Focal Infection - Theory or Reality
Robert Gammal BDS. FACNEM(Dent)
Introduction
In recent years there has been a reawakening of
the dangers of oral infections and their potential disastrous
effects on systemic health. Dead and infected teeth are often
treated 'conservatively' in modern dentistry by performing a treatment
called Root Canal Therapy. As dentists we are indoctrinated that
it is better to save a tooth at any cost - although the real costs
to individual health and the society at large are usually totally
overlooked by the teaching institutions. This may at first seem
surprising considering that dentistry is touted as a health providing
profession. On the other hand, if the dental profession were to
accept the reality of Focal Infection (and the potential sources
of this oral infection), we would have to reassess some of the
fundamental treatment concepts being taught and practiced in dentistry.
Root Canal Therapy must surely be one of the prime candidates
for this reassessment.
With the resurgence of an interest in this area,
there is also a blatant resistance by the dental profession of
the reality of Focal Infection Theory. Both the Australian Dental
Association and the universities have stated that Focal Infection
is a concept dating back 150 years and one, which has been disproven
by recent research. This supposed research has never been cited
by either the Australian Dental Association or the universities.
This attitude flies in the face of published scientific
research some of which is even published in the dental journals.
In 1996 the Journal of Periodontology devoted a whole issue to
this subject relating periodontal disease to a variety of systemic
diseases which included coronary heart disease, diabetes and low
birth weight babies.
Quintessence International is one of the most highly
respected dental journals in the world. They state in 1997:
"The detrimental effect of focal infection
on general health has been known for decades. Chronic dental infections
may worsen the condition of medically compromised patients."
(335)
As is common in these sorts of debates the dental
authorities will mention research which is 100 years old - in
this case the work of people like Billings, Rosenow and Price
- and claim that because it is old research it is no longer relevant.
They completely ignore the research which is more current. Interestingly
all of the research conducted by Dr Weston Price in the 1920's
is fully supported by the recent literature.
It is well accepted in the profession that any form
of oral surgery will produce a bacteremia and that this may cause
infections in susceptible tissues, especially the heart. What
is less accepted is that other sources of sepsis exist in the
mouth. These include;
periodontal infections
NICO lesions
dead teeth.
Dead teeth are impossible to sterilise and remain infected whether
treated with Root Canal Therapy or not. Aside from the actual
infective organisms and their by-products a dead tooth also is
a source of necrotic tissue breakdown products.
The substances that are spread from such a focus
of course include the bacterial, viral and fungal organisms that
survive in such foci. It will also include the endotoxins produced
by anaerobic organisms in the foci. (354-361) Current research
indicates that other toxins produced by anaerobic organisms are
also released into the body - these include hydrogen sulphide
products and methyl mercaptans, both of which are highly poisonous
products. (362-385)
What this means of course is that a dental focus
of infection may not only infect other tissues but also poison
the body with a variety of toxins. Professor Boyd Haley from Kentucky
University has recently demonstrated the presence of these toxins
and has developed techniques to test for them. (You can visit
Prof Haley's site at http://www.altcorp.com/oralartc.htm/)
Distribution of organisms and their toxins throughout
the body is by various routes: (341-353)
blood circulation through out the body
lymphatic distribution locally and then to blood
stream
retrograde axonal transport - transport along nerve
fibres and back to the brain.
In 1951 the problem of focal infection was discussed
at length in the Journal of the American Dental Association. -Mechanism
of Focal Infection J Am Dent Assoc Vol 42 June 1951
Definitions
"A Focus of infection has been defined as a
circumscribed area infected with micro-organisms which may or
may not give rise to clinical manifestations.
A Focal Infection has been defined as sepsis arising
from a focus of infection that initiates a secondary infection
in a nearby or distant tissue or organs."
The article states clearly that "The concept
of focal infection in relation to systemic disease is firmly established"
and that "The origin of many toxic or metastatic diseases
may be traced to primary local or focal areas of infection".
This article also states that there are two major
mechanisms of focal infection:
a) an actual metastasis of organisms from a focus
b) the spread of toxins or toxic products from a
remote focus to other tissues by the blood stream.
Once the infection passes the abscess area about
the tooth:
a) they may multiply in the blood setting up an
acute or chronic septicaemia.
b) they may be carried live to a suitable nidus
where they infect the surrounding tissue.
c) they may produce a slow but progressive atrophy
with replacement fibrosis in various organs of the body.
