181THE LANCET

There is no indication of how often the clinical trials were conductedon the HIV-positive and AIDS patient, and the results thereforehave no statistical significance. The polymerase chain reaction(PCR) technique does not determine the infectivity of any residualvirus. There is no discussion on the clinical significance of HIVbeing found only in the "AIDS" handpiece and only in thenon-sealed "AIDS" prophy angle.The experiments used to determine hepatitis B contamination of

handpieces are so far removed from normal practice that the resultshave no clinical application. Another laboratory experimentdemonstrates that even heat-sterilised handpieces emit viruses intothe environment. Therefore, it could be argued that in addition tomandatory handpiece sterilisation, all dental units must be replacedbetween patients.This investigation has several important design faults, its clinical

basis is very weak, and it has failed to prove that handpieces transmitdisease. Lewis’ fmdings must not be used to promote mandatoryhandpiece sterilisation since to do so-on this evidence-would beempirical behaviour.The definitive investigation! of the only case of possible HIV

transmission during dental treatment has implicated the dentist’sblood as the likely source of transmission, and not dentalinstruments or equipment. The absence of any clinical verificationthat dental instruments spread infectious diseases is sufficient

justification for recommending that the traditional standards

pertaining to dental asepsis be continued.

Department of Dentistry,Vancouver General Hospital,British Columbia’s Health Sciences Centre,Vancouver, British Columbia V5Z 1 M9, Canada J. HARDIE

1. AIDS: CDC’s investigation of HIV transmission by a dentist, September, 1992.Washington: Umted States General Accounting Office, Program Evaluation andMethodology Division, B-249339, 1992.

SIR,-Dr Lewis and colleagues’ studies on HIV, HBV, andphage contamination of the internal surfaces of dental handpiecesafter so-called disinfection question longstanding practices ofdentists world wide who have used disinfection techniques withoutevidence of related viral disease transmission for over 100 years.!Their conclusions about chemical disinfection, the need for heattreatment, and infection dangers seem to be somewhat contrived.The experiments described by Lewis et al are flawed and do notsupport their recommendations.There has never been a reported case of handpiece-related

infection (including the famous Dr Acer AIDS case) in billions ofpatient treatments/ yet Lewis et al warn of real dangers. Lewis’ ownresearch shows that disinfection techniques can kill internalcontamination microbes This study tested weak and unapproveddisinfection agents (chlorhexidine soap in one experiment, ethanolin another) and one poorly described operator-sensitive technique(wiping the handpiece surface), which were then extrapolated tobrand all disinfectants (eg, chlorine, aldehydes, iodophores) anddisinfectant techniques (internal circulation, ultrasonics) as

ineffective. Disinfection is a technique-sensitive operation yet themethod used was poorly described by Lewis et al, who havepreviously expressed a strong bias against all instrumentdisinfection in the public press and journals. 3The testing done did not describe any controls; expecially for the

contamination sensitive PCR tests (eg, no sample splitting, nopositive/negative control gelS)4 that identified microbecontamination. Proper testing and function (check valves, air andwater pressure readings) of equipment were not seriously addressed,although it would substantially affect the results. Presence ofmicrobial DNA particles was assumed to be synonymous withactive infection potential, although dead microbes would give thesame test results. Heat treatment was recommended but not tested.What we need to resolve this issue is a well-controlled series of

tests by several research groups, with HBV and HIV. Brand-namehandpieces should be tested in patient treatment settings, withmodem disinfectants and sterilants (including heat). Until thistesting is done, this issue should not be used as a media/press eventfor career advancement, as has been the case in the USA.

In your accompanying editorial you mention two dentists beingoccupationally infected by HIV-this is incorrect. The confusionarises from the repeated reporting of an assumption of a possibleunproven case by Kline.5 The Centers for Disease Control reportno documented cases of occupational HIV/AIDS in dentalworkers6 and no evidence of instrument contamination (clusters) inthe Acer case.’

