oral health general health summarized

8/3/2019 Oral Health General Health Summarized

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ORAL HEALTH GENERAL HEALTH

JORGE FDO. QUISOBONI E.

Odontlogo P. U. JaverianaPeriodoncista U. del Valle


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Iy Mry


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Oral Health

World HealthOrganizationestablished in 1948

health is a completestate of physical,mental, and socialwell-being, and notjust the absence ofinfirmity.


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The Meaning of Oral Health

What amounts to a asilent epidemic of

dental and oral diseasesis affecting some

population groupsaburden of disease thatrestricts activities inschool, work, and home,and often significantlydiminishes the quality oflife.

National Institute of Dental and Craniofacial Research Chapter 1: The Meaning of Oral Health


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Dental Practice

A dentist must garantee to the public: Him and hisstaff know howto

Prevent the risk of physical, psychological, judicialliability and sanitary damage within the limits of

the practice Offer certified programs of biosecurity for all

procedures under a scheme of good clinicalpractice

Keep good record of medical history and itsconfidenciality Provide patients with a follow up recall and

maintenance program


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if we think of the mouth as a mirror weshould recognize that as dentists in it we couldfind illimited richness ofinformation that couldbe collected from a thorough examination oforal tissues


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Vigorexia or Adonis Complex. The Secret Crisis of Male Body Obssesion


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Periodontal Diseases Etiology

Dental Plaque : Unique Ecosystem : MicrobialBiofilm

once viewed to be the lowest form of existence, occupies a much higher rank in the

scheme of life


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Rodney M. DonlanWilliam Costerton Biofilms: Survival Mechanisms of Clinically Relevant MicroorganismsCLINICAL MICROBIOLOGY REVIEWS, Apr.2002, p. 167193

Size of a micro world


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Location

Thin layerover thesubstrate

PolymereSalivaryand

bacterialmatrix

ngela Toshie ARAKI Er:YAG Laser Irradiation of the Microbiological Apical Biofilm. Braz Dent J 17(4) 2006


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Donlan and Costerton

defintion:

a microbially derived sessile communitycharacterized by cells that are irreversibly

attached to a substratum or interface or to eachother, are embedded in a matrix of extracellularpolymeric substances that they have produced,and exhibit an altered phenotype with respect togrowth rate and gene transcription.

2002

Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002;15(2):167-93.


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Mechanisms of pathogenicity

subgingival species colonization factors

(1) colonize the subgingival area(2) produce damaging factors.

must be able to(1) attach to one or more of the available

surfaces(2) multiply(3) compete successfully against other

species desiring that habitat(4) defend itself from host defense

mechanisms.

Lindhe J. Clinical Periodontology and Implant Dentistry Fifth Edition , pag 245


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A pathogen necessary but not sufficient for a diseaseto occur!

15% Neisseria meningitidis(Caugant et al. 1988), only0.51.1 % occur per 100 000

Mycobacterium tuberculosis5% (Sudre et al. 1992), only2.6 % new cases oftuberculosis per 100 000 ofUS-born / year

1/3 adults Haemophilusinfluenzae (Kilian &

Frederiksen 1981) tiny fractionexhibit disease.

Continuous colonization byperiodontal pathogenssupra or sub gingivaly :show NO evidence ofongoing or previous

periodontal destruction.

Summary of Notifiable Diseases United States 2004, 2006.

Lindhe J. Clinical Periodontology and Implant Dentistry Fifth Edition , pag 245


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Mouth as a microbial habitat

teeth provide hard, non-shedding surfaces for thedevelopment of extensivebacterial deposits.

The accumulation andmetabolism of bacteria onhard oral surfaces isconsidered the primary

cause of dental caries,gingivitis, periodontitis,peri-implant infectionsand stomatitis


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Mouth as a microbial habitat

Philip Marsh Oral Microbiology fourth edition Elsvier limited 2002 chapter 2


17/92Philip Marsh Oral Microbiology fourth edition Elsvier limited 2002 chapter 2

pH average 6.75 7.25


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Only 20 to 25 percent of the oral environment is tooth surface, and mucosal surfaces areimportant contributors to periodontal microbial biofilms. Kerr 1991


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Schillinburg


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Which microorganims?

