EdenteV2, PascalFrancis, Curation, bibRecord, 000B14

Inflammatory mediators of the terminal dentition in adult and early onset periodontitis

Identifieur interne : 000B14 ( PascalFrancis/Curation ); précédent : 000B13; suivant : 000B15

Inflammatory mediators of the terminal dentition in adult and early onset periodontitis

Auteurs : G. E. Salvi [États-Unis, Suisse] ; C. E. Brown [États-Unis] ; K. Fujihashi [États-Unis] ; H. Kiyono [États-Unis] ; F. W. Smith [États-Unis] ; J. D. Becks [États-Unis] ; S. Offenbacher [États-Unis]

Source :

Journal of periodontal research [ 0022-3484 ] ; 1998.

RBID : Pascal:98-0342191

Descripteurs français

Pascal (Inist)
- Parodontite, Edentation, Précoce, Analyse quantitative, Interleukine, Prostaglandine, Inflammation, Monocyte, Lymphocyte, Cellule helper, Réaction chaîne polymérase, Culture cellulaire, Etiopathogénie, Homme, In vivo, In vitro.
Wicri :
- topic : Analyse quantitative, Homme.

English descriptors

KwdEn :
- Cell culture, Early, Edentulousness, Etiopathogenesis, Helper cell, Human, In vitro, In vivo, Inflammation, Interleukin, Lymphocyte, Monocyte, Periodontitis, Polymerase chain reaction, Prostaglandin, Quantitative analysis.

Abstract

Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E₂ (PGE₂), interleukin-1β (IL-1β) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN-y) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 and PGE₂ and Thl, i.e. IL-2 and IFN-y, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1β, PGE₂ and TNFα was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Thl and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Thl cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.

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A08	`01`	`1`	`ENG`	`@1 Inflammatory mediators of the terminal dentition in adult and early onset periodontitis`
A11	`01`	`1`		`@1 SALVI (G. E.)`
A11	`02`	`1`		`@1 BROWN (C. E.)`
A11	`03`	`1`		`@1 FUJIHASHI (K.)`
A11	`04`	`1`		`@1 KIYONO (H.)`
A11	`05`	`1`		`@1 SMITH (F. W.)`
A11	`06`	`1`		`@1 BECKS (J. D.)`
A11	`07`	`1`		`@1 OFFENBACHER (S.)`
A14	`01`			`@1 University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center @2 Chapel Hill, NC @3 USA @Z 1 aut. @Z 2 aut. @Z 5 aut. @Z 7 aut.`
A14	`02`			`@1 University of Berne, School of Dental Medicine @2 Berne @3 CHE @Z 1 aut.`
A14	`03`			`@1 University of Alabama at Birmingham, Department of Oral Biology, Immunobiology Vaccine Center @2 Birmingham, AL @3 USA @Z 3 aut. @Z 4 aut.`
A14	`04`			`@1 University of North Carolina at Chapel Hill, School of Dentistry, Department of Dental Ecology @2 Chapel Hill, NC @3 USA @Z 6 aut.`
A20				`@1 212-225`
A21				`@1 1998`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 15072 @5 354000072315180050`
A44				`@0 0000 @1 © 1998 INIST-CNRS. All rights reserved.`
A45				`@0 58 ref.`
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A60				`@1 P`
A61				`@0 A`
A64		`1`		`@0 Journal of periodontal research`
A66	`01`			`@0 DNK`
C01	`01`		`ENG`	@0 Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E₂ (PGE₂), interleukin-1β (IL-1β) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN-y) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 and PGE₂ and Thl, i.e. IL-2 and IFN-y, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1β, PGE₂ and TNFα was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Thl and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Thl cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.
C02	`01`	`X`		`@0 002B10C01`
C03	`01`	`X`	`FRE`	`@0 Parodontite @5 01`
C03	`01`	`X`	`ENG`	`@0 Periodontitis @5 01`
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C03	`02`	`X`	`FRE`	`@0 Edentation @5 02`
C03	`02`	`X`	`ENG`	`@0 Edentulousness @5 02`
C03	`02`	`X`	`SPA`	`@0 Edentación @5 02`
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C03	`04`	`X`	`SPA`	`@0 Análisis cuantitativo @5 04`
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C03	`05`	`X`	`SPA`	`@0 Interleuquina @5 07`
C03	`06`	`X`	`FRE`	`@0 Prostaglandine @5 08`
C03	`06`	`X`	`ENG`	`@0 Prostaglandin @5 08`
C03	`06`	`X`	`SPA`	`@0 Prostaglandina @5 08`
C03	`07`	`X`	`FRE`	`@0 Inflammation @5 09`
C03	`07`	`X`	`ENG`	`@0 Inflammation @5 09`
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C03	`08`	`X`	`FRE`	`@0 Monocyte @5 10`
C03	`08`	`X`	`ENG`	`@0 Monocyte @5 10`
C03	`08`	`X`	`SPA`	`@0 Monocito @5 10`
C03	`09`	`X`	`FRE`	`@0 Lymphocyte @5 11`
C03	`09`	`X`	`ENG`	`@0 Lymphocyte @5 11`
C03	`09`	`X`	`SPA`	`@0 Linfocito @5 11`
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C03	`10`	`X`	`SPA`	`@0 Célula auxiliar @5 12`
C03	`11`	`X`	`FRE`	`@0 Réaction chaîne polymérase @5 13`
C03	`11`	`X`	`ENG`	`@0 Polymerase chain reaction @5 13`
C03	`11`	`X`	`SPA`	`@0 Reacción cadena polimerasa @5 13`
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C03	`12`	`X`	`ENG`	`@0 Cell culture @5 16`
C03	`12`	`X`	`SPA`	`@0 Cultivo celular @5 16`
C03	`13`	`X`	`FRE`	`@0 Etiopathogénie @5 17`
C03	`13`	`X`	`ENG`	`@0 Etiopathogenesis @5 17`
C03	`13`	`X`	`SPA`	`@0 Etiopatogenia @5 17`
C03	`14`	`X`	`FRE`	`@0 Homme @5 20`
C03	`14`	`X`	`ENG`	`@0 Human @5 20`
C03	`14`	`X`	`SPA`	`@0 Hombre @5 20`
C03	`15`	`X`	`FRE`	`@0 In vivo @5 21`
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C07	`03`	`X`	`FRE`	`@0 Cytokine @5 53`
C07	`03`	`X`	`ENG`	`@0 Cytokine @5 53`
C07	`03`	`X`	`SPA`	`@0 Citoquina @5 53`
C07	`04`	`X`	`FRE`	`@0 Biologie moléculaire @5 69`
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N21				`@1 229`

