The document discusses the oral microbiota and its role in various oral diseases. It begins with an introduction to oral microbiology and a brief history. It then describes the normal microbial flora of the oral cavity including bacteria, fungi and protozoa. Several key bacteria associated with dental diseases like dental caries and periodontal disease are mentioned. The document also discusses the development of oral flora from infancy to adulthood. Various diseases caused by oral microbes like dental plaque, caries, periodontitis and endodontic infections are summarized. Sample collection and diagnostic methods for oral pathogens are also outlined.

1. By
N.Nitya Krishna
1st Year Post Graduate
Department of Public Health Dentistry
1

2.  INTRODUCTION
 HISTORY
 NORMAL MICROBIAL FLORA
 BACTERIAL ORAL FLORA
 FUNGI
 PROTOZOA IN THE ORAL CAVITY
 DENTAL IMPLICATION IN MICROBIOLOGY
1. Dental plaque
2. Dental caries
3. Periodontal disease
4. Endodontic infections
5. Dental abscess
 ROLE OF FLORA IN SYSTEMIC DISEASES
 PREVENTIVE APPROACH TO ORAL INFECTIONS
 ORAL MICROFLORA IN DISEASE
 ROLE OF PUBLIC HEALTH DENTIST TO KNOW ABOUT ORAL
MICOFLORA
 CONCLUSION
2

3.  The mouth is the gateway of the body to the external world and represents
one of the most biologically complex and significant sites in the body.
 This is where the first stages of the digestive process take place and,
consequently, the mouth is richly endowed with sensory functions (taste,
smell, temperature and texture).
 It also plays a critical role in communication, whether by speech or via
facial expressions, and makes a significant contribution to our appearance.
 It has been estimated that the human body is made up of over 1014 cells of
which only around 10% are mammalian. The remainder are the
microorganisms that comprise the resident microflora of the host.
3

4.  Louis Pasteur – Father of Microbiology
 Antony Van Leeuwenhook in 16th century identified bacteria and its
shapes – rods , cocci and spiral forms .
 Willoughby D. Miller proposed that carbohydrate from food were broken
down by oral bacteria and the resulting acids caused dissolution of the
enamel .
 Pierre Fauchard in 1745 described tartar and plaque .
 J.K. Clark in 1942 identified coccus from carious lesion and named as
Streptococcus mutans
4

5.  Normal oral cavity contains a mixture of organisms which include bacteria,
fungi, protozoa and occasionally viruses.
 Types of flora
1. indigenous flora
E.g:- alpha haemolytic strptococci, lactobacilli etc.
2. Transient flora
 E.g:- streptococcus pneumoniae, niesseria meningitidis etc.
3. Supplemental flora
Benefits of Oral Flora
1. Oral bacteria produce certain vitamins and cofactors which are needed by
humans .
2. Prevention of colonization by exogenous pathogens .
3. Helps in maturation of host immune system
5

6.  Bacteria are by far the most predominant type of microorganisms present
in human oral cavity .
 30 genera of bacteria are detected in human mouth and 25 of which are
regular members of the oral flora .
6

7. Bacterial stagnation areas created as a result of :
* shape of the teeth
* the topography of the teeth
{ Occlusal fissures }
* malalignment of teeth
* Poor quality of restorations
{ fillings and bridges }
 Oral bacteria can be classified
Primarily as:
 Gram – positive ( purple )
 Gram – negative ( pink )
 Oral bacteria can be classified
Secondarily as:
 Aerobic
 Anaerobic
7

8. 8

9. Cocci Bacilli
Gram positive cocci
• Streptococcus mutans
• Strept.sanguis
• Strept. mitior
• Strept. milleri
• Enterococcus species
• Peptostreptococcus species
• Micrococcus species
• Staphylococcus species
Gram positive bacilli
•Lactobacilli species
•Actinomyces species
•Propionobacterium species
•Arachnia species
•Bifidobacterium species
•Bacterionema species
•Eubacterium species
Gram negative cocci
•Veilonella species
•Neisseria species
•Branhamella species
Gram negative bacilli
•Actinobacillus species
•Fusobacterium species
•Bacteroides species
•Capnocytophaga species
•Leptotrichia species
•Treponema species
•Haemophilus species
•Stenomona species
•Eikenella species
•Wollinella species
9

