Ahora nos vemos en enero lean libro
CROMOSOMA 6
Tengan excelentes vacaciones y regresen con mucho ánimo para seguir aprendiendo
Saludos
martes, 4 de diciembre de 2012
martes, 27 de noviembre de 2012
jueves, 15 de noviembre de 2012
miércoles, 14 de noviembre de 2012
MONUMENTO A LA REVOLUCION
Tarea cultural:
ir al monumento y museo a la revolución y traer fotografias de la parte de arriba y la plaza de la republica, traer escrito su resumen de que significo la revolución y la biografia de Porfirio Diaz
ir al monumento y museo a la revolución y traer fotografias de la parte de arriba y la plaza de la republica, traer escrito su resumen de que significo la revolución y la biografia de Porfirio Diaz
miércoles, 31 de octubre de 2012
Tarea cultural
Museo de DOLORES OLMEDO
XOCHIMILCO
XOCHIMILCO
Concurso Catrina
12º Concurso de Disfraces de la Calavera Catrina
El Museo Dolores Olmedo te invita a participar en su ya tradicional concurso de disfraces y celebrar el Día de Muertos con La Catrina, uno de los personajes más simpáticos de la temporada. Este año el concurso llevará por tema La Catrina Independiente y Revolucionaria. Bases de participación: 1. El traje deberá inspirarse en alguno de los personajes de la Independencia o de la Revolución de nuestro país.
2. El disfraz puede estar elaborado en cualquier material.
3. El concurso está abierto para mayores de 6 años.
4. Se manejarán dos categorías: niños/jóvenes de 6 a 17 años y adultos de 18 años en adelante.
5. Sólo se aceptará un disfraz por participante.
6. No podrán participar disfraces que se hayan presentado en concursos anteriores.
7. Los participantes deberán:
Los resultados se darán a conocer el mismo día, al finalizar el concurso, y se realizará la entrega de premios.
Premios:
- Los ganadores del primer lugar de ambas categorías serán acreedores a un viaje de 3 días y 2 noches al estado de Chiapas (avión, hotel y recorrido turístico; no incluye alimentos).
- Se otorgarán constancias de participación a todos los concursantes.
Informes: Dirección de Colecciones y Servicios Educativos
T 5555 1221 / 5555 1016 ext. 139 seducat@mdop.org.mx |
Hispanos con el dentista en USA
Medscape Medical News from the:
This coverage is not sanctioned by, nor a part of, the American Dental Association.
Hispanic Patients Challenge Many Dentists
An Expert Interview With Sarita Arteaga, DMD
Topic Alert
Receive an email from Medscape whenever new articles on this topic are available.
Drug & Reference Information
SAN FRANCISCO, California — Editor's note: The percentage of Hispanics in the United States has grown steadily in recent decades, but few dentists are Hispanic.
A presentation on serving this population was featured here at the American Dental Association (ADA) 2012 Annual Session.Medscape Medical News interviewed presenter Sarita Arteaga, DMD, associate professor of dentistry at the University of Connecticut in Hartford, to discuss issues related to this population.
Medscape: How did you get interested in the relationship between dentists and their Hispanic patients?
Dr. Arteaga: I am past president of the Hispanic Dental Association. One of the things we have as our mission is to improve the oral health of Hispanic patients. And many dentists ask about this.
Medscape: What do dentists need to know to work well with Hispanic patients?
Dr. Arteaga: Being able to educate the patient is really important. It is not just a matter of language; it is important to be able to understand the patient.
Medscape: What gets in the way of that understanding?
Dr. Arteaga: A lot of practitioners think that all Hispanics are immigrants who are not going to stay around, so they don't give them a full treatment plan; they just address their urgent issues. They do not think of them as needing a dental home. They may also think the patients are poor, even though in reality many Hispanics make a good living. With that will come the idea that these patients do not have dental insurance, so [the practitioners] will just give them the minimum treatment. That can be a huge detriment to oral health. Practitioners also may think Hispanics do not care about their teeth. For example, they might just do an extraction and not recommend an implant. They may think people who do not understand the language are not intelligent enough to understand other things, so they won't try to educate their patients or explain all the treatment options.
Medscape: Are there any real cultural differences that can affect oral health?
Dr. Arteaga: Some Hispanics arrive late for their appointment — they may stop to socialize on the way — so you might want to ask the patient to come early. Hispanics may prioritize oral health differently. They may feel that they are more knowledgeable than the dentist about oral health. They also may not bring the child to the dentist unless there is a problem. We did a survey in collaboration with Crest and Oral B, and found that two thirds of Hispanics actually thought they could brush cavities away.
Medscape: How can dentists surmount these misunderstandings?
Dr. Arteaga: It is important to educate yourself as much as you can about different cultures, and understand some of the myths.
Medscape: How can you best educate the Hispanic population?
Dr. Arteaga: A lot of Hispanics will look at their mail or media sources, so maybe you can use some of those.
Medscape: Would a brochure in Spanish be helpful?
Dr. Arteaga: A brochure might help. But language is only part of the issue. They are more likely to trust a newspaper or magazine that they already read, so you could show them articles about oral health in these media.
Medscape: Are immigrants from Latin America likely to have different attitudes about fluoridated water?
Dr. Arteaga: It depends on the country. In some places, like Mexico, in many towns they would not drink tap water; they might not be willing to drink it here either.
Medscape: In that case, should you recommend fluoride supplements?
Dr. Arteaga: You could. You would have to explain what it is. You could also offer topical fluoride in the office. But once again, you have to explain the benefits.
Medscape: If no one in the dental office speaks Spanish, what is the best way to communicate?
Dr. Arteaga: There are dental Spanish apps for Android and Apple products. Most Hispanic patients are very grateful if you even try.
Medscape: Do you recommend asking patients to bring their own interpreter?
Dr. Arteaga: There can be HIPAA [Health Insurance Portability and Accountability Act] complications with the patient providing a translator if they are underage. You have to get consent. In most states, you can do this by getting signatures on the appropriate forms.
In certain states, it's illegal for the patient's child to translate. An underage individual might be making decisions, and it is not clear if the patient is giving consent.
Medscape: Are dental schools preparing students to work with Hispanic people?
Dr. Arteaga: At the University of Connecticut dental school, we include cultural awareness as part of the curriculum. We have a whole course on treating diversity. We try to incorporate it as an externship so that the students learn it while they are out in the clinics. The didactic course is about 25 hours. We have standardized patients, who are like patient actors, and we give them sample cases.
Medscape: Are there advantages to working with Hispanic patients?
Dr. Arteaga: Many Hispanic families go together wherever they can. Sometimes dentists are surprised to see the whole family show up for one person's appointment. I sometimes tell dentists that this is an opportunity to recruit the whole family. The Hispanic population is growing and dentists should be aware that they are going to have an Hispanic person in their practice sooner or later.
Dr. Arteaga has disclosed no relevant financial relationships.
Un dia como hoy
Un día como hoy pero hace 400 años Miguel Ángel termino de pintar la Bóveda de la Capilla Sixtina. Para mi una de ls Grandes Obras Maestras, no sólo de Miguel Ángel, sino de la humanidad
El conjunto de pinturas al fresco realizadas para decorar la bóveda de la Capilla Sixtina, en la Ciudad del Vaticano (Roma), fue pintada entre 1508 y 1512 por Miguel Ángel y es una de las obras pictóricas más complejas y más bellas de toda la historia del arte, encargada por el papa Julio II para sustituir la pintura que había en aquel momento a base de un fondo azul con estrellas doradas, que había sido realizada por Piero Matteo d'Amelia, según la tradición de los templos paleocristianos.
