At the end of this session, the student should be able to describe: What is Periodontium and its role Ecology of Dental Crevice and its role Conditions that affect Periodontal tissue Role of Microorganisms in Periodontal Disease Complex relationship between Plaque and periodontal disease

1. MICROBIOLOGY OF
PERIODONTAL DISEASES
Dr. Ali Yaldrum
Faculty of Dentistry, SEGi University.

2. LEARNING OBJECTIVES
• At the end of this session, the student should be able to describe:
What is Periodontium and its role
Ecology of Dental Crevice and its role
Conditions that affect Periodontal tissue
Role of Microorganisms in Periodontal Disease
Complex relationship between Plaque and periodontal disease

3. The term ‘periodontal diseases’ embraces a number of
conditions in which the supporting tissues of the teeth are
attacked.

4. Supporting tissues are
• Gingivae
• Cementum
• Alveolar Bone
• Periodontal Ligament Fibers (PDL)

6. ECOLOGY OF DENTAL
CREVICE
Ecology of dental crevice is different from other sites in the
oral cavity
• more anaerobic
• bathed in gingival crevicular fluid (GCF)
*In diseased state crevice becomes a pocket

7. • In Periodontal pocket
• Low Eh (oxidation reduction potential)
• increased flow of GCF
➡in gingivitis: 147% increase
➡in periodontitis: 30 fold increase

8. GINGIVAL CREVICULAR FLUID
GCF contains
• humoral and cellular defense factors
• proteins & glycoproteins

9. assachrolytic & proteolytic increased growth & enzyme activity of periodontal pathogen Porphyromonas gingivalis
Metabolism
ENVIRONMENT Proteolysis Decreased pH increased temperature
enhanced attachment of microbes with epithelium slight increase during inf lammation
alter the gene expression
alter the competitiveness of P. gingivalis
periodontal pathogens
disturbing the natural balance
of subgingival microflora
growth of proteolytic
gram -ve organisms

10. • Flow of GCF can remove planktonic microorganisms
• Prevotella, Porphyromonas, Fusobacterium spp. adheres to Streptococcus
& Actinomyces colonizing cementum
• Parvimonas micra adhere crevicular epithelial cells

11. C X X
Tissue
destruction
D
D
Gingiva
Tooth C Fluid flow
C
A
A Systemic
A Modulation
of host
defences
Cellular
Immune response –
innate and adaptive
Fig. 6.16 Pathogenic synergy in the aetiology of periodontal diseases. Bacteria capable of causing tissue damage directly (e.g.
species X) may be dependent synergy in the aetiology other cells (e.g. organisms C and D) for essential damage or attachment sites
Pathogenic on the presence of of periodontal diseases. Bacteria capable of causing tissue nutrients
so that they can grow and (e.g. speciesremoval forces provided presence of other cells (e.g. organisms C and D)both of these groups of
directly
resist the X) may be dependent on the by the increased flow of GCF. Similarly, for
essential nutrients or attachment sites so that they can grow and resist the removal forces provided by the
bacteria may be reliant for their survivalSimilarly, both of these groups ofA and C) to be reliant for the host defences. Individual bacteria
increased flow of GCF. on other organisms (e.g. bacteria may modulate their survival on other
may have more than one role(e.g. A and C) to modulatethe host defences. Individual bacteria may have more than one role
organisms (e.g. organism C) in the aetiology of disease.
(e.g. organism C) in the aetiology of disease.
destruction directly (and satisfy Koch’s postulates), that the tongue may act as a reservoir for these peri-
while in other pockets, different bacteria could fill odontal pathogens. Some pathogens may also persist

12. • The main aetiological agent of periodontal disease is microflora
inhabiting subgingival plaque.
• Host tissues and its specific and non- specific host defense
mechanisms play crucial modulating roles.

13. HOST TISSUE
• Dentogingival junction is most vulnerable site for microbial attack
but can be maintained healthy with good oral hygiene
• Plaque accumulates close to the gingival margin, the host
defenses are overcome and gingival inflammation (gingivitis) and
subsequent periodontal inflammation with loss of attachment
ensues (periodontitis).

