JRSM >
Volume 95, Number 4 >
Pp. 178-181
Oral Medicine, Eastman Dental Institute for Oral Health Care Sciences, UCL, University of London, 256 Gray's Inn Road, London WC1X 8LD, UK
E-mail: s.porter{at}eastman.ucl.ac.uk
 | INTRODUCTION |
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 TOP INTRODUCTION PRIONS IN THE DENTAL...GUIDELINES FOR THE DENTAL...CONCLUSIONSREFERENCES |
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| PRIONS IN THE DENTAL HEALTH CARE SETTING |
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TOPINTRODUCTIONPRIONS IN THE DENTAL...GUIDELINES FOR THE DENTAL...CONCLUSIONSREFERENCES |
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Prions in oral tissues
Prions have been detected in the oral and dental tissues of animals with
experimental scrapie, and the finding of neuronal degeneration with probable
prion protein accumulation in the trigeminal ganglia of patients with sporadic
CJD points to a possible route of transmission of prion from the brain to the
oral tissues (and vice
versa)6.
Inoculation of scrapie agent into the peritoneum or dental pulps of hamsters
leads to eventual prion infection of the trigeminal ganglion on the side of
inoculation7, the
estimated rate of travel along the trigeminal nerve being 1 mm per day.
Prion protein was not detected in the pulpal homogenates of 8 US patients with sporadic CJD8; however, intraperitoneal injection of scrapie agent led to infection of the dental pulps of hamsters after about 96 days7. Prions were also detected in the gingival tissues of these animals after about 760 days, the concentration of prion being higher in gingival than in pulpal tissue.
Since prion protein of vCJD is present in tonsillar lymphoid tissue9 it is likely to be present also in lingual tonsil. In addition, the tendency for prion of vCJD to occur at sites outside the central nervous system suggests that it will be present in the trigeminal ganglion—particularly since the prion of bovine spongiform encephalopathy (BSE) can be present in peripheral nerves10.
Infectivity
There is no definitive evidence that prion disease can be transmitted by
oral tissue, although biting is a possible explanation for accidental
transmission of scrapie between encaged
animals11. Gingival
scarification with burrs previously used to scarify scrapie-infected mice did
not lead to
scrapie1, although
intraperitoneal injection of gingival tissue did give rise to astrocytosis of
scrapie in mice. Also, gingival exposure to scrapie-infected brain homogenate
caused scrapie in recipient
mice12. Of note,
while gingival scarification (e.g. with forceps and scissors) caused
transmission to all laboratory animals, disease also developed in 71% of
animals gingivally exposed to brain homogenate but not scarified. Early
studies suggested that gingival extracts have low
infectivity1,
12—for example,
intracerebral inoculation of gingival tissue from scrapie-infected mice only
caused scrapie in 3 of 31
mice12—but
later work revealed substantially greater levels of prion protein in gingival
than in pulpal tissue of scrapie-infected
hamsters7.
There is little information on the precise infectivity of prion-infected oral tissues. One study of scrapie-infected hamsters established that the infectivity of pulpal tissue was 5.6 log LD50 while that of gingival tissue was 72 log LD50. These were lower than the infectivities of trigeminal ganglion and brain tissue.
Likelihood of transmission of prions during dental health care
First a word about experience with nosocomial transmission of non-prion
infectious agents during dentistry. Hepatitis B virus was at one time readily
transmitted during dental care, but contemporary infection control measures
have reduced this risk to almost
zero13. Although 6
patients probably acquired HIV as a consequence of care by an HIV-infected
dentist in the
USA14, lookback
studies of the patients of other HIV-infected dental staff have not disclosed
any patients infected with this virus as a result of dental
treatment15.
Dentists may be liable to hepatitis A virus infection, at least as evidenced
by HAV seroprevalence
studies16, although
they do not seem to be at risk of occupational acquisition of either hepatitis
C virus17 or
Transfusion Transmitted
Virus18. No dental
health care worker (DHCW) is believed to have been infected with HIV as a
consequence of occupational
injury15.
Clearly, these agents are much more easily activated than prions. Epidemiological evidence offers some reassurance that prions are not likely to be transmitted to DHCWs during dental treatment but the possibility cannot be excluded.
