Monday, May 16, 2011

Does Poor Dental Health Have a Role in the Emergence of Variant Creutzfeldt Jakob Disease in the United Kingdom?

Does Poor Dental Health Have a Role in the Emergence of Variant Creutzfeldt Jakob Disease in the United Kingdom?

Robert Burnie, Roland L Salmon, Daniel R Thomas, Nigel Monaghan


Introduction: Variant creutzfeldt jakob disease (vCJD) is the human neurological disease known to be caused by the same proteinaceous infectious agent (“prion”) that causes Bovine Spongiform Encephalopathy or "Mad Cow Disease". Two unusual and unexplained characteristics of the vCJD epidemic are its geographical distribution within the UK (about twice as frequent in Scotland and Northern England) and its median age of onset of 26 years that has remained unchanged over the fifteen years of the epidemic.

The hypothesis: Infection via the dental route as a consequence of poor dental health, most probably the presence of untreated decay may account for the geographical distribution of vCJD in the UK and offer an explanation for the constant median age of onset of the disease by representing a fixed stage in development.

Evaluation of the hypothesis: Analysis of existing data indicates that vCJD incidence by region and an index of dental health by region are positively correlated (r=0.737, p= 0.015). The hypothesis that infection via the dental route may explain the constant median age of onset and geographical distribution of vCJD could be investigated further with a case control study based on individual dental records and by further animal experiments to confirm the biological plausibility of this route.

Key words: Variant creutzfeldt jakob disease; Infection; Dental health; Epidemiology.



An alternative explanation for the asso-ciation between regional dental health and vCJD incidence is that the missing teeth(MT) and filled teeth(FT) components of DMFT scores represent a marker for the number of dental procedures, that is to say for dental treatment. Dental proce-dures, particularly dental extraction, root filling, or gum treatment, may represent a theoretical pathway of secondary trans-mission. The resistance of prions to stan-dard decontamination techniques [19], the potential for instruments to remain con-taminated with protein residue material after cleaning and the potential for endo-dontic instruments to come into intimate contact with peripheral branches of the trigeminal nerve [20] make transmission via this route biologically plausible. The UK National CJD Surveillance Unit re-ports that preliminary data from animal studies carried out by the Health Protec-tion Agency have indicated that the risk of

transmission of vCJD via dentistry may be higher than previously considered [21]. Whilst there is currently no evidence of vCJD having been spread by dentistry, even a very small risk of transmission has significant public health implications due to the considerable number of dental pro-cedures carried out each year [22].

Analysis of the variation in dental health and dental histories of those with vCJD in the UK and France could also be informative. Interestingly, in France the median age of death of 23 cases of vCJD is 36 years [23]. Could this be a reflection of better oral health among children or dif-ferences in treating dental decay in child-hood?


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National CJD Surveillance Unit 2008, ‘Creutzfeldt-Jacob disease surveillance in the UK. Sixteenth Annual Report. Edin-burgh [Accessed May 8, 2011]. Available from:

Griffiths P. Variant CJD epidemiology: joining up the dots. Rev Med Virol 2001;1:203-4.



Ghani A, Ferguson N, Donnelly C, Ander-son R. Predicted vCJD mortality in Great Britain. Nature 2000;406:583-4.



Boëlle P, Cesbron J, Valleron A. Epidemio-logical evidence of higher susceptibility to vCJD in the young. BMC Infect Dis 2004;4:26.


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Cousens, S, Smith, P, Ward, H, Everington, D, Knight, R, Zeidler et al. Geographical distribution of variant Creutzfeldt-Jakob disease in Great Britain, 1994-2000. Lancet 2001;357:1002.


Cousens, S, Everington, D, Ward, H, Huil-lard, J, Will, R & Smith, P. The geographi-cal distribution of variant Creutzfeldt-Jakob disease cases in the UK: what can we learn from it? Stat Methods Med Res 2003;12:235-46.



Jeffrey, M, González, L, Espenes, A, Press C, Martin, S, Chaplin, et al. Transportation of prion protein across the intestinal mucosa of scrapie-susceptible and scrapie-resistant sheep. J Pathol 2006;209:4-14.



Sales, N. What can we learn from the oral intake of prions by sheep? J Pathol 2006;209:1-3.



Bendheim, P, Bockman, J, McKinley, M, Kingsbury, D & Prusiner, S, Scrapie and Creutzfeldt-Jakob disease prion proteins share physical properties and antigenic de-terminants. Proc Natl Acad Sci USA 1985;82:997-1001.


Weissmann C, Enari M, Klöhn P, Rossi D, Flechsig E. Transmission of prions. Proc Natl Acad Sci U S A 2002;99 Suppl 4:16378-83.


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Ingrosso, L, Pisani, F & Pocchiari, M. 'Transmission of the 263K scrapie strain by the dental route. J Gen Virol 1999;80:3043-7.


Pitts NB, Palmer, J. The dental caries ex-perience of 5-, 12-, and 14-year-old child-ren in Great Britain. Surveys coordinated by the British Association for the Study of Community Dentistry in 1991/92, 1992/93, and 1990-91. Community Denl Health 1994; 11, 42-52.