The authors continue to show a relationship to
allergic / immune reactions:
The bacteria at the focus may undergo autolysis
or dissolution. Some of the products of this dissolution, diffusing
into the blood or lymph , may sensitise in an allergic sense,
various tissues of the body."
"A later diffusion of these products on reaching
the sensitised tissue may call forth an allergic reaction."
Considering that the above article was published
in 1951, it may be claimed in the late 90's that this too is old
research. For this reason the first section of references associated
with the this article are taken mainly from the last 40 years
of Medline data bases after combining the search requests 'focal
infection' and 'dentistry'.
Henig and Eliezer state in their paper "Brain
Abscess following Dental Infection" ;
" The elimination of infection from human
tissue is a necessary goal based on fundamental biological principles.
It is even more essential in an environment in which the natural
defense mechanisms of the body are unable to function. Such an
environment is the root canal of a tooth." This statement
is published in the Journal of Oral Surgery in 1978. Although
the authors believed at the time that it is possible to sterilize
a tooth (since disproven) their statement underlies the basic
principles of Focal Infection Theory.
What is most interesting from this search is the
number of reviews of the literature which have been done in this
time. Some of the latest being in 1997.
Published case reports include the following disease
states as being directly related to Oral infections:
Mediastinitis
Maxillary sinusitis
Cavernous Sinus thrombosis
Pharyngeal Cellulitis
Cardiac Problems
Necrotising Fascititis
Necrotising Mediastinitis
Superior Orbital Fissure Syndrome
Proptosis
Opthalmoplegia
Light Reflex Interference
Blindness
Endopthalmitis
Lung Abscess
Aspiration Pneumonia
Brain Abscess
Meningitis
Acute Hemiplagia
Psychotic episodes
Metastatic Paraspinal Abscess
Gasarion Ganglion
Trigeminal Neuralgia
Endocarditis
Septicemia
Myocardial Infection
Deuodenal Ulcers
Splenic Abscess
Leg abscess
Blood disorders
Immune reactions
Inflammatory Bowel Disease
Low birth weight
Infertility
Deaths
Toxic Shock
Arthritis
Rheumatic changes
Infection of artificial joint prosthesis
Kidney Damage
Brain Tumors
Trigeminal Neuralgia
Atypical Facial Pain
In other words all areas of the body may be effected
by the presence of infected foci in the mouth. It has been relatively
easy for the medical profession to distinguish particular micro-organisms
in an infection and relate them to the oral flora. It is only
recently that we have tests, which can demonstrate low molecular
weight toxins, which are produced by these organisms. Interestingly
Dr Weston Price in the 1920's was able to demonstrate the effects
of the toxins although he was not then able to identify or isolate
them - his research, I believe, is as relevant today as it was
when he wrote it.
It is not my intention to do a formal literature
review of focal infections, but merely to present you with a list
of references, which of themselves validate the reality of focal
infection from dental origins. It is my hope that the dental profession
will acknowledge this reality and reassess certain treatment
concepts, which currently disregard the published literature.
All references are available in Medline.
Focal Infection References
Medline 1960 to 1998
General
1. Andra A [Massive infection of odontogenic origin
(author's transl)]: Zentralbl Chir (1978) 103(8):527-32
2565 patients with infections of odontogenic origin
are reported. In only 34,8% of the cases the correct diagnosis
was established. Purulent inflammations of the submaxillar area
mostly occurred (49,9%) followed by the pharyngeal area (19,9%).
Early signs of the spreading of the inflammation must be the indication
to send the patient to the hospital to avoid complications.