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Le document en format XML

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<term>Periodontitis</term>
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<term>Inflammation</term>
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<term>Cellule helper</term>
<term>Réaction chaîne polymérase</term>
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<front><div type="abstract" xml:lang="en">Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E<sub>2</sub>
 (PGE<sub>2</sub>
), interleukin-1β (IL-1β) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN-y) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 and PGE<sub>2</sub>
 and Thl, i.e. IL-2 and IFN-y, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1β, PGE<sub>2</sub>
 and TNFα was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Thl and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Thl cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3484</s0>
</fA01>
<fA03 i2="1"><s0>J. periodontal res.</s0>
</fA03>
<fA05><s2>33</s2>
</fA05>
<fA06><s2>4</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Inflammatory mediators of the terminal dentition in adult and early onset periodontitis</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>SALVI (G. E.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>BROWN (C. E.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>FUJIHASHI (K.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>KIYONO (H.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SMITH (F. W.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>BECKS (J. D.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>OFFENBACHER (S.)</s1>
</fA11>
<fA14 i1="01"><s1>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center</s1>
<s2>Chapel Hill, NC</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>University of Berne, School of Dental Medicine</s1>
<s2>Berne</s2>
<s3>CHE</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>University of Alabama at Birmingham, Department of Oral Biology, Immunobiology Vaccine Center</s1>
<s2>Birmingham, AL</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>University of North Carolina at Chapel Hill, School of Dentistry, Department of Dental Ecology</s1>
<s2>Chapel Hill, NC</s2>
<s3>USA</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>212-225</s1>
</fA20>
<fA21><s1>1998</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>15072</s2>
<s5>354000072315180050</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 1998 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>58 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>98-0342191</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i2="1"><s0>Journal of periodontal research</s0>
</fA64>
<fA66 i1="01"><s0>DNK</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E<sub>2</sub>
 (PGE<sub>2</sub>
), interleukin-1β (IL-1β) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN-y) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 and PGE<sub>2</sub>
 and Thl, i.e. IL-2 and IFN-y, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1β, PGE<sub>2</sub>
 and TNFα was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Thl and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Thl cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B10C01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Parodontite</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Periodontitis</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parodontitis</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Edentation</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Edentulousness</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Edentación</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Précoce</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Early</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Precoz</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Analyse quantitative</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Quantitative analysis</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="GER"><s0>Quantitative Analyse</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Análisis cuantitativo</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Interleukine</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Interleukin</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Interleuquina</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Prostaglandine</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Prostaglandin</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Prostaglandina</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Inflammation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Inflammation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Inflamación</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Monocyte</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Monocyte</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Monocito</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Lymphocyte</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Lymphocyte</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Linfocito</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Cellule helper</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Helper cell</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Célula auxiliar</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Réaction chaîne polymérase</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Polymerase chain reaction</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Reacción cadena polimerasa</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Culture cellulaire</s0>
<s5>16</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Cell culture</s0>
<s5>16</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Cultivo celular</s0>
<s5>16</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Etiopathogénie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Etiopathogenesis</s0>
<s5>17</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Etiopatogenia</s0>
<s5>17</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>In vivo</s0>
<s5>21</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>In vivo</s0>
<s5>21</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>In vivo</s0>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>In vitro</s0>
<s5>22</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>In vitro</s0>
<s5>22</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA"><s0>In vitro</s0>
<s5>22</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Stomatologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Stomatology</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Estomatología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Parodontopathie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Periodontal disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Parodontopatía</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>53</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>53</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>53</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Biologie moléculaire</s0>
<s5>69</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Molecular biology</s0>
<s5>69</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Biología molecular</s0>
<s5>69</s5>
</fC07>
<fN21><s1>229</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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Inflammatory mediators of the terminal dentition in adult and early onset periodontitis

Inflammatory mediators of the terminal dentition in adult and early onset periodontitis

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