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Dental Sealant Toxicity: Neurocutaneous Syndrome (NCS), a dermatological and neurological disorder By Dr. Omar M. Amin, Ph.D. Reprinted with permission Holistic Dental Association Journal The Communicator Volume 2004, number 1 pp. 1 - 15

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Page 1: Dental Sealant Toxicity

Dental Sealant Toxicity: Neurocutaneous Syndrome(NCS), a dermatological and neurological disorder

By Dr. Omar M. Amin, Ph.D.

Reprintedwith permission

Holistic Dental Association JournalThe Communicator

Volume 2004, number 1pp. 1 - 15

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Author

"Dr. Omar M. Amin has!B.Sc., M. Sc. and Ph.D.!degrees in Chemistry, BiologicalSciences, Medical Entomology, Parasitology and Infectious Diseases!from Cairo Univ.,Egypt and Arizona State Univ., USA. He has!held research positions!in the US NavalMedical Research Unit # 3 (NAMRU-3), Cairo, the Centers for Disease Control (CDC),Atlanta, Georgia and the University of Wisconsin, USA where he was a Professor ofParasitology and Epidemiology.! He is the founder and current Director ofthe!Parasitology Center, Inc., and the Institute of Parasitic Diseases, Tempe, Arizona. Heis a nationally and internationally recognized authority in the field with over 135 majorpublications."!

Contact information:

Parasitology Center, Inc.903 S. Rural Rd., # 101-318Tempe, Arizona 85281, USAPhone: 480-767-2522Fax: 480-767-5855E-mail: [email protected] site: www.parasitetesting.com

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Dental Sealant Toxicity: Neurocutaneous Syndrome (NCS),a dermatological and neurological disorder

by Dr. Omar M. Amin, PhD

Abstract: Neurocutaneous syndrome (NCS), a newly discovered toxicity disorder, is describedin light of our new understanding of its relationships with the causative agents included inthe dental liners used in afflicted patients. NCS is characterized by neurological sensations,pain, depleted energy and memory loss as well as itchy cutaneous lesions that may invitevarious opportunistic infections. Components in the calcium hydroxide dental sealants Dycal,Life and Sealapex have been identified as sources of the observed symptoms consideredcompatible with classical sulfa toxicity. Sulfonamide and neurological toxicity issues arediscussed, three case histories are presented and an outline of management protocol isproposed. Additional notes on zinc oxide, Fynal, IRM and Sultan U/P sealants are also included.

Introduction The original description of the neurocutaneous syndrome(NCS)1 was “introductory innature… intended only to bring attention to a new disease entity that has not beenpreviously reported.”1

Examination of many NCS patients and a careful study of their symptoms, exposures,clinical conditions and histories have made it possible to identify the underlying cause ofthe syndrome and proceed with its management. It is now also possible to help NCSclinical cases and to make dentists aware of the adverse impact of some routine dentalprocedures commonly regarded as harmless or safe.

Materials and Methods NCS patients from the United States sought our help after having exhausted all othermeans to resolve their symptoms. Upon signing an informed consent, patients were personallyevaluated and their clinical history, records, symptomology and exposures carefully examined.Fecal and blood specimens provided or collected at the Parasitology Center, Inc. (PCI) werestudied and identified. An NCS status was only determined upon confirming that neurologicaland dermatological symptoms are compatible with those of NCS and that one or more of thesuspect sealants (based on the dental records of hundreds of patients) have been used onprior dates. Sensitivity to sulfa and the level of sulfa in the blood were used as a confirmationof sulfonamide toxicity. Continuing patients followed our recommendations of rehabilitationof their compromised teeth, removed suspect liner(s), and replaced with ethyltoluenesulfonomide (ETS)- and zinc oxide-free sealers. We provided the dentists with a list of vitamin/mineral supplements for the patient to take during the transitional period and another listof substitute sealants. Patients were followed up for weeks/months to monitor the resolutionof all symptoms.

