Eureka - Anyone suffering strange lesions in the mouth or on the face?

I think I have confirmed where my dental and facial skin issues are coming from. Has anyone ever heard of Dr. Omar Amin in Tempe Arizona and his work with toxic dental sealants?

I am almost certain this is what I have. I practically cried as I read this- tears of relief and joy and hope that I will get better.

Be careful of what material you replace your Amalgams with.

Here is an article. It is kind of long.

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
Author
"Dr. Omar M. Amin has!B.Sc., M. Sc. and Ph.D.!degrees in Chemistry, Biological
Sciences, Medical Entomology, Parasitology and Infectious Diseases!from Cairo Univ.,
Egypt and Arizona State Univ., USA. He has!held research positions!in the US Naval
Medical 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 of
Parasitology and Epidemiology.! He is the founder and current Director of
the!Parasitology Center, Inc., and the Institute of Parasitic Diseases, Tempe, Arizona. He
is a nationally and internationally recognized authority in the field with over 135 major
publications."
!
Contact information:
Parasitology Center, Inc.
903 S. Rural Rd., # 101-318
Tempe, Arizona 85281, USA
Phone: 480-767-2522
Fax: 480-767-5855
E-mail: omaramin@aol.com
Web site:
http://www.parasitetesting.com

Communicator - Page 1
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 described
in light of our new understanding of its relationships with the causative agents included in
the 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 invite
various opportunistic infections. Components in the calcium hydroxide dental sealants Dycal,
Life and Sealapex have been identified as sources of the observed symptoms considered
compatible with classical sulfa toxicity. Sulfonamide and neurological toxicity issues are
discussed, three case histories are presented and an outline of management protocol is
proposed. 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 in
nature… intended only to bring attention to a new disease entity that has not been
previously 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 of
the syndrome and proceed with its management. It is now also possible to help NCS
clinical cases and to make dentists aware of the adverse impact of some routine dental
procedures commonly regarded as harmless or safe.
Materials and Methods
NCS patients from the United States sought our help after having exhausted all other
means to resolve their symptoms. Upon signing an informed consent, patients were personally
evaluated and their clinical history, records, symptomology and exposures carefully examined.
Fecal and blood specimens provided or collected at the Parasitology Center, Inc. (PCI) were
studied and identified. An NCS status was only determined upon confirming that neurological
and dermatological symptoms are compatible with those of NCS and that one or more of the
suspect sealants (based on the dental records of hundreds of patients) have been used on
prior dates. Sensitivity to sulfa and the level of sulfa in the blood were used as a confirmation
of sulfonamide toxicity. Continuing patients followed our recommendations of rehabilitation
of their compromised teeth, removed suspect liner(s), and replaced with ethyltoluene
sulfonomide (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 list
of substitute sealants. Patients were followed up for weeks/months to monitor the resolution
of all symptoms.
Results and Discussion
The Neurocutaneous Syndrome
The disorder is a double faceted condition, dermatological and neurological, with clear-cut
symptoms of classical sulfa toxicity. The latter is characterized by abnormal blood and bacterial
flora values, photosensitive reactions, allergic vasculitis sores,and redness of the skin,
Communicator - Page 2
which may lead to liver and kidney failure.2
The neurological aspects of NCS are
characterized by pin-prick and/or creeping,
painful and irritating movement sensations,
often interpreted as parasite movements
subcutaneously or in various body tissues or
cavities including the head. In the latter case,
movement sensations are either unipolar or
bipolar and may proceed horizontally or
vertically. They may manifest as readily
observable variably shaped bruises or waves
of elevated ripples or channels. In no case
was the movement sensation related to
parasites which were always found absent.1
Neurological symptoms may also include loss
of memory, brain fog, lack of concentration
and control of voluntary movements.
