ORAL HEALTH GENERAL HEALTH

JORGE FDO. QUISOBONI E. Odontólogo P. U. Javeriana Periodoncista U. del Valle

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Oral Health
• World Health Organization established in 1948 • “health is a complete state of physical, mental, and social well-being, and not just the absence of infirmity”.

and home.The Meaning of Oral Health • What amounts to a “a silent epidemic” of dental and oral diseases is affecting some population groups—a burden of disease that restricts activities in school. National Institute of Dental and Craniofacial Research Chapter 1: The Meaning of Oral Health . and often significantly diminishes the quality of life. work.

Dental Practice A dentist must garantee to the public: Him and his staff know how to… • Prevent the risk of physical. judicial liability and sanitary damage within the limits of the practice • Offer certified programs of biosecurity for all procedures under a scheme of good clinical practice • Keep good record of medical history and its confidenciality • Provide patients with a follow up – recall and maintenance program . psychological.

“if we think of the mouth as a mirror” we should recognize that as dentists… in it we could find illimited richness of information that could be collected from a thorough examination of oral tissues .

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

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occupies a much higher rank in the scheme of life .Periodontal Diseases Etiology • Dental Plaque : Unique Ecosystem : Microbial Biofilm once viewed to be the lowest form of existence.

p. 167–193 .Size of a micro world Rodney M. Apr.2002. Donlan William Costerton Biofilms: Survival Mechanisms of Clinically Relevant Microorganisms CLINICAL MICROBIOLOGY REVIEWS.

Location • Thin layer over the substrate • Polymere Salivary and bacterial matrix Ângela Toshie ARAKI Er:YAG Laser Irradiation of the Microbiological Apical Biofilm. Braz Dent J 17(4) 2006 .

” 2002 Donlan RM.15(2):167-93. are embedded in a matrix of extracellular polymeric substances that they have produced. . Clin Microbiol Rev 2002. Costerton JW. and exhibit an altered phenotype with respect to growth rate and gene transcription. Biofilms: survival mechanisms of clinically relevant microorganisms.Donlan and Costerton defintion: “a microbially derived sessile community characterized by cells that are irreversibly attached to a substratum or interface or to each other.

Lindhe J. 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. pag 245 .Mechanisms of pathogenicity subgingival species colonization factors (1) colonize the subgingival area (2) produce damaging factors. Clinical Periodontology and Implant Dentistry Fifth Edition .

2006.6 % new cases of tuberculosis per 100 000 of US-born / year • 1/3 adults Haemophilus influenzae (Kilian & Frederiksen 1981) tiny fraction exhibit disease. Lindhe J.5–1. Summary of Notifiable Diseases – United States 2004. only 2. only 0.A pathogen… necessary but not sufficient for a disease to occur! • 15% Neisseria meningitidis (Caugant et al.1 % occur per 100 000 • Mycobacterium tuberculosis 5% (Sudre et al. 1992). Clinical Periodontology and Implant Dentistry Fifth Edition . 1988). pag 245 . • Continuous colonization by periodontal pathogens supra or sub gingivaly : show NO evidence of ongoing or previous periodontal destruction.

periodontitis.Mouth as a microbial habitat • teeth provide hard. nonshedding surfaces for the development of extensive bacterial deposits. gingivitis. peri-implant infections and stomatitis . • The accumulation and metabolism of bacteria on hard oral surfaces is considered the primary cause of dental caries.

Mouth as a microbial habitat Philip Marsh Oral Microbiology fourth edition Elsvier limited 2002 chapter 2 .

75 – 7.25 Philip Marsh Oral Microbiology fourth edition Elsvier limited 2002 chapter 2 .pH average 6.

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

Schillinburg .

Thomas Managing the complexity of a dynamic biofilm JADA. 137 http://jada.Which microorganims? Gram-positive bacteria generally communicate via small diffusible peptides.org November 2006 pgs 10s – 15s . Vol. while many gramnegative bacteria secrete acyl homoserine lactones to communicate John G.ada.

137 http: Jada. Numbers in supragingival plaque can exceed on a single tooth surface not inert / metabolically reduced Exponential growth Maturity (stationary) Dispersal (death) John G. shallow sulci to in deep periodontal pockets. Vol. Managing the complexity of a dynamic biofilm JADA.stages of dental plaque biofilm growth Counts in subgingival sites range from about in healthy.org November 2006 .ada.