Results and Discussion

The Neurocutaneous Syndrome The disorder is a double faceted condition, dermatological and neurological, with clear-cutsymptoms of classical sulfa toxicity. The latter is characterized by abnormal blood and bacterialflora values, photosensitive reactions, allergic vasculitis sores,and redness of the skin,

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which may lead to liver and kidney failure.2

The neurological aspects of NCS arecharacterized by pin-prick and/or creeping,painful and irritating movement sensations,often interpreted as parasite movementssubcutaneously or in various body tissues orcavities including the head. In the latter case,movement sensations are either unipolar orbipolar and may proceed horizontally orvertically. They may manifest as readilyobservable variably shaped bruises or wavesof elevated ripples or channels. In no casewas the movement sensation related toparasites which were always found absent.1

Neurological symptoms may also include lossof memory, brain fog, lack of concentrationand control of voluntary movements. The cutaneous aspects include smallitchy sores (Fig.1), inflamed often elevatedpimples (Figs.2,3) and painful and fully open/amorphous mucoid lesions that often enlargeand coalese (Fig.4). Histopathologicalsections of lesions (Fig.5) in nine biopsiedpatients show superficial and deepperivascular infiltrate of lymphocytes,accompanied by interstitial deposits ofgranular mucin material. Eosonophils areusually present within the inflammatoryinfiltrate and foci of epidermolytichypokeratosis are often identified within theepidermis (Fig.5). Lesions may also be on thescalp where they may be associated withinfestation of springtails (Collembola).1 Inmany cases, lesions are associated withedematous reactions usually in the arms andlegs (Fig.6). Blood vessels may also becomeenlarged and elevated, and the head maybecome hot and turn red. The gum tissue andthe teeth may turn gray and becomecompromised first and stay compromised thelongest. Mucoid secretions from gum andother tissues may also turn gray. Noparasites were ever detected from these, orany other compromised sites.1 The abovecreeping sensation is clearly distinguishedfrom these caused by nematodes such asToxocara canis3 or Dioctophyme sp.4

General symptoms usually include fatigue,compromised immune system andpsychological trauma. Elevated sulfa levelsare also observed in the blood of testedpatients. The depressed immune status pre-empts the patient for opportunistic infections.

Compounding FactorsWhile NCS itself is not a contagious condition,superimposed opportunistic infections onopen sores may be. Initial infection withfungus or bacteria appear to attractsubsequent infestations with many arthropodspecies, especially springtails (Collembola:Insecta).1,5,6,7 Black specks associated withsuch infections appear to be metabolic waste(fecal elements) of these organisms or mycelialmasses of certain fungal species.Staphylococci, e.g., Staphylococcus aureusand S. haemolyticus; actinomycetes, e.g.,Streptomyces spp.; and yeast, e.g., Candidaalbicans; Mycetomas, e.g., Madurella spp.among others, have been identified fromcultured swabs taken from sores of variousNCS patients. Opportunistic infections withthese organisms have been shown toaggrevate the cutaneous symptoms of NCSpatients.8 The black grains of the mycelialmasses of Madurella spp. may be related tothe “black specks” often reported by NCSpatients. Treatment of these sores may resolvethe superimposed infection but does not affectthe NCS condition.

Arthropods identified from sores include fleas(Siphonaptera), caterpillars (Lepidoptera),wasps and ants (Hymenoptra), beetles(Coleoptera), winged flies and midges(Diptera), thrips (Thysanoptera), ticks, mitesand spiders (Arachnida) and springtails(Collembola).1,4 While springtails have closeassociation with sores in many NCS patients,it should be emphasized that they, and otheropportunistic infections representaggravating but not causal factors of NCSsores.Unidentifiable filaments (non-textile fibers)

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have also been observed in many NCSpatients associated with lesions and may berelated to the mycelia of Madurella spp. Thehealing of certain patients lesions,9 however,was observed to be proportional to the exitof remaining fibers from lesions3. Patientsexperiencing complete remission remainsusceptible to fungal promoting conditionsin damp, shaded, moldy places.

The SealantsThe three major calcium hydroxide sealantscausing NCS (Dycal, Life and Sealapex) areconsidered in this study9. While promotedas calcium hydroxide sealants, they onlyinclude about 50% calcium hydroxide in thecatalyst. Other components that areidentical in all three sealants (Table1) arescarcely known or advertised but will,however, impact the patient in the samemanner.

