determinants of host susceptibility in aggressive periodontitis+conference+prof. ricardo benza...
DESCRIPTION
Conferencia: "Determinantes de la susceptibilidad del huèsped en la periodontitis agresiva". Programaciòn Acadèmica Anual de la Asociaciòn Peruana de Periodoncia y Osteointegraciòn. Prof. Ricardo Benza Bedoya DDS, Auditorio del Laboratorio Graxo Smith & Kline. Lima-Peru 2007TRANSCRIPT
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RBBRBBMacchu Picchu. The lost city of the Incas. Cuzco-Perù Song ”Qori kinto ” . Interpreter : Raùl Garcìa Zàrate
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Asociaciòn Peruana de Periodoncia y Oseointegraciòn
Programa acadèmico anual 2007
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Determinantes de la susceptibilidad del huèsped en la periodontitis agresiva
Prof. Ricardo Benza Bedoya DDS
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Pràctica Clìnica de la Asignatura de Periodoncia II (2005). Facultad de Odontologìa de la Universidad de San Martìn de Porres. Profesor Responsable: Ricardo Benza Bedoya RBB
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Pràctica Pre-Clìnica del II Curso de Post-Grado de Implantologìa Oral Bàsica de la Federaciòn Odontològica del Perù. Prof. Responable: Ricardo Benza Bedoya
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OBJETIVOS1. Valorar la responsabilidad que
implica el tratamiento de las PA2. Comprender y analizar las caracterìsticas principales de las
PA
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TEMARIO1. Antecedentes2. Anormalidades radiculares en la
periodontitis agresivas.3. Infecciòn con herpes virus en
periodontitis agresivas.4. Efectos del tabaco y el stress en la
periodontitis agresivas.5. Transmisiòn hereditaria en la
periodontitis agresivas. 6. Conclusiones
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“El sabio puede sentarse en un hormiguero, pero sólo el necio se queda sentado en él.”
Proverbio chino
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Antecedentes
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Periodontitis juvenil
Periodontitis de instalaciòn temprana
Periodontitis de ràpido progreso
PERIODONTITISAGRESIVAS
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PERIODONTITISAGRESIVAS
Caracterìsticas
Destrucciòn periodontal
Personas en su mayorìa jòvenes
Agente primario extrìnseco
ràpida
severasusceptibilidad Bacterias
patògenas
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PERIODONTITISAGRESIVAS
Epidemiologìa
Caucàsicos
Hispanos
Afro-americanosChinos
Mayor prevalencia
0,1%-15%
0,12%-0,47%
Albandar JJ, Brown LJ, Lôe H. Clinical features of early onset periodontitis. J Am Dent Assoc 1997; 128: 1393–1399.Neely AL. Prevalence of juvenile periodontitis in a circumpubertal population. J Clin Periodontol 1992; 19: 367–372.Saxen L. Prevalence of juvenile periodontitis in Finland. J Clin Periodontol 1980; 7: 177–186.Sjôdin B, Matsson L, Unell L, Egelberg J. Marginal bone loss in the primary dentition of patients with juvenile periodontitis. J Clin Periodontol 1993; 20: 32–36.Buremeister JJ, Best AA, Palcanis KK, Caine FA, Ranney RR. Localized juvenile periodontitis and generalized severe periodontitis: clinical findings. J Clin Periodontol1984; 11: 181192.Lôe H, Brown LJ. Early onset periodontitis in the United States of America. J Periodontol 1991; 62: 608–616.Melvin WW, Sandifer JB, Gray JL. The prevalence and sex ratio of juvenile periodontitis in a young racially mixed population. J Periodontol 1991; 62: 330–334. RBB
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PERIODONTITISAGRESIVAS
Variaciones Epidemiologicas
Factores metodològicos
Edad Raza Factores ambientales
Muestras no aletorias
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Factores desusceptibilidad del huèsped en la PA
Family aggregation
Singlenucleotide polymorphisms
Disfunciòn neutrofìlica
Antibody response
Tabaco
StressMorfologìa radicular
Herpes virus
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Root abnormality
in APRBB