Center for Dental AIDS Research,1000 North Avenue,Suite 102,Waukegan, Illinois 60085, USA E. J. NEIBURGER

1. Ciesielski C, Marianos D, Chin-Yih Oui, et al. Transmission of HIV in a dentalpractice. Ann Int Med 1992; 116: 798-805.

2. Lewis D, Boe R. Cross-infection risks associated with current procedures for usinghigh speed dental handpieces. J Clin Microbiol 1992; 30: 404.

3. Editorial: ADA News, Dec 7, 1992: 44. Farley M, Harrington J, eds. Forensic DNA technology. Chelsea, Michigan: Lewis

Publishers, 1991: 76-130.5. Neiburger EJ. Percutaneous injuries. J Am Dental Assoc 1992; 123: 146. Centers for Disease Control. HIV/AIDS surveillance July, 1992. Atlanta, Georgia:

CDC, 1992.

Adenomyosis: time for a reappraisalSIR,-As outlined in your Oct 31 editorial and review articles

(Nov 21, pp 1264, 1267), endometriosis remains an enigmaticdisease. Heterotopic endometrium can be found not only in thepelvic cavity but also in the myometrium and in extrapelvic sites.Heterotopic endometrial glands and stroma deep within themyometrium have been defmed as adenomyosis. Since theintroduction of the regurgitation theory of pelvic endometriosis in1927 adenomyosis and endometriosis have been generally regardedas different nosological entities.However, the histological characteristics of both diseases are

essentially the same and were accurately described by Cullen! as "amatrix of fibrous tissue with typical uterine glands and stromascattered throughout". Another common feature of all types ofheterotopic endometrium is its histological asynchronism whencompared with eutopic endometrium. It is generally accepted thatectopic endometrium responds to cyclic variations in endogenousoestrogen and progesterone. For this reason, the medical

management of endometriosis is based on the belief that

interruption of the hypothalamic-pituitary axis, either directly orindirectly, will promote regression of the disease. However, thephase of adenomyotic foci is delayed with respect to the eutopicendometrium in most specimens, most often presenting a

proliferative picture. Nevertheless, one can sometimes find aprogestational response, including decidualisation of adenomyoticfoci during pregnancy? When endometriotic implants are

histologically dated, only 13% are synchronous with the

corresponding intrauterine endometrium, and both proliferativeand secretory implants are present in fairly constant proportionsthroughout the menstrual cycle.3 Evidence is accumulating thatimmunological mechanisms are implicated in the pathophysiologyof endometriosis, but such data for adenomyosis are sparse.However, a recent study showed that high titres of autoantibodies(in particular to phospholipids) are present in patients withadenomyosis as often as in those with endometriosis 4

Unlike endometriosis, adenomyotic lesions are not characterisedby a pronounced haemorrhagic tendency or inflammatory response.The reason for this difference is not clear, but peritoneal fluid mightplay an important part in the pathogenesis of pelvic endometriosis.Peritoneal macrophages isolated from patients with endometriosisrelease several growth factors in vitro to a greater extent than thoseisolated from women without the disease.5The clinical and scientific interest in adenomyosis, in sharp

contrast with endometriosis, has been marginal in the past fewdecades-undoubtedly partly because of the difficulty in clinicaldiagnosis. Moreover, the use of diagnostic laparoscopy has divertedattention from the uterus to the pelvic cavity. The early exhaustivestudies on direct extension, and on lymphatic and haematogenousmetastasis of viable eutopic endometrium, have been oversimplifiedinto the transtubal regurgitation theory, and this had resulted in theclassification of heterotopic endometrium into two different

nosological entities-adenomyosis and endometriosis.