Of the components common to all threesealants, ethyltoluene sulfonamide as wellas zinc oxide are considered most toxic.Toluene is a known potent nerve toxin10

associated with the neurological symptomsof NCS. The sulfonamide component of thiscompound brings about a sensitivity allergic-toxic reaction ultimately manifesting as thevascular mucoid sores characteristic of theNCS, especially in sulfa sensitive patients.

Zinc oxide was shown to be genotoxic11,cytotoxic12,13, killing macrophages14, andcausing chronic and fibrous inflammatoryreactions,15,16 ulcerations16 andosteosclerosis.17 Additionally, the toxic effectsof zinc oxide and calcium hydroxide wereshown to be similar.18,19 Calcium hydroxidewas shown to cause periapical inflammation,typical granuloma and partial lack ofhealing.20 Titanium dioxide and Barium ions(Table 1) were also shown to provoke strongforeign body and bio-incompatible reactionsin live tissue.21,22

We observed that the toxicity of ethyltoluenesulfonamide is determined by theconcentration of this compound in the sealantused, the amount of sealant used and thenumber of teeth involved. The patient’sreaction will depend on the degree ofsensitivity to the compounds. These variablesdetermine the time after which the patientwill begin to experience symptoms. This timewas observed to vary between one day andmany years after the original dentalprocedure. Neurological and cutaneoussymptoms are not necessarily similar inintensity and the pathology of sores variedbetween unremarkable to extremely overt butthe neurological sensations were usuallysevere especially at night.

Cytotoxicity of Dycal, Life and Sealapex wasclearly demonstrated invivo and invitro invarious tissues.23 Sealapex was shown tocause severe inflammatory infiltration15,24,25

and edema25 accompanied by subcutaneoustissue necrosis15,26 and progressivedifferentiation and reaction of monocytes,macrophages and epithelial cells27. The finalphase of the inflammation is characterized byan intense granulomatous reaction especiallyin epithelial cells causing various intensitiesof irritation.28The cytotoxicity29,30 andneurotoxicity31 of Sealapex was welldemonstrated in various mammaliansystems.

As with Sealapex, Dycal was also shown tocause hemorrhage and acute to consistentinflammatory cell16,32,33 necrosis,16,32,33 tissueloss,33 karyorrhexis,16 neurotoxicity.34 andformation of serous exudates.16 Life has beenthe least researched sealant. It, however, hasthe same toxic ingredients, i.e., ethyltoleunesulfonamide and zinc oxide, as Sealapex andDycal and has been associated with classicalNCS symptoms in some of our patients, e.g.,DB (Fig.6) and MM (Fig.4).

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(Continued on page 6)

Sealants not containing ethyltoluenesulfonamide but including zinc oxide andeugenol have also been associated with NCScases.These include Fynal(>75% zinc oxide),IRM and Sultan U/P(<50% zinc oxide). Fynalwas associated with the cases of MM (Fig.4),and among other cases not discussed here.Fynal has been classified as “hazardous” inthe manufacturer’s (Dentsply caulk) materialsafety data sheet (MSDS) causing “rednessand irritation” upon skin contact and “opensores or wounds of the skin” in persons withknown sensitization to eugenol. Similarly,IRM (by Dentsply caulk) and Sultan U/P(bySultan Chemists) were associated with aclassical NCS case in TS, a 30-year-old whitefemale. Of 19 teeth, which had dental workperformed between 1995-1996, 5 were sealedwith IRM (3) and Sultan U/P(2). In the other14 teeth, Gluma One Bond (by HeraeusKulzer) and Scotch bond (by 3M) were used.The latter two products contain 2-hydroxyethyl methacrylate and the MSDSindicate adverse skin reactions upon contact.The symptoms of TS were most severe in theupper left arm and on the forehead. TheMSDS indicate that the acrylates can cause“skin irritation…redness, swelling,itching..dryness..allergic skin reaction andblistering.”