Biofilms: survival mechanisms of clinically relevant microorganisms. O2 tension.Biofilms characteristics • Adherence • Heterogenicity • Diverse microenvironmentes pH. • Primitive circulatory system • Host immune system resistant • Antimicrobial agents • Quorum sensing Donlan RM. nitrogen. . ions concentration. Clin Microbiol Rev 2002. carbone.15(2):167-93. Costerton JW.

org February 2010 | Volume 5 | Issue 2 | e9321 .Biofilm architecture and the spatial distribution of predominant species / subgingival plaque • Actinomyces sp. Vincent Zijnge Oral Biofilm Architecture on Natural Teeth PLoS ONE | www.plosone. • Tannerella forsythia • Fusobacterium nucleatum • Spirochaetes • Synergistetes • Lactobacillus sp.

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antibodies no longer attach to the bacteria within the microcolonies Bos R. Zaura-Arite E. along with antibodies. . Van Der Mei HC (1997) Physico-Chemical Interactions In Initial Microbial Adhesion And Relevance For BiofilmFormation.Biofilms as model systems • for bacterial adhesion • biofilm development • Resistance to antibiotics. Adv Dent Res 11: 24–32. Busscher HJ (1999) Physico-Chemistry Of Initial Microbial Adhesive Interactions–Its Mechanisms And Methods For Study. are important early host defenses. Once biofilms form. due to their widespread presence and accessibility Toll-like receptors. Ten Cate JM (2001) Conofocal Microscopy Study Of Undisturbed And Chlorhexidine-Treated Dental Biofilm. Van Der Mei HC. Van Marle J. Busscher HJ. J Dent Res 80: 1436–1440. FEMS Microbiol Rev 23: 179–230.

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

Spirochaetes. and Synergistetes in subgingival plaque • Been on close relation to epithelial cells Vincent Zijnge Oral Biofilm Architecture on Natural Teeth PLoS ONE | www. Tannerella forsythia..org February 2010 | Volume 5 | Issue 2 | e9321 .In vivo data • showed convincingly the dominance of Actinomyces sp.plosone. Fusobacterium nucleatum.

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

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

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

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

Etiology and Pathogenesis of Periodontal Disease. L. © Springer-verlag Berlin Heilderberg 2010 .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 the environment A. DOI:10. Dumitrescu.1007/978-3-642-03010_1.

Virulent microbe • Chatacteristic endproducts of bact metab • Chemical composition of bact components • Ability of the bacterium or its parts to overwhelm host defense mechanisms • Invasiveness • Ability to kill Holt and Eversole 2005 .

dozens of integrins. involving hundreds of growth factors. scores of enzymes.Functions of virulence factors • Ability to induce microbe – host interactions (attachment) • Ability to invade the host • Ability to grow in the confines of a host cell • Ability to evade / interfere with host defenses Copyright © Alfred B. Ross. 2001-2008 healing is extremely complex. Eds. Lennox. . and Rockford J. and over ten different cell types. Cunningham. John E.

immunosupressive proteins. L. antibiotic resistance. Fc – binding proteins A. Dumitrescu.Enhance survival chances • Factors that promote colonization and persistance: adhesins. chemotactic inhibitors. DOI:10.1007/978-3-642-03010_1. • Factors that interfere host’s defenses: leucotoxin. © Springer-verlag Berlin Heilderberg 2010 . Etiology and Pathogenesis of Periodontal Disease. invasins. bacteriocins.

Dumitrescu. bone resorption agents. DOI:10. inhibitors of bone formation A. L. © Springer-verlag Berlin Heilderberg 2010 . stimulators of inflammatory mediators • Factors that inhibit host repair tissues: inhibitors of fibroblasts proliferation. Etiology and Pathogenesis of Periodontal Disease. collagenases.Enhance survival chances • Factors that destroy host tissues: cytotoxins.1007/978-3-642-03010_1.

Periodont. Zilm PS and Rogers AH. Fusobacterium nucleatum chemostat-culture supernatants that are potent inhibitors of human gingival fibroblast proliferation. nucleatum are spindle-shaped or fusiform rods of variable length. and the type species for the genus Fuosbacterium. .. Res.Which one is the bandit? Fusobacterium nucleatum is an anaerobic Gram-negative non-spore forming bacterium. The cells of F. 26. 314-322. Gully NJ. Studies in laboratories. Bartold PM. 1991. J. producing butyrate as a major metabolic endproduct. have shown that the organism obtains energy via the fermentation of carbohydrates and specific amino acids.

