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Medizinische Universität Graz

DIE SUCHE NACH DEMDENTOGENEN

Rugani P.Spezialambulanz für Orale MedizinAbteilung für Orale Chirurgie und Kieferorthopädie, Jakse N.

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■ Herd/Focus of infec/on: - Umschriebenes Gebiet mit pathogenen Mikroorganismen - kann überall im Körper vorkommen- üblicherweise keine klinische Manifesta?on

■ Herderkrankung /Focal infec/on- lokalisierte oder generalisierte Infek?on durch die Verbreitung von Mikroorganismen oder deren toxischer Produkte aus einem Herd.

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Herderkrankungen durchEntzündungsherde im Mund?

Focal infection: new age orancient history?THOMAS J. PALLASCH & MICHAEL J. WAHL

A focus of infection is a confined area that: (1) contains

pathogenic microorganisms, (2) can occur anywhere in

the body and (3) usually causes no clinical manifesta-

tions (1). A focal infection is a localized or generalized

infection caused by the dissemination of microorgan-

isms or toxic products from a focus of infection (1).

These concepts have led to the Focal Theory of

Infection (or Theory of Focal Infection) that postulates

a myriad of diseases caused by microorganisms

(bacteria, fungi, viruses) that arise endogenously from

a focus of infection. Some have expanded this to

include the environment via the concept of antigenic

(molecular) mimicry or even to the extent that all

diseases are caused by microbes (2, 3).Foci of infection have historically been postulated to

arise from the tonsils, adenoids, sinuses and oral cavity

with less common foci from the prostate, appendix, gall

bladder and kidney (4, 5). Oral foci have traditionally

been ascribed to pyorrhea alveolaris (periodontitis),

alveolar abscesses and cellulitis, pulpless teeth, apical

periodontitis, general oral sepsis and endodontically

treated teeth with viridans group streptococci (VGS)

being the principal metastatic microbial culprits (1, 4, 5).

Focal infections attributed to foci of infection have

included arthritis, neuritis, myalgias, nephritis, osteo-

myelitis, endocarditis, brain abscesses, prosthetic

joint infections, skin abscesses, pneumonia, asthma,

anemia, indigestion, gastritis, pancreatitis, colitis,

diabetes, emphysema, goiter, thyroiditis, Hodgkin’s

disease, fever of unknown origin, stupidity and

‘nervous diseases of all kinds’ (1, 6–8). Currently,

diseases postulated to be caused by microorganisms

include cancer (9), sarcoidosis, multiple sclerosis,

amyotrophic lateral sclerosis, autism, Guillain–Barre

syndrome, pediatric autoimmune neuropsychiatric

disorders associated with streptococcal infections

(PANDAS), Tourette’s syndrome, myasthenia

gravis, polycystic kidney disease, obesity, Alzheimer’s

disease, diabetes mellitus and, of particular interest to

dentistry, cardiovascular disease (4, 10). Many of these

are proposed to affect the host by antigenic mimicry:

microbial antigens similar to host antigens that induce

an immune response that damages host tissue (11).

The classic pathway of focal infection is by direct spread

via blood or lymphatic metastasis of the infecting

microorganism, its toxic products or tissue-damaging

immunologic reactions to the microorganism.

Several characteristics consistently appear through-

out the long history of focal infection: (1) theories of

disease espoused by authoritative (some might say

autocratic) individuals with little or no science to

support their theses (doctrine without data), (2)

consistent application of focal infection to diseases for

which medicine has no good concepts of etiology and/

or treatment, (3) consistent and pervasive extrapola-

tion beyond the data and (4) a common disregard for

the accepted methodology of science (i.e. controlled

studies). Often, the ‘disregard syndrome’ is apparent:

the unintentional failure to cite previous scientific

works, scorn for previous sound published data that is

not considered ‘cutting edge’, apparently intentional

disregard for already published data that does not

conform or even contradicts the position espoused by

the investigator or an unintentional lack of regard for

relevant literature due to ignorance of the field being

investigated (12). ‘Reverse Investigation’ is not un-

common: start with the conclusion and then gather

only the facts that support it. The tendency to

programmed conferences is common: only those who

are of the samemind are invited and commonly leads to

what Jane’s Defense Weekly terms ‘incestuous ampli-

fication’: a condition in warfare where one only listens

32

Endodontic Topics 2003, 4, 32–45Printed in Denmark. All rights reserved

Copyright r Blackwell MunksgaardENDODONTIC TOPICS 20031601-1538

Hippokrates (460-370 v. Chr.)• Gilt als Begründer der Medizin als Wissenschaft

à Medizin, die auf vernunftgemäßer Naturbeobachtung basiert

... Ausheilung einer ArthriEs nach ZahnextrakEon

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à Keimtheorieà Geburtsstunde der Bakteriologie und Mikrobiologie