John G. Thomas Managing the complexity of a dynamic biofilm JADA, Vol. 137 http://jada.ada.org November 2006 pgs 10s 15s

Gram-positive bacteria generally communicate via small diffusible peptides, while manygramnegative bacteria secrete acyl homoserine lactones to communicate


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stages of dental plaque biofilm growth

not inert / metabolically reduced Exponential growth Maturity (stationary) Dispersal (death)

Counts in subgingival sites range from about in healthy, shallow sulci to in deep periodontalpockets. Numbers in supragingival plaque can exceed on a single tooth surface

John G. Managing the complexity of a dynamic biofilm JADA, Vol. 137 http: Jada.ada.org November 2006


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Biofilms characteristics

Adherence

Heterogenicity

Diverse microenvironmentes pH, O2 tension,

carbone, nitrogen, ions concentration. Primitive circulatory system

Host immune system resistant

Antimicrobial agents Quorum sensing

Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002;15(2):167-93.


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Biofilm architecture

and the spatial distribution ofpredominant species /subgingival plaque

Actinomyces sp. Tannerella forsythia

Fusobacterium nucleatum

Spirochaetes Synergistetes

Lactobacillus sp.Vincent Zijnge Oral Biofilm Architecture on Natural Teeth PLoS ONE | www.plosone.org February 2010 | Volume 5 | Issue 2 | e9321
http://www.plosone.org/http://www.plosone.org/


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Biofilms as model systems

for bacterial adhesion

biofilm development

Resistance to antibiotics, due to theirwidespread presence and accessibility

Bos R, Van Der Mei HC, Busscher HJ (1999) Physico-Chemistry Of Initial Microbial Adhesive InteractionsIts Mechanisms And Methods For Study. FEMS Microbiol Rev 23: 179230.

Busscher HJ, Van Der Mei HC (1997) Physico-Chemical Interactions In Initial Microbial Adhesion And Relevance For BiofilmFormation. Adv Dent Res 11: 2432.

Zaura-Arite E, Van Marle J, Ten Cate JM (2001) Conofocal Microscopy Study Of Undisturbed And Chlorhexidine-Treated Dental Biofilm. J Dent Res 80: 14361440.

Toll-like receptors, along with antibodies, are important early host defenses. Oncebiofilms form, antibodies no longer attach to the bacteria within the microcolonies


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Alfred B. Cunningham, John E. Lennox, and Rockford J. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss , Eds. 2001-2008


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In vivo data

showed convincingly the dominance ofActinomyces sp., Tannerella forsythia,Fusobacterium nucleatum, Spirochaetes, and

Synergistetes in subgingival plaque Been on close relation to epithelial cells

Vincent Zijnge Oral Biofilm Architecture on Natural Teeth PLoS ONE | www.plosone.org February 2010 | Volume 5 | Issue 2 | e9321


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Virulence factors

How do these organisms cause the disease? Virulence: the relative ability of an organism to

cause disease or to interfere with a metabolic or

physiological function of its host Latin: full of poison

Ability to express pathogenicity

Depends upon many extrinsic factors of theenvironment

A. L. Dumitrescu, Etiology and Pathogenesis of Periodontal Disease, DOI:10.1007/978-3-642-03010_1, Springer-verlag Berlin Heilderberg 2010


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Virulent microbe

Chatacteristic endproducts of bact metab

Chemical composition of bact components

Ability of the bacterium or its parts tooverwhelm host defense mechanisms

Invasiveness

Ability to killHolt and Eversole 2005


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Functions of virulence factors

Ability to inducemicrobe hostinteractions(attachment)

Ability to invade the

host Ability to grow in

the confines of ahost cell

Ability to evade /interfere with hostdefenses

healing is extremely complex, involving hundreds ofgrowth factors, dozens ofintegrins,scores ofenzymes, and over ten different cell types.

