This document discusses plaque as a biofilm and the microbiology of periodontal diseases. It begins by introducing the complex microbial flora that inhabits the oral cavity. A key point is that while most of these microbes coexist harmlessly with the host, a subset of organisms can lead to periodontal diseases either through overgrowth or new pathogenic properties. The document then examines historical and modern evidence that supports the infectious nature of periodontal diseases. It discusses the unique features of periodontal infections as biofilms outside of the body on tooth surfaces. Finally, it reviews the current understanding of suspected periodontal pathogens and their role in destructive periodontal disease.
Biofilms on the teeth are the root cause of inflammation on the gums and periodontium. Understanding the formation of biofilms will make improve our treatment modalities towards disruption of biofilms hence provide better periodontal health to our patients at large.
Biofilms on the teeth are the root cause of inflammation on the gums and periodontium. Understanding the formation of biofilms will make improve our treatment modalities towards disruption of biofilms hence provide better periodontal health to our patients at large.
Introduction……
Uterus……..Sterile
After birth……… few facultative & aerobic microorganisms
Second day……... anaerobic
2 weeks …….. Nearly mature microbiota
> 2 years …….. 400 different spp (10 14 )
After tooth eruption …… > 500 spp.
Any individual contains ≥150 spp.
6 Ecological niches
Or
Microbial habitats within the mouth
EARLYCOLONIZERS
Dental plaque
Formation
2. Specific Plaque Hypothesis
Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms.
This concept predicts that plaque harboring specific bacterial pathogens results in periodontal disease because these organisms produce substances that mediate the destruction of host tissues.
3. Ecological plaque hypothesis
In 1990, PD Marsh et al developed the ecologic plaque hypothesis
According to this, both the total no. of dental plaque and the specific microbial composition of plaque may contribute to the transition from health to disease.
A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for overgrowth by pathogens.
pathogens in periodontal microbiology. the red complex bacteria described in detail. recent updates regarding proteases and virulence factors of all pathogens.
Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.
Host microbial interaction in periodontal diseaseAnushri Gupta
Bacterial Evasion of Host Defense Mechanisms
Immunological Aspects of Microbial Host Interaction
Connective Tissue Alterations:Tissue Destruction in Periodontitis
BONE RESORPTION
Introduction……
Uterus……..Sterile
After birth……… few facultative & aerobic microorganisms
Second day……... anaerobic
2 weeks …….. Nearly mature microbiota
> 2 years …….. 400 different spp (10 14 )
After tooth eruption …… > 500 spp.
Any individual contains ≥150 spp.
6 Ecological niches
Or
Microbial habitats within the mouth
EARLYCOLONIZERS
Dental plaque
Formation
2. Specific Plaque Hypothesis
Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms.
This concept predicts that plaque harboring specific bacterial pathogens results in periodontal disease because these organisms produce substances that mediate the destruction of host tissues.
3. Ecological plaque hypothesis
In 1990, PD Marsh et al developed the ecologic plaque hypothesis
According to this, both the total no. of dental plaque and the specific microbial composition of plaque may contribute to the transition from health to disease.
A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for overgrowth by pathogens.
pathogens in periodontal microbiology. the red complex bacteria described in detail. recent updates regarding proteases and virulence factors of all pathogens.
Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.
Host microbial interaction in periodontal diseaseAnushri Gupta
Bacterial Evasion of Host Defense Mechanisms
Immunological Aspects of Microbial Host Interaction
Connective Tissue Alterations:Tissue Destruction in Periodontitis
BONE RESORPTION
Microbiology of Periodontal diseases with its introduction history, plaque hypothesis, Microbial complexes, Individual pathogens, Advances in microbiological diagnosis,
Control of bacterial biofilms.
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
explanation of Dental plaque and its composition, pathogenesis, its classification, structure of subgingival plaque, structure of supragingival plaque formation.
tooth associated plaque, implant associated plaque
Dental plaque biofilm cannot be eliminated permanently.
However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bio burden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing, flossing and rinsing with antimicrobial mouth rinses.
This can result in the prevention or management of the associated squeal, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders.
Osseointegration, definition, history, process of osseointegration, factors influencing osseointegration, methods for evaluation of osseointegration, failure of osseointegration
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Smoking and periodontal disease, smoking as a risk factor, incidence of smoking, effects of smoking on periodontium, smoking and gingivitis and smoking and periodontitis, effect of surgical and non surgical therapy on smokers
Systemic Peridoontology, link between systemic health and periodontology, diabetes and periodontology, Pregnancy and Peridotology,Nutrition and periodontology
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
1. PLAQUE AS A BIOFILM
AND
MICROBIOLOGY OF PERIODONTAL
DISEASES
Navneet Randhawa
MDS Final year
2. INTRODUCTION
• It is estimated that about 700 different spp. are capable of colonizing the
mouth.
• An individual may harbor 150 or more different spp.
• The ecological relationship between periodontal microbiota & host –benign .
• A subset of organisms either introduced, overgrow or exhibit new properties –
leading to periodontal diseases.
3. EVIDENCE OF INFECTIOUS NATURE
OF PERIODONTAL DISEASE
1. Acute periodontal infections: - alleviated by anti microbial therapy.
2. Positive co-relation of plaque levels to gingivitis and amount of bone loss. (Loe et al
1965)
3. Efficacy of antibiotics in treatment of periodontitis:
4 HOST IMMUNOLOGIC RESPONSE: ↑serum antibody response (Taubman et al 1994 )
5. Toxic products (endotoxins, H2S , NH3, indole, amines, leucotoxins ) - demonstrate
pathogenic potential.