1991. Fusobacterium nucleatum chemostat-culture supernatants that are potent inhibitors of human gingival fibroblast proliferation. Zilm PS and Rogers AH. 26. F.. nucleatum is frequently associated with periodontal diseases. nucleatum that may be related to virulence include it's adherence to and invasion of host tissue cells.Which one is the bandit? Properties of F. liver and abdomen. and modulation of the host immune response. Periodont. 314-322. chest. Res. as well as invasive human infections of the head and neck. Nucleatum ability to adhere to a wide range of other plaque microorganisms it is proposed to play a crucial role in plaque development. F. Bartold PM. . Gully NJ. lung. J.

2010. zaremba et al 2007. Chen et al 2008 Pussinen et al 2003. Vol. 54. 222–234 . Periodontology 2000.Periodontal pathogenic bacteria Have been detected in patients with: • various cardiovascular diseases. Zaremba et al 2007 Nakano et al 2008 Iwai et al 2005 KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. including atherosclerosis • Arteriosclerotic aneurysms • Peripheral arterial disease • Coronary heart disease • Heart valves of endocarditis • Buergers disease chiu et al 99. Nakano et al 2008. Kurihara et al 2004. Nakano et al 2008.

Moreillon P. 2010. Janket S. diabetes. Inaba H.Epidemiological studies have implicated… P. and coronary artery disease. Commonality in chronic inflammatory diseases: periodontitis. KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. Periodontol 2000 2000: 40: 130–143. Meurman JH. Zaremba M. DAiuto F. Leishman S. Donald A. Evaluation of the incidence of periodontitis-associated bacteria in the atherosclerotic plaque of coronary blood vessels. Kolltveit KM. Systemic diseases caused by oral infection. Parkar M. 222–234 . Suwalski P. Infective endocarditis. Takahashi T. Olsen I. Sanz M. Tronstad L. Nomura R. Amano A. Cullinan MP. Deanfield J. Relationship between periodontal infections and systemic disease. Taniguchi K. 54. Moss K. diabetes mellitus. Periodontology 2000. 4): 3–10. N Engl J Med 2007: 356: 911–920. Vol. Nibali L. Offenbacher S. Storry C. pre-term low birth weight and rheumatoid arthritis Li X. Oral health. atherosclerosis. Seymour GJ. Detection of cariogenic Streptococcus mutans in extirpated heart valve and atheromatous plaque specimens. Taylor GW. J Periodontol 2007: 78: 322–327. Beck JD. Clin Microbiol Rev 2000: 13: 547– 558. Vallance P. Kowalski J. gingivalis in the development of systemic diseases: • Cardiovascular disease. Suvan J. Treatment of periodontitis and endothelial function. J Clin Microbiol 2006: 44: 3313–3317. Takeda M. Southerland JH. Crit Rev Oral Biol Med 2004: 15: 403–413. Lancet 2004: 363: 139–149. Tonetti MS. Clin Microbiol Infect 2007: 13 (Suppl. Ooshima T. Que YA. and cardiovascular disease. Gorska R. Yoshioka H. Nakano K. Yamazaki K. Nemoto H. Ford PJ. Hingorani AD.