Copyright Alfred B. Cunningham, John E. Lennox, and Rockford J. Ross, Eds. 2001-2008


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Enhance survival chances

Factors that promote colonization and

persistance: adhesins, invasins, bacteriocins,antibiotic resistance.

Factors that interfere hosts defenses:

leucotoxin, chemotactic inhibitors,immunosupressive proteins, Fc binding

proteins



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Enhance survival chances

Factors that destroy host tissues: cytotoxins,collagenases, bone resorption agents,stimulators of inflammatory mediators

Factors that inhibit host repair tissues:

inhibitors of fibroblasts proliferation,inhibitors of bone formation



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Which one is the bandit?

Fusobacterium nucleatum is an anaerobicGram-negative non-spore forming bacterium,and the type species for the genusFuosbacterium.

Bartold PM, Gully NJ, Zilm PS and Rogers AH. 1991. Fusobacterium nucleatum chemostat-culture supernatants that are potent inhibitors of human gingival fibroblast proliferation. J. Periodont. Res., 26, 314-322.

The cells ofF. nucleatum are spindle-shaped orfusiform rods of variable length. Studies in

laboratories, have shown that the organismobtains energy via the fermentation ofcarbohydrates and specific amino acids,producing butyrate as a major metabolic end-product.


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Which one is the bandit?

F. Nucleatum ability to adhere to a wide rangeof other plaque microorganisms it is proposedto play a crucial role in plaque development.F. nucleatum is frequently associated withperiodontal diseases, as well as invasivehuman infections of the head and neck, chest,lung, liver and abdomen.

Bartold PM, Gully NJ, Zilm PS and Rogers AH. 1991. Fusobacterium nucleatum chemostat-culture supernatants that are potent inhibitors of human gingival fibroblast proliferation. J. Periodont. Res., 26, 314-322.

Properties ofF. nucleatum that may be relatedto virulence include it's adherence to andinvasion of host tissue cells, and modulation ofthe host immune response.


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Periodontal pathogenic bacteria

Have been detected in patients with: various cardiovascular diseases, including

atherosclerosis chiu et al 99, zaremba et al 2007, Nakano et al 2008,

Arteriosclerotic aneurysms Kurihara et al 2004, Nakano et al 2008,

Peripheral arterial disease Chen et al 2008

Coronary heart disease Pussinen et al 2003, Zaremba et al 2007

Heart valves of endocarditis Nakano et al 2008 Buergers disease Iwai et al 2005

KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. Periodontology 2000, Vol. 54, 2010,222234


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Epidemiological studies haveimplicated

P. gingivalis in the development of systemic diseases: Cardiovascular disease, diabetes mellitus, pre-term low

birth weight and rheumatoid arthritis

Li X, Kolltveit KM, Tronstad L, Olsen I. Systemic diseases caused by oral infection. Clin Microbiol Rev 2000: 13: 547

558.Meurman JH, Sanz M, Janket S. Oral health, atherosclerosis, and cardiovascular disease. Crit Rev Oral Biol Med

2004: 15: 403413.Moreillon P, Que YA. Infective endocarditis. Lancet 2004: 363: 139149.Nakano K, Inaba H, Nomura R, Nemoto H, Takeda M, Yoshioka H, Takahashi T, Taniguchi K, Amano A, Ooshima T.

Detection of cariogenic Streptococcus mutans in extirpated heart valve and atheromatous plaque specimens. JClin Microbiol 2006: 44: 33133317.

Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K. Relationship between periodontal infections and

systemic disease. Clin Microbiol Infect 2007: 13 (Suppl. 4): 3

10.Southerland JH, Taylor GW, Moss K, Beck JD, Offenbacher S. Commonality in chronic inflammatory diseases:

periodontitis, diabetes, and coronary artery disease. Periodontol 2000 2000: 40: 130143.Tonetti MS, DAiuto F, Nibali L, Donald A, Storry C, Parkar M, Suvan J, Hingorani AD, Vallance P, Deanfield J.