The cutaneous aspects include small
itchy sores (Fig.1), inflamed often elevated
pimples (Figs.2,3) and painful and fully open/
amorphous mucoid lesions that often enlarge
and coalese (Fig.4). Histopathological
sections of lesions (Fig.5) in nine biopsied
patients show superficial and deep
perivascular infiltrate of lymphocytes,
accompanied by interstitial deposits of
granular mucin material. Eosonophils are
usually present within the inflammatory
infiltrate and foci of epidermolytic
hypokeratosis are often identified within the
epidermis (Fig.5). Lesions may also be on the
scalp where they may be associated with
infestation of springtails (Collembola).1 In
many cases, lesions are associated with
edematous reactions usually in the arms and
legs (Fig.6). Blood vessels may also become
enlarged and elevated, and the head may
become hot and turn red. The gum tissue and
the teeth may turn gray and become
compromised first and stay compromised the
longest. Mucoid secretions from gum and
other tissues may also turn gray. No
parasites were ever detected from these, or
any other compromised sites.1 The above
creeping sensation is clearly distinguished
from these caused by nematodes such as
Toxocara canis3 or Dioctophyme sp.4
General symptoms usually include fatigue,
compromised immune system and
psychological trauma. Elevated sulfa levels
are also observed in the blood of tested
patients. The depressed immune status preempts
the patient for opportunistic infections.
Compounding Factors
While NCS itself is not a contagious condition,
superimposed opportunistic infections on
open sores may be. Initial infection with
fungus or bacteria appear to attract
subsequent infestations with many arthropod
species, especially springtails (Collembola:
Insecta).1,5,6,7 Black specks associated with
such infections appear to be metabolic waste
(fecal elements) of these organisms or mycelial
masses of certain fungal species.
Staphylococci, e.g., Staphylococcus aureus
and S. haemolyticus; actinomycetes, e.g.,
Streptomyces spp.; and yeast, e.g., Candida
albicans; Mycetomas, e.g., Madurella spp.
among others, have been identified from
cultured swabs taken from sores of various
NCS patients. Opportunistic infections with
these organisms have been shown to
aggrevate the cutaneous symptoms of NCS
patients.8 The black grains of the mycelial
masses of Madurella spp. may be related to
the “black specks” often reported by NCS
patients. Treatment of these sores may resolve
the superimposed infection but does not affect
the 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, mites
and spiders (Arachnida) and springtails
(Collembola).1,4 While springtails have close
association with sores in many NCS patients,
it should be emphasized that they, and other
opportunistic infections represent
aggravating but not causal factors of NCS
sores.
Unidentifiable filaments (non-textile fibers)
Communicator - Page 3
have also been observed in many NCS
patients associated with lesions and may be
related to the mycelia of Madurella spp. The
healing of certain patients lesions,9 however,
was observed to be proportional to the exit
of remaining fibers from lesions3. Patients
experiencing complete remission remain
susceptible to fungal promoting conditions
in damp, shaded, moldy places.
The Sealants
The three major calcium hydroxide sealants
causing NCS (Dycal, Life and Sealapex) are
considered in this study9. While promoted
as calcium hydroxide sealants, they only
include about 50% calcium hydroxide in the
catalyst. Other components that are
identical in all three sealants (Table1) are
scarcely known or advertised but will,
however, impact the patient in the same
manner.
Of the components common to all three
sealants, ethyltoluene sulfonamide as well
as zinc oxide are considered most toxic.
Toluene is a known potent nerve toxin10
associated with the neurological symptoms
of NCS. The sulfonamide component of this
compound brings about a sensitivity allergictoxic
reaction ultimately manifesting as the
vascular mucoid sores characteristic of the
NCS, especially in sulfa sensitive patients.
Zinc oxide was shown to be genotoxic11,
cytotoxic12,13, killing macrophages14, and
causing chronic and fibrous inflammatory
reactions,15,16 ulcerations16 and
osteosclerosis.17 Additionally, the toxic effects
of zinc oxide and calcium hydroxide were
shown to be similar.18,19 Calcium hydroxide
was shown to cause periapical inflammation,
typical granuloma and partial lack of
healing.20 Titanium dioxide and Barium ions
(Table 1) were also shown to provoke strong
foreign body and bio-incompatible reactions
in live tissue.21,22
We observed that the toxicity of ethyltoluene
sulfonamide is determined by the
concentration of this compound in the sealant
used, the amount of sealant used and the
number of teeth involved. The patient’s
reaction will depend on the degree of
sensitivity to the compounds. These variables
determine the time after which the patient
will begin to experience symptoms. This time
was observed to vary between one day and
many years after the original dental
procedure. Neurological and cutaneous
symptoms are not necessarily similar in
intensity and the pathology of sores varied
between unremarkable to extremely overt but
the neurological sensations were usually
severe especially at night.