Office for National Statistics 2000, Na-tional Food Survey 1997-1999: Household consumption by Government Office Re-gion [Accessed May 8, 2011]. Available from:

Census Dissemination Unit, 2006, Depri-vation Scores 1991 Census [Accessed May 8, 2011]. Available from:

British Fluoridation Society. One in a mil-lion: water fluoridation and dental public health. 2nd edition. United Kingdom: British Fluoridation Society, 2004:55-79.

Everington D, Smith A, Ward H, Letters S, Will R, Bagg J. Dental treatment and risk of variant CJD--a case control study. Br Dent J 2007;202:E19; discussion 470-1.

Carp R. Transmission of scrapie by oral route: effect of gingival scarification. Lancet 1982;1:170-1.


Trevitt C, Singh P. Variant Creutzfeldt-Jakob disease: pathology, epidemiology, and public health implications. Am J Clin Nutr 2003;78:651S-56S.


Smith A, Dickson M, Aitken J, Bagg J. Contaminated dental instruments. J Hosp Infect 2002;51:233-5.



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Deadly vCJD may have a link to tooth decay

by Madeleine Brindley, Western Mail
May 16 2011


A GROUP of Welsh experts believe cases of the human form of mad cow disease could be linked to simple tooth decay.

They have put forward an hypothesis, which suggests tooth decay may be the way in which people became infected with the incurable disease as a result of eating contaminated meat during the 1980s.

Dr Roland Salmon, one of the Public Health Wales professionals involved in developing the idea, said the hypothesis also helps to explain why there have been relatively few cases of variant Creutzfeldt-Jakob disease (vCJD).

It may also explain the geographical spread of the disease – cases are highest in Scotland and the North-East of England, where rates of dental decay are also high.

Between 1990 and the start of May 2011 there have been 171 confirmed and probable vCJD deaths reported to the National Creutzfeldt-Jakob Disease Research and Surveillance Unit in Edinburgh.

A further four people with either definite or probable vCJD are still alive.

Dr Salmon, director of Public Health Wales’ communicable disease surveillance centre, said: “There are three things that are difficult to explain given that, during the 1980s, we must have eaten tonnes of potentially infected meat.

“In many ways it’s remarkable that there have been so few cases, which may be because of the difficulty the disease had of crossing the species barrier and the genetics of humans.

“But given that we had taken all contaminated food out of the equation by 1996, we would have thought that the age of cases would be getting older – they aren’t.

“The median age of onset has remained at around 26.

“Another thing, which is not so widely known, is that it’s twice as common in Scotland and North-East England.”

The correlation between tooth decay and vCJD appeared after analysing regional data on vCJD incidence and historical regional dental health data from 1992-3 in 12-year-old children collected by British Association for the Study of Community Dentistry.

Dr Salmon, who devised the hypothesis with Daniel Thomas and Nigel Monaghan, also from Public Health Wales, and with Cardiff University medical student Robert Burnie, said it appears as if infection with vCJD was via the dental route – through minute gaps in the teeth caused by untreated decay – rather than through the stomach.

Variant Creutzfeldt-Jakob disease is known as the human form of mad cow disease because it is caused by the same prion responsible for bovine spongiform encephalitis – mad cow disease.

Dr Salmon said: “It looks like the relationship between dental health and the risk of getting vCJD has some mileage.

“Our research suggests that it’s not dental treatment but dental decay in the first place which is a risk factor.

“One particularly interesting thing is that the area with the lowest numbers of filled teeth and the lowest incidence of vCJD is the West Midlands, which is also the region with the highest levels of water fluoridation.”

The hypothesis has been published in the journal Dental Hypotheses in the hope that other researchers around the world will carry out further investigations to establish the link between vCJD and tooth decay.

“This does look like an explanation that has some mileage in it,” Dr Salmon added.

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''It was in the cards a long time ago,'' she says. ''We've put it in the hands of God.''

- Crystal Harmon can be reached at 894-9643 or by e-mail at

see full text ;

Tuesday, August 12, 2008

Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)

Thursday, July 08, 2010


Position Statement


Position Statement vCJD and Dentistry
1. The Department of Health (DH) asked SEAC to advise on the findings of preliminary research aimed at informing estimates of the risk of variant Creutzfeldt-Jakob Disease (vCJD) transmission via dentistry.

2. Prions are more resistant than other types of infectious agent to the conventional cleaning and sterilisation practices used to decontaminate dental instruments1. Appreciable quantities of residual material may remain adherent to the surface after normal cleaning and sterilisation2. Therefore, if dental tissues are both infectious and susceptible to infection, then dental instruments are a potential mechanism for the secondary transmission of vCJD. Dentistry could be a particularly significant route of transmission for the population as a whole, due to the large number of routine procedures undertaken and also because dental patients have a normal life expectancy. This is in contrast with other transmission routes, such as blood transfusion and neurosurgery, where procedures are often carried out in response to some life-threatening condition. Additionally, the ubiquity of dental procedures and the lack of central records on dental procedures means that should such transmission occur, then it would be difficult to detect and control.