Treatment of periodontitis and endothelial function. N Engl J Med 2007: 356: 911920.Zaremba M, Gorska R, Suwalski P, Kowalski J. Evaluation of the incidence of periodontitis-associated bacteria in the

atherosclerotic plaque of coronary blood vessels. J Periodontol 2007: 78: 322327.



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Cardiovascular diseases, in particular, appear to bestrongly related to infection by periodontal pathologicalbacteria

Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996: 67: 11231137

Ebersole JL, Cappelli D, Mathys EC, Steffen MJ, Singer RE, Montgomery M, Mott GE, Novak MJ. Periodontitis in humans and non-humanprimates: oral-systemic linkage inducing acute phase proteins. Ann Periodontol 2002: 7: 102111.

Ismail A, Khosravi H, Olson H. The role of infection in atherosclerosis and coronary artery disease: a new therapeutic target. Heart Dis1999: 1: 233240.

Kuramitsu HK, Qi M, Kang IC, Chen W. Role for periodontal bacteria in cardiovascular diseases. Ann Periodontol 2001: 6: 4147.

Matsuura E, Kobayashi K, Lopez LR. Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle.Autoimmunity Rev 2008: 7: 214222.

Mustapha IZ, Debrey S, Oladubu M, Ugarte R. Markers of systemic bacterial exposure in periodontal disease and cardiovascular diseaserisk: a systematic review and metaanalysis. Mustapha IZ, Debrey S, Oladubu M, Ugarte R. Markers of systemic bacterial exposurein periodontal disease and cardiovascular disease risk: a systematic review and metaanalysis. J Periodontol 2007: 78: 22892302. J

Periodontol 2007: 78: 2289

2302.Noll G. Pathogenesis of atherosclerosis: a possible relation to infection. Atherosclerosis 1998: 140 (Suppl. 1): S3S9.

Offenbacher S, Madianos PN, Champagne CM, Southerland JH, Paquette DW, Williams RC, Slade G, Beck JD. Periodontitisatherosclerosis syndrome: an expanded model of pathogenesis. J Periodontal Res 1999: 34: 346352.

Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclesosis, cardiovascular disease, andstroke. A systematic review. Ann Periodontol 2003: 8: 3853.

KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. Periodontology 2000, Vol. 54, 2010,

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Epidemiological studies haveimplicated


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Lindhe J. Clinical Periodontology and Implant Dentistry Fifth Edition , 2009 pag 43


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Biofilms in Health and Medicine

How is the skin healing process affected inchronic wounds?

platelets to form a blood clot, leukocytes to

combat microbial invaders, and mesenchymalcells that develop into fibroblasts



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migratory phase begins

a scab is formed and epithelial cells migrateacross the wound under the scab. Granulation

tissue is formed as fibroblasts produceextracellular matrix and endothelial cells formblood vessels.



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proliferative phase

characterized by extensive growth of epithelialcells, fibroblast deposition of collagen fibers in

random patterns, and continued growth ofblood vessels.



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maturation phase

occurs where collagen fibers become moreorganized, blood vessels are restored to

normal, the scab is shed, and the epidermis isrestored to normal thickness



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Ab l d l i b i


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Absolute and relative barriers tohealing

low blood oxygen content

Infection

lack of perfusion sustained pressure

patient malnutrition

systemic disease such as diabetes treatments such as immunosuppressants


H h h li i di d


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How the healing process is disruptedin chronic wounds

Fibroblasts isolated from chronic woundsshow impairment of synthesis, migration andproliferation


H th h li i di t d


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Endothelial cells from chronic wounds aredeficient in production of enzymes andgrowth factors, and also are impaired in

migration, proliferation, and the formation ofnew capillaries


H th h li i di t d


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keratinocytes are impaired in their migrationand proliferation as well as their ability tosynthesize cytokines, provisional matrix and

basement membrane.