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Anormalidades radicularesen PA
Clasificación
Raìcescònicas
Raìcesdelgadas
Curvaturasradiculares
Relaciòn corono-radiculardesfavorable
Raìces fusionadas
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FACTORES LOCALESCONTRIBUYENTES
De acuerdo a laanchura radicular
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Periodontitisagresiva
Familiares depacientes con PA
Periodontitiscrònica
Pacientesperiodontalmente
sanos
Prevalencia
Anormalidadesradiculares
++++++++++
Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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Herpesvirus infections
in APRBB
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Factores de virulencia
bacterianos
Agente etiològicoprimario
ENFERMEDAD PERIODONTAL
Biofilm
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ENFERMEDAD PERIODONTAL
Destrucciòn del periodonto
Extensiòn Severidad
Composiciòn de lamicroflora
Factoresmodificadores
Susceptibilidad del huèsped
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Factormodificador
PERIODONTITISAGRESIVA
LOCALIZADA
Citomegalovirus
- Slots J. Herpesviruses in periodontal diseases. Periodontol 2000 2005; 38: 33–62.- Cappuyns I, Gugerli P, Mombelli A. Viruses in periodontal disease-a review. Oral Dis 2005; 11: 219–229. Michalowicz
BS, Ronderos M, Camara-Silva R, Contreras- A, Slots J. Human herpesviruses and Porphyromonas gingivalis are associated with early-onset periodontitis. J Periodontol 2000; 71: 981–988.
Pg
Acciòn sinèrgica
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CitomegalovirusHerpessimplex
son predictores
Porfiromonagingivalis
- Kamma JJ, Slots J. Herpesviral–bacterial interactions in aggressive periodontitis. J Clin Periodontol 2003; 30: 420–426.- Saygun I, Kubar A, Ôzdemir A, Yapar M, Slots J. Herpesviral-bacterial interrelationships in aggressive periodontitis. J Periodontal Res 2004; 39: 207–212.- Slots J, Kamma JJ, Sugar C. The herpesvirus-Porphyromonas gingivalis-periodontitis axis. J Periodontal Res 2003; 38: 318–323- Slots J. Update on human cytomegalovirus in destructive periodontal disease. Oral Microbiol Immunol 2004; 19:217–223.-Slots J. Herpesviruses in periodontal diseases. Periodontol 2000 2005; 38: 33–62.
Respuesta inmunològicacoordinada
produce
Replicaciòn
frente a laViral
Bacteriana
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Citomegalovirus(CMVH)
Virus herpes simple (VHS)
Virus Epstein Barr tipo I (VEB-1)
Actividad Enfermedad Periodontal
- Kanma JJ, Contreras A, Slots M. Herpes viruses and periodontopathic bacteria in early-onset periodontitis. J Clin Periodontol 2001; 28: 879-885. - Ling LJ, Ho CC, Wu CY, Chen YT, Hung SL. Association between human herpesviruses and the severity of periodontitis. J Periodontol 2004; 75: 1479-1485. -Yapar M, Saygun I, Ôzdemir A, Kubar A, Sahìn S, Prevalence of human herpesviruses in patients with aggressive periodontitis. J Periodontol 2003; 74: 1634-1640
Citomegalovirus (CMVH)
Virus Epstein Barr tipo I (VEB-1)
PREVALENCIA
Periodontitisagresiva
Encìasana
ALTA
ALTA
BAJA
BAJA
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Citomegalovirus (CMVH)
Núcleo
Envoltura
Càpside
CapsòmeroNùcleo de àcido nucleido DNA
Alta prevalencia de càpsides
Bolsas profundas en
jòvenes
Ting M, Contreras A, Slots J. Herpesviruses in localizedjuvenile periodontitis. J Periodontal Res 2000; 35: 17–25. RBB
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Effects of smoking
and stress in AP
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Schenkein HA, Gunsolley JC, Koertge TE, Schenkein JG, Tew JG. Smoking and its effects on early-onset periodontitis. J Am Dent Assoc 1995; 126: 1107–1113.
INCREMENTO DE LA SEVERIDAD
Tabaquismo
PAG PAL
SI NOSI NO
DISMINUCION RESPUESTA DE ANTICUERPOS
SI NODISMINUCION ANTICUERPOS PARA Aa
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Darby IB, Hodge PJ, Riggio MP, Kinane DF. Clinical and microbiological effect of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients. J Clin Periodontol 2005; 32: 200–206.
