SEARCH VEGSOURCE:

 

 

Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.
  




From: TSS ()
Subject: Dental treatment and risk of vCJD
Date: May 1, 2007 at 1:24 pm PST

Summaries abstract

--------------------------------------------------------------------------------

British Dental Journal 202, 470 - 471 (2007)
Published online: 28 April 2007 | doi:10.1038/bdj.2007.356


Subject Categories: Cross infection control | Infection control

Dental treatment and risk of vCJD
S. R. Porter1


This manuscript is the first attempt to investigate potential links between dental treatment and the development of vCJD using case control methodology.
The results highlight difficulties in collecting retrospective data from relatives of CJD cases regarding dental treatment history.
Access to case and control dental records in the future may provide more useful information.


--------------------------------------------------------------------------------

Abstract
Objective Knowledge of risk factors for variant CJD (vCJD) remains limited, but transmission of prion proteins via re-useable medical devices, including dental instruments, or enhanced susceptibility following trauma to the oral cavity is a concern. This study aimed to identify whether previous dental treatment is a risk factor for development of vCJD.

Design Case control study.

Methods Risk factor questionnaires completed by interview with relatives of 130 vCJD patients and with relatives of 66 community and 53 hospital controls were examined by a dental surgeon. Responses regarding dental treatments were analysed.

Results There was no statistically significant excess of risk of vCJD associated with dental treatments with the exception of extractions in an unmatched analysis of vCJD cases with community controls (p = 0.02). However, this result may be explained by multiple testing.

Conclusions This is the first published study to date to examine potential links between vCJD and dental treatment. There was no convincing evidence found of an increased risk of variant CJD associated with reported dental treatment. However, the power of the study is restricted by the number of vCJD cases to date and does not preclude the possibility that some cases have resulted from secondary transmission via dental procedures. Due to the limitations of the data available, more detailed analyses of dental records are required to fully exclude the possibility of transmission via dental treatment.

Top of page
--------------------------------------------------------------------------------

Professor of Oral Medicine, UCL Eastman Dental Institute

http://www.nature.com/bdj/journal/v202/n8/abs/bdj.2007.356.html


© 2007 Nature Publishing Group

RESEARCH SUMMARY

470 BRITISH DENTAL JOURNAL VOLUME 202 NO. 8 APR 28 2007

ABSTRACT

Objective

Knowledge of risk factors for variant CJD (vCJD) remains limited, but

transmission of prion proteins via re-useable medical devices, including

dental instruments, or enhanced susceptibility following trauma to the

oral cavity is a concern. This study aimed to identify whether

previous dental treatment is a risk factor for development of vCJD.

Design

Case control study.

Methods

Risk factor questionnaires completed by interview with relatives of

130 vCJD patients and with relatives of 66 community and 53 hospital

controls were examined by a dental surgeon. Responses regarding

dental treatments were analysed.

Results

There was no statistically signifi cant excess of risk of vCJD associated

with dental treatments with the exception of extractions in an

unmatched analysis of vCJD cases with community controls

(p = 0.02). However, this result may be explained by multiple testing.

Conclusions

This is the first published study to date to examine potential links

between vCJD and dental treatment. There was no convincing evidence

found of an increased risk of variant CJD associated with reported

dental treatment. However, the power of the study is restricted by the

number of vCJD cases to date and does not preclude the possibility

that some cases have resulted from secondary transmission via dental

procedures. Due to the limitations of the data available, more detailed

analyses of dental records are required to fully exclude the possibility

of transmission via dental treatment.

EDITOR'S SUMMARY

Variant Creutzfeldt-Jakob disease (vCJD) has caused considerable

public concern due to its link with BSE-contaminated beef products

and evidence that it can be transmitted by blood transfusions. The

fact that the prion protein responsible for vCJD can be found and

transmitted in blood raises the question of cross infection during

routine healthcare procedures such as dental treatment. Previous

studies have not shown dental treatment to be a risk factor for the

sporadic form of CJD. This paper by Everington et al. is the first

study to date to look at whether dental treatment is a risk factor for

variant CJD.