Cytotoxicity of Dycal, Life and Sealapex was
clearly demonstrated invivo and invitro in
various tissues.23 Sealapex was shown to
cause severe inflammatory infiltration15,24,25
and edema25 accompanied by subcutaneous
tissue necrosis15,26 and progressive
differentiation and reaction of monocytes,
macrophages and epithelial cells27. The final
phase of the inflammation is characterized by
an intense granulomatous reaction especially
in epithelial cells causing various intensities
of irritation.28The cytotoxicity29,30 and
neurotoxicity31 of Sealapex was well
demonstrated in various mammalian
systems.
As with Sealapex, Dycal was also shown to
cause hemorrhage and acute to consistent
inflammatory cell16,32,33 necrosis,16,32,33 tissue
loss,33 karyorrhexis,16 neurotoxicity.34 and
formation of serous exudates.16 Life has been
the least researched sealant. It, however, has
the same toxic ingredients, i.e., ethyltoleune
sulfonamide and zinc oxide, as Sealapex and
Dycal and has been associated with classical
NCS symptoms in some of our patients, e.g.,
DB (Fig.6) and MM (Fig.4).
Communicator - Page 4
(Continued on page 6)
Sealants not containing ethyltoluene
sulfonamide but including zinc oxide and
eugenol have also been associated with NCS
cases.These include Fynal(>75% zinc oxide),
IRM and Sultan U/P(<50% zinc oxide). Fynal
was associated with the cases of MM (Fig.4),
and among other cases not discussed here.
Fynal has been classified as “hazardous” in
the manufacturer’s (Dentsply caulk) material
safety data sheet (MSDS) causing “redness
and irritation” upon skin contact and “open
sores or wounds of the skin” in persons with
known sensitization to eugenol. Similarly,
IRM (by Dentsply caulk) and Sultan U/P(by
Sultan Chemists) were associated with a
classical NCS case in TS, a 30-year-old white
female. Of 19 teeth, which had dental work
performed between 1995-1996, 5 were sealed
with IRM (3) and Sultan U/P(2). In the other
14 teeth, Gluma One Bond (by Heraeus
Kulzer) and Scotch bond (by 3M) were used.
The latter two products contain 2-
hydroxyethyl methacrylate and the MSDS
indicate adverse skin reactions upon contact.
The symptoms of TS were most severe in the
upper left arm and on the forehead. The
MSDS indicate that the acrylates can cause
“skin irritation…redness, swelling,
itching..dryness..allergic skin reaction and
blistering.”
Case Histories
Case #1.
ME is a Swedish female born in 1951. In
1985 she underwent dental repairs which
included the use of Dycal in 20 teeth. ME is
allergic to sulfonomides, with IGE values
reaching 5000. Every dental treatment was
followed by aggressive skin reactions of
allergic and toxicological nature(Fig.3). All
tests for parasites were negative. Her
symptoms fulminated into full blown typical
sulfa toxicity reactions including oozing skin
sores, which also appeared on the nasal
septum with bloody scabs and smelly
discharge associated with a superimposed
infection with Staphylococcus aureus ( Fig.7).
Other symptoms included loss of memory,
kidney pain and urgency, sensitivity to light
and electricity fields, pin-prick and moving
sensations under the skin, and swelling. After
each treatment, ME had problems breathing
and talking, and was totally exhausted. She
subsequently developed intestinal problems
and the skin sores flared up with unbearable
itching against which no antipruritic agent
helped. Photosensitive reactions presented as
the skin became blotchy ( Fig.7) with severe
burning sensations in the face, throat and
chest and a total loss of quality of life.
Dycal was removed in 1991-1992 and initially
replaced with Harvard cement. The symptoms
were exacerbated with every single removal.
ME was confined to bed with strong pains in
the face and neck, and in her whole musculoskeletal
system, bowel disturbances and signs
of polyneuropathy. A few weeks after the last
of the Dycal was removed in February, 1992,
most of her sores and rashes disappeared and
she could tolerate sunlight (Fig.8). The
Swedish clinical practitioners working with
ME concluded that Dycal was the underlying
cause of her “toxic ulcerative dermatitis.”
Case # 2.