2. Berard R [Special characteristics of infection
spread in temporary molars] Actual Odontostomatol (Paris) (1973
Dec) 27(104):707-18
3. Cros P Freidel A Parret J [3 studies on general
infections with dental etiology and bacteriological proofs] Ann
Odontostomatol (Lyon) (1969 Sep-Oct) 26(5):189-93
4. Cadenat H Marcopoulos A Gely P Fabie M Combelles
R [2 new cases of Melkersson-Rosenthal's syndrome] Rev Stomatol
Chir Maxillofac (1971 Sep) 72(6):635-42
5. Elsner R Koch H [Errors and dangers in treatment
of odontogenic infections with antibiotics] Quintessenz (1977
Oct) 28(10):137-40
6. Gawrzewska B Wedler A Fijal D [Results of studies
on the removal of active infectious foci in the treatment of diseases
caused by odontogenic focal infections] Czas Stomatol (1976 Dec)
29(12):1099-103
7. Huurman PM [Root canal therapy and focal infection]
Dtsch Stomatol (1965 Dec) 15(12):938-40
8. Klammt J [Life endangering complications of acute
odontogenous infections in the era of antibiotics] Dtsch Gesundheitsw
(1969 Sep 4) 24(36):1695-8
9. Hunter N Focal infection in perspective. Oral
Surg Oral Med Oral Pathol (1977 Oct) 44(4):626-7
In this article some of the theoretical possibilities
arising as a result of focal infection are discussed. Rheumatic
fever is discussed as an example of a disease in which a number
of possible mechanisms may act to produce tissue damage at a target
area. The mechanisms examined are direct dissemination of organisms
from the focus to the target area, the induction of L-phase bacteria,
and toxic damage to target tissue. Host-mediated tissue damage
by hypersensitivity or auto-immune mechanisms is considered as
well.
10. Lachard J Cremieu A Jars G Ged S Kaplanski P
[4 cases of Osler's disease] Rev Stomatol Chir Maxillofac (1970
Jul-Aug) 71(5):405-10
11. Reil B Koblin I [Catamnestic surveys in 371
cases of abscess of the maxillofacial region in childhood] Dtsch
Zahnarztl Z (1976 Feb) 31(2):182-4
Catamnestic surveys of 371 children who suffered
from abscesses during the past ten years (1965 to 1974) showed
that type and location of the abscesses and their incidence in
the various age groups are typical and differ from those of abscesses
in adults. These results are discussed and compared with the data
found in the literature.
12. Rouchon [Distant manifestations of bucco-dental
origin in children] Med Infant (Paris) (1965 May) 72(5):341-9
13. Sadowsky C The tooth and periodontium as a site
of focal infection. Diastema (1968) 2(3):43-7
14. Stortebecker TP [Spreading hazards from infection
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15. Sukin L Periodontal disease, focal infection
and systemic health. J N J Dent Assoc (1975 Winter) 46(2):26-9,
47
Cardiac
16. Asikainen S Alaluusua S Bacteriology of dental
infections. Eur Heart J (1993 Dec) 14 Suppl K:43-50
Oral bacteria may spread into the blood stream through
ulcerated epithelium in diseased periodontal pockets and cause
transient bacteraemias, which are regarded as increased risk,
especially for immunocompromised patients or persons with endoprotheses.
17. Droz D Koch L Lenain A Michalski H Bacterial
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France Br Dent J (1997 Aug 9) 183(3):101-5
18. Lieberman MB A life-threatening, spontaneous,
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(1992 Sep) 20(9):37-9
19. Mattila KJ Dental infections as a risk factor
for acute myocardial infarction. Eur Heart J (1993 Dec) 14 Suppl
K:51-3
20. Mattila KJ Valle MS Nieminen MS Valtonen VV
Hietaniemi KL Dental infections and coronary atherosclerosis.
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22. Root TE Silva EA Edwards LD Topp JH Hemophilus
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23. Seymour RA Steele JG Is there a link between
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Br Dent J (1998 Jan 10) 184(1):33-8 Evidence suggests that dental
health, in particular periodontal disease, may be a significant
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36. Guittard P Ducasse JL Jorda MF Eschapasse H
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37. Hendler BH Quinn PD Fatal mediastinitis secondary
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A case of necrotizing mediastinitis that caused
death in a 38-year- old man has been reported. The cause of his
infection was proved, both radiographically and clinically, to
be dental infection associated with the lower molars and their
supporting structures. A diffuse cellulitis involving the submandibular,
masticator, and parapharyngeal spaces ensued. Sudden onset of
severe pleuritic chest pains and a 100% pneumothorax of the left
lung developed, which ultimately led to his death.
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40. Latronica RJ Shukes R Septic emboli and pulmonary
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41. Larik ML van Zanten TE van der Waal I van der
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43. McCurdy JA Jr MacInnis EL Hays LL Fatal mediastinitis
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The pertinent features of life-threatening complications
of dental infections have been briefly reviewed with particular
emphasis on the alterations of the clinical features of these
conditions induced by antibiotic therapy. The clinician who deals
with dental infections must exercise a high index of suspicion
to consistently abort the development of these complications,
especially when treating debilitated patients or individuals with
compromised immune functions.
