1259
EDITORIALS
Risk of HIV transmission during dental treatment The first health care worker reported to have been responsible for the transmission of human immunodeficiency virus (HIV) to patients in clinical practice was a dentist practising in Florida, USA.1 The precise mode of transmission of HIV is uncertain,2but 5 patients are known to have been infected and all had had invasive procedures carried out by the dentist, who had AIDS.3 A "sharps" injury is a possibility because the dentist had, like many health care workers, sustained needlestick injuries. It is also possible that unsterile dental equipment could have led to cross-infection. The dental unit water system might have been a source of infection; bacteria,
including legionellae, can certainly be transmitted by this route, despite placement of check valves.4 Another potential hazard is sucking back of HIVinfected oral material such as blood, gingival fluid,s saliva,6 and tissue from dental handpieces into waterlines. There have been no firm data to support the contention of waterline infection until now. On p 1252, Lewis and colleagues report that HIVinfected material can be sucked back into waterlines and expelled via a dental handpiece. Methods of disinfecting waterlines have included addition of chlorhexidine gluconate,8 sodium hypochlorite,9 or hydrogen peroxide1O to the dental water supply and flushing out the system before and after use for every patient.ll These techniques are not always practicable and have anyway not been shown to be effective against viruses.12 Probably the most effective method is use of a sterile water reservoir combined with regular flushing with povidone-iodine,13 but this approach necessitates ready access to waterlines and is clearly not feasible between patients in a busy dental practice. A centralised chlorination system for the water supplies may be effective for large dental practices. The efficacy of these techniques against HIV is unproven. Transmission of HIV during dental treatment in a US practice is alarming, but world wide, in the decade or so of the recognised HIV pandemic, only these 5 patients in a single dental practice are known to have become infected. None of over 15 000 patients treated by 32 HIV-infected health care workers (including 16 dentists/dental students) has been found
HIV through dental or other treatment. 14-21 Most dental staff are well operative aware of the risks of cross-infection and are generally compliant with current protective guidelines.22 If dentistry were an important source of HIV transmission between patients and dental staff, it is likely that several dental personnel would have acquired HIV by now, whereas only 2 of over 7000 tested dental health care staff, including those from areas of high HIV prevalence, seem to have been infected during dental practice. 23-25 Moreover, dentists have the same risk of occupational acquisition of HIV as do other health care workers. 2-3--25 As with all surgical procedures, there can be areas of weakness in infection control in dental practice, but existing data indicate that the risk of HIV transmission during dental treatment is very small.
to
have
acquired