En la bóveda de cañón rebajada, el artista diseñó una complicada arquitectura simulada donde incluyó el desarrollo de la historia de la humanidad, con historias del Génesis, domo la Creación narradas desde el extremo del altar hasta la puerta de entrada de la capilla en más de 500m2 de espacio. Desde 1508 hasta el otoño de 1512 Miguel Ángel trabajó solo en su realización, sin ayudantes. El 1 de noviembre de 1512 se celebró la primera misa en la capilla, después de acabada la pintura de la bóveda.
Años después Miguel Ángel, terminó entre 1536-1541 el decorado de la Capilla con otra de sus más grandes obras,
El conjunto de pinturas al fresco realizadas para decorar la bóveda de la Capilla Sixtina, en la Ciudad del Vaticano (Roma), fue pintada entre 1508 y 1512 por Miguel Ángel y es una de las obras pictóricas más complejas y más bellas de toda la historia del arte, encargada por el papa Julio II para sustituir la pintura que había en aquel momento a base de un fondo azul con estrellas doradas, que había sido realizada por Piero Matteo d'Amelia, según la tradición de los templos paleocristianos.
En la bóveda de cañón rebajada, el artista diseñó una complicada arquitectura simulada donde incluyó el desarrollo de la historia de la humanidad, con historias del Génesis, domo la Creación narradas desde el extremo del altar hasta la puerta de entrada de la capilla en más de 500m2 de espacio. Desde 1508 hasta el otoño de 1512 Miguel Ángel trabajó solo en su realización, sin ayudantes. El 1 de noviembre de 1512 se celebró la primera misa en la capilla, después de acabada la pintura de la bóveda.
Años después Miguel Ángel, terminó entre 1536-1541 el decorado de la Capilla con otra de sus más grandes obras,
viernes, 19 de octubre de 2012
miércoles, 17 de octubre de 2012
Tarea cultural de finde semana octubre 20 y 21 entregar resumen escrito a mano
1983: Hantavirus (hemorrhagic fever)
1986: Human herpesvirus-6 (multiple diseases)
1988: Hepatitis E virus (hepatitis E)
1993: Sin Nombre virus (hantavirus pulmonary syndrome)
1995: Kaposi sarcoma herpesvirus (Kaposi sarcoma)
1997: Transfusion-transmitted virus (transfusion-transmitted viral disease)
1998: Nipah virus (pig-borne; encephalitis and respiratory disease)
2001: Metapneumovirus (respiratory viral illness)
2009: Influenza H1N1 (pandemic influenza)
2011: Huaiyangshan virus (hemorrhagic fever-like illness)
miércoles, 3 de octubre de 2012
TAREA CULTURAL
FIND E SEMANA DE MUSEO
LA MARCHA DE LA HUMANIDAD
POLYFORUM SIQUEIROS
LUZ Y SONIDO¡¡¡¡¡
LLEVEN SU CREDENCIAL TIENEN DESCUENTO
LA MARCHA DE LA HUMANIDAD
POLYFORUM SIQUEIROS
LUZ Y SONIDO¡¡¡¡¡
LLEVEN SU CREDENCIAL TIENEN DESCUENTO
domingo, 30 de septiembre de 2012
Para buscar el articulo original¡¡¡
Hallan proteínas que causan metástasis
Se identificaron seis proteínas que están involucradas en el crecimiento del tumor de cáncer de mama y en la expansión del mal hacia el pulmón
La inhibición de las proteínas puede usarse cono tratamientos terapeúticos.(Foto: Archivo El Universal )
Domingo 30 de septiembre de 2012Gerardo Del Castillo | El Universal04:05 Un grupo de investigadores españoles hallaron seis proteínas que favorecen la diseminación metastática del cáncer de mama hacia el pulmón. La eliminación de estas soluciones compuestasdisminuye el crecimiento del tumor en la mama, así como su expansión, lo que podría devenir en futuras terapias.
Así mismo lograron identificar una "huella genética" en las células de cáncer de mama que permiten predecir la evolución del tumor, así como recurrencias en la enfermedad y las probabilidades de que se desarrolle la metástasis.
La inactivación de las proteína Vav3 y Vav2, que regularmente se encuentra en altas concentraciones en el cáncer de mama, en modelos animales permitió conocer cuál era el papel que jugaban en un tumor canceroso.
Los resultado mostraron que ambos compuestos, en coordinación, activaban el crecimiento del tumor y posteriormente la metástasis. Los especialistas investigaron si estas proteínas podían ser usadas como indicadores para un diagnostico clínico.
Así se encontraron otras 4 proteínas, Ilk, Inhibina betaA, ciclooxigenasa 2 y Tacstd2, las cuales cuando se inhibían genéticamente disminuía el tumor y se eliminaba el riesgo de metástasis.
La inhibición de estas seis proteínas, de forma conjunta o individual, pueden usarse comoposibles tratamiento terapéuticos.
Con métodos metagenómicos y bioinformáticos, los investigadores confirmaron una "firma genética" en pacientes con cáncer de mama, la cual se limita a 102 genes que podrían predecir los parámetros de evolución del tumor canceroso.
Así se podría conocer el grado de supervivencia de la persona que padece el tumor, su posibilidad de recurrencia de la enfermedad o el posible desarrollo de metástasis, de acuerdo al Consejo Superior de Investigaciones Científicas, de España.
Tal como declara uno de los investigadores José Bustelo, de la Universidad de Salamanca, "este trabajo ha identificado nuevas posibilidades terapéuticas y demostrado a nivel pre-clínico que potencialmente serían de interés (las proteínas) en este tipo de cáncer."
Y agrega "sin embargo, su implementación práctica vendrá condicionada por la capacidad de desarrollar en un futuro próximo fármacos capaces de inhibirlas de manera efectiva y que funcionen sin efectos colaterales tóxicos en los pacientes con cáncer".
En cuanto a la "huella genética", esta podría implementarse rápidamente si es que una empresa está interesada en su comercialización.
Los resultados del estudio, que aparecerán en la revista Science Signaling, ha proporcionado a los investigadores dos patentes que protegen las posibilidades terapéuticas y la "firma genética" de diagnóstico, ambas registradas por la Universidad de Salamanca.
Así mismo lograron identificar una "huella genética" en las células de cáncer de mama que permiten predecir la evolución del tumor, así como recurrencias en la enfermedad y las probabilidades de que se desarrolle la metástasis.
La inactivación de las proteína Vav3 y Vav2, que regularmente se encuentra en altas concentraciones en el cáncer de mama, en modelos animales permitió conocer cuál era el papel que jugaban en un tumor canceroso.
Los resultado mostraron que ambos compuestos, en coordinación, activaban el crecimiento del tumor y posteriormente la metástasis. Los especialistas investigaron si estas proteínas podían ser usadas como indicadores para un diagnostico clínico.
Así se encontraron otras 4 proteínas, Ilk, Inhibina betaA, ciclooxigenasa 2 y Tacstd2, las cuales cuando se inhibían genéticamente disminuía el tumor y se eliminaba el riesgo de metástasis.
La inhibición de estas seis proteínas, de forma conjunta o individual, pueden usarse comoposibles tratamiento terapéuticos.
Con métodos metagenómicos y bioinformáticos, los investigadores confirmaron una "firma genética" en pacientes con cáncer de mama, la cual se limita a 102 genes que podrían predecir los parámetros de evolución del tumor canceroso.
Así se podría conocer el grado de supervivencia de la persona que padece el tumor, su posibilidad de recurrencia de la enfermedad o el posible desarrollo de metástasis, de acuerdo al Consejo Superior de Investigaciones Científicas, de España.
