anÁlisis de artÍculos cientÍficos 3

7/27/2019 ANLISIS DE ARTCULOS CIENTFICOS 3

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ANLISIS DE ARTCULOS CIENTFICOS

CURSO:AVANCES EN ESTOMATOLOGA II

AUTOR:

Bach. Rodrguez Alayo Gerardo A.

DOCENTE:

Dr. Guardia Mndez Gustavo.

UNIVERSIDAD NACIONAL DE TRUJILLOESCUELA DE POSTGRADO

MAESTRA EN ESTOMATOLOGA

Trujillo - Per

2011


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Gingival Crevicular Fluid Myeloperoxidase inPeriodontitis and Pancreatic Cancer

Pesquisa Brasileira em Odontopediatria e Clnica Integrada, Vol. 10, Nm. 1,

enero abril, 2010, pp. 79-82

Universidade Federal da Paraba Brasil


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Objective: To determine the association between levels of GCF myeloperoxidase (GM),periodontitis and pancreatic cancer.

Method: This was a double blind randomized study. Sixty six subjects middle class divided into

four group such as pancreatic cancer with periodontitis, pancreatic cancer without periodonti ti s,non pancreati c cancer with periodonti ti s and normal (33:33 M:F; range 30-65 years) wereselected for the study were recruited for the study and GM levels were analyzed. Periodonti ti s inpatients was defined of the presence of at least seven teeth with probing depth > 5mm anddemonstrable radiographic bone loss >30 percent of tooth sites by a full mouth intraoalradiographic series. Clinical measures of the severity of periodontal disease, such as bleeding onprobing, probing depth (PD) and loss of clinical attachment level (CL) were determined using aconventi onal periodontal probe.

Results: GM levels were significantly higher in pancreatic cancer with periodontitis as comparedto others. The mean GM level in non pancreatic cancer and pancreatic cancer withoutperiodontitis were 0.680.32U/ml and 0.840.32 U/ ml, respectively. A positive correlation wasnoted between GCF meyloperoxidase and percentage of BP, CL and PD. Pancreatic cancer withperiodonti ts, pancreatic exhibited greater BP, PD and CL as compared to non- pancreatic cancer

(p


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Introduction

Periodontal disease, a common chronic oral inflammatorydisease, is characterized by destruction of soft tissue andbone. The crucial casual relation might be established byprospective treatment studies, which elucidate theconnection between treatment of poor dental health andsystemic inflammatory markers 1,2.

The oral cavity provides a gateway between the externalenvironment and the gastrointestinal tract, and it facilitatesboth food ingestion and digestion. Oral hygiene and toothloss can potentially affect gastrointestinal flora andnutritional status, and thus they have implications for thedevelopment of chronic diseases.


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Poor dental health, tooth loss, or both have beenassociated with increased risk for gastrointestinalmalignancies, including oral , esophageal , and gastriccancers3-7. It has been reported a positive association

between self-reported periodontal disease and risk ofpancreatic cancer in a cohort of 51 529 predominantlywhite US men aged 40- 75 years in the HealthProfessionals Follow- Up Study (HPFS)8.

It has been reported that myeloperoxidase levels

increase in pancreatic cancer9. Biomarkers ofperiodontal activity may be obtained from potentialproteolytic and hydrolytic enzymes of inflammatorycell origin10.


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It has been also observed that increasedmyeloperoxidase which is present in azurophilicgranules of polymorphonuclear neutrophils,activity in periodontitis as compared to

controls11. Myeloperoxidase considered apromising marker of periodontal inflammation12,13.

Hence, the present study was planned to

determine the relationship between GCFmyeloperoxidase (GM) levels in periodontitis andpancreatic cancer.


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Material and methods

This was a double blind randomized study. Sixty six subjectsmiddle class (14:12 M:F; range 30-65 years) were selectedfor the study. Patients were excluded from the study if theyhad alcholic or chronic smoker. Thrity five diagnosticpatients middle class non smoker and non alcoholic (20:15;range 33-62 years ) of pancreatic cancer were selected andoral examination were done without any other systemicdiseases.

The middle class periodontal cases comprised 20 subjects(10:10 F:M; range 24-60 years). The control middle class(healthy), non periodontal cases comprised 11 subjects (6:5F:M; range 28-63 years), none of whom exhibited clinicalsigns over 5 mm or any clinical attachment loss. In none ofthe participants was cardiovascular disease or any otherongoing general disease or infections diagnosed.