Reducciòn post-tto PS
Periodontitisagresiva
Fumadores Nofumadores
Menor MayorDetecciòn de Pi
Mayor Menor
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Stress
Factorpredisponente
Alteraciòn de funciones inmunològicas
Enfermedades infecciosas
EPN
Inflamaciòn periodontal
- Herbert TB, Cohen S. Stress and immunity in humans: a meta-analytic review. Psychosom Med 1993; 55: 364–379. - Cohen S, Williamson GM. Stress and infectious disease in humans. Psychol Bull 1991; 109: 5–24.- Monteiro da Silva AM, Oakley DA, Newman HN, Nohl FS, Lloyd HM. Psychosocial factors and adult onset rapidly progressive periodontitis. J Clin Periodontol 1996; 23: 794. RBB
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Stress
Factorpredictivo
Pèrdida de inserciòn
Correlaciòn Enfermedad periodontal
- Breivik T, Thrane PS, Murison R, Gjermo P. Emotional stress effects on immunity, gingivitis and periodontitis. Eur J Oral Sci 1996; 104: 327–334.- Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress and inadequate coping behaviors to periodontal disease. J Periodontol 1999; 70: 711–723.- Monteiro da Silva AM, Newman HN, Oakley DA. Psychosocial factors in inflammatory periodontal diseases. J Clin Periodontol 1995; 22: 516–526. RBB
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Periodontitisagresiva Stress
Pèrdida de inserciòn
P. gingivalis
T. dentìcolaCuadros agudos
Pèrdida de piezas dentarias
Yamazaki K, Tabeta K, Nakajima T, Ohsawa Y, Ueki K, Itoh H, Yoshie H. Interleukin-10 gene promoter polymorphism in Japanese patients with adult and early-onset periodontitis.J Clin Periodontol 2001; 28: 828–832. RBB
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TABACO Stress
Citoquinas Glucocorticoides
Nutrientes de periodontopatògenosPatogènesis de
enfermedadesperiodontales
Genco R. Host responses in periodontal diseases: current concepts. J Periodontol 1992; 63: 338–355.Birkedal-Hansen H. Role of cytokines and inflammatory mediators in tissue destruction. J Periodontal Res 1993; 28: 500–510. RBB
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Interleuquinas
Citoquinas
TABACO
Stress
4, 6 y 8
1beta, 6 y 8
Giannopoulou C, Kamma JJ, Mombelli A. Effect of inflammation, smoking and stress on gingival crevicular fluid cytokine level. J Clin Periodontol 2003; 30: 145– 153. RBB
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Periodonto sano
Gingivitis
Periodontitis crònica
Periodontitisagresiva
Incremento deInterleuquina 1 beta
No se incrementa
3 veces
6 veces
9 veces
Mengel R, Bacher M, Flores-De-Jacoby L. Interactions between stress, interleukin-1beta, interleukin-6 and cortisol in periodontally diseased patients. J Clin Periodontol 2002; 29: 1012–1022 RBB
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Stress
Tipo de citoquinas
Glucocorticoides
No se encuentra correlaciòn
Mengel R, Bacher M, Flores-De-Jacoby L. Interactions between stress, interleukin-1beta, interleukin-6 and cortisol in periodontally diseased patients. J Clin Periodontol 2002; 29: 1012–1022 RBB
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Periodontitisagresiva Depresiòn
Interleuquina 6
Pèrdida de inserciòn
Mengel R, Bacher M, Flores-De-Jacoby L. Interactions between stress, interleukin-1beta, interleukin-6 and cortisol in periodontally diseased patients. J Clin Periodontol 2002; 29: 1012–1022 RBB
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Inflamaciòn periodontal
Crònica Aguda
IL 6 Cèlulas plasmàticas
Garant PR, Mulvihill JE. The fine structure of gingivitis in the beagle. III. Plasma cell infiltration of the subepithelial connective tissue. J Periodontal Res 1972; 7: 161–172.