Tal como declara uno de los investigadores José Bustelo, de la Universidad de Salamanca, "este trabajo ha identificado nuevas posibilidades terapéuticas y demostrado a nivel pre-clínico que potencialmente serían de interés (las proteínas) en este tipo de cáncer."
Y agrega "sin embargo, su implementación práctica vendrá condicionada por la capacidad de desarrollar en un futuro próximo fármacos capaces de inhibirlas de manera efectiva y que funcionen sin efectos colaterales tóxicos en los pacientes con cáncer".
En cuanto a la "huella genética", esta podría implementarse rápidamente si es que una empresa está interesada en su comercialización.
Los resultados del estudio, que aparecerán en la revista Science Signaling, ha proporcionado a los investigadores dos patentes que protegen las posibilidades terapéuticas y la "firma genética" de diagnóstico, ambas registradas por la Universidad de Salamanca.
martes, 25 de septiembre de 2012
MARCHA DE LA HUMANIDAD
Polyforum siqueiros tarea cultural apra este find e semana busquen dia y hora del espectaculo de luz y sonido
Less Smoking and Drinking Tied to Oral Cancers
Other Factors at Play
Roxanne Nelson
September
18, 2012 — The prevalence of smoking and alcohol use has declined over the past
few decades in patients with oral cavity cancer, according to a new
single-institution study. Because these factors are associated with the
disease, it is now considered likely that other causes play a role in the
pathogenesis of oral cancer.
Researchers
from the Memorial Sloan-Kettering Cancer Center in New York City found that
during the past 25 years, there has been a progressive decline in tobacco use
in this cancer population at their institution. From 1985 to 1990, 80% of
patients treated there used tobacco; from 2005 to 2008, 55% did.
In
addition, there was a decline in the daily amount of tobacco used. In the early
cohort, 55% of patients smoked more than 1 pack per day, whereas in the late
cohort, 30% did (P < .001).
The
researchers found that alcohol consumption also declined over the decades, from
80% in the early cohort to 67% in the late cohort (P < .007). In addition,
the percentage of patients who consumed more than 3 drinks per day decreased
from 23% in the early cohort to only 9% in late cohort (P < .001).
These
findings were published in the September
issue of the Archives of Otolaryngology — Head & Neck Surgery.
Not
Quite That Simple
The
worldwide incidence of oral cancer is increasing, explained lead author Ian
Ganly, MD, PhD, a surgeon at the Memorial Sloan-Kettering Cancer Center.
"In the United States, it is actually decreasing, largely due to the
reduction in smoking," he said.
But
it is not quite that simple, he noted. The number of cases seen at his
institution has doubled over what was seen 25 years ago, he reported. "Our
numbers are increasing," Dr. Ganly told Medscape Medical News, "but
the patient population is quite different. Before it was largely a
smoking/alcohol population; now we see more nonsmokers and nondrinkers with
oral cancer than smoker and drinkers," he explained.
The
researchers do not know why the demographics have changed. He pointed out that
the sex and age distribution and disease staging of their patients is the same,
and that survival figures are stable.
However,
they are seeing more oral tongue cancer in patients younger than 60 years. For
patients younger than 60 years, the percentage of oral and nonoral tongue
cancer cases is unchanged, Dr. Ganly said. For those younger than 60 years, the
percentage of oral tongue cases is increasing and the percentage of nonoral
tongue cancer cases is decreasing, he reported.
Other
Causes
A
recent study showed that the incidence of oral tongue squamous cell carcinoma
increased 28% from 1975 and 2007 in people 18 to 44 years of age, as previously reported by Medscape
Medical News (J Clin Oncol. 2011;29:1488-1494). Among white people in this age
group, the incidence increased 67%; among white women, the incidence jumped a
dramatic 111%.
These
data "suggest we are seeing a change in the epidemiology of this disease —
mainly in oral tongue cancer," said Dr. Ganly. "There must be another
cause for this, but we do not know what it is," he acknowledged.
Studies
suggest that human papillomavirus (HPV) might be
the driver behind a rising increase of oropharyngeal squamous cell carcinoma.
Dr. Ganly notes that a change in the oral microbiome might be another cause.
"Clearly, more research is needed to identify what is causing this
change," he said.
Changing
Trends
Oral
cavity cancer is the eighth most frequent cancer in the world, and the
traditional causes are smoking and alcohol consumption. However, major cancer
registries, such as the Surveillance, Epidemiology and End Results (SEER)
database, do not collect information on tobacco and alcohol use in patients
with cancer, and the current literature in head and neck cancer has not
reported on trends in tobacco and alcohol use among patients with oral cancer,
note Dr. Ganly and colleagues.
The
scarcity of these data is important, according to the researchers, because
recent studies of oropharynx cancer have shown a causal change.
After
a review of the medical records of patients with oral cavity cancer from 1985
to 2009, the researchers included data from 1617 patients in their analysis.
To
compare trends in alcohol and tobacco use, the patients were divided into 5
different cohorts, according to the date of initial surgery: 274 patients were
treated from 1985 to 1990; 250 were treated from 1990 to 1994; 315 were treated
from 1995 to 1999; 356 were treated from 2000 to 2004; and 422 were treated
from 2005 to 2009.
The
median age of patients was 62.5 years (range, 15.0 to 97.0 years), 86.5% were
white, and 56.0% were men. The most common cancer subsite was oral tongue
(49.0%), and 72.0% had T1 or T2 tumors. During the study period, there were no
changes in sex or age distribution, but there was an increase in the percentage
of nonwhite patients (9.1% to 16.6%). This change is primarily related to the
increase in the number of patients of Asian origin.
The
researchers report that over time, there was a small increase in the number of
buccal mucosa cancer cases and a reduction in the number of cases of floor of
mouth cancer.
When
stratified by sex, the decrease in the prevalence of alcohol and tobacco use
was larger in women than in men. This decrease was statistically significant
for men and women who used tobacco (P < .05) but not for those who used
alcohol (P = .06).
The
authors have disclosed no relevant financial relationships.
Medscape
Medical News © 2012 WebMD, LLC
Send
comments and news tips to news@medscape.net.
jueves, 20 de septiembre de 2012
Articulo del cancer de Sigmund Freud
Lean ela rticulo de la evolucion y tratamiento del cancer de Sigmun Freud, para el lunes de la proxima semana.
INTRODUCTION
In May 1999 members of the West Kent Medico- Chirurgical Society visited the city of Thessaloniki, in Greece. As part of the activities, we organised a scientific meeting about historical medical subjects. It was sug- gested, that I, an Oral and Maxillofacial Surgeon, should speak to our English colleagues about Sigmund Freud’s oral cancer. Many of those who attended the meeting wanted to see the publication of Freud’s illness, which has elements of a great classical epic (comical at times, but always courageous and tragic).
This great man and maxillofacial surgeon did all the necessary operations (33 procedures in all) and made most of the prostheses required for rehabilitation. For 16 subse- quent years, he provided care and support during Freud’s illness. This meant a great commitment as it required nu- merous and frequent appointments. In 1924 alone 74 ap- pointments were needed. A graphic representation of this period was done in German by Pichler himself, but in an obscure form of shorthand invented by his father. The only other person who understood the shorthand writing was Pichler’s secretary, who copied all the notes in clear handwriting in the German language. The translation into English was done by Dr Lagos Levy and the accuracy of the translation was revised by Dr Maxim Shur, Freud’s faithful friend and physician. The Freud museum at 20, Maresfield Gardens, Swiss Cottage, London was Sigmund Freud’s home for the last year of his life from 1938 to 1939.
martes, 28 de agosto de 2012
lunes, 20 de agosto de 2012
whonamedit.com buscar biografias¡¡¡¡¡
{821} and the Systematized Nomenclature of Medicine (http://snomed.org). Behaviour is coded /0 for benign tumours, /3 for malignant tumours, and /1 for borderline or uncertain behaviour.