14. Specific Host Defense Factors Non-specific Host Defense Factors
Polymorphs
B and T Lymphocytes
Macrophages
Complement system
Proteases
Antibodies: IgA, IgG, IgM
Lyzozyme
Lactoferrin
IgG, Immunoglobulin G.

15. Dental Plaque is an essential aetiological agent in the development
and progression of periodontal diseases and is shown by the
following
— Epidemiological data
— Clinical Studies
— Topical application of antimicrobial agents
— Initiation of disease in gnotobiotic animals by peridontopathogenic bacteria

16. PLAQUE SPECIFIC HYPOTHESIS
— In certain disease states such as necrotizing ulcerative gingivitis the key aetiologic
agents are fusobacteria and spirochaetes. Direct involvement of Aggregatibacter
actinomycetemcomitans in aggressive (juvenile) periodontitis
— Disease can be resolved by appropriate antibiotics active against anaerobes
(metronidazole) and tetracycline.

17. NON-SPECIFIC PLAQUE HYPOTHESIS
— Collective groups or consortia of different bacteria have the total complement
of virulence factors required for periodontal tissue destruction
— some bacteria can substitute for others absent from the pathogenic
consortium.
— This hypothesis implies that plaque will cause disease irrespective of its
composition, and it is supported by the clinical findings of numerous bacterial
species in diseased periodontal pockets.

18. the putative pathogens, but also by interfering with response of the host, and (c) connective tissue and
the environmental factors that drive the changes bone metabolism. These interactions are influenced
in the balance in the microflora, e.g. such as by reduc- by disease modifiers, which may be genetic (e.g.
ing the severity of the inflammatory response, or by neutrophil defects) or environmental (e.g. tobacco
ECOLOGICAL PLAQUE HYPOTHESIS
altering the redox potential of the pocket to prevent
the growth of the obligate anaerobes. Other relevant
changes in the local environment that could perturb
smoking) factors. The clinical signs reflect the sum
of these interactions, and the severity of the disease
can feed back to influence the microbial challenge,
Predominantly
Gingival
Gram positive microflora
health
Plaque Reduced Low GCF flow
reduction inflammation Higher Eh Facultative
anaerobes
Inflammatory Environmental Ecological
response change shift
Predominantly
Gram negative microflora
Plaque Increased High GCF flow
Gingivitis
accumulation inflammation Lower Eh Obligate
anaerobes
Fig. 6.17 A schematic representation of the ‘ecological plaque hypothesis’ in relation to periodontal disease. Plaque
accumulation produces an inflammatory host response; this causes changes in the local environmental conditions which favour
the growth of proteolytic and anaerobic Gram negative bacteria. Disease could be prevented by not only targeting the putative
pathogens, but also by interfering with the factors driving their selection.
134

19. Ecology of Healthy Gingival Crevice

20. Ecology in Gingivitis

21. Ecology in Periodontitis

22. Oral Microbiology
V. parvula
A. odontolyticus
S. oralis C. rectus
S. mitis C. gracillis P. gingivalis
E. corrodens P. intermedia T. forsythia
P. nigrescens E. nodatum T. denticola
Streptococcus spp. S. constellatus P. micros
S. gordonii F. nucleatum
S. intermedius
E. corrodens
Aggregatibacterium (Actinobacillus)
C. gingivalis
actinomycetemcomitans b.
C. sputigena
C. ochraceae
C. concisus
A. a serotype a
Fig. 6.10 The grouping of bacteria into complexes to reflect their relationship with the host in health and periodontal disease.
The ‘red complex’ is found most frequently in deep periodontal pockets, and their presence was usually preceded by members
of the ‘orange complex’. Members of the ‘yellow’, ‘green’ and ‘purple’ complexes were generally associated with healthy sites.
Purple, Yellow, Green: Healthy Gingival sulcus Red, Orange: Periodontal pockets
and Treponema denticola, and their presence was often approaches has identified low levels of many of
preceded by members of the orange complex, which the putative pathogens at healthy sites, while evi-
was also often found in deeper pockets, but was dence of transmission of organisms such as P.
more diverse in membership. In contrast, species gingivalis and A. actinomycetemcomitans between
of the yellow, green and purple complexes, together spouses has been obtained. However, in either sit-