H th h li i di t d


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When matrix metalloproteases are evaluatedin chronic wounds, regardless of the etiology,and regardless of the age, gender, or any other

demographic factor of the patient, they allshow an identical biochemistry.

Up regulated up to 30-fold.


P f i fl t


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Presence of proinflammatorycytokines

The innate immune system is designed to bevigilant and reactive to foreign insults, especiallybacteria.

Toll-like receptors (TLR) 2 and 4 are very sensitiveto lipopolysaccharide (LPS) material produced byGram-negative bacteria as well as teichoic acid,produced by Gram-positive bacteria.

Interleukin 1, tumor necrosing factor alpha andgamma interferon



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Questionsregarding P. gingivalis mediatedmechanisms in vascular diseases

How can P. gingivalis, anobligate anaerobicbacterium, safely travel

through the bloodstreamfrom small vessels in theoral cavity to reach the

central arteries in whichatherosclerotic lesionsdevelop?


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How can P. gingivalisadhere to normalendothelial cells given the

extremely rapid bloodflow in the abdominal orthoracic aorta?


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1 cell thick, 5 10 m


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How can P.gingivalis invadenormal

endothelial cellsof large-sizedarteries?


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confirm whether direct arterial invasion by P. gingivalis is possible and sufficient to causevascular diseases

depth of 1.57 m


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An indirect mechanism of P. gingivalis-mediatedatheroma formation

Various pathological factors such as diabetes

mellitus, hypertension, hyperlipidemia andsmoking can cause endothelial cell dysfunction,resulting in vascular damage



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P.G. Fimbria-Dependent Activation


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P.G. Fimbria Dependent Activationof Inflammatory Genes in Human Aortic

Endothelial Cells

Little is knownregarding genedownregulation during

endothelial cellinfection by bacteria orthe impact of this on

the development ofatherosclerosis

Hsin-Hua Chou. Porphyromonas gingivalis Fimbria-Dependent Activation of Inflammatory Genes in Human Aortic Endothelial Cells. INFECTION AND IMMUNITY, Sept. 2005, Vol. 73, No. 9 p. 53675378


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Aspects of innate host response



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Pathogen associated molecular patterns PAMPs



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Main receptors and signaling pathways

Toll like receptors TLRs

CD14

Nucleotide binding oligomerization domainproteins Nod

G protein coupled receptors

Formyl methionyl peptide receptors

Protease activated receptors



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TLRs in periodontitis lesions

Inn Inm Rec / limited # germline encodedreceptors: pathogen recognition receptors

Conserved molecular patterns PAMPs and

produce inflammatory cytokines viaintracellular signaling

Dendritic cells subsets express sets TLRs

Distinct T-cell subsets

Azuma et al 2006


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Chromosomal localizationGenomic structureAmino acid sequences5 subfamilies


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TLRs signaling pathways


Complex forming

molecules:CD14MD-2MyD 88Mal Tollip

LipopolysaccharideLigand complexed to CD14Includes TLR-4 and MD2

Signal transuction includesRecruitment of MyD88 andIL-1 receptor assoc kinaseIt results in nuclear tanslocAnd gene activation of

specific inflammatorymediatorsIL-1 and TNF-


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Histopatogenesis of gingivitis and periodontitis Page and Schroeder 1982


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sociodemographySystemically ?potencialized


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early and useful sign in order to establish an accuratediagnosis. The main entities are:gingival lesions related to mucocutaneous diseases, gingivallesions related to hormonal levels,

gingival alterations produced by pharmacologicaltreatments,gingival lesions produced by viral infections,gingival alterations related to haematological disordersgingival alterations of genetic origin such as gingivalfibromatosis


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Initiation of inflammationEarly lesion: Evolves from initial lesion 1 week Infiltrate s,m,l lymphocytes (75 %) and

macrophages, plasma cells Accute inflammation persists:

vasculitis and neutrophils at JE Infiltrated area 5 15 % MCT 60 70 % affected collagen Resident fibroblasts pathologically

altered electron lucid nuclei, swollen

mytochondria, vacuolization of theendoplasmic reticulum, rupture of cellmembranes



