The document discusses various hypotheses regarding the role of plaque in periodontal diseases, including the non-specific, specific, updated, ecological, and keystone pathogen hypotheses. It highlights that while all hypotheses acknowledge plaque accumulation leads to gingivitis, the transition to periodontitis remains complex and not fully explained. A new hypothesis is needed to clarify the intricate interactions between oral microbes and host responses that influence disease progression.

1. PLAQUE HYPOTHESIS

3. CONTENTS
• Introduction
• Definitions
• Non specific plaque hypothesis
• Specific plaque hypothesis
• Updated plaque hypothesis
• Ecological plaque hypothesis
• Keystone pathogen plaque hypothesis
• Conclusion

4. INTRODUCTION
• Plaque is the primary etiological factor of
periodontal diseases
• Also evidences support that periodontal disease
acts as contributor factor for various systemic
diseases (Diabetes, Heart Diseases, Lung
Diseases, Preterm low birth weight infants….....)

5. INTRODUCTION
To effectively treat and prevent these diseases, various
hypothesis are proposed to find how healthy plaque
change to pathological plaque

6. PLAQUE HYPOTHESIS-
• Non specific plaque hypothesis
• Specific plaque hypothesis
• Updated plaque hypothesis
• Ecological plaque hypothesis
• Keystone pathogen hypothesis

7. NON-SPECIFIC
PLAQUE HYPOTHESIS

8. Non-specific plaque hypothesis
Described in nineteenth century
when due to lack of technology,
bacteria could not be identified

9. Non-specific plaque hypothesis
Proposed by Miller in 1890;
Name given by Walter Loesche (1976)
States that periodontal disease results from the
noxious products released by entire plaque flora

10. All plaque bacteria
played a role in
periodontal
destruction rather
than any specific
bacteria.
Entire
plaque was
viewed as
bad plaque

11. Plaque induced gingivitis model in support of this theory
• Loe, Theilade, and Jensen in 1965- examined gingival
inflammation in healthy adults who ceased tooth brushing and
any other oral hygiene practices.
• It was observed that as the plaque accumulated, gingivitis
developed
• When plaque was removed by reinstituting adequate oral
hygiene, gingivitis started decreasing

12.  Day 0- Mechanical plaque control stopped, plaque
slowly started forming on the teeth.
 Day 1-6- Plaque composition changed, with a shift
to more gram-negative species and more rods,
filaments
 Day 7- Spirals and spirochetes started appearing

13. • Day 3- First symptoms of gingival
inflammation became visible.
• On re-establishment of proper plaque
control- plaque composition returned
to the initial situation; symptoms of
gingivitis disappeared.

14. Limitations of non- specific plaque
hypothesis
Some individuals with good amount of plaque and
calculus develop gingivitis, but never develop destructive
periodontitis.
Some individuals with periodontitis demonstrate site
specificity in the pattern of disease. Some sites in mouth are
unaffected, whereas deep pockets are found in adjacent sites

15. SPECIFIC
PLAQUE HYPOTHESIS

16. Specific plaque hypothesis
With invent of microscope,
bacterial identification led to this
hypothesis in twentieth century

17. Specific plaque hypothesis
Given by Walter Loesche
(1976)
Specific bacteria in plaque results in
periodontal disease because that
bacteria produces substances that
mediate the host tissues destruction

18. Specific plaque hypothesis was
accepted
• By the recognition of A. actinomycetemcomitans as a
main causative bacteria in Localized Aggressive
Periodontitis.
• By microbial complexes observed by Socransky et al