Biography of Rudolf Ludwig Karl Virchow
Rudolf Virchow is considered the most prominent German physician of the 19th century, his long and successful career reflecting the ascendancy of German medicine after 1840. Virchow pioneered the modern concept of pathological processes by his application of the cell theory to explain the effects of disease in the organs and tissues of the body. He emphasized that diseases arose, not in organs or tissues in general, but primarily in their individual cells. Moreover, he campaigned vigorously for social reforms and contributed to the development of anthropology as a modern science. He worked vigorously to make the methods of natural science supreme in the medical sciences.- Rudolf Ludwig Karl Virchow
1) Lepra cell. 2) the lacunae in osseous tissue containing the bone cells; also the bone cells themselves. 3) connective tissue cells between the laminae of fibrous tissue in the cornea. These are also known as corneal corpuscles..
Description
1) Lepra cell.
2) The lacunae in osseous tissue containing the bone cells; also the bone cells themselves.
3) Connective tissue cells between the laminae of fibrous tissue in the cornea. These are also known as corneal corpuscles.
2) The lacunae in osseous tissue containing the bone cells; also the bone cells themselves.
3) Connective tissue cells between the laminae of fibrous tissue in the cornea. These are also known as corneal corpuscles.
miércoles, 15 de agosto de 2012
PADRE DE LA PATOLOGIA BUCAL
Thomas Bond's New Book of Oral Diseases is dedicated to Thomas E. Bond Jr., M.D., of Baltimore, Maryland, who was the first professor of oral pathology, wrote the first textbook of oral pathology and is considered by some to be the Father of Oral & Maxillofacial Pathology. His text, A Practical Treatise on Dental Medicine, was published from the U.S. in 1848, with second and third editions published in 1850 and 1863. The book was initially produced by Dr. Bond at the request of the first national dental association, the American Association of Dental Surgeons.
Our new 4th edition of Bond's Book is intended as a comprehensive review of the field of oral and maxillofacial pathology, with an emphasis on the clinical features of disease. Diseases are grouped according to common tissues of origin or common etiologies, but alternate indexes are available, including an alphabetical listing and a differential diagnosis listing. Topics and references are updated periodically as new information becomes available. The 4th edition was published on the web in 1999 as an incomplete manuscript. It is expected to be completed by February, 2001.
martes, 14 de agosto de 2012
Que opinan?????
Olympics-Performance Enhancing Dope: Should Sport Ban Cannabis?
By Kate Kelland
LONDON (Reuters) Aug 06 - The expulsion of an American judo player from the London 2012 Olympic Games on Monday after he tested positive for marijuana prompted scientists to question the sense behind the drug's inclusion on the World Anti Doping Agency's (WADA) banned list.
Few experts think marijuana, or cannabis, can do much to enhance the kind of speed, strength, power or precision that Olympic athletes strive for.
And many wonder whether the expensive time and effort of sporting drug testers might be better spent catching serious cheats who top up their blood with EPO or pop anabolic steroids to boost testosterone levels and muscle growth.
"There's no evidence cannabis is ever performance enhancing in sport, and since its use is legal in a number of countries, there's no reason for it to be banned by WADA," said David Nutt, a professor of neuropsychopharmacology at Imperial College London.
"I can't think of any sport in which it would be an advantage. And it seems ludicrous that someone could quite legally smoke cannabis in Amsterdam in the morning and then come over to London in the afternoon and be banned from competing."
The heart of the problem is where to draw the line between performance enhancing drugs - which many experts agree should be prohibited in sports because they make the contest unfair - and recreational drugs, which have little bearing on performance but could give sport a bad image.
SCIENTIFIC OR POLITICAL?
Since marijuana is a forbidden drug on WADA's current list, athletes face a two-year ban if it is found in their system while they are in competition.
But the anti-doping body does not sanction athletes who test positive for marijuana outside of competition times, while they are in training camps or during rest periods.
Scientists say this smacks of double standards and suggests WADA bans cannabis for political rather than scientific reasons.
"The problem is the elite athletes should be seen as role models for young kids, and so they ban cannabis because they don't want to have the image of gold medalists smoking joints," said one British-based sports scientist who asked not to be identified because of the sensitivity of the issue.
A photo of the American swimming champion Michael Phelps smoking marijuana through a glass pipe "bong" in 2009 sparked criticism from the U.S. Olympic Committee.
In a statement released shortly after the picture was published by a British tabloid newspaper, Phelps admitted to smoking pot and apologized for what he described as "bad judgment." But he faced no sporting sanction for his behavior because it was not "in competition."
Experts say that row, as well as Monday's ruling on American judoka Nick Delpopolo - who said he inadvertently ate the drug in a marijuana brownie - is far more to do with the image of sport than any form of cheating.
"It's hard to imagine how smoking a joint or eating marijuana brownies is going to help somebody in judo," said Michael Joyner, a member of the Physiological Society and a researcher at the Mayo Clinic in Minnesota in the United States.
"My advice to WADA is that they should focus on drugs that are clearly performance enhancing in the sports where they are clearly performance enhancing."
SENSITIVE ISSUE
Some national sporting bodies are also kicking back against WADA's stance.
Australia's Coalition of Major Professional and Participation Sports called in May for marijuana to be removed from the list saying it was wrong to group it with performance enhancing drugs like human growth hormone and steroids.
Substances on WADA's banned list should meet two of the following criteria: they are proven to be performance enhancing, they are dangerous to the health of athletes, or they are contrary to the spirit of sport.
While there are few signs that marijuana can enhance sporting performance, there is evidence to suggest it could have a negative impact.
Studies have shown that THC - the ingredient in cannabis that induces the "high" - increases blood pressure and heart rate while also decreasing cardiac stroke volume, leading to diminished peak performance.
It can also slow reaction times, cause problems with coordination, reduce hand-eye coordination, and interfere with visual perception.
Anti-doping authorities were not keen to discuss the issue on Monday. Officials at UK Anti-Doping declined to comment, and an email sent by Reuters to WADA's media relations office asking for a statement on why cannabis is banned got no response.
Reuters Health Information © 2012
martes, 12 de junio de 2012
Para los que les interesa la endodoncia
Experimental evidence supports the abscess theory of development of radicular cysts
P.N.R. Nair, BVSc, DVM, PhD (Hon),a Göran Sundqvist, DDS, PhD,b Ulf Sjögren, DDS, PhD,b Zurich, Switzerland, and Umeå, Sweden UNIVERSITY OF ZURICH AND UMEÅ UNIVERSITY
Objective. The objective of this study was to experimentally induce inflammatory cysts in an animal model so as to test the hypothesis that radicular cysts develop via the “abscess pathway.” Methodology. Twenty-eight perforated custom-made Teflon cages were surgically implanted into defined locations in the back of 7 Sprague Dawley rats. A week after the implantation of the cages, a known quantity of freshly grown, close allogeneic oral keratinocytes in phosphate buffer solution (PBS) was injected into each cage. One cage per animal was treated as the control that received only epithelial cells. The remaining 3 cages of each animal were trials. Seven days post epithelial cell inoculation; a suspension of 0.2 mL of Fusobacterium nucleatum (108 bacteria per mL) was injected into each of the 3 trial cages. Two, 12, and 24 weeks after the inoculation of the bacteria, the cages were taken out, and the tissue contents were fixed and processed by correlative light and transmission electron microscopy. Sixteen of the 21 trial cages could be processed and yielded results.