The paper’s findings are encouraging: the analysis of interviews

with the relatives of 130 vCJD patients and 66 community and 53

hospital controls showed no significant increase in risk of vCJD

associated with dental treatment. The authors acknowledge that the

study is limited by its reliance on reported data from relatives and by

the number of vCJD cases to date, and more detailed research is being

investigated. However, it is important to note that the study assumes

that infection control procedures are in place, fully complied with and

not significantly less effective than they are expected to be. The authors

state that the results do not preclude the possibility that some cases of

vCJD have arisen because of secondary transmission through dental

treatment. If anything, this work emphasises the need for infection

control procedures in dentistry to be carefully considered and strictly

adhered to.

While more detailed studies are required in order to confirm that

dental treatment is not a risk factor for vCJD, this work is an important

first step and goes some way towards reassuring patients and

practitioners that as long as infection control measures are in place and

fully complied with, the risk of a patient contracting vCJD as a result of

dental treatment is extremely small.

The full paper can be accessed from the BDJ website

(www.bdj.co.uk), under ‘Research’ in the table of contents for

Volume 202 issue 8.

Rowena Milan,

Journal Editor

DOI: 10.1038/bdj.2007.356

Dental treatment and risk of vCJD

Dental treatment and risk of variant CJD – a case control study

D. Everington,1 A. J. Smith,2 H. J. T. Ward,3 S. Letters,4 R. G. Will5 and J. Bagg6

VERIFIABLE

CPD PAPER

ONLINE

• This manuscript is the fi rst attempt to investigate potential links between dental

treatment and the development of vCJD using case control methodology.

• The results highlight diffi culties in collecting retrospective data from relatives of CJD

cases regarding dental treatment history.

• Access to case and control dental records in the future may provide more useful

information.

I N B R I E F

© 2007 Nature Publishing Group

BRITISH DENTAL JOURNAL VOLUME 202 NO. 8 APR 28 2007 471

AUTHOR QUESTIONS AND ANSWERS

1. Why did you undertake this research?

The research was undertaken to determine if there was a link

between previous dental treatment and development of vCJD. It has

been postulated that although dental treatment involves contact

with tissues that have low levels of infectious prion proteins, the

large numbers of dental interventions may represent a risk factor at

population levels either through cross contamination and/or trauma

to the oral cavity resulting in an increased susceptibility by an as yet

undetermined aetiology. It is important to exclude dental treatment as

a risk factor for development of vCJD.

2. What would you like to do next in this area to follow on

from this work?

In order to obtain more robust data (as opposed to data obtained

from interview of relatives) we wish to review the dental records of

CJD cases and controls. This exercise is currently underway as a pilot

study to assess the logistics of recovering dental records from a small

cohort of CJD patients and appropriate control.

RESEARCH SUMMARY

COMMENT

Four types of human prion disease are presently recognised,

of which sporadic Creutzfeldt-Jakob disease (CJD) is probably

the most common. Variant CJD (vCJD) has attracted particular

attention in view of its arising principally in young adults,

variable clinical features, geographic clustering of affected

individuals (eg in the UK), wide distribution of prion protein

outside the neural system and probable transmission via blood

transfusions.1,2

Published data suggest that dentistry is a very unlikely

route of transmission of prion disease and this case control

study indicates that there is unlikely to be an association

between previous dental health care and potential acquisition

of prions causing vCJD. Although prions have been detected

in oral tissue of appropriate experimental animals and/or

individuals with vCJD, there is no evidence that prions can be

spread as a consequence of exposure3 to oral fluids, nor via

social or sexual contact. Hence despite the self acknowledged

limitations of their study, the findings of Everington and coworkers

are perhaps unsurprising and potentially reassuring to

both patients and oral health care staff.

While it is not known if a further wave of vCJD infections

will emerge, the present epidemiological data do not support

the notion that prion transmission is likely to occur during

dental care. For now, the risks of prion transmission during

dental care should be considered to be extremely low – as

detailed in the Department of Health’s risk assessment4

– provided of course that currently advised infection control

measures are adhered to.