10.  Besides bacteria, the normal flora of mouth may contain fungi and
protozoa
group Organism
Fungi •Candida albicans
•C. tropicalis
•C. Pseudotropicalis
Protozoa •Entamoeba gingivalis
•Trichomonas tenax
10

11. 11

12. 12

13. •Primary Oral Candidiasis
–ACUTE
•Pseudomembranous
•Erythematous
–CHRONIC
•Hyperplastic
•Erythematous
•Pseudomembranous
–CANDIDA ASSOCIATED LESION
•Denture stomatitis
•Angular stomatitis
•Median rhomboid glossitis
•Secondary candidiasis
–Manifestation of Systematic mucocutaneouscandidiasis–thymic aplasia and
candida endocrinopathy syndrome
13

14. Samples
• Whitish patches from mucous membrane of mouth
• Sputum
Method of collection
• Sterile swabs
Direct examination (Microscopy)
• KOH wet mount
• Gram staining ( Presence of yeast cells and pseudohyphae)
• Other stains: PAS and Gomori’s methenamine silver stain
14

15. Fungal culture
• Sabouraud Dextrose Agar + Antibiotics ( Cream, Pasty, Smooth
colonies in 3-4 days of incubation at 37 C)
• Cornmeal Agar (Characteristic terminal chlamydospores, yeast
cells and pseudohyphae in clusters at 25 C)
• Chrom agar (light green to bluish green colonies)
Germ tube test (Reynold’s-Braude Phenomenon)
• Culture of candida treated with sheep/normal human serum is
incubated at 37 C for 2-4 hours
• No constriction seen at the point of attachment to the yeast cell
• Appear in 2 hours for C.albicans
Chlamydospore formation
• Suspected strain of Candida isolated on rice starch agar and
incubated at 25 C
• Formation of large, highly refractile, thick walled, terminal
chlamydospores in 2-3 days of incubation
15

16. Typing of Candida strains
• Tests include serotyping and isoenzyme profiling
• Southern blotting technique used
Immunodiagnosis
• PCR based tests for candida-DNA detection
• Detection of Candida albican-derived molecules
• ELISA, RIA, CIE, PHA and LPA
16

17. Entamoeba gingivalis Trichomonas tenax
 E. gingivalis –
 found in soft calculus, periodontal pockets and infection of tonsils
 Can become opportunistic pathogen
 T.tenax – only parasitic flagellate in oral cavity
--number increases in periodontitis
17

18.  Saliva is widely used as the main sample to study the microbial flora .
 W.D Miller isolated microrganisms from saliva.
 On an average 750 million microrganisms are present in each ml of saliva
and this number may reach upto 5.5 billion / ml .
 The cultivable organisms in saliva can be 10 – 100 million / ml .
 The organisms present in saliva include veillonella species , streptococcus
oralis , s. salivarius , s.mutans and actinomyces species.
18

19.  At birth infants mouth is microbiologically sterile .
 Within few hours of birth S.Salivarius species establish themselves in the
mouth and these are transmitted from mother through feeding.
 By the end of 1 st year :
Other species of streptococci , staphylococci , nisseriae and
veillonellae develop in the oral cavity .
 Eruption of teeth :
S.mutans , S.sanguis , A.viscous establish on dental hard tissues.
19

20. Adolescence
 The greatest number of organisms in mouth occur when permanent teeth erupt.
 These teeth have deep fissures, larger inter proximal spaces and deeper gingival
crevice, allowing a great increase in anaerobes.
Adulthood
 Its chief characteristic is its complexity of oral flora.
 There is an increase in Bacteroides and Spirochetes with maturity of dental
plaque.
 As the teeth are lost the available sites for microbial colonisation decreases and
several species diminish disproportionately in numbers.
 Edentulous persons harbour few Spirochetes or Bacteroides but carriage of
Yeast increases.
 S.sanguis & mutans disappear.
20

21. 1. Dental plaque
2. Dental caries
3. Periodontal disease
4. Endodontic infections
5. Dental abscess
21