Case HistoriesCase #1. ME is a Swedish female born in 1951. In1985 she underwent dental repairs whichincluded the use of Dycal in 20 teeth. ME isallergic to sulfonomides, with IGE valuesreaching 5000. Every dental treatment wasfollowed by aggressive skin reactions ofallergic and toxicological nature(Fig.3). Alltests for parasites were negative. Hersymptoms fulminated into full blown typicalsulfa toxicity reactions including oozing skinsores, which also appeared on the nasalseptum with bloody scabs and smellydischarge associated with a superimposedinfection with Staphylococcus aureus ( Fig.7).

Other symptoms included loss of memory,kidney pain and urgency, sensitivity to lightand electricity fields, pin-prick and movingsensations under the skin, and swelling. Aftereach treatment, ME had problems breathingand talking, and was totally exhausted. Shesubsequently developed intestinal problemsand the skin sores flared up with unbearableitching against which no antipruritic agenthelped. Photosensitive reactions presented asthe skin became blotchy ( Fig.7) with severeburning sensations in the face, throat andchest and a total loss of quality of life.

Dycal was removed in 1991-1992 and initiallyreplaced with Harvard cement. The symptomswere exacerbated with every single removal.ME was confined to bed with strong pains inthe face and neck, and in her whole musculo-skeletal system, bowel disturbances and signsof polyneuropathy. A few weeks after the lastof the Dycal was removed in February, 1992,most of her sores and rashes disappeared andshe could tolerate sunlight (Fig.8). TheSwedish clinical practitioners working withME concluded that Dycal was the underlyingcause of her “toxic ulcerative dermatitis.”

Case # 2. Born in Chicago in 1965, JM was ahealthy active Caucasian woman until shestarted experiencing her first symptoms in1991. By that time, she already had dentalwork, including 17 fillings. No sealers wereused in one filling; Dycal was used in the other16 fillings. Her earliest symptoms appearedas skin break outs on the face and neck, whichwas recurrent over the following 9 years. Shewas treated with minicycline, tetracycline,and acutane along with topicalpharmaceuticals. The early episodes wereaccompanied by body tremors, sleeplessnessand joint pain with occasional vomiting ofblack bile. Thrush appeared in the mouth andaround the lips. Pain at the teeth rootspersisted throughout the nineties associated

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with rapid major decay. A sensation ofprickling pain with a pressure and movementunder the skin was accompanied by urticariaand skin ulcerations in the same areas thatwould last for weeks or months. JM’s bodyshowed random swelling with red marks inreadily observable serpentine-like shapes.The swellings eventually bottle-necked at theknees and ankles. The chest burned and hurtas strange fits of coughing from the lungsensued. JM then started losing hair as sheexperienced night fevers and sweats, andpeeling of the skin.

During the early 1990’s JM was heavilymedicated, e.g., Diflucan, Rocefin, Vermox(she had a Taenia infection), Praziquantel,Ketokonazol, Metrobendazole, among othermedications. She experienced some anti-inflammatory relief and occasional temporaryclearing of ulcers after which ulcers returnedand lasted longer.

In 1998, massive ulcers appeared on JM’s faceat the nasiolobial area and at the skin( Fig.9). One ulcer did not resolve for years asit grew deeper while the others cleared withinone year. A CBC in 1999 was unremarkableexcept for a high level of Alpha 1-Globulin of0.5 ( normal range 0.2-0.4 ) and low levels ofIgA of 99 ( normal range 60-400 ) and IgG of724 ( normal range 700-1500 ). The rightocular cavity was severely painful and JM wasbeginning to lose her eyesight. JM was thenput on a program of Rocefin, Nizoral, Diflucan,Albendazole, Cefelexen, Praziquantel, and avariety of other anti-parasitics. In late 1999,JM started a frequency generation programusing a Las Vegas “Genesis” machine whileundergoing internal cleansing. This program,along with occasional ozone encephallationhelped resolve JM’s symptoms to some degree.However, many of the symptoms returned forwhich a program of Mexican herbs, e.g. TeeTree, Yerba de Manzo, Yerba de Arnica, as wellas MSM liquid, colloidal silver, Male fernextract, Ketokonazol creme, Lamasil cremeand tablets, and Ceffalexin was followed.