1. Ou C-Y, Ciesielski CA, Myers G, et al. Molecular epidemiology of HIV transmission in a dental practice. Science 1992; 256: 1165-71. 2. Chamberland ME, Bell DM. HIV transmission from health care worker to patient: what is the risk? Ann Intern Med 1992; 116: 871-73. 3. Ciesielski C, Marianos D, Ou C-Y, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med 1992; 116: 798-805. 4. Crawford JJ, Broderius C. Evaluation of a dental unit designed to prevent retraction of oral fluids. Quint Int 1990; 21: 47-51. 5. Holmstrom P, Syrjanan S, Laine P, Suni J. HIV antigens detected in gingival fluid. AIDS 1992; 6: 738-34. 6. Barr CE, Miller LK, Lopez MR, et al. Recovery of infectious HIV-1 from whole saliva. J Am Dent Assoc 1992; 123: 37-45. 7. Glick M, Trope M, Bagasra O, Pliskin M. Human immunodeficiency virus in fibroblasts of dental pulp of seropositive patients. Oral Surg Oral Med Oral Pathol 1991; 71: 733-36. 8. Blake GC. The incidence and control of bacterial infection in dental spray reservoirs. Br Dent J 1963; 115: 413-20. 9. Abel LC, Miller RL, Micik RE, Ryge G. Studies on dental aerobiology: IV. Bacterial contamination of water delivered by dental units. J Dent Res 1971; 50: 1567-69. 10. Kellett M, Holbrook WP. Bacterial contamination of dental handpieces. J Dent 1980; 8: 249-53. 11. Scheid RC, Kin CK, Bright JS, et al. Reduction of microbes in handpieces by flushing before use. J Am Dent Assoc 1982; 105: 658-60. 12. Lewis DL, Boe RK. Cross-infection risks associated with current procedures for using high-speed dental handpieces. J Clin Microbiol
1992; 30: 401-06. SE, Lauderdale PW, Mayhew RB. Reduction of microbial
13. Mills
contamination in dental units with povidone-iodine 10%. J Am Dent Assoc 1986; 113: 280-84. 14. Porter JD, Cruickshank JG, Gentle PH, Robinson RG, Gill ON. Management of patients treated by a surgeon with HIV infection. Lancet 1990; 335: 113-14. 15. Armstrong FP, Miner JC, Wolfe WH. Investigation of a health-care worker with symptomatic human immunodeficiency virus infection: an epidemiologic approach. Milit Med 1987; 152: 414-18. 16. Mishu B, Schaffner W, Horan JM, et al. A surgeon with AIDS: lack of evidence of transmission to patients. JAMA 1990; 264: 467-70. 17. Danila RN, MacDonald KL, Rhames FS, et al. A look-back investigation of patients of an HIV infected physician: public health implications. N Engl J Med 1991; 325: 1406-11. 18. Comer RW, Myers DR, Steadman CD, et al. Management considerations for an HIV positive dental student. J Dent Educ 1991; 55: 187-91. 19. Hamory BH, Zanotti M, Rohrer VG. "Look-back" involving an Ob/Gyn resident. Second meeting of Society for Hospital Epidemiology of America. West Deptford, New Jersey: Society for Hospital Epidemiology of America, 1992: 34 (abstr). 20. Dickinson G, Bisno A, Morhart R, et al. Human immunodeficiency virus infection among patients of a dentist with AIDS. Clin Res 1992; 40: 219A. 21. Centers for Disease Control. Update: investigations of patients who have been treated by HIV-infected health care workers. MMWR 1992; 41: 344-46. 22. Porter SR. Infection control in density. Curr Opin Dent 1991; 1: 429-35.
1260
23. Klein RS, Phelan JA, Freeman K, et al. Lower occupational risks of human immunodeficiency virus infection among dental professionals. N Engl J Med 1988; 318: 86-90. 24. Gruninger SE, Siew C, Chang S-B, et al. Human immunodeficiency virus type 1 infection among dentists. J Am Dent Assoc 1992; 123: 57-64. 25. Capilouto EI, Cotton D, Weinstein MC, et al. What is the dentist’s occupational risk of becoming infected with hepatitis B or the human immunodeficiency virus? Am J Public Health 1992; 82: 587-89.
Bile acid
therapy in the 1990s.
