peter J. Giannini [États-Unis] ; Marian J. Schmid [États-Unis] ; David B. Marx [États-Unis] ; Richard A. Reinhardt [États-Unis]Source :
- Journal of periodontology [ 0022-3492 ] ; 2008.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Histologie, Médicament.
English descriptors
- KwdEn :
Abstract
Background: Topical injection of simvastatin in methylcellulose gel was shown to stimulate bone growth and inflammation over mouse calvaria and in rat mandible models. The purpose of these pilot studies was to evaluate the potential of locally injected simvastatin in human-sized periodontal defects. Methods: Chronic periodontal defects were created bilaterally in seven 1-year-old beagle dogs: 3-walled intrabony defects distal of the mandibular second premolar and mesial of the fourth premolar and Class II furcation defects at the buccal furcation of the mandibular first molars. The edentulous space distal to the mandibular canine was left undisturbed. After 16 weeks of healing, defect sites were treated with scaling and root planing, and mandible sides were randomly selected to receive three weekly injections of 0.5 mg simvastatin in 30 μl methylcellulose gel and contralateral gel alone (n = 3) or 2.0 mg simvastatin/methylcellulose gel and contralateral gel alone (n = 4). Two months following drug application, block sections, including teeth and surrounding tissues, and submandibular lymph nodes were obtained for histomorphometric analysis. Results: Two trends were noted in this pilot study: buccal edentulous ridge thickness was 29% greater with simvastatin, 0.5 mg, compared to gel alone (P= 0.0845), and the simvastatin groups had bone-height loss in interproximal intrabony and furcation defects, but the length of new cementum in the interproximal intrabony defects was greater with simvastatin, 0.5 mg (0.35 ± 0.14 mm), compared to gel alone (0.06 ± 0.15 mm; P= 0.069). No new cementum was found in furcations. Conclusions: Multiple injections of simvastatin are not appropriate for the treatment of intrabony or furcation defects. However, this approach shows potential to augment bone thickness in closed alveolar environments.
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<series><title level="j" type="main">Journal of periodontology</title>
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<term>Bone</term>
<term>Cementum</term>
<term>Cicatrization</term>
<term>Dentistry</term>
<term>Drug</term>
<term>Healing agent</term>
<term>Histology</term>
<term>Hypocholesterolemic agent</term>
<term>Injection</term>
<term>Regeneration</term>
<term>Simvastatin</term>
<term>Tooth alveolus</term>
<term>Treatment</term>
<term>Wound</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Simvastatine</term>
<term>Histologie</term>
<term>Injection</term>
<term>Alvéole dentaire</term>
<term>Os</term>
<term>Régénération</term>
<term>Cément</term>
<term>Médicament</term>
<term>Traitement</term>
<term>Plaie</term>
<term>Cicatrisation</term>
<term>Cicatrisant</term>
<term>Dentisterie</term>
<term>Hypolipémiant</term>
<term>Hypocholestérolémiant</term>
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<front><div type="abstract" xml:lang="en">Background: Topical injection of simvastatin in methylcellulose gel was shown to stimulate bone growth and inflammation over mouse calvaria and in rat mandible models. The purpose of these pilot studies was to evaluate the potential of locally injected simvastatin in human-sized periodontal defects. Methods: Chronic periodontal defects were created bilaterally in seven 1-year-old beagle dogs: 3-walled intrabony defects distal of the mandibular second premolar and mesial of the fourth premolar and Class II furcation defects at the buccal furcation of the mandibular first molars. The edentulous space distal to the mandibular canine was left undisturbed. After 16 weeks of healing, defect sites were treated with scaling and root planing, and mandible sides were randomly selected to receive three weekly injections of 0.5 mg simvastatin in 30 μl methylcellulose gel and contralateral gel alone (n = 3) or 2.0 mg simvastatin/methylcellulose gel and contralateral gel alone (n = 4). Two months following drug application, block sections, including teeth and surrounding tissues, and submandibular lymph nodes were obtained for histomorphometric analysis. Results: Two trends were noted in this pilot study: buccal edentulous ridge thickness was 29% greater with simvastatin, 0.5 mg, compared to gel alone (P= 0.0845), and the simvastatin groups had bone-height loss in interproximal intrabony and furcation defects, but the length of new cementum in the interproximal intrabony defects was greater with simvastatin, 0.5 mg (0.35 ± 0.14 mm), compared to gel alone (0.06 ± 0.15 mm; P= 0.069). No new cementum was found in furcations. Conclusions: Multiple injections of simvastatin are not appropriate for the treatment of intrabony or furcation defects. However, this approach shows potential to augment bone thickness in closed alveolar environments.</div>
</front>
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<fA11 i1="01" i2="1"><s1>MORRIS (Melissa S.)</s1>
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<fA11 i1="02" i2="1"><s1>LEE (Yeonju)</s1>
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<fA11 i1="03" i2="1"><s1>LAVIN (Mark T.)</s1>
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<fA11 i1="04" i2="1"><s1>GIANNINI (Peter J.)</s1>
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<fA11 i1="06" i2="1"><s1>MARX (David B.)</s1>
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<fA11 i1="07" i2="1"><s1>REINHARDT (Richard A.)</s1>
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<fA14 i1="03"><s1>Department of Biometry, University of Nebraska-Lincoln</s1>
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<sZ>6 aut.</sZ>
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<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Odontología</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Hypolipémiant</s0>
<s5>30</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Antilipemic agent</s0>
<s5>30</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Hipolipemiante</s0>
<s5>30</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Hypocholestérolémiant</s0>
<s5>31</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Hypocholesterolemic agent</s0>
<s5>31</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Hipocolesterolemiante</s0>
<s5>31</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Hydroxymethylglutaryl-CoA reductase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Hydroxymethylglutaryl-CoA reductase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Hydroxymethylglutaryl-CoA reductase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Inhibiteur enzyme</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Enzyme inhibitor</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Inhibidor enzima</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Dérivé de la statine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Statin derivative</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Statina derivado</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Inhibiteur de l'HMG-CoA reductase</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>HMG-CoA reductase inhibitor</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Inhibidor HMG-CoA reductase</s0>
<s5>40</s5>
</fC07>
<fN21><s1>252</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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