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73(4):497-500
Potentially lethal consequences can quickly occur
once the mediastinum is subjected to the ravages of an anaerobic
infection. Mediastinitis from odontogenic or deep cervical infections
is extremely rare in the era of antibiotic drugs. We have recently
encountered five such cases, with a rapid spread of the inflammatory
process into the mediastinum resulting in a number of local and
systemic complications. All were caused by anaerobic bacteria.
Awareness of such complications and early roentgenographic diagnosis
lead to prompt surgical drainage, proper antibiotic therapy, and
survival after a stormy clinical course. The anatomic pathways
between the various fascial planes of the neck and ediastinum
will be described.
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50. Petrone JA Mediastinal abscess and pneumonia
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54. Sazonov AM Muromskii IuA Plotnikov NA Zubkova
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55. Siegel EB Friedlander AH Mongiardo JJ Klebsiella
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62. Terezhalmy GT Bottomley WK Pulmonary nocardiosis
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A case of pulmonary nocardiosis associated with
primary nocardial infection of the oral cavity in a compromised
host is presented. Nocardia asteroides, an aerobic, gram-positive,
branching, filamentous fungus, was demonstrated in the sputum
and in pathologic specimens from gingival sulci stained by Gram's
method and the acid- fast method Kinyoun. The organism was identified
in cultures made on Sabouraud's glucose agar. Marked clinical
improvement was noted when the patient received high dosage of
sulfisoxazole diolamine (8 to 12 Gm. per day) for a prolonged
period of time (9 to 12 months). Because of an apparent relative
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on the subject in the dental literature, this article is timely.
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tracts and the mechanisms that interfere in the determinism of
the bronchopulmonary suppurative syndrome, the septic particles
migrating as a rule along the bronchogenic route.
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67. Andersen WC Horton HL Parietal lobe abscess
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68. Andrews M Farnham S Brain abscess secondary
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Frequently the bacteria found by aspiration of the brain abscess
are the only indication of a dental focus.
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The aetiology, diagnosis and treatment of peripheral
facial nerve palsy are discussed. Four cases of facial nerve palsy
following dental procedures are reported. Following a revision
of the world literature during the last 23 years, the 25 cases
of facial nerve palsy documented are analysed and divided into
four groups on the basis of aetiology, speed of onset and recovery
and modes of treatment suggested.
86. Gobel S., Bink J., degenerative changes in primary
trigeminal axons and in neurons in nucleus caudalis following
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88. Hamlyn JF Acute hemiplegia in childhood following
a dental abscess. Br J Oral Surg (1978 Nov) 16(2):151-5
The syndrome of acute hemiplegia in childhood is
described and a case following dental infection reported. The
possible mechanisms responsible for the development of this condition
are considered.
89. Hedstrom SA Nord CE Ursing B Chronic meningitis
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90. Henig EF Derschowitz T Shalit M Toledo E Tikva
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Med Oral Pathol (1978 Jun) 45(6):955-8
A 48-year-old woman underwent root canal treatment
of the upper left lateral incisor and lower right second premolar.
Close to the conclusion of the endodontic treatment she complained
about headaches. Later on, because of aggravation of her condition,
with headaches, fever, malaise, Weakness, and numbness of the
right limbs, she was admitted to the hospital. The disease progressed
to an epileptic state, with appearance of a right hemiparesis.
A brain scan and carotid arteriogram revealed the presence of
a mass occupying the left parietal space. Craniotomy disclosed
an abscess containing yellow pus from which Streptococcus viridans
was cultured. After thorough surgical cleansing of the area, removal
of the bone for decompression, and treatment with ampicillin the
patient improved gradually and slowly regained the mobility of
her right side.
91. Hollin SA Hayashi H Gross SW Intracranial abscesses
of odontogenic origin. Oral Surg Oral Med Oral Pathol (1967 Mar)
23(3):277-93
92. Ingham HR Kalbag RM Tharagonnet D High AS Sengupta
RP Selkon JB Abscesses of the frontal lobe of the brain secondary
to covert dental sepsis. Lancet (1978 Sep 2) 2(8088):497-9
The bacterial species found in pus aspirated from
brain abscesses in two patients were typical of those found in
dental sepsis. Subsequently apical-root abscesses were demonstrated
in the upper jaws of both patients. This evidence strongly suggests
that these cerebral abscesses were secondary to dental sepsis
which could have spread from the teeth to the frontal lobes by
several possible antaomical pathways.