Intense interest in biliary biochemistry and pathophysiology in the 1960s led to the discovery that formation of cholesterol gallstones was largely attributable to cholesterol oversaturation of bile. Reversal of this process by chenodeoxycholic acid (CDCA) therapy was shown to achieve dissolution of some gallstones and similar results were obtained with ursodeoxycholic acid (UDCA). How has bile acid therapy fared subsequently and what are its prospects? These issues were reviewed last month at the Twelfth International Bile Acid meeting in Basel. For gallstone dissolution, UDCA is at least as efficacious as CDCA and is not associated with diarrhoea. Combined treatrnents-lower doses of
UDCA plus CDCA, or CDCA plus "statin" cholesterol synthesis inhibitors-have been proposed but are not clearly advantageous.1,2 Small gallstone size is crucial to success, which is why lithotripsy plus UDCA achieves better results than UDCA alone.3 For good results, patients should have a functioning gallbladder, stones no larger than 15 mm in diameter, and no evidence of radiographic calcification. Even in selected cases treated with UDCA for at least six months the overall success rate-about one in four-is not spectacular 4These results might be improved by computed tomography before treatment to exclude subradiographic calcification,s and by selection of the
very smallest stones. Recurrent gallstones can be expected in about 50% of patients during a five-year follow-up; there is no sure method of prevention although further UDCA therapy may help.66 UDCA reduces cholesterol content of bile but also lengthens nucleation time for cholesterol crystals, a crucial factor in the initiation of stones. This action may explain UCDA’s usefulness in preventing both gallstones induced by periods of rapid weight loss7 and relapsing acute pancreatitis attributed to microlithiasis. For most gallstone patients, cholecystectomy, including the laparoscopic version, is likely to remain the treatment of choice for gallbladder stones. Bile acid therapy will be reserved for cases unsuitable for surgery, and for prevention. For common bileduct stones, endoscopic retrograde cholangiopancreatography and stone extraction are first-line management, although UDCA and lithotripsy make a minor contribution. It was beginning to look as though bile acid therapy would never reach the big league in the pharmacopoeia until the serendipitous discovery that cholestatic liver disease, especially primary biliary cirrhosis (PBC), could be influenced by UDCA
This approach held out the prospect of safe management where there was no well-established alternative. Early and presymptomatic cases of PBC are increasingly recognised-subjects with a mitochondrial antibody titre of 40 or more have PBC until proven otherwise9-and many of these will progress to more serious disease, as indicated by the presence of M2/M4/M8 subfraction mitochondrial treatment.
antibodies (not generally available as a test) and a rising bilirubin concentration.9,10 The only cure for the disease is liver transplantation, and even then post-transplant recurrences have been reported," UDCA is effective both in alleviating symptoms such as pruritus and in reducing serum concentrations of alkaline phosphatase and glutamyl transferase.12,13 Improvement in the histological appearance of the liver has been more difficult to document, and there is no clear evidence of enhanced survival or a reduction in disease progression. The mechanism of action of UDCA was originally thought to be replacement of toxic bile acids by exogenous UDCA;14 several lines of evidence now suggest that an additional (perhaps even main) mode of action is inununomodulation.1-1-11 Not all researchers have been enthusiastic about UDCA therapy in PBC, either failing to show a definite benefit, or documenting progression to liver failure or established cirrhosis in some cases.1S-20 In a few patients symptoms and liver function tests become worse, but this deterioration is usually apparent in the first few days or weeks of therapy. Patients with early disease will probably benefit most, since there is less scope for improvement when cirrhosis is established.18 Despite doubts about the hazards of altering human bile acids,21 UDCA is much the least toxic of the existing drugs for PBC, and should certainly be considered in early cases. UDCA has been tested in many other cholestatic diseases such as primary sclerosing cholangitis22 and benign cholestasis of pregnancy,23 with encouraging results. It has also been used in autoimmune chronic active hepatitis,24 where its main role may be as an adjuvant to conventional therapy with prednisolone and azathioprine. An important fresh initiative reported at the Basel meeting by Kramer and co-workers from Frankfurt is hybridisation of drugs with bile acids to ensure preferential delivery to the liver via the enterohepatic circulation. Thus it may be possible to reduce renal excretion as with chlorambucil/bile acid conjugates, to avoid non-hepatic side-effects as with HMG coenzyme A reductase inhibitor conjugates, and also to encourage intestinal absorption and avoid hydrolysis of peptide conjugates. 1.
Jazrawi RP, Pigozzi MG, Galatola F, Lanzini A, Northfield TC Optimum bile acid treatment for rapid gallstone dissolution. Gut 1992; 33: 381-86.