6. STUDIES IN EXPERIMENTAL ANIMALS: Induce periodontal disease
4. UNIQUE FEATURES OF PERIODONTAL
INFECTIONS
• Mineralized tooth structure passes through the integument so that part of it is
exposed to the external environment while part is within C.T.
• Non shedding tooth surface.- provides ‘sancturies’ in which micro-organisms can
hide.
• Causative agent reside in biofilms outside the body.
• Formidable problem for host and therapist.
6. • 1683 Antonie van Leeuwenhoek
• “Poor oral hygiene – large no. of bacteria”
“I didn’t clean my teeth for three days and
then took the material that had lodged in
small amounts on the gums above my
front teeth…. I found a few living
animalcules…”
7. The search for the etiological agents of periodontal diseases started
in the ‘golden age of microbiology’ [app. 1880-1920]
8. • 1890 W.D. Miller “pyorrhoea alveolaris is not caused by a specific bacterium”
• Invesigators from the period of 1880-1930 suggested four distinct groups of micro-
organisms. Viz; amoeba,spirochetes,fusiforms,sreptococci.
• 1925 -1950
Decline of interest in microorganisms
Bacteria : secondary invaders/contributors to inflammation
Emphasized on occlusal factors,calculus & poor host defense
9. 1950 Waerhaugh : Dental plaque in the initiation & progression of pdl
diseases
• 1950-1975 : Non specific hypothesis
• 1970s : Improvement in anaerobic culture technique.Distinct microfloras in pdl health
&gingivitis-Specific plaque hypothesis
• 1980s : A.a , P.g, P.intermedia , T.forsythus periodontitis
10. These classic studies provided
the initial impetus to perform
large scale studies attempting to
relate specific microorganisms to
the etiology of periodontal
disease
12. BIOFILM
Biofilm
Microbial biofilm: a structured community of bacterial cells
enclosed in a self-produced polymeric matrix and adherent
to an inert or living surface.
‘ Matrix enclosed bacterial populations adherent to each other
and to surfaces or interfaces’
Costerton et al,1994
13. • Biofilms are ubiquitous and form on virtually all surfaces immersed in natural aqueous
environment
14. • Biofilms are the preferred method of growth for most bacteria.
15. • Protection from :
- competing microorganisms
- environmental factors
-toxic substances
• Facilitate :
-processing and uptake of nutrients
-cross feeding
-removal of potentially harmful metabolites
-development of appropriate physicochemical
environment
16. PLAQUE
• Dental plaque as a naturally occuring microbial deposit represents a ‘true
biofilm’
“Highly specific variable structural entity formed by the sequential
colonization of microorganism on tooth surface, epithelium & restorations”.
(WHO)
“Clinically as a structured resilient, yellow greyish substance that adheres
tenaceously to the intraoral hard surfaces, including removable & fixed
restorations”.
17. COMPOSITION OF DENTAL PLAQUE:
• Composed primarily of microorganisms within an intercellular matrix
• 1g 2 * 10 bacteria
Polysaccharides
Proteins
Organic Glycoproteins
Lipid
Intercellular matrix
Calcium
Inorganic Phosphorus
Na,K,F
18. FORMATION OF DENTAL PLAQUE
• Formation of pellicle on tooth surface
• Initial adhesion & attachment of bacteria
• Colonization & plaque maturation
19. FORMATION OF PELLICLE
Initial phase of plaque formation
Forms with in nanosecond - vigorously polished teeth
Derived from components of saliva + crevicular fluid +bacterial & host tissue cell
products Components-
Glycoprotein (mucin)
Proline rich protein
Enzymes (α-amylase)
Other molecules
20. • Studies of early (2-hour) enamel pellicle reveal that its amino acid composition differs
from that of saliva, indicating that the pellicle forms by selective adsorption of the
environmental macromolecules(Scannapieco1990).
• The mechanisms include
• Electrostatic,
• Van der Waals, and
• Hydrophobic forces.
21. hydroxyapatite surface - negatively charged phosphate groups
Interact with positively charged components of salivary and crevicular fluid
macromolecules.
Pellicles function as-
a protective barrier,
providing lubrication
preventing tissue desiccation.
provide a substrate to which bacteria in the environment attach.
22. The specific component of pellicle depend on underlying surface.
Thus the characteristic of the underlying hard surface are transferred through the
pellicle layers and influence initial bacterial adhesion.(Pratt et al 1991)
Absolom et al (1987) even observed a clear relationship between the type of
proteins adsorbed in the pellicle & the free energy of the substratum surface.
23. 2]Initial adhesion and attachment of bacteria:
Phase 1: Transport to the surface
-Brownian motion
-Sedimentation of bacteria
-Liquid flow
-Active bacterial movement
24. Phase 2: Initial adhesion
• Initial adhesion- reversible.
• Initiated by the interaction between the bacterium and the surface.
• Long-range (>50nm):non-specific interaction : Van der Waals
attractive forces.
• Shorter-range (10-20nm) interactions: Van der Waals attraction
forces + electrostatic repulsion →weak area of attraction
→reversible adhesion
25. PHASE 3: ATTACHMENT
• After initial, a firm anchorage -specific interactions (covalent, ionic or hydrogen
bonding)
• This follows direct contact or bridging- true extracellular filamentous appendages
(10nm)
• On a rough surface bacteria are better protected against shear forces so that a
change from reversible to irreversible bonding occurs more easily & more frequently.