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Periodontitis in patients was defined of the presence of at

least seven teeth with probing depth > 5mm anddemonstrable radiographic bone loss >30 percent of toothsites by a full mouth intraoalradiographic series.

All participants had chronic periodontitis who had notreceived any surgical therapy previously. All subjects were

systemically healthy, with no medical conditions that wouldaffect their participation in the study.

The exclusion criteria was a course of anti inflammatory orantimicrobial therapy within the previous 3 months, ahistory of regular use of mouth washes, use of any vitamin

supplementation or mucosal lesions, chemotherapy,radiation therapy, or medications that cause xerostmia.Informed consent was obtained from the subjects.


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Clinical measures of the severity of periodontal disease, such asbleeding on probing, probing depth (PD) and loss of clinicalattachment level (CL) were determined using a conventionalperiodontal probe (Hu-Friedy Chicago, IL). At six sites around eachtooth (Mesio-buccal, midbuccal, disto-buccal, mesio-lingual, mid-lingual and disto-lingual, excluding third molars. The probe wasdirected parallel to the long axis of the tooth.

Clinical loss of attachment measurement were made from thecemento-enamel junction to bottom of the sulcus. GCF samplingand processing were done as has been described in detailelsewhere12. MPO activity (GM) is analysed as previous studies 13.

Relationships between GM; probing depths and bleeding on

probing, were analysed using a performed during SPSS (version11.0, Chicago, USA).


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Results and discussion

The mean GM level in non pancreatic cancer andpancreatic cancer without periodontitis were0.680.32U/ ml and 0.840.32 U/ml respectively (Table1, p


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A positive correlation was noted betweenGCFmeyloperoxidase and percentage of BP, CLand PD(Table 1).

In the present study, pancreatic cancer withperiodontits, pancreatic exhibited greater BP,PD and CL

as compared to non- pancreatic cancer (Table1, p


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Results and discussion

Although MPO is involved in the pathogenesis ofinflammatory periodontal diseases and pancreaticcancer, it is also found in clinically healthy sites in lowerlevels than the periodentally diseases sites.

To the best of our knowledge, there is no publishedstudy determining the effects of pancreatic on GMlevels. Therefore, we could not compare the results ofpresent study with other results. Several mechanismscould potentially explain the observations from this

study. Inflammation appears to play an important rolein pancreatic cancer pathogenesis8, although theinflammatory mediators that lead to the developmentof pancreatic cancer remain poorly defined.


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An association between periodontal disease and systemic inflammationhas been observed using biomarkers. We hypothesize that periodontaldisease may promote pancreatic carcinogenesis through inflammationthrough oxidative enzyme such as myeloperoxidase. While some authorsbelived that periodontal disease could influence pancreatic carcinogenesisthrough increased generation of carcinogens, namely nitrosamines.

Nitrosamines and gastric acidity have been hypothesized to have animportant role in pancreatic cancer; numerous studies support thishypothesis17. We were not included more oxidative stress marker andmore samples size as well as the same marker in saliva and serum toclarified the correlation between two diseases. GCF myeloperoxidase canbe easily measured and may prove to be useful in identifying patients at

risk of pancreatic cancer. Further study is required on large scale whileconsidering the risk factors and effect of periodontitis treatment onmyeloperoxidase level in saliva and serum.


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Conclusion

GM may prove to be useful in detection risk ofpancreatic cancer in periodontitis patients thisstudy also supports the inflammatory

mechanism of pancreatic cancer.


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ANLISIS


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1. Ttulo

NIVELES DE MIELOPEROXIDASA EN FLUIDOCREVICULAR GINGIVAL EN PERIODONTITIS Y

EN CNCER DE PNCREAS

Menciona la variable del estudio.

Describe su contenido de forma clara y precisa, que le permite

al lector identificar el tema fcilmente.


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2. RESUMEN

Tipo estructurado.

Expresa de forma clara y breve: el objetivo, mtodos, los resultados y laconclusin.

Menciona las palabras clave.


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3. INTRODUCCIN Describe de forma breve enfermedad periodontal.