A major dental repair was completed in 2001when Dycal was removed from all 16 teeth.After being opened, the teeth were packedwith a clove/zinc combination before usingzinc oxide and eugenol. Initially, JMexperienced a few episodes of sickness,sweats, and vomiting. Since the second visitshe was feeling better. After the fourth visit,her eyebrow area had a dramatic reductionin swelling and in the sensation of movementand the red hot congestion of her face and skinresolved. JM’s teeth were subsequentlyrebuilt with gold onlays section by section.By the end of the total repair, Nov.2001, JMregained her normal skin ( Fig.10) with nomovement sensations or pain anywhere in herbody. This state of total resolution has lastedfor over one year to the time of this writingwithout regressions or relapses.

Case #3.LG, a medium- built white American born in1957, was in perfect health until the morningof September 18, 1998 when she had a fillingin her tooth no. 18 using Dycal as a liner. Sheexperienced severe headache within 2 hoursand had to leave work. By 6:00 pm that sameevening, she was vomiting and delirious withthe headache persisting. She was admittedto the emergency room where her bloodpressure was monitored at 169/108 andremained high for the following three yearsdespite repeated attempts to control it withAtenenol and Diazide. LG never experiencedhigh blood pressure or headaches before. AnMRI scan was negative. In 1999 LG’s healthdeteriorated progressively. She experiencedarthritis- like symptoms in her back, heartpalpitations, mitral valve prolapse, fatigue,abnormal pap-smears including pre-cancerous cell abnormalities, night sweats,missed periods, and severe depression. HerAtenenol prescription was increased andvarious antibiotics were routinely used. ByMarch, 2001, LG, who normally weighed 120lbs had lost 20 lbs. She was immediatelyplaced on an IV of antibiotics also to combatan abcess near her brain.

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(continued on page 12)

In April, 2001, LG moved to an apartmentwhich was heavily infested with mold andmites. Lesions started appearing on LG’s facewhich quickly became red hot as if on fire.Her legs became swollen and painfullyburning. By May, 2001, LG had several openlesions (6 mm to 2 cm in diameter)accompanied by erythema, on her face andscalp. Her cheek pulsated as the facial lesionsseemed to track to the chin(Fig.11) where themost fulminating lesion was; nearest to herteeth. Springtails (Collembola) and fiberswere recovered from these sites. At that time,a CBC analysis showed low lymphocytes of15.0% (normal 20-43%) and high granulocytesof 77.1% (normal 51-74%), and highrheumatoid factor of 22.6 (normal <20IU/ml).She also tested negative for all communicablediseases at the same time. Her weightdropped to 92 lbs. She started thenexperiencing movement sensations under theskin of her arms, face and scalp. Lesionsstarted to change shape and acquire trackmarks around them. Grayish pustularsecretions oozed and moved down from thebloody lesions on the scalp and face. The lesionthen extended to her legs. At this time LGwas diagnosed with stress, anxiety, self-inflicting wounds, acute endocarditis andscabies. Treatments for these conditions didnot resolve the NCS symptoms.

OMA diagnosed LG with NCS in January,2002. She was allergic to sulfa andsulfonamide compounds. Following ourprotocol, LG had the filling and the Dycal linerremoved from tooth #18 in April, 2002. Thesewere replaced with Starflow and Aria (acombination of Bisgma, Tegdma, Lidma andcatalysts). Our recommended vitaminsupplementation program was then initiated.

By May, 2002, all symptoms were resolved.Once the chin lesion healed, which took alonger time than the rest, the skin of allpreviously compromised sites returned tonormal(Fig.12). Constitutional andneurological functions as well aspsychological, emotional and energy levels

have also been restored to normalcy.ConclusionThe toxicity of Dycal, Life and Sealapex hasbeen well documented invivo and invitrostudies of various animal and human modelsby many workers. The toxicity assumedcytotoxic, genotoxic, neurotoxic, phototoxic,necrotic, and inflammatory reactionscompatible with the pathology and symptomsobserved in NCS patients. Ethyltoluenesulfonamide, common to all three sealants,is considered the primary cause of the NCS.The toluene component, a known nerve toxin,is believed to be responsible, at least in part,for the neurological symptoms. Neurologicalhyperactivity is related to nerve damageassociated with vasomotor reactions due to adirect influence on the peripheral nerveendings.35The sulfonamide component is thecause of the cutaneous symptoms, especiallyin sulfa-sensitive patients and has beendemonstrated in elevated sulfonamide/sulfalevels in CBC blood analyses as well as inskin sensitivity tests. The relationshipbetween sulfonamide and phototoxicity hasbeen well established.29 Resolving thesymptoms (effect) by removing the sealants(cause) in patients undergoing treatments,confirms this cause-effect relationship. Thetoxic effects of other ingredients of these threesealants, e.g., zinc oxide, can not beoverlooked.