26. SECONDARY COLONIZATION & PLAQUE
MATURATION
Secondary colonizers
Prevotella intermedia,
Prevotella loescheii,
Capnocytophaga spp.,
Fusobacterium nucleatum, and
Porphyromonas gingivalis.
adhere to cells of bacteria already in the plaque
COAGGREGATION
27. Highly specific stereochemical interaction -protein and carbohydrate molecules
located on the bacterial cell surfaces
Eg
Fusobacteria coaggregate with all other human bacteria.
Veillonellae, capnocytophagae & prevotella bind to streptococci & actinomycetes.
(Kolenbrader et al1995)
28. Most coaggregation
Mediated by lectinlike adhesins
Inhibited by lactose & other galactosides.
Well characterized interaction include the coaggregation of–
Fusobacterium nucleatum with S.sanguis,
Prevotella loescheii with A. viscosus
Capnocytophaga ochraceus with A. viscosus
Streptococci show intrageneric coaggregationbind to the nascent monolayer of
already bound streptococci.
30. • Sequential colonization :‘bridging species’.
• Thus as plaque matures an ecologic shift occurs in the biofilm from the
early aerobic environment characterized by gram positive facultative
species to a highly oxygen deprived environment where gram negative
anaerobic organisms predominate
32. Supragingival
Direct contact with the gingival margin is referred to as marginal plaque.
Demonstrates stratified organisation of bacteria.
Gram +ve cocci & short rods predominate at the tooth surface.
Gram -ve rods & filaments as well as spirochetes - outer surface of mature plaque
mass.
33.
34. Subgingival:
• Formed below the gingival margin,
• Present between the tooth & sulcular tissue
• Subgingival microbiota differ in composition: Local availablity of blood product
Low redox potential anaerobic environment.
35. • Subgingival plaque can be divided in to
• Attached/tooth associated
• Unattached plaque
• Epithelial associated
• Within CT
• On bone surface
36. PLAQUE HYPOTHESIS
NON SPECIFIC PLAQUE HYPOTHESIS:
• In 1900s Any accumulation of microorganisms at or below the gingival margin would produce
irritants leading to inflammation
• Periodontal disease results from the ‘elaboration of noxious products by the entire plaque flora’.
When only small amount of plaque the noxious product neutralized by
host.
Similarly large amounts of plaque noxious product overwhelm the host
defense.
Limitations
• Some individuals with considerable amount of plaque & gingivitis never developed destructive
periodontitis.
• Site specificity in the pattern of disease
37. SPECIFIC PLAQUE HYPOTHESIS
[WALTER LOESCHE 1979]
• Only certain plaque is pathogenic & its pathogenicity depends on the presence of or
increase in specific microorganism.
• This concept predicts that plaque harboring specific bacterial pathogens results in a
periodontal disease because these organism produce substances that mediate the
destruction of host tissue.
• Acceptance of this hypothesis was spurred by recognition of A.a as a pathogen in
localized aggressive periodontitis.
38. ECOLOGICAL PLAQUE HYPOTHESIS [MARSH 1991]
• A change in a key environmental factor will trigger a shift in the balance of the resident
microflora & this might predispose a site to disease.
Increased Increased High GCF flow, bleeding
plaque inflammation temp
Overgrowth of gram –ve
anaerobes
• Microbial specificity in disease would be due to the fact that only certain species are
competitive under the new environmental condition
ECOLOGICAL
SHIFT
39.
40. Special Bacterial Behaviour in a biofilm:
1)Antibiotic resistance:
a] Slower rate of growth within the biofilm
b] Matrix resists diffusion of antibiotics
acts as an ion exchange resin
c] Beta lactamase,formaldehyde lyase & formaldehyde dehydrogenase may
become conc.
d] Super resistant bacteria with ‘multi drug efflux pumps’
3)High density of cells facilitate exchange of genetic information:
-conjugation
-transformation
-plasmid transfer
-transposon transfer
41. • When within a biofilm bacteria exhibit both favourable & antagonistic relations with the other species
Favourable interactions:
- provides of growth factors
-facilitates attachment
Antagonistic interactions:
-enzymes which inhibit binding
-factors that kill other species
42. QUORUM SENSING
• Quorum sensing in bacteria "involves the regulation of expression of specific
genes through the accumulation of signaling compounds that mediate inter
cellular communication” (Prosser 1999).
• Quorum sensing - dependent on cell density
• Few cells: signaling compounds at low levels
• Auto induction ↑concentration
• Once the signaling compounds reach threshold level (quorum cell density),
gene expression is activated.
43. FACTORS AFFECTING THE COMPOSITION
OF BIOFILM
• Disease status- ↑red and orange complex
• Pocket depth: red and orange complex↑ with ↑ pocket depth
• Transmission:
Two types of transmission are recognized:
• "vertical“- that is transmission from parent to offspring, "horizontal”- passage of an
organism between individuals outside the parent—offspring relationship.
• Acquisition of new strains of pathogenic species can occur at both young and older ages.
If the newly acquired strain is more virulent than the pre-existing strain of that species,
then a change in disease pattern could occur
44. • Host susceptibility
HIV infection and diabetes
• Studies such as these suggest that altered host susceptibility → change the rate of
disease progression(periodontal pathogens –same)
Smoking
• ↑red and orange complex
• Tobacco- diminish the local and systemic immune response
46. ACQUISITION OF MICROFLORA
• Mouth of fetus- sterile.
• No. of organisms
rapidly increase
following 6- 10 hrs
after birth.
• Anaerobic bacteria -
2nd day
Birth
• >2 yrs complex
microflora is formed
• More than 400
different types of
bacteria
Infancy and
early childhood • Greatest increase with
the eruption of
permanent teeth.