22.  According to WHO : Plaque is a highly specific
and selective but structurally variable clinical
entity characterized by sequential colonization
of microorganisms on the surface of teeth,
restoration and other parts of the oral cavity.
 It is made up of mucins, desquamative epithelial
cells and microorganisms embedded in an
extracellular matrix.
22

23. Dental
Plaque
Sub gingival
Tooth
associated
Tissue
associated
Supra gingival
23

24. 24
• Gram +ve cocci and short rods
predominant at tooth surfaces.
• Gram –ve rods, filaments,
spirochetes, at outer surfaces.
Supra gingival
• Filamentus microorganisms
dominate.
• Cocci and rods also present .
• Gram +ve rods and cocci:
• St. mitis, St. sangius
• A. Viscosus , naeslundii
• Eubacterium.
Sub gingival
Tooth associated
Subgingival Tissue
associated
St. oralis, St. intermedius
Peptostreptcoccus micros
P. gingivalis, P. intermedia
T. Forsythis, F.
Nucleatum

25.  Microrganisms don’t colonize on the mineralised tooth surface.
 The teeth are always covered by an acellular proteinaceous film ,the
pellicle that forms on the naked tooth surface within mins to hours.
 The bacteria colonize the tooth surface only when pellicle is in place for
hours.
 The pellicle consists of salivary glycoproteins adsorbed to the enamel
mineral to forma a membranous biofilm
 Attachment of single bacterial cell (0-4h)
 Growth of attached bacteria leading to formation of distinct micro
colonies.
(4-24h)
 Microbial succession and co-aggregation .(1-14 days)
 Climax community plaque.(2 weeks or older)
25

26. 26

27.  Function of pellicle-
 Protect enamel.
 Reduces friction.
 Provide matrix for re-mineralization.
 Pellicle contains-lysozyme,albumin,IgA,IgG.
Early colonisation :
 Plaque builds up first in small defects or pits on the enamel surface and then spreads
over the tooth surface.
 Early succession evolves adhesion between pellicle and pioneer organism.
 S.sanguis ,A.viscosus,A.naeslundii and peptostreptoccous attaches within 1 hr.
27

28. In addition it may also contain epithelial cells, macrophages and leucocytes
1 gram of dental plaque contains approximately 2 * 10 bacteria.
Other microorganisms which may be found in the dental plaque include
Mycoplasma sp., yeast and viruses.
colonization by other bacteria such as Prevotella intermedia, Fusobacterium
nucleatum and Porphyromonas gingivalis.
Later on additional plaque bacteria such as Actinomyces can also bind.
Streptococcus mutans and strept. Sanguis initially colonise the dental pellicle
through adhesins.
28

29. Characteristics Early Mature
Gram reaction + _
Morphotypes branching rods, cocci Cocci, rods, spirochetes
Energy metabolism Facultative aerobic Facultative anaerobic
Tolerated by host Well Can cause caries and
gingivitis
29

30. 1. Calculus formation
Both supragingival and subgingival plaque become calcified.
Calcified plaque is named as dental calculus.
2. Dental caries
Inorganic components of teeth are demineralized by acids produced by the
plaque microflora.
Demineralization leads to weakening of the tooth syructure, cavity formation
and eventual loss of tooth.
3. Periodontal disease
It may affect the marginal gingiva, periodontal ligament, cementum or alveolar
bone.
4. Other oral disease
1. Infections of dental plaque or periapical abscess.
2. Acute necrotizing ulcerative gingivitis.
3. Periodontal abscess.
30

31.  Dental caries is characterised by demineralization of the inorganic
components of the tooth, leading to weakening of tooth structure, cavity
formation and eventual loss of tooth.
 Etiology
 1. Host
 2.Diet
 3.Time
 4. Microbial flora in plaque
1. HOST
 Structure of enamel and the nature of saliva play a significant role in
dental caries.
 Quality and quantity of saliva significantly influences the occurrence and
progression of dental caries.
 High calcium and phosphorous in saliva are important for remineralization
during early stage of the disease.
31