19. MICROBIAL COMPLEXES
• Socransky et al in 1998 described the
presence of specific bacterial complexes
in plaque

20. Complex Microorganism
Blue complex Various Actinomyces species
Purple complex Veillonella parvula,
Actinomyces odontolyticus
Green complex Eikenella corrodens,
Capnocytophaga gingivalis,
Actinobacillus actinomycetemcomitans
Yellow complex Streptococcus mitis,
Streptococcus oralis,
Streptococcus sanguis,
Streptococcus gordonii,
Streptococcus intermedius
Orange complex Campylobacter rectus,
Eubacterium nodatum,
Fusobacterium nucleatum
Prevotella intermedia,
Prevotella nigrescens,
Red complex Porphyromonas gingivalis,
Tannerella forsythensis (Bacteroides
forsythus)
Treponema denticola

21. The primary colonizers (that get attached to
tooth surfaces) are either independent
bacteria (no defined complexes) or member
of yellow, blue or purple complexes.
Secondary colonizers in plaque (that
combine with other bacteria, not on
tooth surfaces) fell into green, orange
or red complexes.
The red complex is particularly associated
with bleeding on probing

22. Socranksy’s complexs
Yellow, blue and
purple associated with
periodontal health
Red, Green and orange
associated with
periodontal disease

23. Limitations
Studies showed that periodontitis occurred even in
absence of pathogens like red/green complex
Sometime these pathogens were found to be present in
absence of disease.

24. UPDATED NON-SPECIFIC
PLAQUE HYPOTHESIS (UNIFIED
HYPOTHESIS)

25. UPDATED NON-SPECIFIC PLAOUE
HYPOTHESIS (UNIFIED HYPOTHESIS)
Described by THEILADE IN 1986
Whole plaque contribute to the pathogenic potential to a
greater or lesser extent (Gingivitis), but presence of some
specific virulent bacteria lead to disease progression
(Periodontitis)

26. All bacteria in plaque is virulent by
either involved in invasion, evasion of
the host defenses and/or aggravation
of tissue destruction
But some specific subgingival
bacteria can become virulent than
others (under some favorable
conditions) and cause periodontitis

27. Thus it combines the key concepts of both
the previous hypothesis

28. Theilade’s statement
“any bacterial colonization
(plaque) of sufficient
quantity in the gingival
crevice (sulcus) always
causes at least gingivitis”
Non-pathogenic plaque not
causing gingivitis (in the
absence of oral hygiene)
had never been reported

29. This hypothesis propose
Presence of plaque always lead to gingivitis
Changes occur in plaque leading to growth
of specific virulent bacteria leading to
periodontitis

30. LIMITATION-
CANNOT ANSWER WHY-
In some people, gingivitis
never progress to periodontitis,
whereas some people rapidly
develop periodontitis

31. ECOLOGICAL PLAQUE
HYPOTHESIS

32. ECOLOGICAL PLAQUE HYPOTHESIS
Expanded the previous hypothesis by
stating that virulence of specific
micro-organism in plaque occurs by
changes in ecological factors like
change in pH, redox potential,
presence of nutrients etc

33. ECOLOGICAL PLAQUE HYPOTHESIS
Given by Philip D. Marsh in 1994
Periodontitis is caused by overgrowth of
specific micro-organisms of dental plaque
when the local microenvironment changes
(ecological changes), but it is not necessarily
the same bacteria in each case

34. • Changes in microbial composition occurs
due to ecological factors such as change
in pH and redox potential, the presence of
nutrients

35. According to ecological
plaque hypothesis both the
total amount of dental plaque
and the specific microbial
composition of plaque
contribute to transition from
health to disease.

36. Early colonisers
are Facultative
anaerobes
With time, use
oxygen; and
release carbon
dioxide and
hydrogen
Leading to
obligate
anaerobes that
cause
periodontitis

37. Plaque
accumulation and
increased
inflammation
Lower redox
potential,
Increase pH,
Increase GCF flow,
High temperature,
Change in nutrients
(ECOLOGICAL
CHANGES)
Predominant
Gram–negative
obligate
anaerobes
(Gingivitis,
Periodontitis)

38. Plaque reduction
and decreased
inflammation
Higher redox
potential,
Decrease pH,
Decrease GCF flow,
Low temperature
(ECOLOGICAL
CHANGES)
Predominant
Gram–positive
facultative
anaerobes
(healthy state)

39. LIMITATION
Like the other hypotheses, it does not address the
role of host genetic factors that contribute to the
composition of plaque and to susceptibility of
periodontitis; as gingivitis don’t lead to periodontitis
in every case and genetic factors can be
responsible in addition to environmental factors.