23. Plaque-associated gingivitis has been separ ated into three stages
• Stage 1: The initial lesion
• Stage 2: The ear ly lesion
• Stage 3: Established lesion

24. STAGE 1:THE INITIAL LESION
• develops within 4 days of plaque accumulation.
• Micro-flor a consists mostly of Gr am-positive cocci (Streptococcus spp.).
• Histologically, there is an acute inflammator y reaction.
• The lesion is char acter ized by increased flow of GCF, migr ation of PMN
leukocytes into the gingival sulcus from the local vasculature .
• Adjacent to the junctional and sulcular epithelia, the inflammator y infiltr ate
occupies approximately 5-10% of the gingival connective tissue .
• This initial lesion is not visible clinically.

25. STAGE 2: THE EARLY LESION
• Appear s after approximately 7 days of plaque accumulation, detectable
clinically as gingivitis.
• lower oxygen tension and the plaque flor a shifts to more Actinomyces spp.,
spirochaetes and capnophilic or ganisms.
• Histologically, the gingival infiltr ate in the ear ly lesion is dominated by
lymphocytes (75%) and macro-phages,few plasma cells
• The infiltr ated area occupies approximately 15% of the mar ginal gingival
connective tissue , with some local destr uction of collagen.
• Migr ation of polymor phonuclear leukocytes into the gingival sulcus and
crevicular fluid peaks at 6 to 12 days following the onset of clinically

26. STAGE 3: ESTABLISHED LESION
• After a var iable per iod of time the subgingival microflor a develops into an
environment that can suppor t the growth of obligate anaerobes such as
Porphyromonas gingivalis and Prevotella inter media.
• Histologically, there is a fur ther increase in the size of the inflammator y
lesion within the affected gingiva, with a shift to a predominance of plasma
cells and B-lymphocytes.
• The junctional and pocket epithelia are heavily infiltr ated with neutrophils.
Plasma cells are found at the per ipher y of die lesion, while macrophages and
lymphocytes are present in the lamina propr ia of the pocket wall.
• Established lesions may per sist for months or year s without progression to
per iodontitis.

27. TYPES OF GINGIVITIS
• Chronic Marginal gingivitis
• Acute Necrotizing Ulcerative gingivitis
• Medication influenced gingivitis
• Gingivitis associated with systemic diseases
• Acute Herpetic gingivostomatitis

28. PERIODONTITIS
Per iodontitis may be defined clinically as inflammation
of the suppor ting tissues of the teeth.

29. • Maintains all the features of the established lesion of gingivitis
• Migr ation of the junctional epithelium down the root surface , alveolar bone
resor ption and subsequent pocket for mation
• Char acter ized by progressively destr uctive changes destroying alveolar bone
and per iodontal ligament, with an attachment loss of more than 3 mm.
• Histologically, the conver sion of the established lesion of gingivitis into
per iodontitis is char acter ized by destr uction of the connective tissue
attachment to the root surface and by alveolar bone loss.

30. FORMATION OF DENTAL POCKET
• Creates highly anaerobic environment
• pH shifts from 6.9 to approximately 7.4 to 7.8 and the pocket is continually
bathed by the protein-r ich GCF, which encour ages growth of proteolytic
bacter ia.
• Subgingival plaque have a dense zone of mostly Gr am-positive bacter ia
attached to the tooth surface and a less densely packed zone of mainly
Gr am-negative or ganisms next to the gingival surface .

31. REFERENCES
Philip D. Marsh, Michael V Martin, “Plaque mediated diseases- Dental Caries and Periodontal
diseases” in Oral Microbiology, 5th Edition, Churchil Livingstone, 2009, pp 117-137
J. Bagg, T. W. Macfarlane, I. R. Poxton and A. J. Smith, “Periodontal Diseases” in Essentials of
Microbiology for Dental Students, 2nd Edition, Oxford University Press, 2006 pp 249-259
Lakshman Samaranayake, “Microbiology of Periodontal diseases” in Essential Microbiology for
Dentistry, 3rd Edition, Churchil Livingstone, Elsevier, pp 275 - 287.