• Bacteria occupy
several niches
Adolescence
50. CURRENT CONCEPT OF THE ETIOLOGY OF
PERIODONTITIS:
SUSCEPTIBLE PRESENCE OF
HOST PATHOGEN
ABSENCE OF
BENEFICIAL Spp.
51. ROLE OF BENEFICIAL SPECIES:
• Occupies the niche
• Limits pathogens’ ability to adhere
• Affects vitality & growth of pathogen
• Affects ability of pathogen to produce virulence factors
• Degrades virulence factors produced by pathogens
54. DEFINING PERIODONTAL
PATHOGENS…
• Periodontal disease occurs in area normally inhabited by many bacteria,
hence – difficult to identify specific microbes.
• KOCH’S POSTULATES 1870
1. The causative agent must be routinely isolated from diseased individuals
2. Be grown in pure cultures in lab.
3. Must produce a similar disease when inoculated in susceptible lab animal.
4. Be recovered from lesions in a diseased lab animal.
55. PROBLEMS IN APPLYING THESE
POSTULATES IN PERIODONTAL
DISEASES…
i. In ability to culture all the micro-organisms that have been associated with the
disease.(eg: oral spirochetes).
ii. Difficulty in defining and culturing the sites of active disease.
iii. Lack of animal model system to study periodontitis.
56. SOCRANSKY (1977) PROPOSED AN ALTERNATIVE CRITERIA
TO IDENTIFY KEY ORGANISMS IN PERIODONTAL
INFECTIONS…
i. Organism must be associated with disease as evident by increase in no. of organism at
disease sites.
ii. Must be eliminated or decreased in sites that demonstrate clinical resolution of disease
with treatment.
iii. Must demonstrate a host response in form of an alteration in the host cellular and
humoral immune response.
iv. Must be capable of causing disease in experimental animal model
v. Must demonstrate virulence factors responsible for enabling the micro organism to cause
destructive periodontal disease.
57. SOCRANSKY ET AL 1987 REVIEWED REASONS
FOR UNCERTAINITY ON DEFINING
PERIODONTAL PATHOGENS…1. Over 500 spp may be cultured from periodontal pockets of different individuals
and one may recover 30-100 spp from a single site.
2. Many spp- difficult to grow and identify.
3. Physical contraints of pocket makes it diffcult to collect a representative sample.
4. Site within a subject do not appear to be progressing equally at all times- time of
sampling may play a critical role.
58. 5. there appears to be multiple destructive periodontal disease that mostly cannot be
differentiated on a clinical basis.
6. opportunistic spp my grow as a result of disease rather than as the cause.
7.some of the infections are mixed- difficult to evaluate the role of single spp.
8.strains of putative pathogens may differ from virulence.
9.more virulent strains of a spp may harbor plasmids that might confer virulence
properties.
59. HILL’S POSTULATES
• Given current obstacles etiology of periodontitis – pathogenic microbial
cummunity concept +hills criteria of causality
60. MICROBIAL COMPLEXES
• Socransky et al 1998 examined over 13000 sub gingival plaque samples from 185 adults and
recognized 6 closely associated groups of bacterial spp using DNA hybridization technique.
61. • Kolenbrander et al 2006 cell to cell recognition in oral bacteria is not random and
each strain has a defined set of partners.
• Functionally similar adhesins found on bacteria of different genera may recognise
the same receptors on other bacterial cells helping in coaggregation.
63. AGGREGATIBACTER
ACTINOMYCETEMCOMITANS
Actinobacillus actinomycetemcomitans.
• Klinger (1912) first isolated from cervicofacial actinomycosis lesions.
• Henrich and Pulverer(1959) were the first to demonstrate that A. a was
part of the normal oral flora and indicated that it could colonize teeth,
mucosa and the oropharyx.
• With respect to periodontal disease, A. a was first implicated as the cause
of juvenile periodontitis in 1976 by Newman et al. and by Slots .
64. Isolated together with A.israelii, hence the name
which means ‘together with actinomyces’.
Gram –ve, small, non-motile, saccharolytic,
capnophilic, round-ended rod .
Culture condition & identification: grows as white,
translucent, smooth, non hemolytic colony on
blood agar with star shaped internal
structure(Actino=star)
65. • The primary oral ecological niche for Aa is dental plaque.
• High levels- in pockets
• Low levels- in other oral surfaces, tongue, saliva
• It has not been cultured from edentulous mouths
• It does not belong to indigenous microbiota of any other body site.
• Can cause non oral infections such as endocarditis, abscess in lungs, head & neck and
abdominal areas.
• Distribution pattern- generally isolated areas, as IgG response to Aa is protective and limit
infection.
66. • Conventional srp is not effective in eliminating Aa due to ability of Aa to invade the
gingival c.t. (christerson et al)
• Hence effective therapy involves antibiotics alone or in combination with surgery (zambon
et al 1986)
67. Adhesin- Aae
binds to CHO
receptor on buccal
epithelial cell
Moves to
supragingival
plaque by Flp 1
Fimbrae along with
CHO polymer PGA
mediate attachment
to hard surface
Moves to sub
gingival plaque
From here may
attach to & invade
epithelial lining of
pocket & enter c.t
Finally may leave
oral cavity &
contribute to or
cause endocarditis
68. SEROTYPES• 6 serotypes- a,b,c,d,e and f.
• Most subjects infected with only one serotype
• Serotype ‘a’ and ‘b’ are most common in oral cavity while serotype ‘c’ is important in
extra oral infections.
• While serotype ‘b’ was more common in LAP individuals serotype ‘a’ was common in
chronic periodontitis.