Born in Chicago in 1965, JM was a
healthy active Caucasian woman until she
started experiencing her first symptoms in
1991. By that time, she already had dental
work, including 17 fillings. No sealers were
used in one filling; Dycal was used in the other
16 fillings. Her earliest symptoms appeared
as skin break outs on the face and neck, which
was recurrent over the following 9 years. She
was treated with minicycline, tetracycline,
and acutane along with topical
pharmaceuticals. The early episodes were
accompanied by body tremors, sleeplessness
and joint pain with occasional vomiting of
black bile. Thrush appeared in the mouth and
around the lips. Pain at the teeth roots
persisted throughout the nineties associated
Communicator - Page 6
with rapid major decay. A sensation of
prickling pain with a pressure and movement
under the skin was accompanied by urticaria
and skin ulcerations in the same areas that
would last for weeks or months. JM’s body
showed random swelling with red marks in
readily observable serpentine-like shapes.
The swellings eventually bottle-necked at the
knees and ankles. The chest burned and hurt
as strange fits of coughing from the lungs
ensued. JM then started losing hair as she
experienced night fevers and sweats, and
peeling of the skin.
During the early 1990’s JM was heavily
medicated, e.g., Diflucan, Rocefin, Vermox
(she had a Taenia infection), Praziquantel,
Ketokonazol, Metrobendazole, among other
medications. She experienced some antiinflammatory
relief and occasional temporary
clearing of ulcers after which ulcers returned
and lasted longer.
In 1998, massive ulcers appeared on JM’s face
at the nasiolobial area and at the skin
( Fig.9). One ulcer did not resolve for years as
it grew deeper while the others cleared within
one year. A CBC in 1999 was unremarkable
except for a high level of Alpha 1-Globulin of
0.5 ( normal range 0.2-0.4 ) and low levels of
IgA of 99 ( normal range 60-400 ) and IgG of
724 ( normal range 700-1500 ). The right
ocular cavity was severely painful and JM was
beginning to lose her eyesight. JM was then
put on a program of Rocefin, Nizoral, Diflucan,
Albendazole, Cefelexen, Praziquantel, and a
variety of other anti-parasitics. In late 1999,
JM started a frequency generation program
using a Las Vegas “Genesis” machine while
undergoing internal cleansing. This program,
along with occasional ozone encephallation
helped resolve JM’s symptoms to some degree.
However, many of the symptoms returned for
which a program of Mexican herbs, e.g. Tee
Tree, Yerba de Manzo, Yerba de Arnica, as well
as MSM liquid, Colloidal Silver , Male fern
extract, Ketokonazol creme, Lamasil creme
and tablets, and Ceffalexin was followed.
A major dental repair was completed in 2001
when Dycal was removed from all 16 teeth.
After being opened, the teeth were packed
with a clove/zinc combination before using
zinc oxide and eugenol. Initially, JM
experienced a few episodes of sickness,
sweats, and vomiting. Since the second visit
she was feeling better. After the fourth visit,
her eyebrow area had a dramatic reduction
in swelling and in the sensation of movement
and the red hot congestion of her face and skin
resolved. JM’s teeth were subsequently
rebuilt with gold onlays section by section.
By the end of the total repair, Nov.2001, JM
regained her normal skin ( Fig.10) with no
movement sensations or pain anywhere in her
body. This state of total resolution has lasted
for over one year to the time of this writing
without regressions or relapses.
Case #3.
LG, a medium- built white American born in
1957, was in perfect health until the morning
of September 18, 1998 when she had a filling
in her tooth no. 18 using Dycal as a liner. She
experienced severe headache within 2 hours
and had to leave work. By 6:00 pm that same
evening, she was vomiting and delirious with
the headache persisting. She was admitted
to the emergency room where her blood
pressure was monitored at 169/108 and
remained high for the following three years
despite repeated attempts to control it with
Atenenol and Diazide. LG never experienced
high blood pressure or headaches before. An
MRI scan was negative. In 1999 LG’s health
deteriorated progressively. She experienced
arthritis- like symptoms in her back, heart
palpitations, mitral valve prolapse, fatigue,
abnormal pap-smears including precancerous
cell abnormalities, night sweats,
missed periods, and severe depression. Her
Atenenol prescription was increased and
various Antibiotics were routinely used. By
March, 2001, LG, who normally weighed 120
lbs had lost 20 lbs. She was immediately
placed on an IV of Antibiotics also to combat
an abcess near her brain.