S. R. Porter, Professor of Oral Medicine,

UCL Eastman Dental Institute

1. Collinge J. Molecular neurology of prion disease. J Neurol Neurosurg

Psychiatry 2005; 76: 906-919.

2. Health Protection Agency. Variant CJD and blood products.

http://www.hpa.org.uk/infections/topics_az/cjd/blood_products.htm

(accessed 28th January 2007).

3. Carp R I. Transmission of scrapie via oral route: effect of gingival

scarifi cation. Lancet 1982; 1: 170-171.

4. Department of Health. Risk assessment for vCJD and dentistry.

www.dh.gov.uk/assetRoot/04/07/83/02/04078302.pdf

(accessed 16 January 2007).

http://www.nature.com/bdj/journal/v202/n8/pdf/bdj.2007.356.pdf

please note, sporadic CJD i.e. iCJD, has been documented to transmit from different routes and sources in the medical and surgical arena;

6. CJD IN FARMERS

The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups.


These relevant details are:-

MEDICAL/PARAMEDICAL/DENTISTRY 7

ANIMAL LABORATORY 1

PHARMACEUTICAL LABORATORY 0

RESEARCH LABORATORY 0

FARMERS/VETERINARY SURGEONS 7

BUTCHERS/ABATTOIR WORKERS/OCCUPATION
INVOLVING DIRECT CONTACT WITH ANIMAL
OR CARCASES 5

OCCUPATION INVOLVING ANIMAL PRODUCTS 9


snip... full text ;

http://www.bseinquiry.gov.uk/files/yb/1993/07/19001001.pdf

PLEASE SEE DENTAL RISK FROM HUMAN AND ANIMAL TSE


http://neurotalk.psychcentral.com/archive/index.php/t-13173.html

Subject: MASTER DENTIST FALLS VICTIM TO CJD
Date: March 31, 2007 at 1:27 pm PST


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&P=19835

Iatrogenic CJD infection is inadvertently transmitted usually from a case with sCJD in the course of medical/surgical treatment, e.g. human pituitary hormone therapy, human dura mater grafts, corneal grafts or neurological instruments.
􀁹 Avoiding iatrogenic exposures:

􀂃 Specific precautions should be taken in the management of persons with confirmed or suspected transmissible spongiform encephalopathy (TSEs) and their tissues.


􀂃 The following persons have been regarded as "at risk" for developing TSE: recipients of human dura mater, of human cadaver-derived pituitary hormones especially human cadaver derived growth hormone, of cornea transplants, persons undergoing neurosurgery and members of families with heritable TSE.


􀂃 When determining the risk of iatrogenic transmission, infectivity of a given tissue should be considered together with the route of exposure. Infectivity is found most often and in the highest concentration in the central nervous system. Precautions to be taken when performing certain interventions (dental, diagnostic, surgical procedures) and when handling instruments, cleaning and decontaminating instruments, work surface and wastes have been proposed.


􀂃 Probable secondary transmission of vCJD via blood transfusion has been reported. The possibility of transfusion transmission of vCJD has important implications for public health and a range of measures have been taken in a number of countries, especially the United Kingdom, to minimize the risk. For further information see Bibliography below.
http://www.who.int/zoonoses/diseases/Creutzfeldt.pdf


Between 1970 and 2000, 42 cases of iatrogenic CJD have been ascertained, six in recipients of dura mater implants, 35 in recipients of human derived growth hormone (hGH), and one in a recipient of human gonadotrophin (hGN). The mean age at death of the hGH/hGN group was 29 years (range 20-45 years) and for the dura mater recipients 43 years (27-59 years). The first recognised case in a dura mater recipient died in 1979, and the first hGH related death was in 1985.

http://www.eurosurveillance.org/ew/2001/010705.asp

Iatrogenic cases (about 260 cases world wide) result from the accidental transmission of the causative agent by contaminated surgical equipment or as a result of cornea or dura mater transplants or the administration of human-derived pituitary growth hormones. The incubation period between the exposure and onset of illness in iatrogenic cases varies from 15 months to 30 years.