32. 2. DIET
 Microflora in the oral cavity ferment dietery carbohydrates with the
production of acid which destroys the dental tissue.
 Highly cariogenic carbohydrate- sucrose-acts as substrate.
3. TIME
 Prior to the ingestion of carbohydrates, the pH in the oral cavity is slightly
acidic or alkaline.
 After ingestion of carbohydrates the plaque pH rapidly drops by 2 or more.
 Length of time that this acidic environment (low pH) is sustained to
damage the enamel is extremely important in occurrence of dental caries.
.
32

33. Initiation of carious lesions.
Demineralisation of the tooth enamel
Continuous acid production
Glucan-adheres to the smooth surfaces of the teeth and thus forms the
matrix of the dental plaque.
converts dietary sucrose to glucan
Produce enzymes called glycosyltransferases
Strept. mutans, Strept. Sobrinus etc.
33

34. 1. Reduction of microbial flora of oral cavity by proper oral hygiene and use
of antimicrobials.
2. Regular brushing and flossing may prevent stagnation of food debris and
thus reducing the incidence of caries.
3. Control of dietary carbohydrate intake especially sucrose rich diet.
4. Improvement of tooth resistance by incorporation of fluorides in water and
by topical fluoride application.
5. Removal of dental plaque by mechanical methods ( scaling).
Microbiological tests to assess dental caries
 Salivary counts of S. mutans and lactobacilli have been advocated for the
detection of patients who are at higher risk for developing caries
34

35.  Periodontal disease is a term used for many pathological conditions of the
gingiva, periodontal ligament, cementum and alveolar bone.
Etiology
1. Multifactorial
2. Induced by dental plaque
3. Appear as a transient, reversible inflammation called gingivitis
 If the disease persists, inflammation extends into deeper tissues and the
gingival connective tissue is progressively destroyed.
 Periodontal microflora, host defences and extrinsic factors play role in
production of disease.
 Since anerobes are the major bacterial species in the subgingival microflora,
they are involved in infections of the periodontium.
35

36.  These include Spirochetes, Bacteroides, Fusobacterium etc.
 Intrinsic factor- nutrition, immunological defects and metabolic disorders-
decrease the host defence against subgingival microflora.
 Extrinsic factor- poor oral hygiene, calculus- accumulation of subgingival
bacteria.
Various periodontal disease
1. Gingivitis
2. Periodontitis
3. Localised juvenile periodontitis
4. Acute necrotizing ulcerative gingivitis
36

37. Gram positive:
 Actinomyces viscosus
 Actinomyces naeslundii
 Streptococcus sanguis
 Streptococcus mitis
 Peptosreptococcus micros
 Gram negative:
 Fusobactecterium nucleatum
 P. intermedia
 Veillonella parvula
 Wolinella
 Haemophilus species
37

38. 2. Chronic Periodontitis
 It is characterised by destruction of connective tissue attached to the teeth.
Etiology
 Bacteroides gingivalis
 B. intermedius
 Streptococcus milleri
 P. gingivalis
 P. Intermedia
 A. Actinomycetemcomitans
3. Localised juvenile periodontitis
 Found in adolescents, especially females
Etiology
 Actinobacillus actinomycetemcomitans
38

39. 4.Acute necrotizing ulcerative gingivitis
 Acute necrotising ulcerative gingivitis is a relatively rare condition and is
characterised clinically by necrosis of the free gingival margin, the crest of
the gingiva and the interdental papillae.
 “Punched-out” erosion of the interdental papillae occurs
Etiology
 Borellia vincenti- fusiform bacillus- spirochete.
Laboratory diagnosis
 It is done by examination of smear prepared from the ulcerated lesion.
 Gram staining of the smear shows spirochetes, fusobacterium and
leycocytes.
Systemic spread of periodontal disease
 Infection of damaged valve of rheumatic heart patients, joint prostheses
and endocardial implants may occur by bacteria derived from periodontal
disease
39

40. 40

41. Source
 Most important source of endodontic infection is infected carious lesion.
 From the carious lesion the bacteria migrates to the pulp.
 Periodontitis is another source of infection of endodontic tissues.
 Endodontic infections can act as source for spreading infection to various
organs through blood.
 Septicemia, bacteremia, endocarditis etc. occur secondary to endodontic
infections.
Lesions
1. Granuloma and cysts
2. Abscesses
3. Cellulitis
4. Osteomyelitis
5. Ludwigs angina
41