• Intrafamilial transmission- family members seem to be infected by the same serotype
69. TRANSMISSION OF A.A
• Vertical or horizontal
• Route of transmission: Salivary and mucosal contact or on inanimate object.
70.
71. VIRULENCE FACTORS PRODUCED BY
A.A…
• Can be classified as_
i. Factors that assist in colonizing the dental plaque and gingival sulcus-bacterial capsule
and fimbrae
ii. Factors helping it to evade host defence mechanism-leukotoxin
iii. Factors causing tissue destruction-LPS endotoxin(bone resorption), Collagenase(
connective tissue breakdown) Reduction in collagen density
72. VESICLES
• Blebs-LPS in nature
• Originate & continuous with outer membrane.
• Vesicles function as delivery vehicles for A.a toxic materials
• vesicles
73. ADHESINS
Among adherence factors there are bacterial capsules and fimbriae .
FIMBRIAE
• Associated with adhesion
Non fimbriated also exhibit adhesive properties
Anaerobically grown Aa produce more fimbriae than the Aa grown in
aerobic environment. (scannoapieco et al)
74. SUSTENINS
BACTERIOCINS
• Proteins produced by bacteria…..lethal to other bacteria
• Active against S.sanguis/A.viscosus
• MOA : permeability of cell membrane of target bacteria
• Leakage of DNA/RNA/macromolecules essential for growth
75. EVASINS
CYTOTOXINS
• (-) fibroblast proliferation
• Leukotoxin : heat labile factor, that can destroy PMNs
• Aa strains from LAP pts exhibited higher leukotoxin production than from
healthy subjects
• More common in young patients
76. LEUKOTOXIN
Species specific / cell specific
Binds to neutrophils/monocytes/lymphocytes
Pores in the membrane of target cells
Hampers the ability of cell to sustain osmotic
homeostasis
77. IMMUNOSUPPRESSIVE FACTORS
• A.a produces protein
• Inhibits DNA/RNA synthesis in T cells
• Inhibits IgG & IgM synthesis by lymphocytes
79. PORPHYROMONAS GINGIVALIS
• Gram-negative, anaerobic, non-motile, asaccharolytic rods - member of the much
investigated "black-pigmented Bacteroides" group.
• Initially grouped into a single species, B. melaninogenicus.
• At present only known porphyromonas spp isolated from humans that produce
phenylacetic acid as metabolic end product.
• Non-oral infections- endocarditis
80. • Habitat :
• Mouth with poor oral hygiene preferred over clean tooth surface, need G+ve bacteria.
• Not seen in edentulous mouth
• Levels increase with age so infrequent in children, acquired in later life
Association:
• Commonly encountered in sites with destructive periodontal disease
• Refractory sites (haffajee et al, 1988)
• Advanced periodontal disease (Slots 1977)
• Highly inflamed gingivitis lesions (mayrand 1981)
• Acute periodontal abscess (newman and sims 1979)
• Able to invade human gingival epithelial cells (duncan et al 1993) -found in higher number in epithelial cells
recovered from periodontal pocket (dzink et al, 1989)
81. VIRULENCE FACTORS
1. Capsule: polysaccharide capsule helps in protection against phagocytosis.
2. Fimbriae: helps in binding to host cells and saliva coated tooth
3. Proteinases: a large no. of hemolytic, proteolytic and lipolytic substances are produced.
• 4 proteolytic substances are recognized.
• Serine
• Aspartate
• Thiol
• Metalloprotienases
• Out of these collegenase, aminopeptidase, trypsin like protease are critical.
82. Cysteine proteinases (gingipains)
• Cleave polypeptides after arginine and lysine residue and classified as
• Arginine (Arg-) specific proteinases
• Lysine (Lys-) specific proteinases
Effects:
• ↑ vascular permeability ---↑ GCF
• Chemotactic for PMNL so ↑ conc.of PMNL at sites of tissue destruction
• Arg- gingipain distrupts oxidative burst mechanism of PMNLs.
• Only known prokaryote to inhibit this PMN function.
83. PATHOGENICITY OF P.GINGIVALIS
ADHESION & COAGGREGATION
• 1st step
• Fimbriae(major adhesive determinant)
• Proteases
• Hemagglutinins
• LPS
• Arg – gingipain also helps in binding of fimbriae to host cells
• Capable of coaggregating- strept. Spp & actinomyces spp.
• Vesicles- bridges non aggregating spp like S.aureus, certain types of candida
84. SUSTENINS• Sustenance of spp is crucial for its survival
• Biomolecules released to physiologic requirements of these bacteria
• Critical virulent factors
• Proteases- nutrition for bacterial growth in confines of their ecological environ.
• Important for survival of bacterias and collateral damage to host.
85. • Gingipains-originally considered as trypsin like protease
• Comprises of a group of cysteine endopeptidases that account for 85% of
proteolytic activity of P. gingivalis.
• Soluble and cell associated and product of 3 genes rpg A, rpg B, kpg encoding
these proteinases.