Chen W. 2010. Debrey S. Mathys EC. Ann Periodontol 2002: 7: 102–111. Champagne CM. Heiss G. and stroke. Paquette DW. Kuramitsu HK. J Periodontol 1996: 67: 1123–1137 Ebersole JL. Ugarte R. Paju S. Ann Periodontol 2001: 6: 41–47. Role for periodontal bacteria in cardiovascular diseases. Ismail A. Markers of systemic bacterial exposure in periodontal disease and cardiovascular disease risk: a systematic review and metaanalysis. Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle. Singer RE. Cappelli D. Associations between periodontal disease and risk for atherosclesosis. Olson H. Bush RB. Mustapha IZ. Heart Dis 1999: 1: 233–240. J Periodontal Res 1999: 34: 346–352. Offenbacher S. Novak MJ. Lopez LR. Atherosclerosis 1998: 140 (Suppl. Markers of systemic bacterial exposure in periodontal disease and cardiovascular disease risk: a systematic review and metaanalysis. in particular. Slade G. A systematic review. Oladubu M. Scannapieco FA. The role of infection in atherosclerosis and coronary artery disease: a new therapeutic target. Kang IC. Williams RC. Offenbacher S. 222–234 .Epidemiological studies have implicated… • Cardiovascular diseases. Pathogenesis of atherosclerosis: a possible relation to infection. Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins. 1): S3–S9. Madianos PN. Periodontal disease and cardiovascular disease. Kobayashi K. Beck JD. Vol. Mott GE. Khosravi H. Vokonas PS. J Periodontol 2007: 78: 2289–2302. Periodontitis– atherosclerosis syndrome: an expanded model of pathogenesis. Ugarte R. Montgomery M. Matsuura E. Southerland JH. Debrey S. Oladubu M. J Periodontol 2007: 78: 2289–2302. KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. Ann Periodontol 2003: 8: 38–53. Steffen MJ. Qi M. Autoimmunity Rev 2008: 7: 214–222. Garcia R. cardiovascular disease. Periodontology 2000. Noll G. 54. appear to be strongly related to infection by periodontal pathological bacteria Beck J. Mustapha IZ.

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

2001-2008 . John E. Cunningham. and mesenchymal cells that develop into fibroblasts Alfred B. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Lennox. Eds. and Rockford J.Biofilms in Health and Medicine • How is the skin healing process affected in chronic wounds? • platelets to form a blood clot. leukocytes to combat microbial invaders.

Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Eds. Cunningham.Biofilms in Health and Medicine • migratory phase begins • a scab is formed and epithelial cells migrate across the wound under the scab. 2001-2008 . Lennox. John E. Granulation tissue is formed as fibroblasts produce extracellular matrix and endothelial cells form blood vessels. and Rockford J. Alfred B.

Biofilms in Health and Medicine
• proliferative phase • characterized by extensive growth of epithelial cells, fibroblast deposition of collagen fibers in random patterns, and continued growth of blood vessels.

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

Biofilms in Health and Medicine
• maturation phase • occurs where collagen fibers become more organized, blood vessels are restored to normal, the scab is shed, and the epidermis is restored to normal thickness

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

2001-2008 . John E. Cunningham. and Rockford J. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Eds.Absolute and relative barriers to healing • • • • • • • low blood oxygen content Infection lack of perfusion sustained pressure patient malnutrition systemic disease such as diabetes treatments such as immunosuppressants Alfred B. Lennox.

2001-2008 . and Rockford J. Cunningham. Eds. John E.How the healing process is disrupted in chronic wounds • Fibroblasts isolated from chronic wounds show impairment of synthesis. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Lennox. migration and proliferation Alfred B.

Cunningham. Lennox.How the healing process is disrupted in chronic wounds • Endothelial cells from chronic wounds are deficient in production of enzymes and growth factors. John E. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . and the formation of new capillaries Alfred B. 2001-2008 . and also are impaired in migration. and Rockford J. Eds. proliferation.

Lennox.How the healing process is disrupted in chronic wounds • keratinocytes are impaired in their migration and proliferation as well as their ability to synthesize cytokines. and Rockford J. Eds. Alfred B. provisional matrix and basement membrane. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Cunningham. John E. 2001-2008 .

and regardless of the age. • Up regulated up to 30-fold. and Rockford J. Lennox. 2001-2008 . Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . they all show an identical biochemistry. Alfred B. regardless of the etiology. gender. Eds. or any other demographic factor of the patient.How the healing process is disrupted in chronic wounds • When matrix metalloproteases are evaluated in chronic wounds. Cunningham. John E.

and Rockford J. 2001-2008 . Cunningham. tumor necrosing factor alpha and gamma interferon Alfred B. Ross Chapter 3 Biofilms in Health and Medicine Section 1 Biofilms and Chronic Infectionss . Eds. especially bacteria. John E.Presence of proinflammatory cytokines • The innate immune system is designed to be vigilant and reactive to foreign insults. produced by Gram-positive bacteria. Lennox. • Toll-like receptors (TLR) 2 and 4 are very sensitive to lipopolysaccharide (LPS) material produced by Gram-negative bacteria as well as teichoic acid. • Interleukin 1.