The nature of causation of NCS precludescontagious transmission. Any similarities ofsymptoms among partners within the samehousehold are traceable to the transmissionof opportunistic infections, especially fungi.

The proper diagnosis of NCS can only bemade upon the examination of patients,confirmation of their neurological and dermalsymptoms, and the study of their clinicalhistory and medical records, especially dentalcharts. Additional diagnostic aides includeskin tests for allergy to sulfa and blood

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analysis for elevated levels of sulfa. Upon thesatisfactory diagnosis of an NCS case, and thedetermination of which teeth have the toxicsealants, arrangements for dentalrehabilitation are made. Those include theremoval of fillings and of all traces of sealantsand replacing them with bio-compatibledental products not containing ethyltoluenesulfonamide or zinc oxide.

It is recommended not to do more than two orthree teeth per month. The patient is given alist of vitamins and other supplements to takeduring the procedure and for the following fewweeks until symptoms are completelyresolved. The list includes vitamins B12, B6,B5, E, C and folic acid, zinc, calcium,magnesium, omega 3 fish oil or linseed oil,amino acids, Acidofilus, Bifidus,Lactobacillus, digestive enzymes andselenium. After reaching the state ofnormalcy, the patient may still retain somesensitivity to moldy places lacking sun andfresh air circulation. The sealants reportedabove are still in common usage throughoutthe world. The “small” amounts continuallyleaching into the live tissues of the bodypromote a cumulative progressive damagingpathology over a long period of time. Dentalpractitioners should be aware of the adverseeffects of these products and employ thisknowledge to safeguard the well being of their

clients.

Acknowlegment

I am grateful to Marie Erixon, Nordea, Sweden for

her contributions to the better understanding of

issues related to NCS.

References1.Amin OM. Neuro-cutaneous Syndrome(NCS); a new disorder. Explore 2001; 10: 55-56.2.Ockert K. Filling caused serious reactions.Trandlakartidningen 1994; 86: 470. (inSwedish).3.Garcia LS. Diagnostic Medical Parasitology.

Wash, DC: Am Soc Microbiol Press, 2001.

4.Urano Z, Hasegawa H, Katsumata T,Toriyama K, Aoki Y. Dioctophymatidnematode larva found from human skin withcreeping eruption. J Parasitol 2001;87: 462-465.5.Amin OM. Facial cutaneous dermatitisassociated with arthropod presence. Explore1996; 7: 62-64.6.Frye FL. In search for the haphazardlyelusive: a follow-up report on an investigationinto the possible role of collembolans inhuman dermatitis. Vet Invert Soc Newsletter1997; 13: 10-13.7.Janssens F. Checklist of the Collembola:Collembola in association with man. < http//www.collembola.org/publicat/sidney.htm>1999-2003; 10pp, and per comm..8.Mahon CR, Manuselis G Jr. DiagnosticMicrobiology. Philadelphia: WB Saunders Co,1995.9.Draheim RN, Murray AJ. Compressivestrength of two calcium hydroxide bases. JProthet Dent 1985; 54: 365-366.10.Burry MB. Neurodevelopmental toxicity oftoluene.M. Sc. Thesis: Seattle, Univ Wash,2001.11.Tai KW, Huang FM, Huang MS, Chang YC.Assessment of the genotoxicity of resin andzinc-oxide eugenol-based root canal sealers,using an in vitro mammalian test system. JBiomed Mater Res 2002; 59: 73-77.12.Wright KJ, Barbosa SV, Araki K,Spangberg LS. In vitro antimicrobial cytotoxiceffects of Kri 1 paste and zinc oxide eugenolused in primary tooth pulpectomies. PediatrDent 1994; 16: 102-106.13.Pissiotis E, Spangberg LS. Toxicity ofpulpisad using four different cell types. IntEndod J 1991; 24: 249-257.14.Sadeghein A, Bolhari B, Sarafnejad A. Acomparison of the effects of three endodonticsealers on adherence of mouse peritonealmacrophages. J Calif Den Assoc 2001; 29: 673-677.15.Soares I, Goldberg F, Massone EJ, Soares