2. Sackmann
M, Pauletzki J, Aydemir U,
et al. Efficacy and safety of for dissolution of gallstone fragments: comparison with the combination of ursodeoxycholic add and chenodeoxycholic add. Hepatology 1991; 14: 1136-41.
ursodeoxycholic add
EDITORIALS
Risk of HIV transmission during dental treatment The first health care worker reported to have been responsible for the transmission of human immunodeficiency virus (HIV) to patients in clinical practice was a dentist practising in Florida, USA.1 The precise mode of transmission of HIV is uncertain,2but 5 patients are known to have been infected and all had had invasive procedures carried out by the dentist, who had AIDS.3 A "sharps" injury is a possibility because the dentist had, like many health care workers, sustained needlestick injuries. It is also possible that unsterile dental equipment could have led to cross-infection. The dental unit water system might have been a source of infection; bacteria,
including legionellae, can certainly be transmitted by this route, despite placement of check valves.4 Another potential hazard is sucking back of HIVinfected oral material such as blood, gingival fluid,s saliva,6 and tissue from dental handpieces into waterlines. There have been no firm data to support the contention of waterline infection until now. On p 1252, Lewis and colleagues report that HIVinfected material can be sucked back into waterlines and expelled via a dental handpiece. Methods of disinfecting waterlines have included addition of chlorhexidine gluconate,8 sodium hypochlorite,9 or hydrogen peroxide1O to the dental water supply and flushing out the system before and after use for every patient.ll These techniques are not always practicable and have anyway not been shown to be effective against viruses.12 Probably the most effective method is use of a sterile water reservoir combined with regular flushing with povidone-iodine,13 but this approach necessitates ready access to waterlines and is clearly not feasible between patients in a busy dental practice. A centralised chlorination system for the water supplies may be effective for large dental practices. The efficacy of these techniques against HIV is unproven. Transmission of HIV during dental treatment in a US practice is alarming, but world wide, in the decade or so of the recognised HIV pandemic, only these 5 patients in a single dental practice are known to have become infected. None of over 15 000 patients treated by 32 HIV-infected health care workers (including 16 dentists/dental students) has been found
HIV through dental or other treatment. 14-21 Most dental staff are well operative aware of the risks of cross-infection and are generally compliant with current protective guidelines.22 If dentistry were an important source of HIV transmission between patients and dental staff, it is likely that several dental personnel would have acquired HIV by now, whereas only 2 of over 7000 tested dental health care staff, including those from areas of high HIV prevalence, seem to have been infected during dental practice. 23-25 Moreover, dentists have the same risk of occupational acquisition of HIV as do other health care workers. 2-3--25 As with all surgical procedures, there can be areas of weakness in infection control in dental practice, but existing data indicate that the risk of HIV transmission during dental treatment is very small.
to
have
acquired