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222–234 . gingivalis mediated mechanisms in vascular diseases How can P. an obligate anaerobic bacterium. 54.Questions regarding P. Periodontology 2000. gingivalis. 2010. Vol. safely travel through the bloodstream from small vessels in the oral cavity to reach the central arteries in which atherosclerotic lesions develop? KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease.

Periodontology 2000. gingivalis adhere to normal endothelial cells given the extremely rapid blood flow in the abdominal or thoracic aorta? 1 cell thick. 2010. Vol. 222–234 . 54.Questions regarding P. gingivalis mediated mechanisms in vascular diseases • How can P. 5 – 10 μm KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease.

Periodontology 2000.57 μm confirm whether direct arterial invasion by P. gingivalis is possible and sufficient to cause vascular diseases KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. gingivalis mediated mechanisms in vascular diseases How can P. 2010. 222–234 .Questions regarding P. 54. gingivalis invade normal endothelial cells of large-sized arteries? depth of 1. Vol.

resulting in vascular damage KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. 2010. hyperlipidemia and smoking can cause endothelial cell dysfunction. Periodontology 2000. gingivalis-mediated atheroma formation • Various pathological factors such as diabetes mellitus. 222–234 . Vol.• An indirect mechanism of P. hypertension. 54.

Periodontology 2000. 54.KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. Vol. 2010. 222–234 .

No.P. Porphyromonas gingivalis Fimbria-Dependent Activation of Inflammatory Genes in Human Aortic Endothelial Cells. Sept. 9 p.G. Vol. 2005. 5367–5378 . 73. INFECTION AND IMMUNITY. Fimbria-Dependent Activation of Inflammatory Genes in Human Aortic Endothelial Cells • Little is known regarding gene downregulation during endothelial cell infection by bacteria or the impact of this on the development of atherosclerosis Hsin-Hua Chou.

Etiology and Pathogenesis of Periodontal Disease. © Springer-verlag Berlin Heilderberg 2010 . DOI:10. Dumitrescu.Aspects of innate host response A.1007/978-3-642-03010_1. L.

L. Etiology and Pathogenesis of Periodontal Disease. © Springer-verlag Berlin Heilderberg 2010 .1007/978-3-642-03010_1.Pathogen – associated molecular patterns PAMPs A. DOI:10. Dumitrescu.

© Springer-verlag Berlin Heilderberg 2010 . Etiology and Pathogenesis of Periodontal Disease.1007/978-3-642-03010_1. L. DOI:10. Dumitrescu.Main receptors and signaling pathways • Toll like receptors TLRs • CD14 • Nucleotide – binding oligomerization domain proteins Nod • G – protein – coupled receptors • Formyl – methionyl peptide receptors • Protease activated receptors A.

TLRs in periodontitis lesions • Inn Inm Rec / limited # germline encoded receptors: pathogen recognition receptors • Conserved molecular patterns PAMPs and produce inflammatory cytokines via intracellular signaling • Dendritic cells subsets express ≠ sets TLRs • Distinct T-cell subsets Azuma et al 2006 A. Etiology and Pathogenesis of Periodontal Disease. DOI:10.1007/978-3-642-03010_1. © Springer-verlag Berlin Heilderberg 2010 . L. Dumitrescu.

DOI:10.Chromosomal localization Genomic structure Amino acid sequences 5 subfamilies A.1007/978-3-642-03010_1. Etiology and Pathogenesis of Periodontal Disease. Dumitrescu. L. © Springer-verlag Berlin Heilderberg 2010 .

© Springer-verlag Berlin Heilderberg 2010 . Dumitrescu. Etiology and Pathogenesis of Periodontal Disease. L. DOI:10.TLRs signaling pathways Complex forming molecules: CD14 MD-2 Lipopolysaccharide MyD 88 Ligand complexed to CD14 Mal Tollip Includes TLR-4 and MD2 Signal transuction includes Recruitment of MyD88 and IL-1 receptor assoc kinase It results in nuclear tansloc And gene activation of specific inflammatory mediators IL-1 and TNF-α A.1007/978-3-642-03010_1.

Histopatogenesis of gingivitis and periodontitis Page and Schroeder 1982 .