3. No cases of vCJD transmission arising from dental procedures have been reported to date 3 . Previous DH risk assessments4,5 have focused on two possible mechanisms for the transfer of vCJD infectivity via dental instruments; accidental abrasion of the lingual tonsil and endodontic procedures that involve contact with dental pulp. In considering these assessments, SEAC agreed that the risk of transmission via accidental abrasion of the lingual tonsil appears very low. However, the risk of transmission via endodontic procedures may be higher and give rise to a self sustaining vCJD epidemic under circumstances where (i) dental pulp is infective, (ii) transmission via endodontic instruments is efficient and (iii) a large proportion of vCJD infections remain in a subclinical carrier state (SEAC 91, February 2006). In light of this, SEAC advised that restricting endodontic files and reamers to single use be considered 6. SEAC recommended reassessment of these issues as new data emerge.

New research
4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease.

5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases7. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases , the relationship between levels of infectivity and abnormal prion protein is unclear8. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model9 .

6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered.

7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures. Implications for transmission risks

8. The new findings help refine assumptions made about the level of infectivity of dental pulp and the stage of incubation period when it becomes infective in the risk assessment of vCJD transmission from the reuse of endodontic files and reamers10. For example, if one patient in 10 000 were to be carrying infection (equivalent to about 6 000 people across the UK – the best current estimate11), the data suggest that in the worst case scenario envisaged in the risk assessment, re-use of endodontic files and reamers might lead to up to 150 new infections per annum. It is not known how many of those infected would go on to develop clinical vCJD. In addition, transmission via the re-use of endodontic files and reamers could be sufficiently efficient to cause a self-sustaining vCJD epidemic arising via this route.

9. These results increase the importance of obtaining reliable estimates of vCJD infection prevalence. Data that will soon be available from the National Anonymous Tonsil Archive may help refine this assessment and provide evidence of the existence and extent of subclinical vCJD infection in tonsillectomy patients. Further data, such as from post mortem tissue or blood donations, will be required to assess prevalence in the general UK population12.

10. Recent guidance issued by DH to dentists to ensure that endodontic files and reamers are treated as single use13 is welcomed and should, as long as it is effectively and quickly implemented, prevent transmission and a self-sustaining epidemic arising via this route. However, the extent and monitoring of compliance with this guidance in private and National Health Service dental practice is unclear.

11. The new research also suggests that dental procedures involving contact with other oral tissues, including gingiva, may also be capable of transmitting vCJD. In the absence of a detailed risk assessment examining the potential for transmission via all dental procedures, it is not possible to come to firm conclusions about the implications of these findings for transmission of vCJD. However, given the potential for transmission by this route serious consideration should be given to assessing the options for reducing transmission risks such as improving decontamination procedures and practice or the implementation of single use instruments.

12. The size of the potential risk from interactions between the dental and other routes of secondary transmission, such as blood transfusion and hospital surgery, to increase the likelihood of a self-sustaining epidemic is unclear.

13. It is likely to be difficult to distinguish clinical vCJD cases arising from dietary exposure to BSE from secondary transmissions via dental procedures, should they arise, as a large proportion of the population is likely both to have consumed contaminated meat and undergone dentistry. However, an analysis of dental procedures by patient age may provide an indication of the age group in which infections, if they occur, would be most likely to be observed. Should the incidence of clinical vCJD cases in this age group increase significantly, this may provide an indication that secondary transmission via dentistry is occurring. Investigation of the dental work for these cases may provide supporting data. There is no clear evidence, to date, based on surveillance or investigations of clinical vCJD cases, that any vCJD cases have been caused by dental procedures but this possibility cannot be excluded.

14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.

15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.

16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.

June 2007

1Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775.

2Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241.

3Everington et al. (2007) Dental treatment and risk of variant CJD – a case control study. Brit. Den. J. 202, 1-3.

4Department of Health. (2003) Risk assessment for vCJD and dentistry.

5 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished.

6SEAC (2006) Position statement on vCJD and endodontic dentistry.

7Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343.

8SEAC 90 reserved business minutes.

9Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047.

10Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished.

11Clarke & Ghani (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility R. J. Soc. Interface. 2, 19-31.

12SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.

13DH (2007) Precautionary advice given to dentists on re-use of instruments

Page updated: 8 June, 2007

Monday, December 31, 2007

Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation

Subject: CJD: update for dental staff Date: November 12, 2006 at 3:25 pm PST

1: Dent Update. 2006 Oct;33(8):454-6, 458-60.

CJD: update for dental staff.

Friday, February 19, 2010

Creutzfeldt-Jakob disease (CJD) biannual update (2010/1)

Tuesday, March 29, 2011


Tuesday, April 26, 2011

sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)

Friday, May 13,

2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans

Sunday, May 01, 2011

STUDY OF ATYPICAL BSE 2010 Annual Report May 2011


Saturday, March 5, 2011



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