A. v. Leeuwenhoek L. Pasteur R. Koch I. Semmelweis J. Lister

09.10.19

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Focal infection: new age orancient history?THOMAS J. PALLASCH & MICHAEL J. WAHL

A focus of infection is a confined area that: (1) contains

pathogenic microorganisms, (2) can occur anywhere in

the body and (3) usually causes no clinical manifesta-

tions (1). A focal infection is a localized or generalized

infection caused by the dissemination of microorgan-

isms or toxic products from a focus of infection (1).

These concepts have led to the Focal Theory of

Infection (or Theory of Focal Infection) that postulates

a myriad of diseases caused by microorganisms

(bacteria, fungi, viruses) that arise endogenously from

a focus of infection. Some have expanded this to

include the environment via the concept of antigenic

(molecular) mimicry or even to the extent that all

diseases are caused by microbes (2, 3).Foci of infection have historically been postulated to

arise from the tonsils, adenoids, sinuses and oral cavity

with less common foci from the prostate, appendix, gall

bladder and kidney (4, 5). Oral foci have traditionally

been ascribed to pyorrhea alveolaris (periodontitis),

alveolar abscesses and cellulitis, pulpless teeth, apical

periodontitis, general oral sepsis and endodontically

treated teeth with viridans group streptococci (VGS)

being the principal metastatic microbial culprits (1, 4, 5).

Focal infections attributed to foci of infection have

included arthritis, neuritis, myalgias, nephritis, osteo-

myelitis, endocarditis, brain abscesses, prosthetic

joint infections, skin abscesses, pneumonia, asthma,

anemia, indigestion, gastritis, pancreatitis, colitis,

diabetes, emphysema, goiter, thyroiditis, Hodgkin’s

disease, fever of unknown origin, stupidity and

‘nervous diseases of all kinds’ (1, 6–8). Currently,

diseases postulated to be caused by microorganisms

include cancer (9), sarcoidosis, multiple sclerosis,

amyotrophic lateral sclerosis, autism, Guillain–Barre

syndrome, pediatric autoimmune neuropsychiatric

disorders associated with streptococcal infections

(PANDAS), Tourette’s syndrome, myasthenia

gravis, polycystic kidney disease, obesity, Alzheimer’s

disease, diabetes mellitus and, of particular interest to

dentistry, cardiovascular disease (4, 10). Many of these

are proposed to affect the host by antigenic mimicry:

microbial antigens similar to host antigens that induce

an immune response that damages host tissue (11).

The classic pathway of focal infection is by direct spread

via blood or lymphatic metastasis of the infecting

microorganism, its toxic products or tissue-damaging

immunologic reactions to the microorganism.

Several characteristics consistently appear through-

out the long history of focal infection: (1) theories of

disease espoused by authoritative (some might say

autocratic) individuals with little or no science to

support their theses (doctrine without data), (2)

consistent application of focal infection to diseases for

which medicine has no good concepts of etiology and/

or treatment, (3) consistent and pervasive extrapola-

tion beyond the data and (4) a common disregard for

the accepted methodology of science (i.e. controlled

studies). Often, the ‘disregard syndrome’ is apparent:

the unintentional failure to cite previous scientific

works, scorn for previous sound published data that is

not considered ‘cutting edge’, apparently intentional

disregard for already published data that does not

conform or even contradicts the position espoused by

the investigator or an unintentional lack of regard for

relevant literature due to ignorance of the field being

investigated (12). ‘Reverse Investigation’ is not un-

common: start with the conclusion and then gather

only the facts that support it. The tendency to

programmed conferences is common: only those who

are of the samemind are invited and commonly leads to

what Jane’s Defense Weekly terms ‘incestuous ampli-

fication’: a condition in warfare where one only listens

32

Endodontic Topics 2003, 4, 32–45Printed in Denmark. All rights reserved

Copyright r Blackwell MunksgaardENDODONTIC TOPICS 20031601-1538

Um 1890 WD Miller:

Begriff “focal infecAon“ ...