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potencialized Systemically ? sociodemography .

early and useful sign in order to establish an accurate diagnosis. The main entities are:
gingival lesions related to mucocutaneous diseases, gingival lesions related to hormonal levels, gingival alterations produced by pharmacological treatments, gingival lesions produced by viral infections, gingival alterations related to haematological disorders gingival alterations of genetic origin such as gingival fibromatosis

Initiation of inflammation
Early 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 the endoplasmic reticulum, rupture of cell membranes

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

Host’s mechanisms
• Epithelial cells’ regular shedding • Washing effect of saliva and GCF • Phagocytic action of neutrofils JE – sulcus Maintain normal, non irritating environment
A. L. Dumitrescu, Etiology and Pathogenesis of Periodontal Disease, DOI:10.1007/978-3-642-03010_1, © Springer-verlag Berlin Heilderberg 2010

DOI:10. L. Dumitrescu. Etiology and Pathogenesis of Periodontal Disease.First cells to be challenged • Disturbance of equilibrium by appareance of pathogenic bacteria in the P niche • Bacterial adhesion through fimbriae activates Epithelial cells A. © Springer-verlag Berlin Heilderberg 2010 .1007/978-3-642-03010_1.

1007/978-3-642-03010_1.A. L. © Springer-verlag Berlin Heilderberg 2010 . Dumitrescu. DOI:10. Etiology and Pathogenesis of Periodontal Disease.

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54.Tobacco impact • Smoking induces the release of an abundance of reactive oxygen species into the blood with the potential to cause injury to the endothelial cells KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. 222–234 . Vol. 2010. Periodontology 2000.

2010. facilitating P. 54. Periodontology 2000.Injured endothelium • Dysfunction or detachment of the endothelial cells lead to direct exposure of the vascular smooth muscle cell layer. Vol. gingivalis invasion KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease. 222–234 .

Ohata et al 2004 KOICHIRO WADA & YOSHINORI KAMISAKI Molecular dissection of Porphyromonas gingivalisrelated arteriosclerosis: a novel Mechanism of vascular disease.Thromboangiitis obliterans • trigger for the onset of Buerger’s disease. Periodontology 2000. Roncon-albuquerque et al 2002. which occurs despite the absence of elevated plasma cholesterol levels Mishima et al 96. 2010. Vol. 222–234 . 54.

Diabetes .

There is low predictive value of clinical assesments Diagnosis Treatment Plan Det microbial incidence / simple & economical methods M. PERIODONCIA Y OSTEOINTEGRACIÓN Volumen 15 Número 4Octubre-Diciembre 2005 . Frías López Métodos de diagnóstico clínicoen periodoncia.C.

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

34 2004. 9 -21 . Periodntology 2000. Periodontal diagnoses and classification of periodontal diseases. vol.Diagnostic criteria • Under the best circumstances a periodontal diagnosis is a clinician’s best guess as to what condition or disease the patient has. Armitage G.

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

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

L J Jin Are periodontal diseases risk factors for certain systemic disorders—what matters to medical practitioners? Hong Kong Med J 2003.9:31-7 .

Over eighty different types of HPV have been identified. . is the human papilloma virus. Different types of the human papilloma virus are known to infect different parts of the body.One of the most common virus groups in the world today affecting the skin and mucosal areas of the body.

et al. 2009 • together with our microbiota. distal gut. we form superorganisms to exchange energy and metabolites Gill. mucosal surfaces. 2006 • homeostasis is maintained by the immune system Eberl.nature. E.Where’s the equilibrium? • trillions of bacteria / complex and sitespecific communities Skin. et al. K. encode hundreds of genes that are absent in the human genome Costello. G. S.com/reviews/immunol 735 – 744 | oCToBER 2010 | voLuME 10 . R. A 2010 Nadine Cerf-Bensussan and Valérie Gaboriau-Routhiau The immune system and the gut microbiota: friends or foes? www.

loss-of-function mutations that affect the interleukin-10 receptor (iL-10r) Nadine Cerf-Bensussan and Valérie Gaboriau-Routhiau The immune system and the gut microbiota: friends or foes? www.nature.Where’s the equilibrium? secretory immunoglobulins in patients with common variable immunodeficiency (cviD) a key regulatory pathway (for example.com/reviews/immunol 735 – 744 | oCToBER 2010 | voLuME 10 .

Lots of Enough Little .

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