93. King R. Interaction of noxious and nonnoxious
stimuli in primary sensory nuclei Adv Neurol 1974; 4:659-63
94. Larkin EB Scott SD Metastatic paraspinal abscess
and paraplegia secondary to dental extraction. Br Dent J (1994
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95. Lewandowski L Serafinowska A [Peripheral facial
nerve palsy caused by focal dental infection] Czas Stomatol (1970
Dec) 23(12):1357-60
96. Lutsik LA [Streptococcal chroniosepsis complicated
by meningoencephalitis with a fatal outcome] Stomatologiia (Mosk)
(1979 Nov-Dec) 58(6):55-6
97. Martinez Garcia W Aleman Lopez ST [Septic thrombosis
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Odontol (1971 Sep-Oct)(171):25-7
98. Marks PV Patel KS Mee EW Multiple brain abscesses
secondary to dental caries and severe periodontal disease. Br
J Oral Maxillofac Surg (1988 Jun) 26(3):244-7
99. Mojseowicz K Czerwinski F Linnik-Kabat A [Intracranial
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101. Mucke L Clinical management of neuropathic
pain Neurol clin 1987;5:649-63
102. Mukharinskaia VS Antadze ZI Devidze NV Emchenko
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103. Ogundiya DA Keith DA Mirowski J Cavernous sinus
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(1989 Dec) 47(12):1317-21
104. Perna E Liguori R Petrone G Mannarino E Actinomycotic
granuloma of the Gasserian ganglion with primary site in a dental
root. Case report. J Neurosurg (1981 Apr) 54(4):553-5
105. Pompians-Miniac L [Apropos of 2 cases of endocranial
abscesses of dental origin. Propagation by venous route of apical
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106. Renton TF Danks J Rosenfeld JV Cerebral abscess
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Aust Dent J (1996 Feb) 41(1):12-5
107. Ries P Turk R [Histopathologic changes in bone
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Dtsch Z Mund Kiefer Gesichtschir (1984 Jul-Aug) 8(4):301-4
108. Ruzin GP Zakharov IuS Bolgov DF [A case of
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109. Saal CJ Mason JC Cheuk SL Hill MK Brain abscess
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110. Selby G., Diseases of the fifth cranial nerve.
In Dyke PJ., Thomas PK., Peripheral Neuropathy. Philadelphia.
W.B. Saunders 1984;1224-65
111. Schotland C Stula D Levy A Spiessl B [Brain
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112. Steiner G J Neuropath. 1952;11:343-72 Multiple
Sclerosis "sinus mucosa may become repeatedly infected from
diseased teeth, gums and tonsils"
113. Stevenson GW Gossman HH Dental and intracranial
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114. Strauss SI Stern NS Mendelow H Spatz SS Septic
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115. Struzak-Wysokinska M [Peripheral paralysis
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Mar) 20(3):283-8
116. Taicher S Garfunkel A Feinsod M Reversible
cavernous sinus involvement due to minor dental infection. Report
of a case. Oral Surg Oral Med Oral Pathol (1978 Jul) 46(1):7-9
Described is a case of a cavernous sinus involvement
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117. Tassarotti B [A case of spheno-palatine ganglionic
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118. Unteanu G Solacolu VI [Problems concerning
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The data supplied by analysis of more than 1 000
patients pointed to the wide range of the causal factors, the
role of focal infections of the upper respiratory and digestive
tracts and the mechanisms that interfere in the determinism of
the bronchopulmonary suppurative syndrome, the septic particles
migrating as a rule along the bronchogenic route.
119. Urbani G Ferronato G Bertele GP [Trigeminal
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120. Urmosi J Wittmann K Tamus I [Successful treatment
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121. Urmosi J [Thrombophlebitis of the sinus cavernosus]:
Stomatol DDR (1975 Nov) 25(11):776-8
A short survey of the relevant literature is followed
by the description of the clinical course of a thrombophlebitis
of the cavernous sinus. In this case, the initial focus was an
infection of a canine which caused thrombophlebitis via the anterior
facial vein. The healing must be attributed to the immediate application
of broad spectrum antibiotics and removal of the primary focus.
122. Uppgaard RO Tic douloureux--multicauses include
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123. Vitzthum HE Erle A Lambrecht R [Intracranial
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124. Valachovic R Hargreaves JA Dental implications
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There is a high morbidity and mortality associated
with brain abscesses in children with congenital cyanotic heart
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treated primary molar in the etiology of a brain abscess in a
boy with congenital cyanotic heart disease.