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IM. Periapical tissue response to two calciumhydroxide-containing endodontic sealers. JEndod 1990; 16: 166-169.16.McShane CJ, Stimson PG, Bugg JL,Jennings RE. Tissue reactions to Dycal. JDent Childr 1970; 37: 466-474.17.Erausquin J. Periapical tissue reaction toroot canal fillings with zinc, titanium, lead,and aluminum oxides. Oral Surg Oral MedOral Pathol 1970; 30: 545-554.18.Berman DS. Pulpal healing followingexperimental pulpotomy. Brit Dent J 1958;105: 7-16.19.Berman DS, Massler M. Experimentalpulpotomies in rat molars. J Dent Res 1958;37: 229-242.20.Weinstein R, Goldman M. Apical hard-tissue deposition in adult teeth of monkeyswith use of calcium hydroxide. Oral Surg OralMed Oral Pathol 1977; 43: 627-630.21.Bennatti-netto C, Bramante CM, Ber-BertA, Lia RCC. Reacao do tecido conjuntivosubcutaneo de rato ante a implantacao dosmaterials components do cimento AH-26. RevBras Odontol 1982; 39: 11-20.22.Smith JW, Leeb IJ, Torney DL. Acomparison of calcium hydroxide and bariumhydroxide as agents for inducing apicalclosure. J Endod 1984; 10: 64-70.23.Topalian M. Effecto Citotoxico de loscementos selladores utilizados en endodonciasobre et Tejido periapical. Endodocia-Caracas2002, < http://www.carlosboveda.com>; 48pp,and per comm.24.Buntak-Kobler D, Prpic-Mehicic, Najzar-Fleger D, Katunaric M, Talan-Hranilovic J,Suman L. Cytotoxicity of Ca(OH)2 endodonticsealers on connective, muscle and bone tissues.Acta Stomatol Croat 1993; 27: 175-180.25. Sonat B, Dalat D, Gunhan O. Periapicaltissue reaction to root fillings with Sealapex.Intern Endod J 1990; 23: 46-52.26.Bezerra LA, Leonardo MR, Faccioli MR,Faccioli LH, Figueiredo F. Inflammatoryresponse to calcium hydroxide based rootcanal sealers. J Endod 1997; 23: 86-90.

27.Tronstad L, Barnett F, Flax M. Solubilityand biocompatibility of calcium hydroxide-containing root canal sealers. Endod DentTraumatol 1988; 4: 152-159.28. Zmener O, Guglielmotti MB, Cabrini RL.Biocompatibility of two calcium hydroxide-based endodontic sealers: a quantitative studyin the subcutaneous connective tissue of therat. J Endod 1988; 14: 229-232.29.Beltes B, Koulaouzidou E, Kotoula V,Kortsaris AH. In vitro evaluation of thecytotoxicity of calcium hydroxide-based rootcanal sealers. Endod Dent Traumatol 1995;11: 245-249.30.Guertsen W, Leinenbach F, Krage T,Leyhausen G. Cytotoxicity of four root canalsealers in permanent 3T3 cells and primaryhuman periodontal ligament fibroblastcultures. Oral Surg Oral Med Oral PatholOral Radiol 1998; 85: 592-597.31.Serper A, Ucer O, Onur R, Etikan I.Comparative neurotoxic effects of root canalfilling materials on rat sciatic nerve. J Endod1998; 24: 592-594.32.Good DL. Effects of materials used inpediatric dentistry on the pulp: a review ofthe literature. J Calif Dent Assoc 1999; 27:861-867.33.Heys DR, Heys RJ, Cox CF, Avery JK. Theresponse of four calcium hydroxides onmonkey pulp. J Oral Pathol 1980; 9: 372-379.34.Norrsells N. Aven svenska tandlakaretillats nu sedan EU-intradet att anvanda deneffektiva N2-metoden for rotfyllig. Med dennametod kan 500 miljoner kr sparas arligen atpatientena och lidandet minskas. EndodSverige 2002; 5p.35. Hensten-Pettersen A. Skin and mucosal

reactions associated with dental materials. Eur J

Oral Sci 1998; 106: 707-712.