http://chppm-www.apgea.army.mil/madcowdisease/ProviderQA.doc


Creutzfeldt–Jakob Disease in health professionals in Slovakia


Journal European Journal of Epidemiology
Publisher Springer Netherlands
ISSN 0393-2990 (Print) 1573-7284 (Online)
Issue Volume 16, Number 4 / April, 2000
DOI 10.1023/A:1007601313133
Pages 353-355
Subject Collection Medicine
SpringerLink Date Tuesday, November 02, 2004

Eva Mitrová1 and Girma Belay1

(1) Institute of Preventive and Clinical Medicine, Limbová 14, 833 01 Bratislava, Slovakia


Abstract Creutzfeldt–Jakob disease (CJD) is the most important human transmissible spongiform encephalopathy (prion disease), recognised in sporadic, genetic but also iatrogenic forms. The identification of 8 health care workers in a group of 114 definitive CJD patients in Slovakia suggested the possibility of professionaly acquired CJD and induced the investigation of potential endo- and exogenous risk factors. In CJD-affected health professionals special attention was paid to a detailed occupational history, including a possible professional contact with CJD patient and to the findings characteristic for iatrogenic CJD: early cerebellar symptomatology, long duration of the disease, absence of typical EEG finding and homozygosity of PRNP gene at codon 129. Analysis of epidemiological, clinical and molecular biological data in investigated group of CJD-affected health professionals gave no evidence of an occupational risk for CJD.
Creutzfeldt–Jakob disease - Health professionals - Iatrogenic

http://www.springerlink.com/content/v2361482271k2371/

Creutzfeldt-Jakob Disease (CJD) Policy

the management of patients with definite, probable

and possible CJD or variant CJD

Author: Johanna Hill

Department: Infection Control

Date of issue: June 2006

Date of review: June 2008

Policy number: ICC 18

http://www.westminster-pct.nhs.uk/pdfs/ICC18WCJD.pdf

PRIONS AND THE ORAL CAVITY

snip...

Case Reports

There have been two reports of clusters of CJD cases with a

possible connection through dentistry, but there is no strong

epidemiological evidence to link the dental treatment in these

cases with transmission of prions (Will and Matthews, 1982;

Arakawa et al., 1991).

Case Control Studies in sCJD

Many series and case control studies have searched for risk

factors such as diet, exposure to animals, surgical treatment

including dentistry, and occupational exposures. A

retrospective case-controlled study (Kondo and Kuroiwa, 1982)

of 60 definite cases of sporadic CJD, occurring in Japan

between 1975 and 1977, found no association with dental

extractions. However, the authors did report a significant

association with physical injuries, including surgical

operations, but not including dental treatment, blood

transfusions, or lumbar punctures. More recently, an Australian

study has reported that surgical procedures were significantly

associated with the development of sCJD, although they found

no significant risk associated with a history of major dental

treatment (Collins et al., 1999). An analysis of 26 CJD cases

and 40 matched controls from the United States (Davanipour et

al., 1985) failed to discover a significant odds ratio for

endodontic surgery, though these workers did note statistically

significant odds ratios for intra-ocular pressure testing, injury to

or surgery on the head, face, or neck, and trauma to other parts

of the body.

Infectivity in Human Trigeminal Nerve and Oral Tissues

PrPsc has been detected by polyclonal antibodies to scrapieassociated

fibril/prion protein in the trigeminal ganglion of one

patient with fCJD and one patient with sCJD (Table 3) (Guiroy

et al., 1989). These workers also noted the presence of specific

immunostaining of dystrophic axons in the nerve roots and

around the degenerating ganglion cells of the trigeminal

ganglion, suggesting centripetal or centrifugal extension of the

disease process along the axons. Positive immunochemistry for

PrP has been reported for the trigeminal ganglion in vCJD

(Ironside et al., 2002) but was not detected in cranial nerves or

salivary gland tissue.