86. END PRODUCTS OF METABOLISM
• P.g utilizes peptides
• Produce ammonia & organic acids
• Used by other members in subgingival biofilm
P.g peptidylarginine deiminase
NH4
• –ve impact on neutrophil function
• Pathogen growth
88. EVASINS
• P.g alters the secretion & accumulation of selected chemokines
• Interefers with MCP-1
• IL-8 expression
• chemokine level : Ability of host to recognise bacterial species
• Ability of PMNs to remove bacterial cell
• Destruction of neutrophils before it can act-----this provides the bacteria with
proteolytic nutrients for metabolism & growth
• Attack & degrade C3a & C3b
89. • Directly activates C5 C5a
• P.g forms small outer membrane vesicles that contains bacterial proteases
• Degrade host C5a receptors that are present on the surface of attacking neutrophils
• Neutrophil loses its phagocytic function
• PMNs death & degranulation
• Release PMNs associated hydrolytic enzymes
• Further affect host cell & tissue destruction
90. • Gingipain R from P.g
• Cleaves CD14
• LPS induced IL-8 secretion from gingival fibroblast
• Immune evasion by
92. • LPS of P.g causes increase in IL1,TNFα, PGE2 capable of activating osteoclasts.
• Putrify salivary glycoproteins
• Undermining their function in maintaining homeostasis
Effects on blood factors , coagulation and clotting
• Gingipain –activates blood clotting pathways
• PMNs accumulation in actively resorbing periodontitis site
93. • LPS thrombin & IL-I in GCF tissue destruction
• Gingipain R activates factor IX, X, prothrombin
• Gingipain degrade fibrinogen very rapidly (Pike et al)
• Results non clotting host condition
• Active against fibrin gel
94. OTHER VIRULENCE FACTORS….
• Various other factors are collagenases, endotoxins, trypsin like enzyme,
fibrinolysin, proteases that destroys Ig, fatty acids, NH3, hydrogen
sulphide.
• Induces elevated systemic and local immune response in periodontitis
subjects.not seen in normal individual
95. TANERELLA FORSYTHUS
• Previously known as B. forsythus
• First described in 1979 (Tanner et al. 1979) as a "fusiform" Bacteroides at The Forsyth Institute.
• Gram-negative, anaerobic, spindle-shaped, highly pleomorphic rod.
• Difficult to grow, often requiring 7–14 days for minute colonies to develop.
• The growth of the organism was shown to be enhanced by co-cultivation with F. nucleatum and
commonly occurs with this species in subgingival sites (Socransky et al. 1988).
• The species was shown to have an unusual requirement for N-acetylmuramic acid (Wyss 1989).
96.
97. ASSOCIATION:
• Found in higher numbers
• in sites of destructive periodontal disease or
• periodontal abscesses than in gingivitis or healthy sites (Lai et al. 1987).
• in active periodontal lesions than inactive lesions (Dzink et al. 1988)
• Refractory periodontitis cases. (Listgarten et al,1993).
• Subjects who harbored T. forsythus were at greater risk for alveolar bone loss, attachment
loss and tooth loss (Machtei et al. 1999
98. • Studies using checkerboard DNA–DNA hybridization techniques to examine subgingival
plaque samples demonstrated that T. forsythus was the most common species detected from
periodontal pockets (Dibart et al. 1998).
• Listgarten et al 1993 found that T. forsythia was the spp most frequently detected in refractory
periodontitis.
• Serum Ab to this organism was often extremely elevated in subset of refractory periodontitis
subjects.
99.
100. S LAYER- MEDIATES HEME AGGLUTINATION, ADHESION/INVASION OF
EPITHELIAL CELLS, MURINE SUBCUTANEOUS ABSCESS FORMATION.
101. ADHESINS
• Coaggregates with F.nucleatum
• Increase colonisation in subgingival biofilms
SUSTENINS
• Produces enzymatic peptidase
• Degrades BANA
• Described as trypsin like proteases : ( - ) by serine protease
102. • Sialidase from T.f
• Cleaves α-ketosidic linkages between sialic acid & glycosyl residues of host
glycoproteins/glycolipids
• Modified / degraded proteoglycans : nutrition for members of oral microbiota
103. EVASINS
• T.f produce lipoproteins
• Activates gingival fibroblasts
• increase IL-6 & TNF-alpha
• Also kappa B production by fb
104. TREPONEMA DENTICOLA
ADHESINS
• Coaggregation b/w P.g & T.d is mediated by fimbriae binding protein-DENTILYSIN
• Helps transport of Pg to deeper regions
• Binds to ECM proteins like laminin fibronetin /heparin
• And host cells like gingival fibroblast
• Collagen binding proteins of T.d binds Type I,IV,V----------adherence /colonozation (Li et al)
105. • Produces major outer sheath proteins
host cells
• lectin like proteins
• Binding activity (-) mannose/galactose residues
• This protein might have porin activity –enables transportation of molecules into /out of host
cells
106. SUSTENINS
• Possess peptidases associated with its outer sheath
• Chymotripsin like protease ( Uilto et al )
• T.denticola + erythrocyte---resulting in cell lysis & competing with host for available hemin derived iron
• Synthesize 2 low iron induced outer membrane proteins : HbpA & HbpB—binds hemin
107. EVASINS
• Chymotrypsin like protease + proteins on outer sheath
• Chymotrypsin like protease complex
• Adhesion
• Degradation of humoral proteins ( basement membrane components)
• Activates MMPs
• Forms vesicles with hyaluronidase
108. Effects on host innate & immune mechanism
• T.denticola on fibroblast
• Cell rounding
• Formation of surface blebs
• Detachment from cell surface (Weinberg & Holt)
109. • Major sheath protein complex of T.d interferes with collagen attachment via β-integrin
• Direct effect on host response
• T.d produces immunosuppressive proteins (Sip)
• Lymphocyte proliferation
• By inducing an arrest at G1 phase in human T-cells
• Irreversible
• Activates apoptotic pathway in these cells
• May be resistant to β-defensins -1 & -2
110. PREVOTELLA INTERMEDIA
• Second black-pigmented Bacteroides to receive considerable interest
• Gram-negative, short, round-ended anaerobic rod
• Association:
• acute necrotizing ulcerative gingivitis ( Loesche et al. 1982),
• certain forms of periodontitis (Tanner et al. 1979, Herrera et al)
• progressing sites in chronic periodontitis (Tanner et al)
• rapidly progressive periodontitis subjects (Hillmann)
• Elevated serum antibodies to this species have been observed in some but not all subjects
with refractory periodontitis (Haffajee et al. 1988b).