Communicator - Page 7
(continued on page 12)
In April, 2001, LG moved to an apartment
which was heavily infested with mold and
mites. Lesions started appearing on LG’s face
which quickly became red hot as if on fire.
Her legs became swollen and painfully
burning. By May, 2001, LG had several open
lesions (6 mm to 2 cm in diameter)
accompanied by erythema, on her face and
scalp. Her cheek pulsated as the facial lesions
seemed to track to the chin(Fig.11) where the
most fulminating lesion was; nearest to her
teeth. Springtails (Collembola) and fibers
were recovered from these sites. At that time,
a CBC analysis showed low lymphocytes of
15.0% (normal 20-43%) and high granulocytes
of 77.1% (normal 51-74%), and high
rheumatoid factor of 22.6 (normal <20IU/ml).
She also tested negative for all communicable
diseases at the same time. Her weight
dropped to 92 lbs. She started then
experiencing movement sensations under the
skin of her arms, face and scalp. Lesions
started to change shape and acquire track
marks around them. Grayish pustular
secretions oozed and moved down from the
bloody lesions on the scalp and face. The lesion
then extended to her legs. At this time LG
was diagnosed with stress, anxiety, selfinflicting
wounds, acute endocarditis and
scabies. Treatments for these conditions did
not resolve the NCS symptoms.
OMA diagnosed LG with NCS in January,
2002. She was allergic to sulfa and
sulfonamide compounds. Following our
protocol, LG had the filling and the Dycal liner
removed from tooth #18 in April, 2002. These
were replaced with Starflow and Aria (a
combination of Bisgma, Tegdma, Lidma and
catalysts). Our recommended vitamin
supplementation program was then initiated.
By May, 2002, all symptoms were resolved.
Once the chin lesion healed, which took a
longer time than the rest, the skin of all
previously compromised sites returned to
normal(Fig.12). Constitutional and
neurological functions as well as
psychological, emotional and energy levels
have also been restored to normalcy.
Conclusion
The toxicity of Dycal, Life and Sealapex has
been well documented invivo and invitro
studies of various animal and human models
by many workers. The toxicity assumed
cytotoxic, genotoxic, neurotoxic, phototoxic,
necrotic, and inflammatory reactions
compatible with the pathology and symptoms
observed in NCS patients. Ethyltoluene
sulfonamide, 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. Neurological
hyperactivity is related to nerve damage
associated with vasomotor reactions due to a
direct influence on the peripheral nerve
endings.35The sulfonamide component is the
cause of the cutaneous symptoms, especially
in sulfa-sensitive patients and has been
demonstrated in elevated sulfonamide/sulfa
levels in CBC blood analyses as well as in
skin sensitivity tests. The relationship
between sulfonamide and phototoxicity has
been well established.29 Resolving the
symptoms (effect) by removing the sealants
(cause) in patients undergoing treatments,
confirms this cause-effect relationship. The
toxic effects of other ingredients of these three
sealants, e.g., zinc oxide, can not be
overlooked.
The nature of causation of NCS precludes
contagious transmission. Any similarities of
symptoms among partners within the same
household are traceable to the transmission
of opportunistic infections, especially fungi.
The proper diagnosis of NCS can only be
made upon the examination of patients,
confirmation of their neurological and dermal
symptoms, and the study of their clinical
history and medical records, especially dental
charts. Additional diagnostic aides include
skin tests for allergy to sulfa and blood
Communicator - Page 9
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Communicator - Page 12
analysis for elevated levels of sulfa. Upon the
satisfactory diagnosis of an NCS case, and the
determination of which teeth have the toxic
sealants, arrangements for dental
rehabilitation are made. Those include the
removal of fillings and of all traces of sealants
and replacing them with bio-compatible
dental products not containing ethyltoluene
sulfonamide or zinc oxide.
It is recommended not to do more than two or
three teeth per month. The patient is given a
list of vitamins and other supplements to take
during the procedure and for the following few
weeks until symptoms are completely
resolved. 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 and
selenium. After reaching the state of
normalcy, the patient may still retain some
sensitivity to moldy places lacking sun and
fresh air circulation. The sealants reported
above are still in common usage throughout
the world. The “small” amounts continually
leaching into the live tissues of the body
promote a cumulative progressive damaging
pathology over a long period of time. Dental
practitioners should be aware of the adverse
effects of these products and employ this
knowledge 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.