Results. Inoculations of epithelial cells followed 1 week later by F. nucleatum into tissue cages resulted in the development inflammatory cysts in 2 of the 16 cages. The 2 cages contained a total of 4 cystic sites. None of the control cages showed the presence of any cyst-like pathology. Conclusions. Inflammatory cysts were induced by initiating acute inflammatory foci (abscess/necrotic area) by bacterial injection that got enclosed by a proliferating epithelium. This finding provides strong experimental evidence in support of the “abscess theory” of development of radicular cysts. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;xx:xxx)
martes, 22 de mayo de 2012
entren y vean este caso
http://www.medscape.com/viewarticle/761811?src=mp&spon=38
medscape. tiene mucha informacion
medscape. tiene mucha informacion
lunes, 21 de mayo de 2012
Articulo
Articulo que nos envia Gerardo Jasso
The Laryngoscope
VC 2011 The American Laryngological, Rhinological and Otological Society, Inc.
Case Report
A Case of Preoperative ‘‘First-Bite Syndrome’’ Associated with Mucoepidermoid Carcinoma of the Parotid Gland
Gillian R. Diercks, MD; David E. Rosow, MD; Mukesh Prasad, MD; William I. Kuhel, MD
First-bite syndrome, characterized by excruciating pain in the parotid region after the first few bites of food, can be seen after surgery of the parapharyngeal space. Herein we describe a patient with no prior surgical history who presented with facial pain consistent with first-bite syndrome. Imaging and ultrasound-guided FNA revealed a nonpalpable mucoepider- moid carcinoma of the parotid gland, which was removed surgically with facial nerve preservation. After surgical intervention, the patient’s symptoms resolved. An extensive literature review demonstrated that this is the first description of a preopera- tive first-bite syndrome, or first-bite syndrome associated with the presence a parotid mass.
Laryngoscope, 121:760–762, 2011
viernes, 2 de marzo de 2012
Para la duda de las rugas palatinas¡¡¡¡¡¡
J Am Dent Assoc. 2008 Nov;139(11):1471-8.
Palatine rugae and their significance in clinical dentistry: a review of the literature.
Patil MS, Patil SB, Acharya AB.
Source
Department of Oral and Maxillofacial Pathology, Mahatma Gandhi Dental College and Hospital, RIICO Institutional Area, Sitapura, Jaipur, Rajasthan, India. sbpatilmanu@gmail.com
Abstract
BACKGROUND:
The palatine rugae have interested dentists not only because of their typical pattern of orientation but also because of their usefulness as a reference landmark in various dental treatment modalities. The pattern of orientation is formed by the 12th to 14th week of prenatal life and remains stable until the oral mucosa degenerates after death. The palatine rugae possess unique characteristics that could be used in circumstances in which it is difficult to identify a dead person according to fingerprints or dental records.
TYPES OF STUDIES REVIEWED:
The authors reviewed the literature by using key words regarding the anatomy, development, classification, clinical significance and forensic aspects of palatine rugae.
CONCLUSION AND CLINICAL IMPLICATIONS:
Palatine rugae are permanent and unique to each person, and clinicians and scientists can use them to establish identity through discrimination. If particular rugae patterns could be established for different ethnic groups, they would assist the forensic odontologist in the identification of a person. Because they are a stable landmark, the palatine rugae also can play a significant role in clinical dentistry.
________________________________________
jueves, 23 de febrero de 2012
miércoles, 22 de febrero de 2012
articulo recomendado
CLINICO PATHOLOGIC CONFERENCE
An incidentally discovered radiolucency in the posterior mandible
Stephen B. Hutton, BS,a Sabah Kalamchi, BDS, DDS, LDSRCS, FFDRCS,a and John M. Wright, DDS, MSc,b Arizona School of Dentistry and Oral Health, Mesa, Arizona; and Baylor College of Dentistry, Dallas, Texas (Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113:17-20)
lunes, 30 de enero de 2012
Cone Beam CT of Carotid Artery Densities
Robert A. Danforth, DDS; Edward E. Herschaft, DDS, MA
Posted: 01/10/2012
Cone Beam CT
This case report describes the history and significance of regional neck calcifications commonly observed on panoramic and cone beam (CB) CT radiographs in dental practice. CBCT is a low-dose cross-sectional technique for visualizing bony structures in the head and neck and is increasingly used for point-of-service head, neck, and dentomaxillofacial imaging.[1]Imaging characteristics and differentiation of anatomic regional neck hyperdensities from calcified carotid artery atheroma (CCAA) are discussed in this case. Proper identification and assessment of these calcifications can assist the clinician in determining appropriate medical referral and dental management for the patient.
CCAA on Dental Radiographs
In 1981 Friedlander and Lande[2] reported the ability to observe CCAA plaques on panoramic radiographs. In the sagittal plane, represented by the panoramic radiograph, these radiopacities were described as being located just superior to the carotid bifurcation and approximately 1.5-2.5 cm on a posterior incline from the angle of the mandible to a region adjacent to cervical vertebra C3-C5. CCAA must be differentiated from other anatomic and pathologic structures that may also be visible in this location (Figure 1).
Figure 1. Panoramic dental radiograph showing several bilateral oblong radiopacities of varied density (arrows).
The radiopacities appear to be superimposed on the outlines of the lower pharyngeal airway spaces and the anterior portions of the C3-C5 cervical vertebrae. These opacities are most likely the posterior portions of the greater horns of the hyoid bone and the partially calcified thyroid cartilage. However, in this location on panoramic radiographs, CCAA must be included in a differential interpretation of the image.
Significance of CCAA Findings
Subsequent reports[3-6] indicate that CCAAs are commonly discovered on panoramic radiographs and may be associated with systemic diseases, including stroke, hypertension, and type 2 diabetes. However, the diagnostic value of these observations remains controversial. The conclusions of other studies call into question the significance of CCAA on panoramic radiographs. For example:
Although CCAA discovered on panoramic radiographs may be related to previous vascular disease, it is not considered a useful marker for future vascular disease in 80-year-old individuals.[7]
When compared with ultrasonography, panoramic radiography does not reliably detect CCAA.[8] This finding supported the results of a previous study indicating that ultrasonography screening should be recommended for patients with CCAA on panoramic radiographics.[9]
In a literature review of 54 studies, Mupparapu and Kim[10] concluded that, "data supporting the hypothesis that radiographically detectable CCAA is associated with an increased risk of stroke are incomplete and inconclusive. Further research is needed, as clinical guidelines for risk prediction using panoramic radiographs cannot be established on the basis of the current evidence."
Among dental patients, a history of obesity, smoking, and hypertension might provide more correlative information about the potential for an acute vascular event than CCAA observed on panoramic radiographs.[11-13]
Although first used clinically in 1982, CBCT technology did not become commercially available in the United States until 2001.[14] CBCT technology allowed dental practitioners to visualize CCAA densities in the 3 orthogonal projections (coronal, axial, and sagittal) (Figure 2).
Figure 2. Composite view of selected cone beam CT images shows bilateral linear and curvilinear hyperdense masses at the level of the larynx. Note: These are positioned lateral to the lower pharyngeal airway and cervical spine. These findings are interpreted as being consistent with external carotid artery calcifications.
The dentist reviewing CBCT images should have an understanding of the anatomic positions in which CCAA lesions appear. Other anatomic and pathologic hyperdensities can be differentiated from CCAA in these views.
