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News Bulletin : ADA News Bulletin April 2011
17 APRIL 2011 AN UPDATE ON THE Creutzfeldt–Jakob diseases committee report Transmissible spongiform encephalopathies or prion diseases have attracted considerable attention in dentistry, and until relatively recently there was a suggestion that dental procedures could play a role in the transmission of the various forms of Creutzfeldt–Jakob disease (CJD) (sporadic, familial, iatrogenic and variant). This view has now been discounted, which greatly simplifies the clinical management of such patients when they present for routine dental treatment. CLASSICAL fORMS Of CJd There are very few patients in Australia with classical forms of CJD (sporadic, familial, and iatrogenic) as the incidence is only 1.0–1.5 per million individuals. 2 The 2006 WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies laid the groundwork for the subsequent Australian guidelines from the Special Expert Committee on Transmissible Spongiform Encephalopathies (SECTSE) which now recognise that because of the absence of prions outside the central nervous system (and thus from the oral cavity), transmission of classical forms of CJD through dental instruments does not occur. This has led to a simplification to the management of patients with classical CJD, who can now be treated in office practice with standard precautions, without the need for disposable dental instruments and disposable handpieces as was the case in the past. The exception to this rule is for maxillofacial surgical procedures involving the trigeminal ganglia or other parts of the central nervous system, during which contact with neural tissue is likely to occur. In such cases, use of disposable instruments or special protocols for cleaning and sterilization of objects potentially contaminated with central neural tissue must be followed.1 The same limitations apply to neurosurgery, posterior eye surgery and some fibroscopic endoscopy procedures where there is a high likelihood of contact with brain tissue. vARIAnT CJd Variant CJD has a clinical and pathological presentation which is quite distinct from classical forms of CJD, with a propensity for patients of a younger age, who tend to suffer more in terms of psychiatric symptoms than patients with classical forms of CJD who tend to be older adults (aged 50-70 years) and who present with dementia, confusion, disorientation and problems with walking. Moreover, the agent which causes vCJD is more heat sensitive than the agent responsible for classical forms of CJD. The heat stability of vCJD against temperatures including the standard autoclave cycle (134 oC with a 3 minute holding time, as used in standard dental autoclaves) is relatively poor, with reductions of 300-fold to 1,000-fold in infectivity from autoclaving.3 The origins of vCJD can be traced back to bovine spongiform encephalopathy (BSE) in cattle in the United Kingdom. The source of human exposure to BSE was consumption of contaminated meat products.3 When allowances have been made for asymptomatic infections, it has been estimated that up 3 million infected cattle may have entered the UK human food chain in the early 1990s. Given the large scale of the exposure to the British population, it appears that those who travelled to or lived in the UK between 1980 and 1996 had only a very low risk of contracting vCJD despite having eating contaminated beef. The first cases of vCJD were reported in the UK in 1996. The number of newly diagnosed cases of vCJD has fallen steadily each year since 2000 when the primary outbreak peaked in the UK. By February 2010, a total of 172 confirmed cases of vCJD had been reported in the UK, with 47 additional cases outside the UK, spread across 10 other countries (41 of these cases were in Europe). Of note, all confirmed cases of vCJD share a genetic subtype (methionine homozygosity at codon 129 in the prion protein gene) indicating a genetic predisposition. Some 39% of the population have this genetic predisposition. Nevertheless, no cases of vCJD have been reported in Australia. The three major reasons for this are: (1) Beef imports into Australia from the UK have been banned since 1998, and Australia has since banned imports from other countries whose cattle are affected by BSE. (2) No cases of BSE have been reported in Australian livestock. (3) Australia has taken measures to prevent blood donation from patients at risk for either classical forms of CJD or variant CJD. Recent ‘worse case’ estimates place the prevalence of individuals infected with vCJD in the UK at 1 per 10,000, which is much higher than the current case number would suggest (because not all patients may manifest symptoms).3 Such estimates of ‘background’ vCJD in the UK population underpin the decision of the Australian Red Cross Blood Service not to allow blood donations from people who have resided in the UK between 1980 and 1996 for a total (cumulative) time of 6 months or more, or who have received blood transfusions in the UK since 1 January 1980. In keeping with an oral route of infection, abnormal proteins and infectivity for vCJD have been found for lymphoid tissues, such as tonsils, lymph nodes, spleen and gut associated lymphoid tissue. The levels of infectivity in lymphoid tissues are some 100–1,000 times less than brain tissue. There is indirect evidence that lymphocytes may carry infectivity in blood during the incubation period of vCJD. However, the condition cannot be transmitted by saliva.
ADA News Bulletin March 2011
ADA News Bulletin May 2011