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Hosts mechanisms

Epithelial cells regularshedding

Washing effect of saliva

and GCF Phagocytic action of

neutrofils JE sulcus

Maintain normal, nonirritating environment



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First cells to be challenged

Disturbance of equilibrium by appareance ofpathogenic bacteria in the P niche

Bacterial adhesion through fimbriae activates

Epithelial cells



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Tobacco impact

Smoking induces the release of an abundanceof reactive oxygen species into the blood withthe potential to cause injury to the endothelial

cells



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Injured endothelium

Dysfunction ordetachment of theendothelial cells lead to

direct exposure of thevascular smooth musclecell layer, facilitating

P. gingivalis invasion


h b bl


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Thromboangiitis obliterans

trigger for the onset ofBuergers disease, whichoccurs despite the absence of

elevated plasma cholesterollevelsMishima et al 96, Roncon-albuquerque et al 2002,

Ohata et al 2004


b


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Diabetes


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M.C. Fras Lpez Mtodos de diagnstico clnicoen periodoncia. PERIODONCIA Y OSTEOINTEGRACIN Volumen 15 Nmero 4Octubre-Diciembre 2005

There is low predictive valueof clinical assesments

DiagnosisTreatment PlanDet microbial incidence /

simple & economical methods


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Niklaus P. Lang / Maurizio S. Tonetti Periodontal Risk Assessment (PRA) for Patients in Supportive Periodontal Therapy (SPT). Oral Health & Preventive Dentisty 1/2003, S. 7-16

Di i i i


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Diagnostic criteria

Under the bestcircumstances aperiodontaldiagnosis is aclinicians best

guess as to whatcondition or

disease the patienthas.

Armitage G. Periodontal diagnoses and classification of periodontal diseases. Periodntology 2000, vol, 34 2004, 9 -21


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Gary C. Armitage Development of a Classification System for Periodontal Diseases and Conditions Ann Periodontol Volume 4 Number 1 December 1999 pag 1-6


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Gary C. Armitage Development of a Classification System for Periodontal Diseases and Conditions Ann Periodontol Volume 4 Number 1 December 1999 pag 1-6


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L J Jin Are periodontal diseases risk factors for certain systemic disorderswhat matters to medical practitioners? Hong Kong Med J 2003;9:31-7

One of the most


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One of the mostcommon virus groupsin the world todayaffecting the skin and

mucosal areas of thebody, is the humanpapilloma virus. Overeighty different typesof HPV have beenidentified. Differenttypes of the humanpapilloma virus areknown to infectdifferent parts of thebody.

Wh th ilib i ?


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Wheres the equilibrium?

Nadine Cerf-Bensussan and Valrie Gaboriau-RouthiauThe immune system and the gut microbiota: friends or foes? www.nature.com/reviews/immunol 735

744 | oCToBER 2010 | voLuME 10

trillions of bacteria / complex and site-

specific communitiesSkin, mucosal surfaces, distal gut.encode hundreds of genes that are absent inthe human genome

Costello, E. K. et al. 2009

together with our microbiota, we formsuperorganisms to exchange energy andmetabolites

Gill, S. R. et al. 2006

homeostasis is maintained by the immunesystem

Eberl, G. A 2010

Wh th ilib i ?
http://www.nature.com/reviews/immunolhttp://www.nature.com/reviews/immunol


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Wheres the equilibrium?

Nadine Cerf-Bensussan and Valrie Gaboriau-RouthiauThe immune system and the gut microbiota: friends or foes? www.nature.com/reviews/immunol 735 744 | oCToBER 2010 | voLuME 10

secretory immunoglobulins in

patients with commonvariable immunodeficiency(cviD)a key regulatory pathway (forexample, loss-of-functionmutations that affect the

interleukin-10 receptor(iL-10r)
http://www.nature.com/reviews/immunolhttp://www.nature.com/reviews/immunol


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Lots of

Enough

Little


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oral health general health summarized

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