42. Etiology
 Strptococcus milleri- most common
 Bacteroides endodontalis and B. gingivalis- predominant anaerobes
 Other bacteria- Fusobacterium sp. , anaerobic streptococci, lactobacillus
species etc.
Laboratory diagnosis
 Specimens from root canal are collected under aseptic conditions.
 Anaerobic transport medium is used for transport of the specimen
 Both aerobic and anerobic culures are done according to conventional
methods.
Dental abscess
 Types-
 Periodontal
 Gingival
 periapical
42

43. PERIODONTAlABSCESS GINGIVALABSCESS
PERIAPICALABSCESS
43

44.  It has been recognized that plaque related oral diseases, especially
periodontitis, may alter the course and pathogenesis of a number of
systemic diseases.
44

45.  Cardiovascular disease
1. Atherosclerosis etc.
 Cerebrovascual disease
1. Stroke
 Pregnancy outcome
1. low birth weight infants
 Respiratory system
1. Chronic obstructive pulmonary disease
2. Bacterial pneumonia
 Diseases of connective tissues, bones and joints
1. Rheumatoid arthritis
45

46.  Cardiovascular disease (CVD) is a class of
diseases that involve the heart or blood
vessels which includes coronary heart
diseases (CAD).
 Most of the coronary heart diseases are caused by
atherosclerosis.
 Genetic factors include age, lipid metabolism,
obesity, hypertension, diabetes etc.
 Environmental risk factors include
socioeconomic status, exercise stress, diet,
smoking, and chronic infection etc.
 Evidence linking chronic infection such as
periodontal disease has shown to be capable of
causing cardiovascular disease.
.
46

47. Thromboembolic events
Vessel wall thickening,
Atheroma formation
Thrombus formation
Cytokine/growth factor production
Monocyte infiltration/proliferatioon
platelet adhesion/aggregation,
Endothelial damage,
Gram negative bacteria
Porphyromonas gingivalis Actinobacillus actinomycetocomitans
Periodontal infection
47

48. Author And Journal Aim OfThe Study Materials And Methods Results
Mahendra J et al
Indian J Dent
Res 2015 Mar-
Apr;26(2):189-
95
to assess the
prevalence of
eight putative
periodontal
pathogens in
atherosclerotic
plaque of
coronary artery
disease patients
and comparing
them with non
cardiac
subjects.
250 patients with CAD were
screened.
51 cardiac and non cardiac
subjects within the age
group of 40-80 years,who
met the eligibility criteria,
were selected and
categorized as the
experimental and control
group respectively.
Plaque Index and Oral
Hygiene Index (OHI).
Periodontal pocket depth
and clinical attachment level
were assessed.
Both, subgingival and the
coronary atherosclerotic
plaque samples were
subjected to polymerase
chain reaction (PCR)
analysis for identification of
the periodontal bacteria.
Association of Tannerella
forsythia (T.f),
Campylobacter rectus
(C.r), Eikenella corrodens
(E.c), Porphyromonas
gingivalis (P.g),
Treponema denticola
(T.d), Prevotella
nigrescens (P.n)
,Aggregatibacter
actinomycetemcomitans
(A.a), P.g (fi mA gene) and
Prevotella intermedia
(P.i), was significantly
associated.
A. Actinomycetocomitans
was present only in the
experimental group
48

49. Author And
Journal
Aim OfThe Study Materials And Methods Results
Khatri et al
Singapore
Dent J 2016
Dec;37:9-13
to assess the
interrelationship
between periodontitis and
atherosclerosis by
comparing the ultrasound
and clinical markers
of atherosclerosis in
systemically healthy
patients with and
without periodontitis and
whether periodontitis can be
an independent risk factor
for atherosclerosis.
Total 40 subjects, of
same socioeconomic
status, belonging to
age group of 35-65
years, were recruited
and divided into two
groups –
Group I (Chronic
Generalised Periodo
ntitis without any
systemic disease: CP-
SH),
Group II (Normal
healthy patients
without periodontitis
and any systemic
disease - SH)
Carotid ultrasound
revealed right and
left intima media
thickness (IMT) of
0.626±0.016mm and
0.715±0.037mm
respectively in cases
and 0.495±0.009mm
and 0.518±0.009mm
respectively in
controls, with the
difference being
statistically
significant. In cases,
mean diastolic blood
pressure (DBP) was
83.45±4.07mmHg
and
79.25±3.63mmHg in
controls, with the
difference being
statistically
significant. 49