111. Elimination:
Berglundh et al. (1998) demonstrated that improved clinical parameters after the use of
mechanical therapy and systemically administered amoxicillin and metronidazole were
associated with a decrease of periodontal pathogens including P. intermedia.
Successful treatment of peri-implantitis with local delivery of tetracycline also significantly
decreased the frequency of detection of P . intermedia (Mombelli et al. 2001)
112. • This species appears to have a number of the virulence properties exhibited
by P . Gingivalis
• shown to induce mixed infections on injection in laboratory animals (Hafstrom
& Dahlen 1997).
113. Pregnancy gingivitis
Physiological level of steroid hormone increases
vascular permeability increases
E/P substitute menadione as a growth factor in P.i
• P. intermedia can utilize albumin, mucin and glucose as sources of energy
• Modify its pathogenic factors (proteolytic activity, depending on the nutrients in the
environment)
• This nutritional flexibility may explain why P.intermedia resides in both subgingival
/supragingival areas
114. SPIROCHETES
• Gram-negative, anaerobic, helical shaped, highly motile microorganisms
• implicated as the likely etiologic agent of acute necrotizing ulcerative gingivitis by
its presence in large numbers in tissue biopsies from affected sites (Listgarten &
Socransky 1964, Listgarten 1965)
Cultural studies suggested that T. denticola and a "large treponeme" were found
more frequently in patients with severe periodontitis than in healthy or gingivitis
sites (Moore et al. 1982).
115. FUSOBACTERIUM NUCLEATUM
• Gram-negative, anaerobic, spindle shaped rod
• Association:
• periodontitis (Papapanou,Socransky)
• periodontal abscesses (Herrera et al. 2000).
• Elimination: Successful treatment of peri-implantitis with local delivery of tetracycline was associated
with a significant reduction in frequency of detection in several species including F. nucleatum
(Mombelli et al. 2001).
• Invasion of this species into human gingival epithelial cells in vitro was accompanied by an increased
secretion of IL-8 from the epithelial cells (Han et al. 2000).
116. CAMPYLOBACTER RECTUS
• Earlier called Wolinella rectus
• Gram-negative, anaerobic, short, motile vibrio.
• Utilizes H2 or formate as its energy source.
• It was first described as a member of the "vibrio corroders", a group of
short nondescript rods that formed small convex, "dry spreading" or
"corroding" (pitting) colonies on blood agar plates.
117. • Association:
• Higher numbers in disease sites as compared with healthy sites (Moore et al. 1983)
• In sites exhibiting active periodontal destruction (Dzink et al. 1985)
• In periodontitis patients with NIDDM.
• Elimination: found in lower numbers
• After successful periodontal therapy (Tanner et al. 1987)
• Treatment of peri-implantitis with local delivery of tetracycline (Mombelli et al.)
• Shown to produce a leukotoxin (Gillespie et al. 1992)
• Capable of stimulating human gingival fibroblasts to produce IL- 6 and IL-8
118. EIKENELLA CORRODENS
• Gram-negative, capnophilic, asaccharolytic, regular, small rod with blunt ends
• Also found in osteomyelitis, RC infections, CNS infections
• Association:
• periodontal destruction as compared with healthy sites (Savitt & Socransky 1984)
• active sites (Dzink et al. 1985, Tanner et al. 1987)
• in sites of subjects who responded poorly to periodonal therapy (Haffajee et al. 1988)
• with Aa in some lesions of LJP (Mandell 1984)
• Stimulate the production of matrix metalloproteinases (Dahan et al. 2001) and IL-6 and IL-8 (Yumoto et al.
1999).
119. PEPTOSTREPTOCOCCUS MICROS
• Gram-positive, anaerobic, small, asaccharolytic coccus.
• associated with mixed anaerobic infections in the oral cavity and other parts of the body (Finegold
1977).
• Two genotypes
• smooth genotype (associated with periodontitis lesions)
• rough genotype
• Association:
• periodontal destruction as compared with gingivitis or healthy sites (Moore et al. 1983)
• actively breaking down sites (Dzink et al. 1988).
120. EUBACTERIUM SPECIES
• G+ve, strictly anaerobic, small, somewhat pleomorphic rods
• Possible periodontal pathogens due to their increased levels in disease sites, particularly those of severe
periodontitis (Moore et al. 1982)
• Difficult to cultivate, particularly on primary isolation, and appear to grow better in roll tubes than on blood
agar plates
• Elicited elevated antibody responses in subjects with different forms of destructive periodontitis (Tew et al.
1985a,b, Vincent et al. 1986, Martin et al. 1988)
121. OTHER SPECIES
• All periodontal pathogens have not yet been identified.
• Particularly in individuals who have responded poorly to periodontal
therapy, there are chances of infection with unusual species.
• Emphasis has been placed on enteric organisms, staphylococcal species
125. PREGNANCY GINGIVITIS• Dramatic increase in levels of P.intermedia.
• Other microbes reported : P.melaninogenica, F.nucleatum, T. forsythia.