Anatomic and Pathologic Hyperdensities of Interest
Several studies describe the panoramic radiographic appearances and locations of the stylohyoid ligament complex,[15,16]calcified triticeous cartilage,[17,18] and ossified laryngeal cartilages.[19] When these anatomic structures become calcified, they might be confused with CCAA. Additionally, pathologic calcifications of the palatine tonsillar region have been described. The 3 most common soft tissue calcifications observed on CBCT images have been identified as CCAA, calcification of the triticeous cartilage, and calcifications of the tonsil.[20,21]
Scarfe and Farman[22] describe the relationships between CBCT images of CCAA and calcifications of the stylohyoid chain, superior cornu of the thyroid cartilage, triticeous cartilage, and tonsil. Figures 3 and 4 illustrate some of these associations observed in coronal, axial, and sagittal CBCT images and reconstructed models.
Figure 3. Reconstructed visual models showing configurations and locations of bilateral curvilinear hyperdense masses interpreted as being consistent with external carotid artery calcifications.
Figure 4. Comparative views of selected reconstructed axial, coronal, and sagittal visual models created from cone beam CT images. Note: Arrows in Figure 4 identify anatomic opacities that should be differentiated from calcified carotid artery atheroma (CCAA). The upper composite series of selected hyoid and thyroid images highlights the superiorly positioned hyoid bone and the partially calcified thyroid cartilage with its prominent posterior cornu (horns) projecting toward the hyoid bone. The lower axial carotid views show the presence of CCAA, which are curvilinear hyperdensities laterally positioned to the midline curvature of the hyoid bone and the lateral extensions of the cervical vertebrae.
Bilateral Carotid Artery Hyperdensities Observed on CBCT Radiographs: Case Reports
Patient 1, a 56-year-old man of European ancestry with a history of hepatitis B, hypertension, and coronary artery disease, presented to the general practice residency dental clinic saying, "I am missing several teeth and would like to replace them with dental implants." The patient was diagnosed with pericarditis in 2006 and had bilateral carotid stents placed in 2008. He was taking multiple medications for his systemic health conditions.
Intraoral examination revealed no mucosal soft tissue pathology. However, both dental arches exhibited numerous missing teeth bilaterally. As part of the diagnostic workup to assess the efficacy of dental implant placement in this patient, CBCT radiographs were obtained (Figures 5 and 6). These images revealed bilateral "meshlike," hyperdense areas consistent with carotid artery stents and surgical fixation clips. These CBCT radiographic findings are consistent with the patient's medical history of bilateral carotid artery stent placement in 2008.
Figure 5. A composite view of selected cone beam CT images of the patient in this case shows bilateral, somewhat symmetrical, hyperdense objects (arrows). Note: In the axial view, the objects have ring configurations, whereas in the coronal and right and left sagittal views, these objects appear as vertically aligned "meshlike" cylinders. Additionally, these cylinders are bordered by several small rectangular hyperdense objects. These findings are consistent with the presence of bilateral carotid artery stents and surgical fixation clips.
Figure 6. Selected reconstructed visual models of axial, coronal, and sagittal cone beam CT images from Figure 5 show improved visualization of the configurations and locations of the bilateral carotid artery stents (arrows).
The images in Figure 5 and 6 were compared with those from another patient (Patient 2) who exhibited bilateral hyperdense masses suggestive of CCAA on axial CBCT radiographs (Figure 7). The purpose of this comparison was to use the images of the stents observed in patient 1 to help pinpoint the location of the CCAA-like hyperdensities in patient 2 to the location of the carotid arteries. Measurements relating the positions of the CCAA densities to those of the carotid artery stents indicated similar lateral-horizontal distances of the calcifications from the sagittal midline. Similar distances along acute line-angles radiating from the posterior midpoint of the cervical vertebrae were also found for the CCAA densities and the stents. Thus, the anatomic locations of the carotid stents and those of the bilateral hyperdensities supported the interpretation of the latter as CCAA.
Figure 7. a. Axial cone beam CT images of patient 2 show bilateral hyperdense masses interpreted as being consistent with carotid artery calcifications. b. Bilateral carotid artery stents observed in patient 1. Comparison of the measurements obtained from these images indicates similar lateral-horizontal distances of the calcifications from the sagittal midline and similar distances along acute line-angles radiating from the posterior midpoint of the cervical vertebrae (arrows).
Summary: Next Steps
CBCT radiographic findings suggestive of CCAA may be associated with medical histories that include obesity, cardiovascular disease, hypertension, transient ischemic attack, stroke, hypercholesterolemia, type 2 diabetes, sleep apnea, and male gender.[22] Although attempts to correlate CCAA with risk for a cardiovascular event have limitations, dental practitioners must be able to differentiate possible CCAA lesions from anatomic and pathologic structures that also appear as hyperdensities in the neck.[13]
An understanding of the relationships and anatomic positions of hyperdensities that need to be distinguished from CCAA can be facilitated by CBCT because this radiologic technique offers visualization of suspected lesions in all 3 orthogonal projections. Despite the controversy concerning the prognostic value of these findings, dentists should inform patients about radiographic results suggestive of CCAA. Patients should be referred to their primary care physician, with copies of the radiographs, for appropriate medical evaluation and radiologic consultation. If the patient is not currently under a physician's care for known cardiovascular disease, the dentist should make every effort to ensure that the patient is referred to a physician for proper evaluation.
Acknowledgment
The authors wish to acknowledge the contributions of Dr. George McAlpine, Director of the General Practice Dental Residency Program at the University of Nevada Las Vegas-School of Dental Medicine in the preparation of this manuscript.
References
Miracle AC, Mukherji SK. Conebeam CT of the head and neck, part 2: clinical application. AJNR Am J Neuroradiol. 2009;30:1285-1292. Abstract
Friedlander AH, Lande A. Panoramic radiographic identification of carotid arterial plaques. Oral Surg Oral Med Oral Pathol. 1981;52:102-104. Abstract
Friedlander AH, Manesh F, Wasterlain CG. Prevalence of detectable carotid artery calcifications on panoramic radiographs of recent stroke victims. Oral Surg Oral Med Oral Pathol. 1994;77:669-673. Abstract
Friedlander AH. Identification of stroke prone patients by panoramic and cervical spine radiography. Dentomaxillofac Radiol. 1995;24:160-164. Abstract
Friedlander AH, Garrett NR, Norman DC. The prevalence of calcified carotid artery atheromas on the panoramic radiographs of patients with type 2 diabetes mellitus. J Am Dent Assoc. 2002;133:1516-1523. Abstract
Carter LC, Tsimidis K, Fabiano J. Carotid calcifications on panoramic radiography identify an asymptomatic male patient at risk for stroke. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998;85:119-122. Abstract
Tanaka T, Morimoto Y, Ansai T, et al. Can the presence of carotid artery calcification on panoramic radiographs predict the risk of vascular diseases among 80-year-olds? Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101:777-783. Abstract
Madden RP, Hodges JS, Salmen CW, et al. Utility of panoramic radiographs in detecting cervical calcified carotid atheroma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007;103:543-548. Abstract
Almog DM, Horey T, Illig KA, Green RM, Carter LC. Correlating carotid artery stenosis detected by panoramic radiography with clinical relevant carotid artery stenosis determined by duplex ultrasound. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94:768-773. Abstract
Mupparapu M. Kim IH. Calcified carotid artery atheroma and stroke: a systematic review. J Am Dent Assoc. 2007;138:483-492. Abstract
Goldstein LB, Adams R, Alberts MJ, et al. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council. Stroke. 2006;37:1583-1633. Abstract
Fatahzadeh M, Glick M. Stroke: epidemiology, classification, risk factors, complication, diagnosis, prevention and medical and dental management. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;102:180-191. Abstract
Taheri JB, Moshfeghi M. Prevalence of calcified carotid artery on panoramic radiographs in postmenopausal women. J Dent Res Dent Clin Dent Prospect. 2009;3:46-51.