No describe porqu los niveles de MP aumentan en ambas enfermedades. (periodontitis y cncer pancretico)

Muestran un asociacin:

Refieren un estudio: Enfermedad periodontal como riesgo para desarrollarcncer pancretico.

Niveles de MP est aumentada en cncer pancretico y tambin enenfermedad periodontal.

Por lo que quieren demostrar la relacin entre niveles de MP inPeriodontitis y cncer de pncreas.

Slo mencionan un antecedente que no est relacionado directamente

con la MP.

NO describen importancia

El objetivo de acuerdo al ttulo.


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4. Material y mtodos: Estudio aleatorio a doble ciego. No menciona pero es estudio transversal analtico.

No menciona dnde se realiz el estudio.

Criterios de exclusin eliminan sesgos.

No describe el procedimiento. NO menciona el instrumento.

Menciona pero no describe los ndices

Validez slo para su estudio.

NO menciona la prueba estadstica.

5. Resultados: Muestra una tabla, de acuerdo a los objetivos planteados.


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6. Discusin:

No comparan sus resultados por que refieren ser los primeros

en hacer esta relacin. Discuten el porqu estaran asociados los niveles altos de MP

con CP.

Describen sus limitaciones.

7. Conclusiones: NO est de acuerdo a su objetivo, porque mencionan que los

niveles de MP podra resultar til en deteccin de riesgo CP.

8. Referencias:

Segn Vancouver

Tienen ms de 5 aos de antigedad (1983)


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FUNDAMENTO TERICO

Mieloperoxidasa Es la protena ms abundante en los neutrfilos y es la nica

peroxidasa que cataliza la conversin del perxido de

hidrgeno y cloruro a cido hipocloroso

Dado el amplio espectro de reactividad, el cido hipoclorosoes un mediador de dao hstico en numerosos procesos

inflamatorios.


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La MPO reacciona con el H2O2 proveniente delas clulas fagocitarias activadas por contactocon partculas extraas, formando un

complejo enzima-sustrato con una fuertecapacidad oxidativa.

Este complejo se combina con el haluro,

generalmente cloruro, que se oxida paraformar el cido hipocloroso (HOCl).


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El cido hipocloroso es un potente agente oxidante que sibien contribuye al mecanismo de defensa contra los agentes

infecciosos, puede actuar sobre las clulas del hospedero loque provocara inactivacin de a-antiproteinasa,entrecruzamientos de protenas y reaccin con cidos grasosinsaturados para formar clorohidrinas, las cuales pueden

desestabilizar las membranas celulares. De aqu que el HOCles un candidato a causar mucho del dao mediado porneutrfilos en enfermedades inflamatorias.


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Cncer Pancretico

El cncer de pncreas es el quinto ms frecuente en occidente, conincidencia de 9 por cada 100 000 habitantes. Este tumor es solo superadoen frecuencia por el cncer de pulmn, colo rectal, mama y prstata. Setrata de una enfermedad en la que, a pesar de las mltiples modalidadesteraputicas que se han desarrollado, el pronstico sigue siendo sombro.

Menos de 20 % de los pacientes afectados sobreviven 1 ao despus deldiagnstico y la supervivencia global a 5 aos es solo 3 %.


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Aproximadamente 95 % de los tumores malignos se originan en elpncreas

exocrino y generalmente son clasificados histolgicamente comoadenocarcinomas,

los que en su mayora provienen del sistema ductal (ms de 90 % de lostumores

malignos del de la porcin exocrina del rgano).

Las neoplasias qusticas comprenden los cistoadenomas, loscistoadenocarcinomas

y el carcinoma de clulas acinares; todos ellos pueden derivarse de laporcin

exocrina. El resto de las neoplasias malignas del pncreas son: los tumores

endocrinos o de los islotes, y los linfomas pancreticos que son

extraordinariamente raros.


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Segn la Sociedad Americana de cncer, los factores deriesgo para desarrollar cncer pancretico son:

Personas mayores de 45 aos.

Hombres ligeramente ms frecuentes.

Raza negra.

Fumar cigarrillos.

Obesidad.

Sedentarismo.

Diabetes.

Pancreatitis crnica.

Antecedentes familiares.

Antecedentes genticos.

Alimentacin rica en grasas carnes rojas.

Caf.

Alcohol

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