• Periodontal abscess
• F. nucleatum, P. intermedia, P. gingivalis, P. micros, and B. forsythus
126. CHRONIC PERIODONTITIS• High percentages of anaerobic (90%) gram-negative (75%) bacterial species
• Bacteria most often cultivated at high levels include P. gingivalis, B. forsythus, P. intermedia, C. rectus, Eikenella
corrodens, F. nucleatum, A. actinomycetemcomitans, P. micros, and Treponema and Eubacterium
• C. rectus, P. gingivalis, P. intermedia, f. nucleatum, and B. forsythus were found to be elevated in the active sites
• Recent studies have documented an association between chronic periodontitis and viral microorganisms of the herpes
viruses group, most notably Epstein-Barr Virus-1 (EBV-1) and human cytomegalovirus (HCMV).
127. AGGRESSIVE PERIODONTITIS
• predominantly gram-negative, capnophilic, and anaerobic rods.
• almost all LJP sites harbor A. actinomycetemcomitans, which may comprise as much as 90% of the total
cultivable microbiota.
• Other organisms found in significant levels include P. gingivalis, E. corrodens, C. rectus, E nucleatum, B.
capillus, Eubacterium ,and Capnocytophaga spp. and spirochetes
• Herpes viruses, including EBV-1 and HCMV, also have been associated
128. NECROTIZING PERIODONTAL
DISEASE:
• Microbiologic studies indicate that high levels of P. intertmedia and spirochetes in necrotizing
ulcerative gingivitis lesions.
• Spirochetes are found to penetrate necrotic tissue and apparently unaffected connective
tissue.
• In NUG F. nucleatum is also found in association
129. PERIODONTITIS IN MEDICALLY COMPROMISED
PATIENTS
• HIV PERIODONTITIS
• HIV periodontitis lesions reveal spirochetes, Fusobacterium species, A.a, W.recta, P.micros and P.intermedia each averaging
5-20% of the subgingival microflora.
• Some lesions also yield B.fragilis, F.necrophorum, E.aerofaciens, Clostridium species, enterococci and P.aeuroginosa and
C.albicans.
• DIABETES MELLITUS
• Capnocytophaga species and P. intermedia have been related to the initial breakdown in periodontium.
• W. recta, A.actinomycetemcomitans and P. gingivalis may also play a role
130. PERIODONTAL ENDODONTIC
LESION
• Reflects microbiota of the separate endodontic and periodontal lesions
(Legoff 1997)
• Accordingly it might be impossible to obtain a sample that is
representative of either of the lesion.
131. PERIIMPLANTITIS
• Healthy perimplant pockets : high proportions of coccoid cells, a low ratio of anaerobic/aerobic
species, low detection frequencies for pathogens.
• Around failing implants : A.a., P.gingivalis, T. forsythia, P.micros, C.rectus, Fusobacterium and
Capnocytophaga
• Implant associated with refractory periodontitis : P.aeruginosa, C.albicans, staphylococci aureus
132. PARASITES
Entamoeba gingivalis
• Protozoan & normal commensal
• ↑elderly individuals and in diseased mouths.
• Earlier- critical role
Now- opportunistic pathogen
• Found in soft calculus, periodontal pockets and with diseased tonsils.
Trichomonas tenax
• Only parasitic flagellate found in the oral cavity.
• Numbers are seen to increase in periodontal pockets.
133.
134.
135. VACCINE ???
• Conventional therapy : painful & frequently unsuccessful
• Recurrence of destructive process
• Prevention & control of periodontitis
136. • The three types of vaccine that were employed for the control of
periodontal disease-
1. Vaccines prepared from pure cultures of streptococcus & other oral
micro organism
2. Autogenous vaccines prepared from plaque of patients with
destrucive periodontal disease
3. Stock vaccines such as Van Cott’s vaccine, Goldenberg’s vaccine,
Inava endocorp vaccine-adminstered systemically/locally.
137. • A recent report suggested that the hemagglutinin domain was implicated in the nuclear targeting of this
protease
• Vaccines are mainly peptide & DNA vaccines (Scragg 2002)
• DNA vaccine induces cellular immunity & humoral immunity
• Peptide vaccine induces humoral immunity
138. • Further analysis is required to evaluate at which stage these immune
responses prevent P. gingivalis infection
• Recent data indicate that the gingipains (RgpA and Kgp) of P.
gingivalis are potential candidates for a vaccine
139. CLINICAL IMPLICATIONS• Aid in designing the measure to prevent these diseases
• Determination of risk factors,
• e.g. high levels of p.gingivalis in a smoker
• To monitor and evaluation of treatment outcome
• Declining level of suspected pd pathogen
• To target therapy
• Development of vaccine
• Use of antimicrobials
140. ADVANCES IN MICROBIOLOGY
• DNA based methodology for identification and detection of specific
bacteria and virus offers remarkable advantage
• No. of samples examined and no of micro organisms identified have
increased dramatically
• Also recognition of beneficial activity of several groups such as
probiotics might open new strategies in Pdl therapy.
141. CONCLUSION
• A full understanding of the microbial factors, their
pathogenicity as well as host factors are of the essential importance for
pathogenesis of periodontal disease
• Microbial diagnosis may play a vital role in treating cases of refractory
periodontitis / periodontitis related to specific microorganisms
142. REFERENCES1. Contemporary Oral Microbiology and Immunology – Slots & Taubman.
2. Clinical periodontology and implant dentistry: jan lindhe 4th edition
3. Clinical periodontology: carranza 10th edition
4. Periodontology 2000, vol 38
5. Periodontology 2000, vol 55
6. Text book of Microbiology : Ananth Narayanan, C.K. Jayram Paniker.