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Inheritance mode of AP
(family aggregation)
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Modo hereditariode transmisiòn
Algunos tipos
Periodontitisagresivas
siguen
Leyesmendelianas
Transmisiònde la
susceptibilidad
- Hart TC, Marazita ML, Schenkein HA, Diehl SR. Re-interpretation of the evidence for X-linked dominant inheritance of Juvenile periodontitis. J Periodontol 1992; 63: 169–173.- Melnick M, Shields ED, Bixler D. Periodontosis: a phenotypic and genetic analysis. Oral Surg Oral Med Oral Pathol 1976; 42: 32–41.Page RC, Vandesteen GE, Ebersole JL, Williams BL, Dixon LI, Altman LC. Clinical and laboratory studies of a family with a high prevalence of juvenile periodontitis. J Periodontol 1985; 56: 602–610.- Spektor MD, Vandesteen GE, Page RC. Clinical studies of one family manifesting rapidly progressive, juvenile and prepubertal periodontitis. J Periodontol 1985;
56:93–101.
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Modo hereditariode transmisiòn
raramentePeriodontitis
agresivas
No siguen
Leyesmendelianas
Transmisiònde la
susceptibilidad
Mutaciones de novo
HIROMASA YOSHIE, TETSUO KOBAYASHI, HIDEAKI TAI & JOHNAH C. GALICIA. The role of genetic polymorphisms in periodontitis. Periodontology 2000, Vol. 43, 2007, 102–132 RBB
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Cromosomas
Estructuras filiformes
ProteinasAcidos nucleicos
formado por
ADN
conforman el
formado por
Genes
pequeñas unidadesCaracterìsticas
hereditarias determinan
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Citogenética: FISH
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Leyesmendelianas
UniformidadDistribuciòn
independiente
Principios
Segregaciòn independiente
1ra. Ley 2da. Ley 2da. LeyRBB
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Principio deuniformidad
- Toda la 1ª filial, muestra el carácter dominante
- Cuando se cruzan 2 líneas puras todos los descendientes son iguales.
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F1
Progenie
Alelo dominante
Alelo recesivo
Alelo: Formas alternativas de un gen en un mismo locus, con diferentes secuencias de ADN
Locus: es el lugar específico de un gen en un cromosoma.
Si se cruzan dos razas puras para un determinado carácter, los descendientes de la primera generación son todos iguales entre sí y, a su vez, iguales a uno de sus progenitores, que es el poseedor del alelo dominante
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Principio desegregaciòn
independiente
- Los genes se presentan en parejas
- Sòlo un miembro de este par se transmite a la descendencia.
- Los factores apareados se separan durante la formación de los gametos, cada gameto recibe uno u otro factor durante su formación.
- Los organismos portan dos alelos por cada carácter.
Segregaciòn Separaciòn de loscromosomas
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F1
Progenie
F2
Progenie
Los alelos recesivos que, al cruzar dos razas puras, no se manifiestan en la primera generación (denominada F1), reaparecen en la segunda generacion (denominada F2) resultante de cruzar los individuos de la primera. Ademas la proporción en la que aparecen es de 1 a 3 respecto a los alelos dominantes.
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Principio detransmisiòn
independiente
Los genes de loci diferentes se transmiten de forma independiente
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F1
Progenie
F2
Progenie
Los alelos recesivos que, al cruzar dos razas puras, no se manifiestan en la primera generación (denominada F1), reaparecen en la segunda generacion (denominada F2) resultante de cruzar los individuos de la primera. Ademas la proporción en la que aparecen es de 1 a 3 respecto a los alelos dominantes.
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F1
Progenie
F2
Progenie
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F1
Progenie
F2
Progenie
Los caracteres que se heredan son independientes entre si y se combinan al azar al pasar a la descendencia, manifestandose en la segunda generacion filial o F2
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Herenciamendeliana
Autosòmica
Clasificaciòn
Ligada a loscromosomas
sexuales
Dominante Recesiva RBB
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Periodontitisagresiva
Autosòmicarecesiva
Autosòmicadominante
Tipos de herencia mendeliana
Ligada a los cromosomassexuales
Afroamericanos Caucàsicos
Màs prevalente
Marazita ML, Burmeister JA, Gunsolley JC, Koertge TE, Lake K, Schenkein HA. Evidence for autosomal dominant inheritance and race-specific heterogeneity in early-onset periodontitis. J Periodontol 1994; 65: 623–630. RBB
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PeriodontitisAgresiva localizada
Cromosoma 1q25
Vinculante
DIS492
?