Die

Mikroorganismen der Mundhöhle.

Die örtlichen und allgemeinen Erkrankungen,

welche durch dieselben hervorgerufen werden.

Von

W. D. Müler,Dr. med. et phil.,

Professor am zalinärztlichen Institute der Universität Berlin.

Mit 134 Abbildungen im Texte und 18 Photogramnaen.

Zweite umgearteitete uud stark erweiterte Auflage.

Verlag

Leipzig.

von Georg1892.

T h i e m e.

© Biodiversity Heritage Library, http://www.biodiversitylibrary.org/; www.biologiezentrum.at

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Es ist mit Sicherheit nachgewiesen worden, dass nicht allein bei weitem die

grösste Mehrzahl derjenigen Erkrankungen der Zähne und der

angrenzenden Theile, für welche die Hülfe des Zahnarztes in Anspruch

genommen wird, ihre Entstehung den im Munde vorkommenden Bacterien

zu verdanken hat, sondern dass auch anderweitige örtliche und allgemeine

Erkrankungen von verschiedenster Natur und höchster Bedeutung auf

dieselbe Ursache zurückzuführen sind.

09.10.19

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Focal infection: new age orancient history?THOMAS J. PALLASCH & MICHAEL J. WAHL

A focus of infection is a confined area that: (1) contains

pathogenic microorganisms, (2) can occur anywhere in

the body and (3) usually causes no clinical manifesta-

tions (1). A focal infection is a localized or generalized

infection caused by the dissemination of microorgan-

isms or toxic products from a focus of infection (1).

These concepts have led to the Focal Theory of

Infection (or Theory of Focal Infection) that postulates

a myriad of diseases caused by microorganisms

(bacteria, fungi, viruses) that arise endogenously from

a focus of infection. Some have expanded this to

include the environment via the concept of antigenic

(molecular) mimicry or even to the extent that all

diseases are caused by microbes (2, 3).

Foci of infection have historically been postulated to

arise from the tonsils, adenoids, sinuses and oral cavity

with less common foci from the prostate, appendix, gall

bladder and kidney (4, 5). Oral foci have traditionally

been ascribed to pyorrhea alveolaris (periodontitis),

alveolar abscesses and cellulitis, pulpless teeth, apical

periodontitis, general oral sepsis and endodontically

treated teeth with viridans group streptococci (VGS)

being the principal metastatic microbial culprits (1, 4, 5).

Focal infections attributed to foci of infection have

included arthritis, neuritis, myalgias, nephritis, osteo-

myelitis, endocarditis, brain abscesses, prosthetic

joint infections, skin abscesses, pneumonia, asthma,

anemia, indigestion, gastritis, pancreatitis, colitis,

diabetes, emphysema, goiter, thyroiditis, Hodgkin’s

disease, fever of unknown origin, stupidity and

‘nervous diseases of all kinds’ (1, 6–8). Currently,

diseases postulated to be caused by microorganisms

include cancer (9), sarcoidosis, multiple sclerosis,

amyotrophic lateral sclerosis, autism, Guillain–Barre

syndrome, pediatric autoimmune neuropsychiatric

disorders associated with streptococcal infections

(PANDAS), Tourette’s syndrome, myasthenia

gravis, polycystic kidney disease, obesity, Alzheimer’s

disease, diabetes mellitus and, of particular interest to

dentistry, cardiovascular disease (4, 10). Many of these

are proposed to affect the host by antigenic mimicry:

microbial antigens similar to host antigens that induce

an immune response that damages host tissue (11).

The classic pathway of focal infection is by direct spread

via blood or lymphatic metastasis of the infecting

microorganism, its toxic products or tissue-damaging

immunologic reactions to the microorganism.