50. A. Acute infective endocarditis
 S. aureus
 Aerobic Gram negative bacilli- Pseudomonas
B. Sub acute infective endocarditis
 Viridans strain of Streptococci
 Enterococci
 Fungi
 HACEK (Haemophilus,
Actinobacillus, Cardiobacterium,
Eikenella and Kingella)
50

51. 51

52.  A stroke is a rapid loss of brain function due to disturbance in the blood
supply to the brain. This can be due to ischemia (lack of blood flow) caused
by blockage (thrombosis, arterial embolism), or a haemorrhage
 Ischemic cerebral infarction or stroke is often preceeded by systemic
baterial or viral infection.
 Bacterial pathogens, antigens, endotoxins, and inflammatory cytokines of
periodontitis contributes to atherogenesis and thromboembolic events.
52

53. Author And Journal Aim OfThe Study Materials And Methods Results
Hashemipour MA
et al
Dent Res J
(Isfahan) 2013
Sep;10(5):613-9
To investigate
the gingivitis
and
periodontitis as
a risk factor of
stroke in
Iranian
population.
A case-control study
was conducted on 100
patients suffering
from stroke as case
group, and 100
hospitalized patients as
control group.
case group - 42 males
58 females,
control group -44 males
56 females.
Clinical attachment
level, periodontal
pocket, were recorded
by gingival and
periodontal indexes.
The average of gingival
index in men and women
of case group in order was
1.22 ± 0.55 and 1.31 ± 0.55
with this fact that this
number in women is more
than men.
Periodontal index in both
groups in men was more
than women and there
was significant
relationship between this
index and gender (P =
0.031). Furthermore,
periodontal index in case
group was more than
control group (P = 0.001).
Relationship between age
and periodontal disease in
case group was significant
(P = 0.03)
53

54. Author And Journal Aim OfThe Study Materials And Methods Results
Grau AJ et al
Stroke 2004; 35(2);
87-95.
investigated whether
periodontal disease,
including periodontitis
and gingivitis, is a risk
factor for cerebral
ischemia.
a case-control study
with 303 patients
examined within 7
days after acute
ischemic stroke or
transient ischemic
attack, 300 population
controls, and 168
hospital controls with
nonvascular and
noninflammatory
neurological diseases
Results revealed
that Patients had
higher clinical
attachment loss than
population (P<0.001)
and hospital
(P=0.010) controls.
Subjects with severe
periodontitis (mean
clinical attachment
loss >6 mm) had a
4.3-times-higher risk
of cerebral ischemia
than subjects with
mild or without
periodontitis (≤3 mm).
54

55. Vaginal colonization with group B streptococci or bacteroides increase the risk of
preterm delivery, low birth weight infants.
Four organisms associated with mature plaque and progressing periodontitis,
Bacteroides forsythus, P. gingivalis, A. actinomycetemcomitans, and Treponema
denticola, are detected at higher levels in mothers of preterm low-birth-weight infants
than in controls.
Low birth weight, defined as a birth weight of 2,500 grams.
Changes in hormone levels during pregnancy promote an inflammation termed
pregnancy gingivitis.
55

56. Author And Journal Aim OfThe Study Materials And Methods Results
Jacob PS et al
J Periodontal
Implant
Sci. 2014
Apr;44(2):85-
93
To determine
whether
periodontitis
among mothers in
the rural
population of india
is a risk factor for
low birth weight
babies.
A hospital-based case control
study was conducted among
340 postpartum mothers.
The cases consisted of 170
women who had given birth
to babies weighing <2,500 g,
while the control group
consisted of 170 women who
had given birth to babies
weighing ≥2,500 g.
Low Birth Weight
cases had a
significantly worse
periodontal status
than the controls,
having an odds ratio
(OR) of 2.94
(P=0.01).
56