Robb RA. The dynamic spatial reconstructor: an x-ray video-fluoroscopic CT scanner for dynamic volume imaging of moving organs. IEEE Trans Med Imaging. 1982;1:22-33. Abstract
Winkler S, Sammartino FJ Sr, Sammartino FJ Jr, Monari JH. Stylohyoid syndrome. Report of a case. Oral Surg Oral Med Oral Pathol. 1981;51:215-217. Abstract
Langlais RP, Miles DA, Van Dis ML. Elongated and mineralized stylohyoid ligament complex: a proposed classification and report of a case of Eagle's syndrome. Oral Surg Oral Med Oral Pathol. 1986;61:527-532. Abstract
Carter LC. Discrimination between calcified triticeous cartilage and calcified carotid atheroma on panoramic radiography. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90:108-110. Abstract
Ahmad M, Madden R, Perez L. Triticeous cartilage: prevalence on panoramic radiographs and diagnostic criteria. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005;99:225-230. Abstract
Hatly W, Evison G, Samuel E. The pattern of ossification in the laryngeal cartilages: a radiological study. Br J Radiol. 1965;38:585-591. Abstract
Aspestrand F, Kolbenstvedt A. Calcifications of the palatine tonsillary region: CT demonstration. Radiology. 1987;165:479-480. Abstract
Khan Z, Wells A, Scarfe W, Farman A. Cone beam CT isolation of calcifications in the maxillofacial and cervical soft tissues: a retrospective analysis. Int J Computer Assist Radiol Surg. 2008;3(Suppl 1):S221-S222.
Scarfe WC, Farman AG. Soft tissue calcifications in the neck: maxillofacial CBCT presentation and significance. AADMRT Newsletter. 2010;2:1-15.
Medscape Dentistry & Oral Health © 2012 WebMD, LLC
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Robert A. Danforth, DDS; Edward E. Herschaft, DDS, MA
Posted: 01/10/2012
Cone Beam CT
This case report describes the history and significance of regional neck calcifications commonly observed on panoramic and cone beam (CB) CT radiographs in dental practice. CBCT is a low-dose cross-sectional technique for visualizing bony structures in the head and neck and is increasingly used for point-of-service head, neck, and dentomaxillofacial imaging.[1]Imaging characteristics and differentiation of anatomic regional neck hyperdensities from calcified carotid artery atheroma (CCAA) are discussed in this case. Proper identification and assessment of these calcifications can assist the clinician in determining appropriate medical referral and dental management for the patient.
CCAA on Dental Radiographs
In 1981 Friedlander and Lande[2] reported the ability to observe CCAA plaques on panoramic radiographs. In the sagittal plane, represented by the panoramic radiograph, these radiopacities were described as being located just superior to the carotid bifurcation and approximately 1.5-2.5 cm on a posterior incline from the angle of the mandible to a region adjacent to cervical vertebra C3-C5. CCAA must be differentiated from other anatomic and pathologic structures that may also be visible in this location (Figure 1).
Figure 1. Panoramic dental radiograph showing several bilateral oblong radiopacities of varied density (arrows).
The radiopacities appear to be superimposed on the outlines of the lower pharyngeal airway spaces and the anterior portions of the C3-C5 cervical vertebrae. These opacities are most likely the posterior portions of the greater horns of the hyoid bone and the partially calcified thyroid cartilage. However, in this location on panoramic radiographs, CCAA must be included in a differential interpretation of the image.
Significance of CCAA Findings
Subsequent reports[3-6] indicate that CCAAs are commonly discovered on panoramic radiographs and may be associated with systemic diseases, including stroke, hypertension, and type 2 diabetes. However, the diagnostic value of these observations remains controversial. The conclusions of other studies call into question the significance of CCAA on panoramic radiographs. For example:
Although CCAA discovered on panoramic radiographs may be related to previous vascular disease, it is not considered a useful marker for future vascular disease in 80-year-old individuals.[7]
When compared with ultrasonography, panoramic radiography does not reliably detect CCAA.[8] This finding supported the results of a previous study indicating that ultrasonography screening should be recommended for patients with CCAA on panoramic radiographics.[9]
In a literature review of 54 studies, Mupparapu and Kim[10] concluded that, "data supporting the hypothesis that radiographically detectable CCAA is associated with an increased risk of stroke are incomplete and inconclusive. Further research is needed, as clinical guidelines for risk prediction using panoramic radiographs cannot be established on the basis of the current evidence."
Among dental patients, a history of obesity, smoking, and hypertension might provide more correlative information about the potential for an acute vascular event than CCAA observed on panoramic radiographs.[11-13]
Although first used clinically in 1982, CBCT technology did not become commercially available in the United States until 2001.[14] CBCT technology allowed dental practitioners to visualize CCAA densities in the 3 orthogonal projections (coronal, axial, and sagittal) (Figure 2).
Figure 2. Composite view of selected cone beam CT images shows bilateral linear and curvilinear hyperdense masses at the level of the larynx. Note: These are positioned lateral to the lower pharyngeal airway and cervical spine. These findings are interpreted as being consistent with external carotid artery calcifications.
The dentist reviewing CBCT images should have an understanding of the anatomic positions in which CCAA lesions appear. Other anatomic and pathologic hyperdensities can be differentiated from CCAA in these views.
Anatomic and Pathologic Hyperdensities of Interest
Several studies describe the panoramic radiographic appearances and locations of the stylohyoid ligament complex,[15,16]calcified triticeous cartilage,[17,18] and ossified laryngeal cartilages.[19] When these anatomic structures become calcified, they might be confused with CCAA. Additionally, pathologic calcifications of the palatine tonsillar region have been described. The 3 most common soft tissue calcifications observed on CBCT images have been identified as CCAA, calcification of the triticeous cartilage, and calcifications of the tonsil.[20,21]
Scarfe and Farman[22] describe the relationships between CBCT images of CCAA and calcifications of the stylohyoid chain, superior cornu of the thyroid cartilage, triticeous cartilage, and tonsil. Figures 3 and 4 illustrate some of these associations observed in coronal, axial, and sagittal CBCT images and reconstructed models.
Figure 3. Reconstructed visual models showing configurations and locations of bilateral curvilinear hyperdense masses interpreted as being consistent with external carotid artery calcifications.
Figure 4. Comparative views of selected reconstructed axial, coronal, and sagittal visual models created from cone beam CT images. Note: Arrows in Figure 4 identify anatomic opacities that should be differentiated from calcified carotid artery atheroma (CCAA). The upper composite series of selected hyoid and thyroid images highlights the superiorly positioned hyoid bone and the partially calcified thyroid cartilage with its prominent posterior cornu (horns) projecting toward the hyoid bone. The lower axial carotid views show the presence of CCAA, which are curvilinear hyperdensities laterally positioned to the midline curvature of the hyoid bone and the lateral extensions of the cervical vertebrae.
Bilateral Carotid Artery Hyperdensities Observed on CBCT Radiographs: Case Reports
Patient 1, a 56-year-old man of European ancestry with a history of hepatitis B, hypertension, and coronary artery disease, presented to the general practice residency dental clinic saying, "I am missing several teeth and would like to replace them with dental implants." The patient was diagnosed with pericarditis in 2006 and had bilateral carotid stents placed in 2008. He was taking multiple medications for his systemic health conditions.