Several characteristics consistently appear through-

out the long history of focal infection: (1) theories of

disease espoused by authoritative (some might say

autocratic) individuals with little or no science to

support their theses (doctrine without data), (2)

consistent application of focal infection to diseases for

which medicine has no good concepts of etiology and/

or treatment, (3) consistent and pervasive extrapola-

tion beyond the data and (4) a common disregard for

the accepted methodology of science (i.e. controlled

studies). Often, the ‘disregard syndrome’ is apparent:

the unintentional failure to cite previous scientific

works, scorn for previous sound published data that is

not considered ‘cutting edge’, apparently intentional

disregard for already published data that does not

conform or even contradicts the position espoused by

the investigator or an unintentional lack of regard for

relevant literature due to ignorance of the field being

investigated (12). ‘Reverse Investigation’ is not un-

common: start with the conclusion and then gather

only the facts that support it. The tendency to

programmed conferences is common: only those who

are of the samemind are invited and commonly leads to

what Jane’s Defense Weekly terms ‘incestuous ampli-

fication’: a condition in warfare where one only listens

32

Endodontic Topics 2003, 4, 32–45Printed in Denmark. All rights reserved

Copyright r Blackwell Munksgaard

ENDODONTIC TOPICS 20031601-1538

• 1900 William Hunter:

„Sepsis als Ursache von Erkrankungen“ ...

...“ Gold fillings, crowns and bridges, fixed dentures, builton an about diseased tooth roots form a veritable mausoleum over a mass of sepsis to which there is noparallel in the whole realm of medicine and surgery.

à 100 percentersà ExtrakHon aller Wurzelkanal - behandelten Zähne

à ExtrakHon aller nicht durchbluteten oder verdächHgen Zähne

à ExtrakHon aller Zähne als Behandlung bzw. PrävenHon

(„therapeuHc edentulaHon“ oder „clean sweap“)

à Wurzelkanalbehandlung in den USA nicht mehr gelehrt

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■ 1930er und 1940er ...Gegens:mmen zur Fokustheorie

...Grossman: Kri:k am Studiendesign

...Edmund Kells: wahlloses Extrahieren ist ‘das Verbrechen des Zeitalters’

...Cecil and Angevine (1935): no benefit of tonsillectomie or dental extrac:ons in 200 cases

... Vaizey and Clark- Kennedy (1939): medizinisch zahnlose Pa:enten leiden unter Arthri:s und Dyspepsie – Extrak:onen führen zu Verdauungsstörungen und heilen sie nicht

... Reimann und Havens (1940): kein Beweis für Fokustheorie

A focusof infectio

n is

„anything readily

accessible to surgery“

.

Cecil andAngevin

e

... Unzulässiges Studiendesign

... Kein Vorteil durch Wahlloses Extrahieren und Tonsillektomieren

... Verdauungsstörungen durch Extrak:onen

... Keine s:chhal:gen Beweise für die Fokustheorie

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Biologic den6stry

Quelle: h;p://www.swiss-biohealth.com, 08.03.2018

Mundflora – das orale Mikrobiom

• Gesamtheit der Mikroorganismen, die die Mundhöhle besiedeln

• Kolonisierung beginnt sofort nach der Geburt

• Plaque: 1011 Keime / Gramm

• Speichel 109 Keime / Gramm

• bis zu 770 Keimarten

Meyer F., Enax J. Die Mundhöhle als ÖkosystemBiol. Unserer Zeit 1/2018 (48) Escapa et al. New insights into human nostril microbiome from theexpanded human oral microbiome database.(eHOMD)

Zahn

DIE POLYMIKROBIELLE PLAQUE ZWISCHEN ZAHNOBERFLÄCHE UND ZAHNFLEISCH

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Zahn

DIE POLYMIKROBIELLE PLAQUE ZWISCHEN ZAHNOBERFLÄCHE UND ZAHNFLEISCH

J Periodont Res. 2019;54:405–412. wileyonlinelibrary.com/journal/jre | 405

Received:11June2018  |  Revised:18December2018  |  Accepted:13January2019DOI:10.1111/jre.12642

O R I G I N A L A R T I C L E

Qualitative and quantitative differences in the subgingival microbiome of the restored and unrestored teeth

Steven W. H. Rademacher1 | Egija Zaura2 | Cornelis J. Kleverlaan3 | Mark J. Buijs2 |  Wim Crielaard2 | Bruno G. Loos1 | Marja L. Laine1