1. Ou C-Y, Ciesielski CA, Myers G, et al. Molecular epidemiology of HIV transmission in a dental practice. Science 1992; 256: 1165-71. 2. Chamberland ME, Bell DM. HIV transmission from health care worker to patient: what is the risk? Ann Intern Med 1992; 116: 871-73. 3. Ciesielski C, Marianos D, Ou C-Y, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med 1992; 116: 798-805. 4. Crawford JJ, Broderius C. Evaluation of a dental unit designed to prevent retraction of oral fluids. Quint Int 1990; 21: 47-51. 5. Holmstrom P, Syrjanan S, Laine P, Suni J. HIV antigens detected in gingival fluid. AIDS 1992; 6: 738-34. 6. Barr CE, Miller LK, Lopez MR, et al. Recovery of infectious HIV-1 from whole saliva. J Am Dent Assoc 1992; 123: 37-45. 7. Glick M, Trope M, Bagasra O, Pliskin M. Human immunodeficiency virus in fibroblasts of dental pulp of seropositive patients. Oral Surg Oral Med Oral Pathol 1991; 71: 733-36. 8. Blake GC. The incidence and control of bacterial infection in dental spray reservoirs. Br Dent J 1963; 115: 413-20. 9. Abel LC, Miller RL, Micik RE, Ryge G. Studies on dental aerobiology: IV. Bacterial contamination of water delivered by dental units. J Dent Res 1971; 50: 1567-69. 10. Kellett M, Holbrook WP. Bacterial contamination of dental handpieces. J Dent 1980; 8: 249-53. 11. Scheid RC, Kin CK, Bright JS, et al. Reduction of microbes in handpieces by flushing before use. J Am Dent Assoc 1982; 105: 658-60. 12. Lewis DL, Boe RK. Cross-infection risks associated with current procedures for using high-speed dental handpieces. J Clin Microbiol
1992; 30: 401-06. SE, Lauderdale PW, Mayhew RB. Reduction of microbial
13. Mills
contamination in dental units with povidone-iodine 10%. J Am Dent Assoc 1986; 113: 280-84. 14. Porter JD, Cruickshank JG, Gentle PH, Robinson RG, Gill ON. Management of patients treated by a surgeon with HIV infection. Lancet 1990; 335: 113-14. 15. Armstrong FP, Miner JC, Wolfe WH. Investigation of a health-care worker with symptomatic human immunodeficiency virus infection: an epidemiologic approach. Milit Med 1987; 152: 414-18. 16. Mishu B, Schaffner W, Horan JM, et al. A surgeon with AIDS: lack of evidence of transmission to patients. JAMA 1990; 264: 467-70. 17. Danila RN, MacDonald KL, Rhames FS, et al. A look-back investigation of patients of an HIV infected physician: public health implications. N Engl J Med 1991; 325: 1406-11. 18. Comer RW, Myers DR, Steadman CD, et al. Management considerations for an HIV positive dental student. J Dent Educ 1991; 55: 187-91. 19. Hamory BH, Zanotti M, Rohrer VG. "Look-back" involving an Ob/Gyn resident. Second meeting of Society for Hospital Epidemiology of America. West Deptford, New Jersey: Society for Hospital Epidemiology of America, 1992: 34 (abstr). 20. Dickinson G, Bisno A, Morhart R, et al. Human immunodeficiency virus infection among patients of a dentist with AIDS. Clin Res 1992; 40: 219A. 21. Centers for Disease Control. Update: investigations of patients who have been treated by HIV-infected health care workers. MMWR 1992; 41: 344-46. 22. Porter SR. Infection control in density. Curr Opin Dent 1991; 1: 429-35.
1260
23. Klein RS, Phelan JA, Freeman K, et al. Lower occupational risks of human immunodeficiency virus infection among dental professionals. N Engl J Med 1988; 318: 86-90. 24. Gruninger SE, Siew C, Chang S-B, et al. Human immunodeficiency virus type 1 infection among dentists. J Am Dent Assoc 1992; 123: 57-64. 25. Capilouto EI, Cotton D, Weinstein MC, et al. What is the dentist’s occupational risk of becoming infected with hepatitis B or the human immunodeficiency virus? Am J Public Health 1992; 82: 587-89.
Bile acid
therapy in the 1990s.