Intraoral examination revealed no mucosal soft tissue pathology. However, both dental arches exhibited numerous missing teeth bilaterally. As part of the diagnostic workup to assess the efficacy of dental implant placement in this patient, CBCT radiographs were obtained (Figures 5 and 6). These images revealed bilateral "meshlike," hyperdense areas consistent with carotid artery stents and surgical fixation clips. These CBCT radiographic findings are consistent with the patient's medical history of bilateral carotid artery stent placement in 2008.
Figure 5. A composite view of selected cone beam CT images of the patient in this case shows bilateral, somewhat symmetrical, hyperdense objects (arrows). Note: In the axial view, the objects have ring configurations, whereas in the coronal and right and left sagittal views, these objects appear as vertically aligned "meshlike" cylinders. Additionally, these cylinders are bordered by several small rectangular hyperdense objects. These findings are consistent with the presence of bilateral carotid artery stents and surgical fixation clips.
Figure 6. Selected reconstructed visual models of axial, coronal, and sagittal cone beam CT images from Figure 5 show improved visualization of the configurations and locations of the bilateral carotid artery stents (arrows).
The images in Figure 5 and 6 were compared with those from another patient (Patient 2) who exhibited bilateral hyperdense masses suggestive of CCAA on axial CBCT radiographs (Figure 7). The purpose of this comparison was to use the images of the stents observed in patient 1 to help pinpoint the location of the CCAA-like hyperdensities in patient 2 to the location of the carotid arteries. Measurements relating the positions of the CCAA densities to those of the carotid artery stents indicated similar lateral-horizontal distances of the calcifications from the sagittal midline. Similar distances along acute line-angles radiating from the posterior midpoint of the cervical vertebrae were also found for the CCAA densities and the stents. Thus, the anatomic locations of the carotid stents and those of the bilateral hyperdensities supported the interpretation of the latter as CCAA.
Figure 7. a. Axial cone beam CT images of patient 2 show bilateral hyperdense masses interpreted as being consistent with carotid artery calcifications. b. Bilateral carotid artery stents observed in patient 1. Comparison of the measurements obtained from these images indicates similar lateral-horizontal distances of the calcifications from the sagittal midline and similar distances along acute line-angles radiating from the posterior midpoint of the cervical vertebrae (arrows).
Summary: Next Steps
CBCT radiographic findings suggestive of CCAA may be associated with medical histories that include obesity, cardiovascular disease, hypertension, transient ischemic attack, stroke, hypercholesterolemia, type 2 diabetes, sleep apnea, and male gender.[22] Although attempts to correlate CCAA with risk for a cardiovascular event have limitations, dental practitioners must be able to differentiate possible CCAA lesions from anatomic and pathologic structures that also appear as hyperdensities in the neck.[13]
An understanding of the relationships and anatomic positions of hyperdensities that need to be distinguished from CCAA can be facilitated by CBCT because this radiologic technique offers visualization of suspected lesions in all 3 orthogonal projections. Despite the controversy concerning the prognostic value of these findings, dentists should inform patients about radiographic results suggestive of CCAA. Patients should be referred to their primary care physician, with copies of the radiographs, for appropriate medical evaluation and radiologic consultation. If the patient is not currently under a physician's care for known cardiovascular disease, the dentist should make every effort to ensure that the patient is referred to a physician for proper evaluation.
Acknowledgment
The authors wish to acknowledge the contributions of Dr. George McAlpine, Director of the General Practice Dental Residency Program at the University of Nevada Las Vegas-School of Dental Medicine in the preparation of this manuscript.
References
Miracle AC, Mukherji SK. Conebeam CT of the head and neck, part 2: clinical application. AJNR Am J Neuroradiol. 2009;30:1285-1292. Abstract
Friedlander AH, Lande A. Panoramic radiographic identification of carotid arterial plaques. Oral Surg Oral Med Oral Pathol. 1981;52:102-104. Abstract
Friedlander AH, Manesh F, Wasterlain CG. Prevalence of detectable carotid artery calcifications on panoramic radiographs of recent stroke victims. Oral Surg Oral Med Oral Pathol. 1994;77:669-673. Abstract
Friedlander AH. Identification of stroke prone patients by panoramic and cervical spine radiography. Dentomaxillofac Radiol. 1995;24:160-164. Abstract
Friedlander AH, Garrett NR, Norman DC. The prevalence of calcified carotid artery atheromas on the panoramic radiographs of patients with type 2 diabetes mellitus. J Am Dent Assoc. 2002;133:1516-1523. Abstract
Carter LC, Tsimidis K, Fabiano J. Carotid calcifications on panoramic radiography identify an asymptomatic male patient at risk for stroke. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998;85:119-122. Abstract
Tanaka T, Morimoto Y, Ansai T, et al. Can the presence of carotid artery calcification on panoramic radiographs predict the risk of vascular diseases among 80-year-olds? Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101:777-783. Abstract
Madden RP, Hodges JS, Salmen CW, et al. Utility of panoramic radiographs in detecting cervical calcified carotid atheroma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007;103:543-548. Abstract
Almog DM, Horey T, Illig KA, Green RM, Carter LC. Correlating carotid artery stenosis detected by panoramic radiography with clinical relevant carotid artery stenosis determined by duplex ultrasound. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94:768-773. Abstract
Mupparapu M. Kim IH. Calcified carotid artery atheroma and stroke: a systematic review. J Am Dent Assoc. 2007;138:483-492. Abstract
Goldstein LB, Adams R, Alberts MJ, et al. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council. Stroke. 2006;37:1583-1633. Abstract
Fatahzadeh M, Glick M. Stroke: epidemiology, classification, risk factors, complication, diagnosis, prevention and medical and dental management. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;102:180-191. Abstract
Taheri JB, Moshfeghi M. Prevalence of calcified carotid artery on panoramic radiographs in postmenopausal women. J Dent Res Dent Clin Dent Prospect. 2009;3:46-51.
Robb RA. The dynamic spatial reconstructor: an x-ray video-fluoroscopic CT scanner for dynamic volume imaging of moving organs. IEEE Trans Med Imaging. 1982;1:22-33. Abstract
Winkler S, Sammartino FJ Sr, Sammartino FJ Jr, Monari JH. Stylohyoid syndrome. Report of a case. Oral Surg Oral Med Oral Pathol. 1981;51:215-217. Abstract
Langlais RP, Miles DA, Van Dis ML. Elongated and mineralized stylohyoid ligament complex: a proposed classification and report of a case of Eagle's syndrome. Oral Surg Oral Med Oral Pathol. 1986;61:527-532. Abstract
Carter LC. Discrimination between calcified triticeous cartilage and calcified carotid atheroma on panoramic radiography. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90:108-110. Abstract
Ahmad M, Madden R, Perez L. Triticeous cartilage: prevalence on panoramic radiographs and diagnostic criteria. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005;99:225-230. Abstract
Hatly W, Evison G, Samuel E. The pattern of ossification in the laryngeal cartilages: a radiological study. Br J Radiol. 1965;38:585-591. Abstract
Aspestrand F, Kolbenstvedt A. Calcifications of the palatine tonsillary region: CT demonstration. Radiology. 1987;165:479-480. Abstract
Khan Z, Wells A, Scarfe W, Farman A. Cone beam CT isolation of calcifications in the maxillofacial and cervical soft tissues: a retrospective analysis. Int J Computer Assist Radiol Surg. 2008;3(Suppl 1):S221-S222.
Scarfe WC, Farman AG. Soft tissue calcifications in the neck: maxillofacial CBCT presentation and significance. AADMRT Newsletter. 2010;2:1-15.
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