1DepartmentofPeriodontology,AcademicCentreforDentistryAmsterdam(ACTA),UniversityofAmsterdamandVUUniversity,Amsterdam,TheNetherlands2DepartmentofPreventiveDentistry,AcademicCentreforDentistryAmsterdam(ACTA),UniversityofAmsterdamandVUUniversity,Amsterdam,TheNetherlands3DepartmentofDentalMaterials,AcademicCentreforDentistryAmsterdam(ACTA),UniversityofAmsterdamandVUUniversity,Amsterdam,TheNetherlands

CorrespondenceMarjaL.Laine,DepartmentofPeriodontology,AcademicCentreforDentistryAmsterdam(ACTA),UniversityofAmsterdamandVUUniversity,Amsterdam,TheNetherlands.Email:M.Laine@acta.nl

Funding informationACTAAmsterdamandtheUniversityofAmsterdamforthefocalpoint“Oralinfectionandinflammation”,Grant/AwardNumber:2010CU1746

Background and Objective: Metal-baseddentalrestorationswithasubgingivaloutlinemayenhanceplaqueaccumulationandbacterialcolonization.Thisstudyaimedtoinvestigatewhethermetal-basedrestorationsinfluencethecompositionofsubgingivalmicrobiome.Material and Methods: Persubjectonesitewithametal-basedrestorationandonecontra-lateralsitewithoutarestorationwereselectedonbasisofradiographicboneloss≤2mm, restorationoutlineat sulcus level/subgingivally,pocketdepth≤4mm,andnorootcanaltreatments.Subgingivalsampleswerecollectedwithsterilepaper-points,andmicrobialprofileswereobtainedby16SrRNAgeneampliconsequencing.RestorationsweresampledwithanArkansas-stoneandthemetalcompositionwasdeterminedusingenergy-dispersiveX-rayspectroscopy.Results: Atotalof22sitesfrom11subjectswereincluded.Nosignificantdifferencesfortheclinicalparameterswerefoundbetweentherestoredandunrestoredsites.Theaverageageof the restorationswas14.9±7.1years.Firmicuteswas themostprevalentphylumattherestoredsites(32%vs20%ofthereadsoftheunrestoredsites,P=0.016),andActinobacteriaattheunrestoredsites(33%vs18%ofthereadsof the restored sites,P=0.01).Overall, sequences clustered into 573operationaltaxonomic units (OTUs). Species richness of the restored sites was significantlyhigher than species richnessof theunrestored sites (117±32 and96±20OTUs,respectively,P=0.013).Noassociationsbetweenthemetalcompositionandbacte-rialprofileswerefound.Conclusion: Thisstudyshowsthatmetal-basedrestorationsmayenhancecoloniza-tion ofFirmicutes and the neighboring pocketmay harbormore diversemicrobialcommunities.

K E Y WO RD S

16SrRNAsequencing,bacteria,metal-based,restoration

ThisisanopenaccessarticleunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsuse,distributionandreproductioninanymedium,providedtheoriginalworkisproperlycited.©2019TheAuthors.Journal of Periodontal ResearchPublishedbyJohnWiley&SonsLtd

https://doi.org/10.1177/0022034519877150

Journal of Dental Research 1 –8© International & American Associations for Dental Research 2019Article reuse guidelines: sagepub.com/journals-permissionsDOI: 10.1177/0022034519877150journals.sagepub.com/home/jdr

Research Reports: Biological

IntroductionThe association between dysbiosis of the oral microbiome and periodontitis is now well established (Mira et al. 2017). Although there are significant individual-to-individual varia-tions in the microbial composition of subgingival biofilms in health (Hall et al. 2017), the development of disease coincides with a characteristic population shift. Consistently, the change involves not only an increase in the overall microbial biomass but also the emergence of bacterial species that are only pres-ent in low abundance in health and a proportionate decrease in the abundance of others (Marsh 1994; Socransky et al. 1998; Diaz et al. 2016). Although culture-based studies originally indicated that the emergent bacterial populations in the disease-associated communities may represent only a relatively small number of different taxa (Socransky et al. 1998; Holt and Ebersole 2005), the application of more advanced technologies has demonstrated that a wider range of organisms should be considered (Griffen et al. 2012; Abusleme et al. 2013). This, in turn, has led to the concept of a community-wide perturbation in the composition of the microbiome associated with peri-odontal disease (Hajishengallis and Lamont 2012; Curtis 2014). However, it remains controversial to what extent the

observed shift in the microbial population structure in peri-odontitis is the primary cause of pathology or simply a conse-quence of the altered environmental conditions induced in an inflammatory disease.