182 THE LANCET

After more than sixty years of neglect maybe it is time for areappraisal of adenomyosis. New imaging techniques allow thediagnosis of adenomypsis without having to do a hysterectomy.Magnetic resonance imaging has proved highly accurate in

diagnosis 6 In addition, recent studies have suggested an importantrole for transvaginal ultrasound in distinguishing between

adenomyosis and leiomyomata.’ Refocusing our attention on theuterus may not only improve our understanding of endometriosisbut also might contribute to the development of new therapeuticstrategies for this enigmatic disease.8

Reproductive Medicine,Royal Postgraduate Medical School,Hammersmith Hospital,London W12 0NN, UK JAN J. BROSENS

Pathology,Hammersmith Hospital FRED G. BARKER

1. Cullen TS. The distribution of adenomyomata containing uterine mucosa. Arch Surg1919; 80: 130-38.

2. Azziz R. Adenomyosis: current perspectives. Obstet Gynecol Clin North Am 1989; 16:221-25.

3. Metzger DA. Cyclic changes in endometriosis implants (abstr 011). Presented at 3rdworld congress on endometriosis; Brussels; June 1-3, 1992.

4. Ota H, Maki M, Shidara Y, et al. Effects of danazol at the immunologic level in patientswith adenomyosis, with special reference to autoantibodies: a multicenter

cooperative study. Am J Obstet Gynecol 1992; 167: 481-86.5. Surrey ES, Halme J. Effect of platelet-derived growth factor on endometrial stromal

cell proliferation in vitro: a model for endometriosis? Fertil Steril 1991; 56: 672-79.6. Togashi K, Ozasa H, Konishi I, et al. Enlarged uterus: differentation between

adenomyosis and leiomyoma with MR imaging. Radiology 1989; 171: 531-34.7. Fedele L, Bianchi S, Dorta M, et al. Transvaginal ultrasonography in the differential

diagnosis of adenomyoma versus leiomyoma. Am J Obstet Gynecol 1992; 167:603-06.

8. Igarashi M. A new therapy for pelvic endometriosis and uterine adenomyosis: localeffect of vaginal and intrauterine danazol application. Asia-Oceania J ObstetGynaecol 1990; 16: 1-12.

Hypertonic saline solution as disinfectantSIR,-Dr Mangete and colleagues (Nov 28, p 1351) suggest that

normal saline wound dressing can be made more effective simply byincreasing their salinity to 1 -5 osmol/L. However, it was perhapssurprising that in-vitro tests at this strength (24 h incubation) failedto inhibit bacterial growth.A possible explanation for these results is that the gauze dressings

were left uncovered (as would seem to be the case) and that thisallowed more water to evaporate from the dressings (especiallylikely in a hot climate) than was possible under the laboratoryconditions described. The evaporative effect (in vivo) should resultin a more or less stable situation whereby the outer layers of thedressing are strongly hypertonic but, as wound exudate escapesthrough the gauze, there is a gradient of reducing salinity as thewound surface is approached. This effect may similarly explain thereputed success of normal saline wound dressings.!The lack of success with increasing strengths of saline (greater

than 1.5 osmol/L) suggests that the wound is stimulated to produceso much exudate that the beneficial effects of the hypertonicgradient are quickly lost; the extra salt being washed out of thedressing.Our clinical experience indicates that both the construction of a

wound dressing and the frequency of dressing renewal influencesthe healing rate of a wound, and that different wounds needdifferent dressing constructions and renewal times to encourageoptimum healing.

Royal National Orthopaedic Hospital Trust,Stanmore, Middlesex HA7 4LP, UK

PETER LOWTHIANSHERAN OKE

1. Svedman P. Irrigation treatment of leg ulcers. Lancet 1983; ii: 532-34.

SIR,-Dr Mangete and colleagues describe the value of

hypertonic saline for wound dressing and quantify the optimumconcentration at 4-4 g salt per 100 mL (or g) water. One of us (N. S.)has long recommended the use of a teaspoonful of salt in a glass ofwater for minor infection and soreness of the gums as well as forsmall ulcers and cuts-this concentration is similar to that of

Mangete et al.

