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From: TSS ()
Subject: Dental treatment and CJD risk DOH FUNDED STUDY ON WHAT?
Date: November 15, 2005 at 6:49 pm PST

Dental treatment and CJD risk DOH FUNDED STUDY ON WHAT?
Tue Nov 15, 2005 20:55

Dental treatment and CJD risk DOH FUNDED STUDY ON WHAT?


British Dental Journal (2005); 199, 545. doi: 10.1038/sj.bdj.4812914

Dental treatment and CJD risk

Sir, we wish to inform readers of a forthcoming Department of Health funded study to investigate the possibility of retrieving the dental case records of patients affected by CJD (sporadic and variant) and to note the types of treatment undertaken. We stress that we have no reason to suspect that dental treatment is linked in any way to the development of CJD. This work is part of a process of eliminating another potential risk factor to provide a clearer understanding of how CJD develops. This project forms part of the portfolio of work being undertaken by the National CJD Surveillance Unit (NCJDSU) investigating potential risk factors for the development of CJD.

The project is a small-scale study to identify how difficult or easy it is to access the dental records from CJD patients and a control group of unaffected people, who have given consent. If the study is successful then there is a possibility that we will examine many more case records. At present we plan to look at dental records from 16 patients who have had CJD across Scotland, England, Wales and Northern Ireland and 32 unaffected people as controls.

The study has full ethical approval from Lothian Multi-centre Research Ethics Committee as part of the NCJDSU's ongoing case control study examining risk factors for variant and sporadic CJD.

We would welcome any comments that readers may have on this study. Please feel free to contact us at the address below.

A. Smith
A. P. Matthewson

Infection Research Group, Level 9, Glasgow Dental Hospital & School, 378 Sauchiehall Street, Glasgow G2 3JZ
0141 211 9747

> We stress that we have no reason to suspect that dental treatment is

> linked in any way to the development of CJD.

famous last words.

> The project is a small-scale study to identify how difficult or easy it is to

> access the dental records from CJD patients and a control group of

> unaffected people, who have given consent.

i guess they all think we fell off a shrimp boat yesterday. ...TSS

J Hosp Infect 2002 Jul;51(3):233-5 Related Articles, Links [Click here to
read] Contaminated dental instruments.

Smith A, Dickson M, Aitken J, Bagg J.

Infection Research Group, Glasgow Dental Hospital & School, 378 Sauchiehall
Street, Glasgow, UK.

There is current concern in the UK over the possible transmission of prions
via contaminated surgical instruments. Some dental instruments (endodontic
files) raise particular concerns by virtue of their intimate contact with
terminal branches of the trigeminal nerve. A visual assessment using a
dissecting light microscope and scanning electron microscopy of endodontic
files after clinical use and subsequent decontamination was performed. The
instruments examined were collected from general dental practices and from a
dental hospital. Seventy-six per cent (22/29) of the files retrieved from
general dental practices remained visibly contaminated, compared with 14%
(5/37) from the dental hospital. Current methods for decontaminating
endodontic instruments used in dentistry may be of an insufficient standard
to completely remove biological material. Improved cleaning methods and the
feasibility of single use endodontic instruments require further

PMID: 12144804 [PubMed - indexed for MEDLINE]

J Gen Virol 1999 Nov;80 ( Pt 11):3043-7

Transmission of the 263K scrapie strain by the dental route.

Ingrosso L, Pisani F, Pocchiari M

Laboratory of Virology, lstituto Superiore di Sanita, Viale Regina Elena
299, 00161 Rome, Italy.

Apart from a few cases of iatrogenic and familial human transmissible
spongiform encephalopathies (TSEs) or prion diseases, the cause of
Creutzfeldt-Jakob disease (CJD) remains unknown. In this paper we
investigated the possibility that dental procedures may represent a
potential route of infection. This was assessed by using the experimental
model of scrapie in hamster. In the first part of this study we found that
after intraperitoneal inoculation, oral tissues commonly involved in dental
procedures (gingival and pulp tissues) bore a substantial level of
infectivity. We also found high scrapie infectivity in the trigeminal
ganglia, suggesting that the scrapie agent had reached the oral tissues
through the sensitive terminal endings of the trigeminal nerves. In the
second part of the study we inoculated a group of hamsters in the tooth pulp
and showed that all of them developed scrapie disease. In these animals, we
detected both infectivity and the pathological prion protein (PrPsc) in the
trigeminal ganglion homolateral to the site of injection but not in the
controlateral one. This finding suggests that the scrapie agent, and likely
other TSE agents as well, spreads from the buccal tissues to the central
nervous system through trigeminal nerves. Although these findings may not
apply to humans affected by TSEs, they do raise concerns about the possible
risk of transmitting these disorders through dental procedures. Particular
consideration should be taken in regard to new variant CJD patients because
they may harbour more infectivity in peripheral tissues than sporadic CJD

PMID: 10580068

a simple auto-claving just will not kill this agent, considering the fact
this agent can survive ashing to 600 degrees celsius;

New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*,
Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, and Dagger Environmental Protection
Branch, Division of Safety, Office of Research Services, National Institutes
of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre
National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999


One-gram samples from a pool of crude brain tissue from hamsters infected
with the 263K strain of hamster-adapted scrapie agent were placed in covered
quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at
temperatures ranging from 150°C to 1,000°C. Residual infectivity in the
treated samples was assayed by the intracerebral inoculation of dilution
series into healthy weanling hamsters, which were observed for 10 months;
disease transmissions were verified by Western blot testing for
proteinase-resistant protein in brains from clinically positive hamsters.
Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to
150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to
300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C
completely ashed the brain samples, which, when reconstituted with saline to
their original weights, transmitted disease to 5 of 35 inoculated hamsters.
No transmissions occurred after exposure to 1,000°C. These results suggest
that an inorganic molecular template with a decomposition point near 600°C
is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical waste |


The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure
(i.e., autoclaving). As a means of decontamination, dry heat is used only at
the extremely high temperatures achieved during incineration, usually in
excess of 600°C. It has been assumed, without proof, that incineration
totally inactivates the agents of TSE, whether of human or animal origin. It
also has been assumed that the replication of these agents is a strictly
biological process (1), although the notion of a "virus" nucleant of an
inorganic molecular cast of the infectious beta -pleated peptide also has
been advanced (2). In this paper, we address these issues by means of dry
heat inactivation studies.

see full text:

cjd dental


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