In previous studies, using a mouse model of periodontal dis-ease, we demonstrated that the introduction of Porphyromonas gingivalis into the oral microbiome of specific pathogen-free (SPF) mice led to significant alterations in both the quantity

877150 JDRXXX10.1177/0022034519877150Journal of Dental ResearchHorizontal and Vertical Transfer of Oral Microbial Dysbiosis and Periodontal Diseaseresearch-article2019

1Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK2Department of Biomedical Sciences, College of Dentistry, King Faisal University, Al-Ahsa, Saudi Arabia3Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, Tower Wing, Guy’s Hospital, London, UK4Department of Microbiology, Forsyth Institute, Cambridge, MA, USA

A supplemental appendix to this article is available online.

Corresponding Author:M.A. Curtis, Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, Tower Wing, Guy’s Hospital, Floor 18 Faculty Office, London SE1 9RT, UK. Email: mike.curtis@kcl.ac.uk

Horizontal and Vertical Transfer of Oral Microbial Dysbiosis and Periodontal Disease

M.A. Payne1, A. Hashim2, A. Alsam1, S. Joseph3, J. Aduse-Opoku3, W. Wade3,4, and M.A. Curtis3

AbstractOne of the hallmark features of destructive periodontal disease, well documented over the last 50 y, is a change to the quantitative and qualitative composition of the associated microbiology. These alterations are now generally viewed as transformational shifts of the microbial populations associated with health leading to the emergence of bacterial species, which are only present in low abundance in health and a proportionate decrease in the abundance of others. The role of this dysbiosis of the health associated microbiota in the development of disease remains controversial: is this altered microbiology the driving agent of disease or merely a consequence of the altered environmental conditions that invariably accompany destructive disease? In this work, we aimed to address this controversy through controlled transmission experiments in the mouse in which a dysbiotic oral microbiome was transferred either horizontally or vertically into healthy recipient mice. The results of these murine studies demonstrate conclusively that natural transfer of the dysbiotic oral microbiome from a periodontally diseased individual into a healthy individual will lead to establishment of the dysbiotic community in the recipient and concomitant transmission of the disease phenotype. The inherent resilience of the dysbiotic microbial community structure in diseased animals was further demonstrated by analysis of the effects of antibiotic therapy on periodontally diseased mice. Although antibiotic treatment led to a reversal of dysbiosis of the oral microbiome, in terms of both microbial load and community structure, dysbiosis of the microbiome was reestablished following cessation of therapy. Collectively, these data suggest that an oral dysbiotic microbial community structure is stable to transfer and can act in a similar manner to a conventional transmissible infectious disease agent with concomitant effects on pathology. These findings have implications to our understanding of the role of microbial dysbiosis in the development and progression of human periodontal disease.

Keywords: periodontitis, oral microbiome, bone loss, Porphyromonas gingivalis, keystone, microbiology

DYSBIOSE

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(modifiziert nach Wilson W.; 2007)

... incidence of bacteremia from tooth brushing (32%) was high enough to strongly suggestthat bacteremia from various acFviFes of daily living (chewing food as well) may occurhundreds of Fmes more oGen than bacteremia from dental office procedures ...

Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani- Mougeot FK. Bacteremia associated withtoothbrushing and dental extracFon. Circula(on. 2008;117:3118–3125.

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Blutkulturen■ MAYO Clinic:

■ 281.747 konsekuBve Blutkulturen

■ 20.456 posiBv für Mikroorganismen

-2,8% VGS-4,4% insg. obligate AnaerobierObligate orale Aerobier:

0,1% Prevotella0,2% Fusobaterium nucleatum0,2% Peptostreptokokkus0,1% Veillonella0,4% Abiotrophia

Cockerill FR III et al. Analysis of 281,797 consecuBve blood cultures performed over an eight-year period: trends in microorganisms isolated and the value of anaerobic cultureof blood. Clin Infect Dis 1997: 24: 403–418.

Orale Mikroorganismen kommen in Blutkulturen in geringem %satz vor

Me

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Associa'on between dental health andacute myocardial infarc'on.

Brit Med J. 1989;298:779-781.