57. Author And Journal Aim OfThe Study Materials And Methods Results
Moliterno LF et al
J Clin Periodontol
2005
Aug;32(8):886-90.
To verify a
possible
association
between
periodontitis and
low-birth-weight
babies
151 mothers were
examined.
Cases- 76 mothers with
( mean age 25.6 years),
babies birth weight -
<2500 g.
Control- 75 mothers with
( mean age 24.4 years),
baies birth weight - >
2500 g.
Probing pocket depth
(ppd) and clinical
attachment loss (cal) in
six sites were measured.
The median number and
percentage of sites with
PPD>4 and CAL>3 mm
was 8% and 5.6%,
respectively, in the case
group. The corresponding
numbers for the control
group were 4% and 2.5%,
respectively.
The mean weight at birth
was 1924 ( 417)g in the
case group and 3253 (
412) g in the control
group.
The results of the present
study showed that the
adjusted OR for the
association between
periodontitis and LBW
was 3.48.
57

58. Aspiration of oral pathogens into lungs,
Aspiration of oral pathogens such as P.gingivalis into lungs
Adhesion and colonization of respiratory pathogens
bacterial interactions (Plaque bacteria Respiratory
pathogens )
Periodontal disease associated enzymes may destroy
salivary pellicle on respiratory bacteria
Cytokines released during periodontal disease may alter
respiratory epithelium and promote respiratory diseases
58

59. Author And
Journal
Aim OfThe Study Materials And Methods Results
Prasanna SJ
J Indian Soc
Periodontol
2011
Oct;15(4):35
9-65
To evaluate the
potential
association
between
periodontal
health and
COPD and to
assess the
potential health
status of patients
with and without
COPD
Observational study
100 patients
Group A - 50
COPD patients
Group B - 50 patients
without COPD.
Gingival Index (GI)
and Papilla Bleeding
Index (PBI) were used
to assess the gingival
status.
Periodontal indices
included Russell's
Periodontal Index (PI)
and Periodontal Index
were assessed.
The mean indices of all
variables between groups were
found to be highly significant
(P<0.001). The scores were
highly significant in COPD
group than in non-copd group.
59

60.  Pneumonia is an infection of pulmonary parenchyma caused by a wide
variety of infectious agents, including bacteria, fungi, parasites, and
viruses.
 Failure of host defense mechanisms to eliminate them, multiplication of
the microorganisms, result in subsequent tissue destruction.
 Anerobic organism from periodontal pockets may serve as the primary
inoculum respiratory diseases
 Among the oral bacterial species implicated in pneumonia are
A. actinomycetemcomitans, Actinomyces israelii , Capnocytophaga spp. ,
Eikenella corrodens , Prevotella intermedia, and Streptococcus
constellatus are found in subgingival plaque
 Potential respiratory pathogens (prps) such as Streptococcus pneumoniae,
Mycoplasma pneumoniae, and Haemophilus influenzae can colonize the
oropharynx and can be aspirated into the lower airways.
60

61.  Rheumatoid arthritis is a chronic destructive inflammatory disease
characterized by the accumulation and persistence of an inflammatory
infiltrate in the synovial membrane that leads to synovitis and the
destruction of the joint architecture resulting in impaired function.
Joints like ankles, knees, elbow, wrists
are involved
61

62. 62

63. Author And Journal Aim OfThe Study Materials And Methods Results
Ranade SB et al
J Indian Soc
Periodontol.201
2 Jan;16(1):22-7
To investigate
any
relationship
between
periodontitis
and
rheumatoid
arthritis
The study was done in parts:
Part A: The study population
comprised of 80 individuals
between the ages 20-70 years,
which were divided into two
groups of 40 each.
Group I: Subjects diagnosed with
rheumatoid arthritis (RA group)
Group II: Subjects in control
group without rheumatoid
arthritis Non-RA group
Part A of the study evaluated and
compared the periodontal
condition of individuals having
RA those who don′t have it.
Part B: Complete periodontal
treatment was done for 10
patients of group suffering
from periodontitis. All
parameters of periodontal indices
were measured pre-operatively
and weeks after completion of
periodontal treatment.
The prevalence of
periodontitis in RA
group was
significantly high
(97.5%). Only 1 - no
periodontitis, 5
(12.5%) - mild
periodontitis, 30
(75%) - moderate
periodontitis, 4
(10%) had -severe
periodontitis.
There was
statistically,
significant reduction
in parameters
postoperatively with
concomitant decrease
in periodontal
parameters in RA
group.
63