Parasitology Center, Inc.Dr. Omar M. Amin, Ph.D.903 S. Rural Rd.#101-318

Tempe, AZ 85281(480) 767-2522 • Fax (480) 767-5855

www.parasitetesting.com

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Figs. 1-6. Cutaneous symptoms in NCS patients. 1. Early NCS sores on the thigh of KM. She was born in 1964,compromised with Dycal in two teeth in 1982 and in one tooth in 2002. Neurological symptoms in upper quadrantstarted in 1997. Cutaneous symptoms began in Spring 2002 preceded by extensive treatment with topical sulfapreparations for possible “mite infestation.” Dycal was removed in December, 2002 and recovery is in progress.2. Elevated sores on the forehead of KM (Fig.1); note the hot red color of the skin. 3. Diffuse NCS sores coveringthe whole body of ME given Dycal in 1985 (case no.1). 4. Mucoid NCS/lesions on the face of MM. She was bornin 1950, given Fynal in six teeth in 1981 and in one tooth in 1986 as well as with Life in two teeth in 1985 and1988. 5. Histopathological section of one of the roughly 300 sores covering the body of SK. She was born in 1956and reacted with typical NCS symptoms to a zinc oxide cement (combined with Durelon) underneath a totalveneer job in 1982. The section shows hyperkeratosis –like perivascular dermatitis with eosinophils. 6. Cutaneoussores and swelling in the right hand and arm of DB. Born in 1965, DB had 10 amalgam restorations in 1982and 1983 using Life. She started experiencing symptoms including ulcerated rash all over the body, unilateraledema and pin-prick and subcutaneous movement sensations in 2001-2002. Life is being removed and recoveryis in progress.

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Figs. 7-12. Facial appearance of the three presented cases before and after recovery from NCS. 7,8(ME; case no.1); note the hot red face (Fig.7). 9,10 (JM; case no.2); note the lesion on the right cheekand the hot red face (Fig.9). 11,12 (LG; case no.3); note the return of the natural “baby” skin back(Fig.12) after the healing of all facial lesions (Fig.11).

For diagnosis and management of parasitic infectionsParasitology Center, Inc.Dr. Omar M. Amin, Ph.D.

(480) 767-2522e-mail: [email protected]

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Table 1- Components in catalysts (C) and bases (B) of Dycal, Life andSealapex._______________________________________________________________ ____________

Material Dycal* Life* Sealapex______________________________________________________________

Calciumhydroxide

51% ( C ) 51% ( B ) NG ( B )**

Zinc oxide 9.23% ( C ) 13.75% ( B ) NG ( B )

Zinc stearate 0.29% ( C ) 0.25% ( B ) ________

Ethyltoluene sulfonamide 39.48% ( C ) 34% ( B ) NG ( B )

Silicon dioxide ________ ________ NG ( B )_______________________________________________________________

Titanium dioxide pigment ________ 10.0% ( C ) NG ( C )

Pigment 0.1% ( B ) 0.1% ( C ) ________

Calcium phosphate 31.0% ( B ) ________ ________

Barium sulphate ________ 37.90% ( C ) NG ( C )

Zinc oxide 9.0% ( B ) ________ ________

Methyl silicate ________ 12.0% ( C ) ________

Silicon dioxide ________ ________ NG ( C )

Calcium tungstate 17.0% ( B ) ________ ________

Butylene glycol disalicylate 43% ( B ) ________ ________

Polymethylene mythylsalicylate

________ 38.0% ( C ) ________

Isobutyl salicylate ________ ________ NG ( C )_______________________________________________________________* See Draheim and Murrey.9** NG = Percentages not given in the manufacturer's ( Kerr Corp.) Material Safety Data Sheet published July 28, 2000.