Oral manifestations of prion disease
Oral manifestations of human transmissible spongiform encephalopathies are
dysphagia and dysarthria (due to pseudobulbar palsy), and in vCJD patients
there may be orofacial dysaesthesia or
paraesthesia19.
Loss of taste and smell has been reported in one patient with
vCJD20.
Possible routes of transmission of prions during dental care
Since prion protein of vCJD is likely to be in perioral lymphoid tissue,
and prions of scrapie can be transmitted via pulpal and gingival tissue, we
must assume that there is some risk, albeit small, of prion protein
transmission during dental care. The most likely means of transmission would
be via contaminated dental instruments; thus measures to reduce this risk are
essential in the dental surgical care of patients with known prion
disease.
| GUIDELINES FOR THE DENTAL MANAGEMENT OF PATIENTS WITH PRION DISEASE |
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TOPINTRODUCTIONPRIONS IN THE DENTAL...GUIDELINES FOR THE DENTAL...CONCLUSIONSREFERENCES |
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Instruments must not be reused but discarded appropriately
The current UK guidance is that all health care instruments employed in the
treatment of a patient with known prion disease should be
discarded21,
22. Single-use
instruments are preferred, and these will come into increasing use for all
patients as new legislation comes into force.
Dental unit waterlines must not be activated
Dental unit waterlines can become contaminated with prions when the dental
handpiece is connected to the waterline. Thus, in view of the present
impossibility of inactivating prions, a sensible policy is to avoid the risk
of retraction of prions into the waterlines by instead using a coolant
provided by syringe.
Dental unit waterlines are a potential source of nosocomial infection. Dental staff have an excess seroprevalence of influenza A and B viruses and respiratory syncytial virus24, this possibly being due to the generation of aerosols25 and the development of biofilms within the lines. Dental staff also have an increased seroprevalence of legionella, and titres may correlate with duration of dental practice26. Although the frequency of legionella seropositivity does not correlate with rates of clinical disease27, fatal Legionella dumoffii in one dentist may have been due to acquisition of infection from bacteria within the waterline28. The precise risk of acquisition by patients or dental health care staff of infection from waterlines is not known, but since two immunosuppressed patients developed nonfatal infection of Pseudomonas aeruginosa derived from dental unit waterlines29 there is clearly a risk.
Biofilms of microorganisms derived from both the water source of the unit and retracted oral fluids develop within 8 hours within waterlines30. The rapid biofilm formation reflects the low diameter to surface area of the lines, the ease of adherence of bacteria to the hydrophobic polyurethane or polyvinyl surface, the low rate of flow of water and the frequent long periods of no flow within the line31, 32.
Retraction of oral fluids into dental handpieces and the waterline is common, indeed as much as 800 µL of fluid can pass into the handpiece33. Bacteria (e.g. Ps. aeruginosa) and viruses (e.g. HIV, hepatitis B, herpes simplex, bacteriophage 174) have been found to be retracted into the waterlines34. Flushing even for 10-20 minutes does not remove the biofilm35,36,37,38 (since the pressure at the tubing wall is almost zero31) and currently no antiretraction system, filtering mechanism32, or biocide has been reported to remove biofilms consistently from dental unit waterlines.
Thus, since there is a risk of retraction of prions in oral fluids, it would seem sensible not to activate waterlines when patients with known prion disease require restorative dental care. There is little information on the possible retraction of materials into the air lines of dental units.
An independent suction and spittoon other than those of the dental
unit should be used
In view of the difficulties of disinfection, the suction system of the
dental unit cannot be used; instead a stand-alone suction unit should be used.
The reservoir of the suction unit should be disposable. Patients should
expectorate into a disposable bowl, not a spittoon, and this should be
discarded directly into the clinical waste bin for incineration.
| CONCLUSIONS |
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TOPINTRODUCTIONPRIONS IN THE DENTAL...GUIDELINES FOR THE DENTAL...CONCLUSIONSREFERENCES |
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| REFERENCES |
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TOPINTRODUCTIONPRIONS IN THE DENTAL...GUIDELINES FOR THE DENTAL...CONCLUSIONSREFERENCES |
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