Intense interest in biliary biochemistry and pathophysiology in the 1960s led to the discovery that formation of cholesterol gallstones was largely attributable to cholesterol oversaturation of bile. Reversal of this process by chenodeoxycholic acid (CDCA) therapy was shown to achieve dissolution of some gallstones and similar results were obtained with ursodeoxycholic acid (UDCA). How has bile acid therapy fared subsequently and what are its prospects? These issues were reviewed last month at the Twelfth International Bile Acid meeting in Basel. For gallstone dissolution, UDCA is at least as efficacious as CDCA and is not associated with diarrhoea. Combined treatrnents-lower doses of
UDCA plus CDCA, or CDCA plus "statin" cholesterol synthesis inhibitors-have been proposed but are not clearly advantageous.1,2 Small gallstone size is crucial to success, which is why lithotripsy plus UDCA achieves better results than UDCA alone.3 For good results, patients should have a functioning gallbladder, stones no larger than 15 mm in diameter, and no evidence of radiographic calcification. Even in selected cases treated with UDCA for at least six months the overall success rate-about one in four-is not spectacular 4These results might be improved by computed tomography before treatment to exclude subradiographic calcification,s and by selection of the
very smallest stones. Recurrent gallstones can be expected in about 50% of patients during a five-year follow-up; there is no sure method of prevention although further UDCA therapy may help.66 UDCA reduces cholesterol content of bile but also lengthens nucleation time for cholesterol crystals, a crucial factor in the initiation of stones. This action may explain UCDA’s usefulness in preventing both gallstones induced by periods of rapid weight loss7 and relapsing acute pancreatitis attributed to microlithiasis. For most gallstone patients, cholecystectomy, including the laparoscopic version, is likely to remain the treatment of choice for gallbladder stones. Bile acid therapy will be reserved for cases unsuitable for surgery, and for prevention. For common bileduct stones, endoscopic retrograde cholangiopancreatography and stone extraction are first-line management, although UDCA and lithotripsy make a minor contribution. It was beginning to look as though bile acid therapy would never reach the big league in the pharmacopoeia until the serendipitous discovery that cholestatic liver disease, especially primary biliary cirrhosis (PBC), could be influenced by UDCA
This approach held out the prospect of safe management where there was no well-established alternative. Early and presymptomatic cases of PBC are increasingly recognised-subjects with a mitochondrial antibody titre of 40 or more have PBC until proven otherwise9-and many of these will progress to more serious disease, as indicated by the presence of M2/M4/M8 subfraction mitochondrial treatment.
antibodies (not generally available as a test) and a rising bilirubin concentration.9,10 The only cure for the disease is liver transplantation, and even then post-transplant recurrences have been reported," UDCA is effective both in alleviating symptoms such as pruritus and in reducing serum concentrations of alkaline phosphatase and glutamyl transferase.12,13 Improvement in the histological appearance of the liver has been more difficult to document, and there is no clear evidence of enhanced survival or a reduction in disease progression. The mechanism of action of UDCA was originally thought to be replacement of toxic bile acids by exogenous UDCA;14 several lines of evidence now suggest that an additional (perhaps even main) mode of action is inununomodulation.1-1-11 Not all researchers have been enthusiastic about UDCA therapy in PBC, either failing to show a definite benefit, or documenting progression to liver failure or established cirrhosis in some cases.1S-20 In a few patients symptoms and liver function tests become worse, but this deterioration is usually apparent in the first few days or weeks of therapy. Patients with early disease will probably benefit most, since there is less scope for improvement when cirrhosis is established.18 Despite doubts about the hazards of altering human bile acids,21 UDCA is much the least toxic of the existing drugs for PBC, and should certainly be considered in early cases. UDCA has been tested in many other cholestatic diseases such as primary sclerosing cholangitis22 and benign cholestasis of pregnancy,23 with encouraging results. It has also been used in autoimmune chronic active hepatitis,24 where its main role may be as an adjuvant to conventional therapy with prednisolone and azathioprine. An important fresh initiative reported at the Basel meeting by Kramer and co-workers from Frankfurt is hybridisation of drugs with bile acids to ensure preferential delivery to the liver via the enterohepatic circulation. Thus it may be possible to reduce renal excretion as with chlorambucil/bile acid conjugates, to avoid non-hepatic side-effects as with HMG coenzyme A reductase inhibitor conjugates, and also to encourage intestinal absorption and avoid hydrolysis of peptide conjugates. 1.
Jazrawi RP, Pigozzi MG, Galatola F, Lanzini A, Northfield TC Optimum bile acid treatment for rapid gallstone dissolution. Gut 1992; 33: 381-86.
2. Sackmann
M, Pauletzki J, Aydemir U,
et al. Efficacy and safety of for dissolution of gallstone fragments: comparison with the combination of ursodeoxycholic add and chenodeoxycholic add. Hepatology 1991; 14: 1136-41.
ursodeoxycholic add