125. Westrum LE., Canfield RC., Black R., Transganglionic
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126. Westrum LE., Canfield RC., Electron microscopy
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127. Yun MW Hwang CF Lui CC Cavernous sinus thrombosis
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128. Zachariades N Vairaktaris E Mezitis M Triantafyllou
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129. Bayer D. et al Trigeminal Neuralgia an overview.
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130. Fromm G., et al Trigeminal Neuralgia. Current
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1204-7
131. King R. Interaction of noxious and nonnoxious
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132. Mucke L Clinical management of neuropathic
pain Neurol clin 1987;5:649-63
133. Selby G., Diseases of the fifth cranial nerve.
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W.B. Saunders 1984;1224-65
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134. Artis JP Artis M Bowyer M Durivaux S [On uveitis
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135. Boyer R Fourel J Martin R Barkat A [Eye manifestations
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136. Bermanowa G Pietrowa N Lalek A Bujalska H [Dental
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137. Bocca M Zombolo L Coscia D Moniaci D [The correlation
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138. Cordier J Vexler C Watrin E Barisain P [Ocular
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139. Francois J Van Oye R [Eye diseases and odontologic
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140. Harris M Dental infection and the eyes. Dent
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141. Harris M Dental infection and the eyes. Pak
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144. May DR Peyman GA Raichand M Friedman E Metastatic
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145. Murphy NC Mahar PJ Fair R Uveitis and its relation
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A 46-year-old man developed symptoms of a chronic
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a dental procedure. The patient's intraocular inflammation was
not diminished by massive treatment with topical and systemic
corticosteroid therapy or intravenously administered adrenocorticotropic
hormone. The inflammatory process progressed to an overt endophthalmitis
during a period of three weeks and the eye eventually required
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146. Niho M [2 cases of rhinogenic retrobulbar optic
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147. Nemetz U [Ophthalmology and focal infections]
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148. Papakonstantinou A Papakonstantinou P [Dental
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149. Rousselie F [Eye infections of dental origin]
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150. Rubin et al Oral Surg 1976 Vol 41 No 1 Abscess
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152. Sela M Sharav Y The dental focal infection
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153. Stone A Straitigos GT Mandibular odontogenic
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Orbital cellulitis usually begins as an infection
of the paranasal sinuses. While a small percentage of cases are
of dental origin, these usually involve the maxillary teeth. In
the case reported here orbital cellulitis originated from an infection
in the mandible and spread through the pananasal sinuses, deep
facial circulation, and orbital tissues, resulting in unilateral
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154. Szak O Belan J [Endogenous uveitis in 4-year-material
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156. Takahashi T [A case of retrobulbar neuritis
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158. Zoltan N Gyula M [Odontogenic orbital phlegmon]
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159. Carter TB Blankstein KC White RP Jr Severe
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161. Marculescu A Ursuleac S Pralea E Anghel I [Vascular
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162. Madeira AA Lopes GV [Study of the hematological
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164. Salgarelli A Morana G Beltramello A Nocini
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165. Shurin SB Socransky SS Sweeney E Stossel TP
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We recovered capnocytophaga, a gram-negative anaerobe
implicated in the pathogenesis of periodontal disease, from two
patients with a history of dental infections. Neutrophils from
both patients failed to acquire the asymmetric shape characteristic
of normal neutrophils. Fluorescein staining of the patients' living
neutrophils remained diffuse and patchy instead of showing the
normal pattern in which the fluorescence is swept into the rear
of the cell. The locomotion of one patient's neutrophils in vitro
was less than 50 per cent of that of normal neutrophils, and migration
of this patient's neutrophils into dermal abrasions was reduced,
although phagocytosis and nitroblue tetrazolium reduction were
normal. All abnormalities of neutrophil morphology and function
disappeared after eradication of the capnocytophaga infections.
Sonicates and culture medium of capnocytophaga contained a dialyzable
substance that caused normal neutrophils to behave like neutrophils
obtained from the infected patients.