à Pa>enten mit Herzinfarkten leiden häufiger an

oralen Krankheiten wie Gingivi>s, Parodon>>s oder

endodon>schen Problemen.

DeStefano F, Anda RF, Kahn HS, et al.

Dental disease and risk of coronary heart disease and mortality. BMJ. 1993;306:688-691.

à Pa>enten mit Parodon>>s haben ein 24% erhöhtes KHK-Risiko

MaTla KJ, Nieminen MS, Valtonen VV et al.

Li et al. CLINICAL MICROBIOLOGY REVIEWS 2000

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Herderkrankungen ...?

■ Gehirnabszess

■ Infek;on von Gelenksendoprothesen

■ Bakterielle Endokardi;s

Olsen & van Winkelhoff Period.2000; 2014

Pallasch und Wahl 2003

... Und der Zusammenhang mit zahnärztlichen Eingriffen

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Horstkotte D et al. 2004 Pallasch und Wahl 2003

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Leitlinien zur Endokarditisprophylaxe 2007: (DGK, AHA, ESC)

1) Angeborene Herzfehler o Zyanotische Herzfehler, die nicht operiert wurden, oder palliativ mittels systemisch-pulmonalem Shunt versorgt wurden o Operierte Herzfehler mit Implantation von Conduits (mit/ohne Klappe) oder zurückgebliebenen Defekten o Alle operativ oder interventionell behandelten Herzfehler in den ersten 6 Monaten 2) überstandene Endokarditis3) Klappenersatz o Rekonstruierte Klappen unter Verwendung von alloprothetischem Material innerhalb der ersten 6 Monate nach der Operation 4) o Herztransplantation, die eine kardiale Valvulopathie entwickelt

Europ. Society of Cardiology 2009 und Update DKG 2009: AB-Prophylaxe bei herztransplantierten Patienten, die eine Valvulopathie entwickeln, nicht nötig

Baumgartner H. 2011, Naber C. 2007

Risikopa6enten

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01.12.1998

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01.12.1998

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01.12.1998

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Befunde mit möglicher Herdwirkung

... Höhere Bakteriämiewahrscheinlichkeit

P. Kessler, Herderkrankungen aus Mund-, Kiefer- und Gesichtschirurgischer Sicht , Springer 2006

■ PulpiFs, Pulpanekrose■ Apikale ParodonFFs, Zysten■ DenFFo difficilis, PerikoroniFs■ Bakt. WeichgewebsinfiltraFon... Phlegmone / Abszess

■ ParodonFFs■ PeriimplanFFs■ Potent. mikrobiell besiedelte Fremdkörper

© Rugani

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■ Klinischer Befund

■ Röntgen – Summa=onsbildverfahren

■ Schni@bilddiagnos=k

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71

435

850

11451344

16021795

2256

2009 2010 2011 2012 2013 2014 2015 2016

2009 2010 2011 2012 2013 2014 2015 2016 totalDVT 71 435 631 279 274 270 281 385 2557DVT – Med. Ind. 219 866 1070 1332 1514 1871 6872

71 435 850 1145 1344 1602 1795 2256 9498

Univ. Klinik für Zahnmedizin und Mundgesundheit

à Häufiger Nebenbefund

st.p. Knochenaufbau...

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Estrela et al J Endod 2008

…apikale ParodontitisEndodontie

von 109 Läsionen, die im DVT erkannt wurden, wurden 34% im KB nicht entdeckt. (P<0.001)

Comparison of Periapical Radiography and Limited Cone-Beam Tomography in Posterior Maxillary Teeth Referred for Apical Surgery

Low et al., J Endod 2008

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Therapieschema Herdsanierung Oralchirurgie GrazGeringes Risiko

èvor Stent/Herzklappen-OPèvor Gelenksendoprothesen-OP èbei dermatologischen Erkrankungen unklarer Geneseèbei febrilen Zuständen unklarer Geneseèvor Bisphosphonat/Denosumab-Therapie (Osteoporose-Indikation)Mittleres Risikoèvor Organtransplantation (Niere, Herz, Leber, Lunge, Pankreas)èvor Chemotherapieèvor Bisphosphonat/Denosumab-Therapie (onkologische Indikation)

Hohes Risikoèvor Kopf-Hals-Bestrahlungèvor Knochenmarkstransplantationèvor Ganzkörperbestrahlung

Konventionell

Semiradikal

RadikalRugani, P. HERDSANIERUNG BEI RISIKOPATIENTEN GRUNDLAGEN ZU DIAGNOSTIK UND THERAPIE. ÖGZMK e- Newsletter 2018(2).