OR 3,48
LOCUS
Li Y, Xu L, Hasturk H, Kantarci A, DePalma SR, Van Dyke TE. Localized aggressive periodontitis is linked to human chromosome 1q25. Hum Genet 2004: 114: 291–297.
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1q24.3Periodontitis agresiva 1q25
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OMIN• PERIODONTITIS, LOCALIZED
AGGRESSIVE• Alternative titles; symbols • PDLA
LOCALIZED AGGRESSIVE PERIODONTITIS; LAPPERIODONTITIS, LOCALIZED JUVENILE
• Gene map locus 1q25
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PeriodontitisAgresiva localizada
Cromosoma 4q
Vinculante No vinculante
Locus delReceptor vit D
?
- Boughman JA, Halloran SL, Roulston D, Schwartz S, Suzuki JB, Weitkamp LR, Wenk RE, Wooten R, Cohen MM. An autosomal-dominant form of juvenile periodontitis: its localization to chromosome 4 and linkage to dentinogenesis imperfecta and Gc. J Craniofac Genet Dev Biol 1986; 6: 341–350.- Hart TC, Marazita ML, McCanna KM, Schenkein HA, Diehl SR. Reevaluation of the chromosome 4q candidate region for early onset periodontitis. Human Genet 1993; 91: 416–422.
OR 3,0
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Periodontitisprepuberal
Cromosoma 11q14
Vinculante
?
Hart TC, Hart PS, Michalec MD, Zhang Y, Marazita ML, Cooper M, Yassin OM, Nusier M, Walker S. Localisation of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation. J Med Genet 2000: 37: 95–101. RBB
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HIROMASA YOSHIE, TETSUO KOBAYASHI, HIDEAKI TAI & JOHNAH C. GALICIA. The role of genetic polymorphisms in periodontitis. Periodontology 2000, Vol. 43, 2007, 102–132
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Poligènica
Mutaciones en varios loci
Se estima alrededor de 50 genes principales relacionados con la periodontitis
La frecuencia de marcadoreS genèticos muestran gran heterogenicidad entre las razas
La periodontitis agresiva y la periodontitis crònica podrìan presentar polimorfismos genèticos comunes
CONCLUSIONES
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CASOS
CLINICOS
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Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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Huanxin Meng, Li Xu, Qiyan Li, Jie Han & Yibing Zhao. Determinants of host susceptibility in aggressive periodontitis. Periodontology 2000, Vol. 43, 2007, 133–159
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• H.C. Nº= 25112006• Fecha= 25/XI/06• Edad= 35• Ocupaciòn= Electricista• Motivo de la Consulta= Dificultad masticatoria
Inflamación gingival, • Expectativas= Alivio de la inflamación gingival• AMF= Madre padece de inflamación gingival y
Mal de Parkinson, niega antecedentes mèdicos de importancia en otros familiares
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• AMP= Niega • AMO= Tratamiento
protèsico, RAR, endodoncias, profilaxis, restauraciones
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• Síntomas= Hipermovilidad dentaria, dificultad fonètica, inflamación gingival, èstos síntomas desde hace 3 semanas no progresivo, sequedad oral leve, sangrado al cepillado zona anterior, desde hace 1 año y progresivo, dificultad masticatoria por la movilidad aumentada de dientes anteriores, impacciòn alimenticia en el sector anteroinferior, ha observado retracciòn gingival progresiva, problema estètico del sector anterior, nota cambio en su engrama muscular. niega halitosis.