Most households now have small scales and graduatedcontainers. 44 g (1 5 oz) in 1L of water contained in a plastic 1L juicebottle provides five mouth washes per day. The value of this is that itcan be prepared as required, costs practically nothing, can be used asfrequently as wished, and has no side-effects (provided that thepatient has no condition for which salt is adversely indicated), tastesnot unpleasant, is not dangerous to children, and has obviousadvantages over phenolic and other proprietorial products from thepharmacist. It is also valuable as a gargle for throat infections and wewonder whether it might be useful for ear infections?

School of Pathology,Middlesex Hospital,London W1P 7PN, UK

N. SACOORIVOR SMITH

Prevention of nosocomial respiratorysyncytial virus infection

SIR,-P. Madge and colleagues (Oct 31, p 1079) reducednosocomial respiratory syncytial virus (RSV) infection from 6 (4%)of 152 children to 12 (0-9%) of 1311 with cohort nursing and the useof gloves and gowns. Our study in Oxford used cohort nursing andhandwashing to reduce the frequency from 18 (4-2%) of 425children in one year to 11 (0-8%) of 1392 over the next two years.’Given such similar results, it is unfortunate that Madge’s study,which aimed to dissect out the contribution of different infectioncontrol strategies, omitted handwashing. Handwashing is cheap,well tolerated, and easily implemented at a level of compliancesufficient to be as effective as gloves.1,2The size of the study groups varied, with 152 in the no special

precautions group, 265 in the cohort nursing group, 337 in thegowns and gloves group, and 1311 in the combined group. Withsmall groups the confidence intervals are wide and overlap(12-2-47-2, 15-7-44-4, 9-6-35-3, and 0-4-18-6) so Madge’s studylacks the power to discriminate between the individual modes ofintervention. Moreover, table in contains errors; 19 plus 33 makes52 (not 33) and 1 plus 1 is 2 (not 1), yielding an infection rate ofnearly 4% not 3%. This would produce even more overlappingconfidence intervals.The number of at-risk patients rose twofold, from 58 in the first

year to 89 then 103 in the subsequent years. Why did this changehappen? The study period started arbitrarily with 5 cases in 7 days,yet finished 3 months later regardless of the caseload. The pattemand timing of RSV epidemics may vary considerably from year toyear3 and to eliminate unintentional bias we studied whole years ofRSV infection from the first to the last case.

Madge et al recommend that all children be screened for RSV,but provide no evidence for this view. We achieved similar resultswithout screening and without segregating cardiovascular patients.How many cases would be missed if screening is not used? Wesuspect that Madge and colleagues, like us, would not have missed asingle case in three years of clinician-directed testing.Renal Unit,Guy’s Hospital,London SE1 9RT, UK C. A. O’CALLAGHAN

1. Isaacs D, Dickson H, O’Callaghan CA, Sheaves R, Winter A, Moxon ERHandwashing and cohorting in prevention of hospital acquired infections withrespiratory syncytial virus. Arch Dis Child 1991; 66: 227-31.

2. Doebbeling BN, Stanley SL, Sheetz CT, et al. Comparative efficacy of alternativehandwashing agents in reducing nosocomial infections in intensive care units.N Engl J Med 1992; 327: 88-93.

3. Wilcox HH, Williams O, Camp SJ, Spencer RC, Ball I. Characteristics of successiveepidemics of respiratory syncytial virus infection. Lancet 1991; 338: 943.

SIR,-P. Madge and colleagues report that cohort nursing andthe wearing of gowns and gloves reduced the incidence ofnosocomial RSV infections yet the rate of nosocomial infectionremained at about 10%. Additional strategies are clearly required.An obvious one is to stop viral replication so that viral sheddingceases and patient secretions become less infectious. Englund et afrecorded more than 98% reduction in viral titres in respiratorysecretions by the third day of therapy with ribavirin, and others havedocumented similar reductions.2,3 RSV is a major cause of fatalrespiratory tract disease during the first year of life.4 The American