40. KEYSTONE PATHOGEN
HYPOTHESIS

41. KEYSTONE PATHOGEN HYPOTHESIS
Certain low-abundant micro-organisms can cause
periodontitis by changing the composition and increasing
the quantity/number of the normal micro-organisms
Given by Hajishengallis et al., 2012
For example Porphyromonas gingivalis ( in small quantities)
has shown to cause periodontitis by manipulating the host
immune system

42. STUDIES
Studies in mouse models showed
Very low amount of P.gingivalis
(<0.01% of total bacteria in plaque)
altered the plaque composition,
causing periodontitis (Hajishengallis et
al.,2011)

43. STUDIES
But in germ-free mice models
P.gingivalis colonized but could
not cause the disease; indicating
the importance of commensal
bacteria in causing the disease

44. P.GINGIVALIS CAUSES three effects
1. “Local chemokine paralysis”
by blocking production of IL-8
produced by gingival epithelial
cells.
Delays the recruitment of
neutrophils, facilitating initial
microbial colonization in
periodontium
Madianos et al.,
1997;
Darveau et al;1998

45. P.GINGIVALIS CAUSES
2. “Manipulate toll like receptor
(TLR) response”
Decrease level of TLR4 activity,
thus facilitate survival and
multiplication of micro-organisms in
periodontium

46. P.GINGIVALIS CAUSES
3. “Inactivate Complement”
Gingipains release by P.Gingivalis
cleave complement factors C3 and
C5 into active C3a and C5a (active
in phagocytosis of microbes). But
these gingipains degraded C3a and
C5a, causing loss of their functions
thus increasing survival of micro-
organisms.

47. P.GINGIVALIS CAUSES
Increasing number of micro-
organisms increase GCF. Increased
GCF is source of more proteins
(utilized as nutrient for other micro-
organisms) and iron (utilized as
source of P.gingivalis)
Thus a vicious cycle is formed in
which P.gingivalis increases
number of other micro-organisms
and its own levels

48. LIMITATION
Like the other hypotheses, it does not address
the role of host genetic factors that contribute to
the composition of plaque and to susceptibility
of periodontitis
Also this hypothesis has yet to be proved in
humans

49. SUMMARY
• Non specific plaque hypothesis: Whole plaque
responsible for disease.
• Specific plaque hypothesis: Specific bacteria in
plaque responsible for disease.
• Updated plaque hypothesis: Whole plaque cause
gingivitis; but progression to periodontitis occurs
by growth of specific bacteria.

50. SUMMARY
• Ecological plaque hypothesis: Whole plaque cause
gingivitis; but progression to periodontitis occurs by
growth of specific bacteria by some ecological
changes in biofilm (like temperature, pH etc.)
• Keystone pathogen hypothesis: Low-abundant micro-
organism like P.gingivalis cause periodontitis by
changing the composition and increasing the quantity
of the normal micro-organisms.

51. Conclusion
It is a proven fact by all hypothesis
that accumulation of plaque always
lead to gingivitis.

52. But progression of disease
from gingivitis to
periodontitis—do not fit to
any hypothesis
‘In some individuals
disease never progress,
whereas in others it rapidly
progress to periodontitis’,
need to be answered

53. Till now, all hypothesis fail to describe actual
relationship between oral microbes and host
response that lead to maintenance of health or its
shift to the disease (periodontitis)

54. A hypothesis is needed, but this is only
possible when complex interaction of
bacteria with the host innate immune
response is fully explored