64.  As a public health dentist it is very important to in detail about the oral
microflora, as we commonly come across these micro organisms while
treating the diseases like dental caries ,periodontitis etc.
 We also should know about the various types of microflora in oral cavity,
the mechanism by which they cause various diseases so that we can
effectively prevent the disease.
 Also, there are microoraganisms which are beneficial for the body thus
treatment planning of any disease should not interfere with these
microorganisms.
70

65.  The mouth has a resident microflora with a characteristic composition that
exists, for the most part, in harmony with the host.
 This microflora is of benefit to the host and contributes to the normal
development of the physiology and host defences of animals and humans.
Components of this microflora can act as opportunistic pathogens when the
habitat is disturbed or when microorganisms are found at sites not normally
accessible to them.
 Dental diseases, caused by imbalances in the resident microflora, are highly
prevalent and extremely costly to treat.
 An understanding of the relationship between the oral microflora and the
host, and how this relationship can be perturbed by exogenous and
endogenous factors, is critical to understanding oral diseases and in
developing new preventative strategies.
71

66.  RRB Russell. Microbiological aspects of caries prevention. In:John J.
Murray, June H Nunn, James G Steele. The Prevention of Oral Disease.6th ed.
Oxford university press; 2003. p. 31-61.
 Ananthanarayan and Paniker's .Textbook of Microbiology. 8TH ed .Oxford
Universities Press;2009. p.1-370.
 Sivapathasundharam B. Microbial diseases of oral cavity. In: Shafer W.G, Hine
M.K, Levy B.M. Shafer’s text book of Oral Pathology. 6th ed. Noida: Reed
Elsevier India;2009.p.311-389.
 Oral microbiolgy. In: Baveja CP. Textbook of microbiology. 2nd ed. CBS
Publishers; 2008.p.333-338.
 Marsh PD, Martin MV. Oral microbiology.5th ed. Noida: Reed Elsevier
India;2009.p.1-160.
 Brain.L, Mealey, Perry R.Klokkevold. Periodontal medicine: Impact of
periodontal infection on systemic health.In: Michael G. Newman, Henry H.
Takei, Perry R. Klokkevold. Carranza’s Clinical Periodontology. 10th ed.
Noida:Reed Elsevier India; 2007.p.318- 330.
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67. .
 Khatri R, Deshmukh J, Shrivastava R, Gupta S, Kawadkar A, Vinaya
Kumar K. Is periodontitis an independent risk factor for subclinical
atherosclerosis?. Singapore Dent J. 2016 Dec;37:9-13.
 Ranade SB, Doiphode S. Is there a relationship
between periodontitis and rheumatoid arthritis? J Indian Soc
Periodontol.2012 Jan;16(1):22-7.
 Prasanna SJ. Causal relationship between periodontitis and chronic
obstructive pulmonary disease. J Indian Soc Periodontol. 2011
Oct;15(4):359-65.
 Moliterno LF, Monteiro B, Figueredo CM, Fischer RG. Association
between periodontitis and low birth weight: a case-control study. J Clin
Periodontol.2005 Aug;32(8):886-90
73

68.  Jacob PS, Nath S. Periodontitis among poor rural Indian mothers increases
the risk of low birth weight babies: a hospital-based case control study. J
Periodontal Implant Sci. 2014 Apr;44(2):85-93.
 Mahendra J, Mahendra L, Nagarajan A, Mathew K. Prevalence of eight
putative periodontal pathogens in atherosclerotic plaque of coronary artery
disease patients and comparing them with noncardiac subjects: A case-
control study. Indian J Dent Res. 2015 Mar-Apr;26(2):189-95.
 Grau AJ, Becher H, Ziegler CM, Lichy C, Buggle F, Kaiser C et al.
Periodontal Disease as a Risk Factor for Ischemic Stroke. Stroke 2004;
35(2): 87-95.
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