166. Stypulkowski C Lagan W Stypulkowska J [Chronic
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171. Oral Surg. 1977 Vol 43 No 3 Immune Reaction
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172. Andriutsa VI Ketrar' GI Kuria VI [Odontogenic
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Three patients with parapharyngeal cellulitis arising
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period of ten months. Respiratory distress and/or pharyngeal discomfort
prompted all patients to seek medical aid. The extent of infection
within the parapharyngeal space, the potential for life-threatening
complications, and the significance of the dental lesions were
not appreciated initially in all cases. Despite early antibiotic
therapy, one patient died and one incurred severe neurologic sequelae.
Early recognition, use of antibiotics effective against anaerobic
bacteria, and prompt surgical drainage are mandatory to prevent
considerable morbidity and mortality. Control of the airway is
the most important therapeutic maneuver leading to a favorable
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175. Perovic J Piscevic A [Chronic subcutaneous
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176. Valdazo A [Peripharyngeal abscesses: various
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181. Janicke S Kettner R Kuffner HD A possible inflammatory
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182. McAndrew PG Davies SJ Griffiths RW Necrotising
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183. Mruthyunjaya B Necrotizing faciitis: report
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184. Roberson JB Harper JL Jauch EC Mortality associated
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188. Stoykewych AA Beecroft WA Cogan AG Fatal necrotizing
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189. Schroeder DC Sarha ED Hendrickson DA Healey
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190. Tasar F Tumer C Yulug N Bayik S Cervicofacial
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J Deep neck infections. Int J Oral Surg (1979 Dec) 8(6):407-11
From January 1967 to August 1978, 65 patients with
cervical abscesses were referred to the ENT Clinic of Turku University
Hospital. The origin of these deep neck infections was odontogenic
in 19, tonsillitis or tonsillectomy in 14, trauma in seven, salivary
glands in five and branchiogenic cysts in five and other known
causes in three cases. In 12 cases the origin was unknown. The
cervical abscesses of odontogenic origin were located mostly in
the submandibular space (11/19). The rest of the deep cervical
infections were mostly found in the parapharyngeal space (25/46).
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AJR Am J Roentgenol (1996 May) 166(5):1219-23
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195. Azimov M Ermakova FB [Role of focal odontogenic
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Evidence of a direct link between chronic sinusitis
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"spirochaetal hypothesis" This hypothesis has not been
shown to be eroneous and a spirochaetal infection of the central
nervous system could explain the specific pathological, immunological,
and epidemiological features of M.S.
200. Gay D et al Lancet 1986;i:815-19 Multiple Sclerosis
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In an analysis of general practice records the rate
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with M.S. than in matched controlls. M.S. and chronic sinus infection
were also significantly associated in the timing of attacks, in
the age at which the patient suffered their attacks, and in the
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201. Guglani L Maxillary sinusitis due to dental
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205. Ivankievicz D Schumacher GH Ethmoidal complications
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206. Maloney PL Doku HC Maxillary sinusitis of odontogenic
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207. Nortje CJ Farman AG de V Joubert JJ Pathological
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213. Strauss SI Stern NS Mendelow H Spatz SS Septic
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216. Yamazaki Y Shimada K Sakuma M Kawashima Y Kobayashi
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218. Borowsky SA Hasse A Wiedlin R Lott E Dental
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A patient with alcoholic cirrhosis had multiple
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for the source of infection finally revealed the organism in the
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219. Dierks EJ Meyerhoff WL Schultz B Finn R Fulminant
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224. Laine PO Lindqvist JC Pyrhonen SO Strand-Pettinen
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225. Loesche WJ Association of the oral flora with
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226. Marques AP Walker PO Intraoral etiology of
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227. Mitchell CS Nelson MD Jr Orofacial abscesses
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228. Navazesh M Mulligan R Systemic dissemination
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232. Thoden van Velzen SK Abraham-Inpijn L Moorer
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Fever
233. Berry E Silver J Pyorrhoea as cause of pyrexia.
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Three patients with fever and malaise, one of whom
also had joint pains, were extensively investigated before their
condition was attributed to dental sepsis. Each patient recovered
fully after appropriate dental treatment. Dental sepsis should
be added to the list of possible causes of pyrexia of ndetermined
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234. Hyjek K Mateja W [Rare case of odontogenic
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235. Levinson SL Barondess JA Occult dental infection
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Three patients with prolonged unexplained fevers
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initial examination failed to elicit symptoms or signs of dental
infection, and extensive in-hospital evaluation was nonproductive,
dental consultation with roentgenograms provided the diagnosis.
All three patients underwent dental extractions with periapical
or peridontal debridement; following a brief postoperative febrile
period, all three responded with defervescence, without subsequent
recurrence of fever. These cases emphasize the importance of periapical
and peridontal infection as causes of fever of obscure origin.