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Examen clìnico= Tumefacción gingival zona antero inferior vestibular y lingual, dolorosa a la palpaciòn, supura a la palpación, severo apiñamiento, secesión, enrojecimiento y movilidad con dolor, tambien en zona palatina anterior superior
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• ATM= Ruidos tipo clicking no recìprocos durante la apertura no síntomas a la palpacion y movimientos excursivos
• ATM der chasquido leve al cierre, movimientos laterales limitados
• ATM izq ruidos tipo crepitacion a la apertura ruido tipo clicking lat dere
• SNM= no hay dolor ni otros síntomas ni signos al examen clìnico a la palpaciòn
• Cierta hiperactividad muscular zona mentoniana
• Al examen con resistencia presenta mucha dificulatad para movimiento laterales
• Sonrisa gingival baja
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Diagnòstico Periodontal presuntivo:
1. Periodontitis agresiva generalizada
2. Periodontitis crònica generalizada
3. DDCA, Factores locales predisponentes de periodontitis
4. Trauma oclusal secundario pzas. 3,1, 3,2, 4,1, 4,2
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• 11/I/2007• Evolución: Paciente manifiesta que no ha progresado la
sintomatologìa• Tratamiento: Ferulizaciòn RAR, exodoncia pza. 3.1• Procedimiento: Se coloca anestesia infiltrativa a nivel de
fondo de surco de caninos inferiores, luego se coloca en lingual de caninos, no se consigue anestesia completa, se refuerza pero persiste dolor en la pza. 3,1, se vuelve a anestesiar en las zonas vestibular y lingual se produce entonces anestesia completa. Se raspa, el sextante anteroinferior, se realiza la extracción de la 3, 1 se desgasta borde incisal, se termina de raspar, se hace ajuste oclusal por desgaste selectivo dejando en anoclusion los dientes, luego se feruliza con resina fotocurable se pule por anterior, se da ATB a base de amoxicilina y analgesico antiinflamatorio diclofenaco+paracetamol, colutorios a base de clorhexidina y recomendaciones postoperatorios se cita a 7 dìas.
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• 18/I/2007• Evolución: Manifiesta estar
asintomático, no siente hipermovilidad dentaria, ha mejorado notablemente la dificultad fonètica, no siente inflamación gingival, siente alivio y frescor al enjuague bucal con clorhexidina, no siente sequedad bucal, no siente sangrado al cepillado, y observa leve retracciòn gingival
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• Tratamiento: Control y reraspado• Procedimiento: Se toma fotografìa,
se empieza a raspar, se nota sensibilidad al raspado, se cambia ATB por doxiciclina, se prescribe cepillo periodontal e interproximal y pasta dental a base de clorhexidina,
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Neutrophil defects in
APRBB
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Sistema Inmunológico
Antiinfecciosa Antitumoral
defensa
Innata Adaptativa
clasificación
Respuesta inmune
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Respuesta inmuneInnata
Cèlulas fagocìticas
Proteìnas sanguìneas
Citoquinas
Barreras quìmicas
Barreras fìsicas
comprende a las
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Cèlulas madre pluripotenciales
(steam cells)
Mèdula òsea
Linajes
se diferencian
en
Mieloide Linfoide
Granulocitos
Mastocitos Fagocitos
Megacariocitos Cèlulas dendrìticas
Linfocitos
Plaquetas EosinòfilosBasòfilos
NEUTROFILOS Monocitos
Macròfagos
B T NK
Th Tc RBB
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Neutròfilo
Linaje mieloide
+ abundante en sangre60 -75 %
Vida media corta
(Horas o pocos dìas)
Leucocito
Glòbuloblànco
Micròfago
Granulocito
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Neutròfilo
Funciòn
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FagocitosisActividad enzimàtica
Fagocitina
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AP
Neutrophil defects
Adherencia Quimiotaxis
Fagocitosis Generaciónde
superóxido
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Single nucleotide
polymorphisms
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1. Interleukin-1 gene polymorphisms in AP2. Interleukin-4 gene polymorphisms in AP3. Interleukin-10 gene polymorphisms in AP4. Tumor necrosis factor-a polymorphisms AP5. Fc gamma/alpha receptors gene
polymorphisms in AP6. Human leukocyte antigen polymorphisms in
AP7. Vitamin D receptor gene polymorphisms in
AP8. N-formylpeptide receptor gene
polymorphisms in AP9. Other gene polymorphisms in AP
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AP
Single nucleotide polymorphisms
IL
TNF alfa
Fc receptors HLA Vit D receptors
N-formilpèptide receptor
1,4,10 ganma, alfa
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