References
1.Amin OM. Neuro-cutaneous Syndrome
(NCS); a new disorder. Explore 2001; 10: 55-
56.
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Trandlakartidningen 1994; 86: 470. (in
Swedish).
3.Garcia LS. Diagnostic Medical Parasitology.
Wash, DC: Am Soc Microbiol Press, 2001.
4.Urano Z, Hasegawa H, Katsumata T,
Toriyama K, Aoki Y. Dioctophymatid
nematode larva found from human skin with
creeping eruption. J Parasitol 2001;87: 462-
465.
5.Amin OM. Facial cutaneous dermatitis
associated with arthropod presence. Explore
1996; 7: 62-64.
6.Frye FL. In search for the haphazardly
elusive: a follow-up report on an investigation
into the possible role of collembolans in
human dermatitis. Vet Invert Soc Newsletter
1997; 13: 10-13.
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http://www.collembola.org/publicat/sidney.htm>

1999-2003; 10pp, and per comm..
8.Mahon CR, Manuselis G Jr. Diagnostic
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9.Draheim RN, Murray AJ. Compressive
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10.Burry MB. Neurodevelopmental toxicity of
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11.Tai KW, Huang FM, Huang MS, Chang YC.
Assessment of the genotoxicity of resin and
zinc-oxide eugenol-based root canal sealers,
using an in vitro mammalian test system. J
Biomed Mater Res 2002; 59: 73-77.
12.Wright KJ, Barbosa SV, Araki K,
Spangberg LS. In vitro antimicrobial cytotoxic
effects of Kri 1 paste and zinc oxide eugenol
used in primary tooth pulpectomies. Pediatr
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13.Pissiotis E, Spangberg LS. Toxicity of
pulpisad using four different cell types. Int
Endod J 1991; 24: 249-257.
14.Sadeghein A, Bolhari B, Sarafnejad A. A
comparison of the effects of three endodontic
sealers on adherence of mouse peritoneal
macrophages. J Calif Den Assoc 2001; 29: 673-
677.
15.Soares I, Goldberg F, Massone EJ, Soares
Communicator - Page 13
IM. Periapical tissue response to two calcium
hydroxide-containing endodontic sealers. J
Endod 1990; 16: 166-169.
16.McShane CJ, Stimson PG, Bugg JL,
Jennings RE. Tissue reactions to Dycal. J
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2002, <
http://www.carlosboveda.com>;
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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

http://www.parasitetesting.com

Communicator - Page 14
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 quadrant
started in 1997. Cutaneous symptoms began in Spring 2002 preceded by extensive treatment with topical sulfa
preparations 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 covering
the whole body of ME given Dycal in 1985 (case no.1). 4. Mucoid NCS/lesions on the face of MM. She was born
in 1950, given Fynal in six teeth in 1981 and in one tooth in 1986 as well as with Life in two teeth in 1985 and
1988. 5. Histopathological section of one of the roughly 300 sores covering the body of SK. She was born in 1956
and reacted with typical NCS symptoms to a zinc oxide cement (combined with Durelon) underneath a total
veneer job in 1982. The section shows hyperkeratosis –like perivascular dermatitis with eosinophils. 6. Cutaneous
sores and swelling in the right hand and arm of DB. Born in 1965, DB had 10 Amalgam restorations in 1982
and 1983 using Life. She started experiencing symptoms including ulcerated rash all over the body, unilateral
edema and pin-prick and subcutaneous movement sensations in 2001-2002. Life is being removed and recovery
is in progress.
Communicator - Page 15
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 cheek
and 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 infections
Parasitology Center, Inc.
Dr. Omar M. Amin, Ph.D.
(480) 767-2522
e-mail: omaramin@aol.com
19
Table 1- Components in catalysts (C) and bases (B) of Dycal, Life and
Sealapex.
_______________________________________________________________ ____________
Material Dycal* Life* Sealapex
______________________________________________________________
Calcium
hydroxide
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 mythyl
salicylate
________ 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. Tweet