The pathogenesis, characteristics and bacteriology of periapical
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236. Samra Y Barak S Shaked Y Dental infection as
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237. Shinoda T Mizutani H Kaneda T Suzuki M Fever
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238. Urmosi J [Clinical and laboratory data supporting
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239. Donoff RB Guralnick W Shock due to odontogenic
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240. Egbert GW Simmons AK Graham LL Toxic shock
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241. Quinn P Guernsey LH The presentation and complications
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242. Currie WJ Ho V An unexpected death associated
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243. Gotte P [Death after a dental infection] Minerva
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The pertinent features of life-threatening complications
of dental infections have been briefly reviewed with particular
emphasis on the alterations of the clinical features of these
conditions induced by antibiotic therapy. The clinician who deals
with dental infection must exercise a high index of suspicion
to consistently abort the development of these complications,
especially when treating debilitated patients or individuals with
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244. Ocampo Flores P Limon Mejia AL Bustillos Lucas
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245. Kolb H [Spontanous remission of severe backache
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246. Biberman IaM [Clinical aspects of odontogenic
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248. McGinnis JP Keene RD Focal osteoporotic bone
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252. Advisory statement. Antibiotic prophylaxis
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253. Mulligan R Late infections in patients with
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254. Jacobsen PL Murray W Prophylactic coverage
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255. Rubin R Salvati EA Lewis R Infected total hip
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Three cases are reported in which there was a worrisome
association between dental work and an infected total hip replacement.
The patients had long asymptomatic intervals subsequent to Implantation
of prosthetic hip joints. After dental procedures, infections
became apparent in these hips. Such infections carry an enormous
and crippling morbidity. The potential complications of transient
bacteremia in the patient with a cardiac valvular prosthesis are
appreciated and the importance of prophylactic antibodies for
dental work in such patients is well known. Although we emphasize
that there is no proof that the infections in our patients were
metastatic from the mouth, the sequence of events is suggestive.
We recommend prophylactic antibiotics for dental work in the Patient
with a total hip replacement.
256. Schurman DJ Aptekar RG Burton DS Infection
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257. N. Tani et al J. Endo 18:2 1992 Infected total
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258. Hess JC Victor M [Relation between rheumatology
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263. Moses JJ Lange CR Arredondo A Septic arthritis
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266. Wallace DE Chronic periodontitis and a chronic
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270. Zivkovic S [Endodontic treatment in the therapy
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271. Arellano Ocampo F Rojas Rodriguez J Rosales
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272. Bruszt P Vegh T [Incidence of facial fistulae
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274. Roser SM Chow AW Brady FA Necrotizing fasciitis.
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tissue. Recent advances in anaerobic culture techniques have allowed
identification of anaerobic organisms, which are now considered
to have a vital role in the pathogenesis of this soft tissue infection.
Therapy requires both rapid institution of a high level of antibiotics
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275. Samant A Malik CP Chhabra SK Tewari A Bilateral
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276. Sinclair RJ Oral infection in connective tissue
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277. Abu-Dallo KI Manny Y Penchas S Eyal Z Clinical
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An exploratory laparotomy was performed, and the spleen, being
found enlarged, was removed. The other patient showed no peritoneal
signs. Laparotomy was done for pyrexia of unknown origin, and
the removal of a normal-sized spleen was elected on the suspicion
of lymphosarcoma. The spleen was abscessed, apparently because
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and selective angiography, not used in these two patients, is
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278. Dugois P Amblard P Gagnaire J Imbert R [Leg
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280. Perna E et al. "Actinomycotic Granuloma
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281. Black R., laboratory model for Trigeminal Neuralgia.
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282. Westrum LE., Canfield RC., Black R., Transganglionic
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283. Westrum LE., Canfield RC., Electron microscopy
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284. Gobel S., Bink J., degenerative changes in
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285. Sowell SB Dental care for patients with renal
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Prostate / Infertility
288. Bieniek KW Riedel HH [Diseases of the masticatory
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289. Linossier A Thumann A Bustos-Obregon E Sperm
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292. J Periodontol 1996 Oct;67(10 Suppl):1138-1142
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298. Daniel MA et al Alterations in Phagocyte Function
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316. Freyberger P [Electropotential differences
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324. Maresch O [Area of disturbances--reaction area
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