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Therapieschema Herdsanierung Oralchirurgie GrazGeringes Risiko

èvor Stent/Herzklappen-OPèvor Gelenksendoprothesen-OP èbei dermatologischen Erkrankungen unklarer Geneseèbei febrilen Zuständen unklarer Geneseèvor Bisphosphonat/Denosumab-Therapie (Osteoporose-Indikation)Mittleres Risikoèvor Organtransplantation (Niere, Herz, Leber, Lunge, Pankreas)èvor Chemotherapieèvor Bisphosphonat/Denosumab-Therapie (onkologische Indikation)

Hohes Risikoèvor Kopf-Hals-Bestrahlungèvor Knochenmarkstransplantationèvor Ganzkörperbestrahlung

Konventionell

Semiradikal

RadikalRugani, P. HERDSANIERUNG BEI RISIKOPATIENTEN GRUNDLAGEN ZU DIAGNOSTIK UND THERAPIE. ÖGZMK e- Newsletter 2018(2).

Kriterien: • Risiko für Herderkrankung

• Risikofaktoren für die zahnärztliche Therapie zu diesem bzw. zu

einem späteren Zeitpunkt

• Management von potentiell auftretenden Komplikationen

• Zeitfenster / Dringlichkeit

Herdsanierung – Gruppen - KriterienNiedriges Risiko

§ Meist ausreichend Zeit zur adäquaten zahnärztlichen Therapie

§ Zahnärztliche Maßnahmen können auch nach der geplanten OP unter Befolgung spezieller Richtlinien durchgeführt werden (Gerinnungskontrolle, AB-Abdeckung)

Mittleres Risiko

§ Möglichst konservatives und zahnerhaltendes Vorgehen bei strengerer Indikationsstellung

§ u.U. bereits bestehende Risikosituation à adaptiertes Vorgehen (Gerinnungseinstellung, AB-Abdeckung 24h prä- und 7 Tage postoperativ, primär plast. Wundverschluss )

§ Die Sanierung sollte mind. 2 Wochen vor der geplanten OP/Therapie abgeschlossen sein

Hohes Risiko

§ Radikales Vorgehen mit strenger Indikationsstellung

§ Häufig wenig Zeit

§ u.U. bereits bestehende Risikosituationà adaptiertes Vorgehen (Gerinnungseinstellung, AB-Abdeckung 24h prä- und 7 Tage postoperativ, primär plast. Wundverschluss )

§ Die Sanierung sollte 2 Wochen vor der geplanten Therapie abgeschlossen sein

Rugani, P. HERDSANIERUNG BEI RISIKOPATIENTEN GRUNDLAGEN ZU DIAGNOSTIK UND THERAPIE. ÖGZMK e- Newsletter 2018(2).

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Revision der WKB/WSR

Revision der WKB/WSR

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Extraktion

Evtl. zahnerhaltende Parotherapie

Weiblich 60 JahreMyelodysplastisches SyndromKnochenmarkstransplantation geplant

à Bestehende Risikosituationà Hohes Risiko für lokale Komplikationen

sowie für Herdgeschehenà Enges Zeitfensterà Eher radikales Vorgehen

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„zahnloser Patient“

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Häufige Probleme bei der Herdsanierung

■ Häufig multimorbide Patienten

■ Enges Zeitfenster

■ evtl. großer Sanierungsbedarf

■ u.U. nach Zahnextraktionen begrenzte Möglichkeiten zur prothetischen Rehabilitation nach erfolgter

Therapie der Grunderkrankung (antiresorptive Therapie, Strahlentherapie)

■ Prognose quoad vitam? – Abwägung von Nutzen-Risiko in Hinsicht auf die Lebensqualität des

Patienten

■ wenig wissenschaftliche Evidenz

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Medizinische Universität Graz

DIE SUCHE NACH DEMDENTOGENEN HERD

Rugani P.Spezialambulanz für Orale MedizinAbteilung für Orale Chirurgie und Kieferorthopädie, Jakse N.