One study has investigated the levels of prion protein in

pulpal tissue from eight patients with sCJD (Blanquet-Grossard

et al., 2000). By Western blotting, using a specific monoclonal

antibody, this group was unable to detect any prion protein in

pulpal tissue. However, the authors suggested that since the

method used was relatively insensitive, the potential for

transmission of CJD via dental procedures, although low, could

not be dismissed. These workers calculated that 1 g of sCJDinfected

pulp would be expected to contain 40 log10 LD50/g of

infectivity, compared with 108-9 LD50/g of infectivity in brain

tissue.

Implications for Dental Treatment

There are few experimental data on which to base risk

assessments for potential transmission of CJD via dental

procedures. Animal models provide useful data, but, by

virtue of differing genetic susceptibilities and the varied

properties of the different strains of prions used, this

information cannot be directly extrapolated to the clinical

setting. However, there is a general consensus that all

instruments, including dental handpieces, used for treatment

774 Smith et al. J Dent Res 82(10) 2003

on known or suspected cases of CJD of any type should not

be re-used on other patients (WHO, 2000), but rather should

be incinerated.

The situation is less clear-cut for treatment of healthy

patients deemed to be "at risk" of developing CJD. These

include recipients of contaminated dura mater grafts or relatives

of patients with fCJD, for which there is significant variation

between different sets of official recommendations, from

stringent decontamination protocols for instruments, including

extended periods of autoclaving in a vacuum autoclave

(ACDP/SEAC, 1998), to no special precautions at all (WHO,

2000). There is no evidence that TSEs can be transmitted by

aerosol routes or contaminated surfaces; therefore, the only

components of infection control procedures that merit special

consideration are those relating to re-usable instruments.

Routine surgery protocols for surgery surface and

environmental cleaning, which are used to limit transmission of

blood-borne viruses, are sufficient for treatment of known,

suspected, or "at-risk" cases. At the time of writing, there is no

evidence in humans to suggest that oral tissues carry high levels

of PrPsc (see note below). Since it is not possible to identify

patients who may be asymptomatic carriers of PrPsc, particularly

vCJD, the most important recommendation is to ensure that the

quality of pre-sterilization cleaning of instruments used on all

patients is of the highest standard, and that instruments which

cannot be reliably cleaned are treated as single-use.

CONCLUSION

The last five years have seen the emergence of a new human

TSE termed "variant CJD", which results from exposure to the

BSE agent. This has been accompanied by a wealth of

scientific data on the responsible infectious agents called

prions. However, data concerning the distribution of PrPsc and

infectivity in the oral cavity are sparse. The available animal

model evidence illustrates a potential for transmission via the

dental route, but differences in patterns of disease and in

strains of the agent make it difficult to extrapolate these

findings directly to humans. Data concerning the distribution

of PrPsc and infectivity in the human oral cavity are urgently

required to determine the risk, if any, of cross-infection during

common dental procedures.

http://jdr.iadrjournals.org/cgi/reprint/82/10/769.pdf

TOPICAL DENTAL PRODUCTS WOULD ALSO BE OF CONCERN, since there was a suggestion that kuru had been transmitted through the gums and/or gum abrasions.

http://www.bseinquiry.gov.uk/files/yb/1989/04/17005001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/03/21015001.pdf

NOT FOR PUBLICATION

COMMITTE ON DENTAL AND SURGICAL MATERIALS

http://www.bseinquiry.gov.uk/files/yb/1991/11/20006001.pdf

NOT FOR PUBLICATION (and they meant it...tss)

COMMITTEE ON DENTAL AND SURGICAL MATERIALS

http://www.bseinquiry.gov.uk/files/yb/1988/11/16006001.pdf

http://www.bseinquiry.gov.uk/files/yb/1993/11/01005001.pdf


http://www.bseinquiry.gov.uk/files/yb/1993/11/17005001.pdf


USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...

64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...

http://www.seac.gov.uk/minutes/95.pdf


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535


JOURNAL OF NEUROLOGY

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

flounder@wt.net

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

http://www.neurology.org/cgi/eletters/60/2/176#535


TSS




Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: