chronic periodontitis History Introduction Definition Classification Overall Characteristics Clinical Features Disease Distribution Disease Severity Clinical Course Of Chronic Periodontitis Progression Of Chronic Periodontitis Prevalence Pathogenesis Risk factors for Chronic Periodontitis Treatment

1. CHRONIC
PERIODONTITIS
BY: Dr Shreeja Nair
PG 2
Dept of Periodontia
GDCH Ahmedabad
GUIDED BY
DR NEETA V BHAVSAR
PROFESSOR AND HOD
PERIODONTIA DEPT

2. Contents• History
• Introduction
• Definition
• Classification
• Overall Characteristics
• Clinical Features
• Disease Distribution
• Disease Severity
• Clinical Course Of Chronic Periodontitis
• Progression Of Chronic Periodontitis
• Prevalence
• Pathogenesis
• Risk factors for Chronic Periodontitis
• Treatment
• Bibliography

3. HISTORY
• FAUCHARD recognised the relationship
between oral hygiene and the aetiology
of periodontal disease.
• JOHN W RIGGS (1811-1885) Leading
authority on periodontal disease and
its treatment in fact, at the time,
periodontitis was known as “Riggs’
disease”

4. • The classic study demonstrating the cause effect
relationship of plaque and gingivitis was done in 1965 by
H. Loe
• Plaque causes decay and periodontal disease. This was the
paradigm until the early 1980s.
• Goodson, Haffajee, Socransky et al (1982) -described
initiation and progression of periodontal disease as
measured by attachment loss
• Disease activity is episodic
• Disease activity is characterized by bursts of activity
• The best predictor of an at risk site……a deep pocket

5. World work shop, 1989
Refinement of the classification systems proposed by Page &
Schroeder, 1982; Grant, Stern & Listgarten, 1988; Suzuki 1988
Based mostly on the age of onset of the disease – “Adult
periodontitis”
Michalowicz studies of the early 1990s using data from twins
raised together and apart really started to identify genetic links in
periodontitis

6. AAP International workshop for the classification of Periodontal
diseases, 1999. -“Chronic Periodontitis”
The AAP and EFP 2017 joint workshop agreed that,
consistent with current knowledge on pathophysiology, three
forms of periodontitis can be identified: necrotizing
periodontitis, periodontitis as a manifestation of systemic
disease, and the forms of the disease previously recognized
as “chronic” or “aggressive”, now grouped under a single
category, “periodontitis”.

7. Historical names of periodontitis
• Alveolodental periostitis
• Smutz pyorrhea
• Riggs disease
• Periodontoclasia
• Pyorrhea alveolaris

8. INTRODUCTION
• Chronic Periodontitis is considered to be a complex slowly
progressing disease. However, in the presence of systemic,
environmental factors that may modify the host response to
plaque accumulation, such as diabetes, smoking or stress,
disease progression may become more aggressive.
• Chronic periodontitis most frequently observed in the adults,
may occur in children and adolescents in response to chronic
plaque and calculus accumulation. Hence, the more universal
description of “chronic” periodontitis can occur at any age.

9. DEFINITION
• Chronic periodontitis has been defined as “an
infectious disease resulting in inflammation within
the supporting tissues of the teeth, progressive
attachment loss, and bone loss.”(Flemming T.F 1999)
• This definition outlines the major clinical and
etiologic characteristics of the disease:
1. microbial biofilm formation (dental plaque);
2. periodontal inflammation (e.g., gingival
swelling, bleeding on probing);
3. attachment as well as alveolar bone loss.

10. CLASSIFICATION

11. Overall Characteristics
• Prevalent in adults but may occur in children.
• Amount of destruction of the periodontal tissues
commensurate with the oral hygiene and plaque levels,
local predisposing factors, smoking, stress, and systemic
risk factors.
• Host factors determine the severity and rate of
progression of the disease.
• The rate of progression of chronic periodontitis is, slow
to moderate; sometimes with periods of rapid tissue
destruction.

12. Clinical features
Colour and texture alterations of Marginal gingiva
clinical attachment loss (CAL)
alveolar bone loss (BL)
Periodontal pockets
bleeding of the gingiva
enlargement or recession of the gingiva
Furcation involvement
Increased mobility, drifting, and/or tooth exfoliation may
occur

13. Disease Distribution
Chronic periodontitis is site specific and it
can be classified as:
• When less than 30% sites assessed
have attachment loss & bone loss.
I) Localized
periodontitis
• Greater than 30% sites.
II) Generalized
periodontitis

14. Disease Severity
Based on the severity of destruction
• when 1 to 2 mm of clinical
attachment loss has occurred.
I) Slight(mild)
periodontitis :
• 3 to 4 mm.
II) Moderate
periodontitis:
• more than 5 mm
III) Severe
periodontitis :

15. Clinical Course Of Chronic
Periodontitis
I. Role Of Gingivitis
II. Incidence, Characteristics And Time Of
Occurrence Of The Initial Periodontal Lesion
III. Patterns, Variations Of Attachment Loss
M Schätzle , LJ Heitz-Mayfield - 2003

16. I. Role Of Gingivitis
• Epidemiological studies - gingival inflammation is
invariably a component of chronic periodontitis, and
that gingivitis precedes the onset of periodontitis.
• Two conditions - separate disease entities,
• bacterial plaque challenge induces overt gingivitis
• but the degree of host response (susceptibility) will
determine whether or not chronic periodontitis will
develop.
• Findings from epidemiologic studies and prospective
clinical trials have indicated that the presence of
gingivitis may be regarded as a risk factor for chronic
periodontitis.

17. II. Incidence,CharacteristicsAnd Time Of
OccurrenceOf The Initial PeriodontalLesion
The prevailing clinical concept of the pathogenesis of the
early lesion in chronic periodontitis included :
1. The formation and maturation of the supra-gingival
plaque and the development of gingivitis,
2. The extension of the bacterial plaque and the chronic
inflammatory process into the subgingival area and the
initial destruction of the connective tissue attachment of
the teeth
3. The apical extension of the junctional epithelium and
the formation of the periodontal pocket and loss of
alveolar bone.

18. III. Patterns and Variations Of
Attachment Loss
• Initial attachment loss in combination with pocket
formation may be seen primarily in interproximal
areas, often in combination with gingival recession.
• Pocket formation increases slowly by deepening of
the initial lesions and the addition of new sites.
• Gingival recession in combination with pockets may,
as indicated before, be caused by factors inherent in
the pathogenesis of periodontal destruction.

19. Disease Progression
• The rate of disease progression is usually slow but
may be modified by systemic or environmental and
behavioural factors.
• More rapidly progressive lesions occur most
frequently in interproximal areas and may also be
associated with areas of greater plaque
accumulation and inaccessibility to plaque control
measures (e.g., furcation areas, overhanging
margins, sites of malposed teeth, areas of food
impaction).

20. Proposedmodelstodescribetherateofdiseaseprogression.
Progression is measured by determining the amount of attachment loss
during a given period, as follows:
• The continuous model suggests that disease progression is slow and
continuous, with affected sites showing a constantly progressive rate
of destruction throughout the duration of the disease.
• The random model, or episodic-burst model, Socransky et al, 1984,
proposes that periodontal disease progresses by short bursts of
destruction followed by periods of no destruction. This pattern of
disease is random with respect to the tooth sites affected and the
chronology of the disease process.
• The asynchronous, multiple-burst model of disease progression,
1989, Manji and Nagelkerke, suggests that periodontal destruction
occurs around affected teeth during defined periods of life, and that
these bursts of activity are interspersed with periods of inactivity or
remission. The chronology of these bursts of disease is asynchronous
for individual teeth or groups of teeth.

21. A. Some sites show a progressive loss of
attachment over time, whereas others
show no destruction. The time of onset
and the extent of destruction vary
among sites.
B. Random burst model. Activity occurs at
random in any site. Some sites show no
activity, whereas others show one or
several bursts of activity. The cumulative
extent of destruction varies among sites.
C. Asynchronous multiple burst model.
Several sites show bursts of activity over
a finite period followed by prolonged
periods of inactivity. Occasional bursts
may occur infrequently at certain sites
at later periods. Other sites show no
periodontal disease activity at any time.
S. Socransky, A. Haffajee, M. Goodson and J. Lindhe .

22. Periods of Destruction
• Periodontal destruction occurs in an episodic,
intermittent manner, with periods of inactivity
or quiescence.
• Periods of destructive activity are associated
with subgingival ulceration and an acute
inflammatory reaction, resulting in rapid loss of
alveolar bone; it was hypothesized that this
coincide with the conversion of a
predominantly T-lymphocyte lesion to one with
a predominantly B-lymphocyte–plasma cell
infiltrate.

23. • Periods of exacerbation are associated
with an increase of the loose, unattached,
motile, gram negative, anaerobic pocket
flora.
• Periods of remission coincide with the
formation of a dense, unattached, non
motile, gram-positive flora with a
tendency to mineralize.
• Tissue invasion by one or several bacterial
species is followed by an advanced local
host defence that controls the attack.

24. Prevalence
• Chronic periodontitis increases in prevalence and severity with
age.
• Affects both the gender equally.
• The worldwide prevalence for severe chronic periodontitis is
estimated at 10.5% to 12% of the world's population. (Global
burden of severe periodontitis in 1990-2010: A systematic
review and meta-regression. J Dent Res. 2014;93:1045–1053.)
• Shah observed that for periodontal diseases, the prevalence at
present is 45% for age group 15+. Due to rampant use of pan
masala and guthka by the persons of all age groups, the
proportion of population with the disease could be 80-90%.
(prevalance of periodontitis in the Indian population : a
literature review; jp shah 2011)

25. PATHOGENESIS

26. Histological features
• The development of gingivitis and subsequently of
the chronic periodontitis lesion has been classically
described as progressing through a series of stages,
i.e. initial, early, established, and advanced. (Page
And Schroeder 1976)
• These stages are not always discernible as distinct
entities in their own right, but provide a useful
framework to compare and contrast the
histopathological processes of periodontitis.

27. • The initial lesion of chronic periodontitis
• subclinical entity occurring within the first 4 days of plaque accumulation.
Page and Schroeder 1976

28. • the presence of an organized plaque biofilm
induces the neutrophils to release their
lysosomal agents, in an act of phagocytosis.
• Perivascular loss of collagen- local connective
tissue disruption
• not clinically discernible
• only occupies 5–10% of the surrounding
connective tissues.

29. • The early lesion becomes discernible after 4–7 days
of uninterrupted plaque accumulation.
• increasing numbers of lymphocytes and
macrophages, development of a perivascular
inflammatory infiltrate.
• Junctional epithelium may resemble microabscess,
with severe leukocyte infiltration.
• Lymphoid cells dominate subjacent connective
tissue. Early T lymphocyte predominance later B
cell abundance
• Vascular proliferation
• Increased collagen loss- 70% collagen destroyed
around cellular infiltrate.

30. • In established lesion
• 2 types: stable and active form (Lindhe et
al 1965)
• The junctional epithelium reveals
widened intercellular spaces filled with
granular cellular debris, including
lysosomes derived from disrupted
neutrophils, lymphocytes, and
monocytes.
• The lysosomes contain acid hydrolases
that can destroy tissue components.
•The junctional epithelium develops rete pegs or ridges that protrude
into the connective tissue, and the basal lamina is destroyed in some
areas.
•In the connective tissue, collagen fibers are destroyed around the
infiltrate of plasma cells, neutrophils, lymphocytes, monocytes, and mast
cells. Junctional epithelium gets substituted by pocket epithelium.

31. •The advanced lesion
• inflammatory cell infiltrate further extends
apically
•There are relatively few macrophages in the
advanced lesion, and it is thought that B cells
may be the major source of IL-1 and other
proinflammatory cytokines that in turn lead to
the production of MMPs, especially by
fibroblasts, resulting in degradation of the
surrounding extracellular matrix.
•An abundance of plasma cells in gingival
connective tissue. (Garant and Mulvihill 1972,
Berglund et al 2005)
•This is typical of both chronic and aggressive
periodontitis.

32. • There is apical migration of plaque on the root surface,
accompanied by subgingival calculus formation.
• The alveolar bone is observed to be destroyed within 2 mm of
the plaque front. (waerhaug et al)
• A predominance of plasma cells is characteristic of this lesion,
and while there is capacity in the region of the lesion for
healing and stability, repair or regeneration does not usually
occur naturally.
• Seymour et al. outlined the development of a perivascular
lymphocyte ⁄ macrophage lesion, with T lymphocytes
dominating with a CD4:CD8 ratio of 2:1, which was confirmed
by subsequent observations.

33. MICROBIOLOGY
• Elevated levels of spirochetes
• Anaerobic 90% & gram negative 75%
• Detected in high levels are: P. gingivalis, T. forsythia,
P. intermedia, P. nigrescens, C. rectus, E corrodens, F.
nucleatum, A. actinomycetemcomitans (often
serotype b), P. micra, E. nodatum, Leptotrichia
buccalis, Treponema (T. denticola), Selenomonas
spp. (S. noxia), and Enterobacter spp.
• high proportions of Actinomyces spp., Rothia spp.,
and Streptococcus spp. are correlated with health.

34. • C. rectus, P. gingivalis, P. intermedia, F. nucleatum,
and T. forsythia were found to be elevated in the
active sites.
• detectable levels of P. gingivalis, P. intermedia, T.
forsythia, C. rectus, and A. actinomycetemcomitans
are associated with disease progression
• P. gingivalis and A. actinomycetemcomitans are
known to invade host tissue cells
• presence of subgingival EBV-1 and hCMV are
associated with high levels of putative bacterial
pathogens, including P. gingivalis, T. forsythia, P.
intermedia, and T. denticola.

36. Human viruses in periodontitis
• Evidence from a variety of sources supports a co-infection
hypothesis in which the development and progression of
periodontal disease is associated with dual infection by
certain human viruses (e.g. Herpes virus, Epstein– Barr virus
and cytomegalovirus) in conjunction with an increase in
opportunistic pathogenic bacteria residing in the
endogenous subgingival microbiota.

37. Periodontitis
cytomegalo
virus
Epstein–
Barr virus
Herpes
simplex
virus 1 & 2

38. Infection with herpes viruses
Local increase in proinflammatory cytokines
Disrupts the homeostatic balance between the resident
periodontal microbiota and the host.
Members of the subgingival microbiota that thrive under
inflammatory conditions - proliferate
• Porphyromonas gingivalis , Tannerella forsythia, Treponema spp
Development and progression of periodontitis.

39. Bone Destruction Caused by the
Extension of Gingival Inflammation
• The most common cause of bone destruction in
periodontitis is the extension of inflammation from
the marginal gingiva into the supporting periodontal
tissues.
• As stated previously, the transition from gingivitis to
periodontitis is associated with changes in the
composition of the bacterial biofilm. In advanced
stages of disease, the number of motile organisms
and spirochetes increases, whereas the number of
coccoid rods and straight rods decreases.
• The cellular composition of the infiltrated connective
tissue also changes with increasing severity of the
lesion.

41. Periodontal Pocket Formation
• The transformation of a gingival sulcus
into a periodontal pocket creates an area
in which plaque removal becomes
impossible.
• Pocket formation starts as an
inflammatory change in the connective
tissue wall of the gingival sulcus.
• The cellular and fluid inflammatory
exudate causes degeneration of the
surrounding connective tissue, including
the gingival fibers.
• Just apical to the junctional epithelium,
collagen fibers are destroyed and the area
is occupied by inflammatory cells and
edema.

42. Development of Periodontal
Pocket

43. Pocket Formation
The two mechanisms associated with collagen loss are as follows:
1. collagenases and other enzymes secreted by various cells in
healthy and inflamed tissue, such as fibroblasts, PMNs and
macrophages, become extracellular and destroy collagen
(enzymes that degrade collagen and other matrix
macromolecules into small peptides are called matrix
metalloproteinases); and
2. fibroblasts phagocytize collagen fibers by extending
cytoplasmic processes to the ligament–cementum interface
and degrading the inserted collagen fibrils and the fibrils of
the cementum matrix.
• As a consequence of the loss of collagen, the apical cells of the
junctional epithelium proliferate along the root surface and
extend finger-like projections that are two or three cells in
thickness

44. Correlation of clinical & Histopathological
features of chronic periodontitis
s.no Clinical features Histopathologic features
1 Gingival wall of pocket presents a
various degrees of bluish red
discoloration; flaccidity; a smooth,
shiny surface; and pitting on
pressure.
The discolouration is caused by
circulatory stagnation,
the flaccidity by destruction of gingival
fibers and surrounding tissues;
the smooth, shiny surface ,by atrophy
of epithelium and oedema,
the pitting on pressure, by edema and
degeneration
2 Less frequently, gingival wall may be
pink and firm
In such cases, fibrotic changes
predominate over exudation and
degeneration

45. 4 Bleeding is elicited by gently
probing soft tissue wall of pocket
Ease of bleeding results
from increased vascularity,
thinning and degeneration
of epithelium, and proximity
of engorged vessels to inner
surface.
5 When explored with a probe,
inner aspect of pocket is generally
painful
Pain on tactile stimulation is
caused by ulceration of
inner aspect of pocket wall
6 In many cases, pus may be
expressed by applying digital
pressure.
Pus occurs in pockets with
suppurative inflammation of
inner wall.

46. Risk factors
for Chronic
Periodontitis

47. I. Prior history of Periodontitis
• A disease predictor (associated with, not causative of) rather than a true
risk factor. Puts the patient at the greater risk for developing further loss
of attachment and bone, given a challenge from bacterial plaque
accumulation.
• A chronic periodontitis patient who has been successfully treated will
develop continuous disease if plaque is allowed to accumulate.
• This emphasizes the need for continuous monitoring and maintenance of
periodontitis patients to prevent recurrence of disease.
• Factors associated with the initiation of chronic periodontitis may also
influence disease progression.
• Furthermore, the extent and severity of disease within an individual are
good predictors of future disease occurrence.

48. II. Microbiologic Aspects
• Plaque accumulation on tooth and gingival
surfaces (dental biofilm formation) at the
dentogingival junction is considered the primary
initiating agent in the etiology of gingivitis and
chronic periodontitis.
• Attachment and bone loss are associated with an
increase in the proportion of gram-negative
organisms in the subgingival biofilm,with specific
increases in organisms known to be pathogenic
and virulent.

49. • Porphyromonas gingivalis, Tannerella forsythia,
and Treponema denticola, otherwise known as
the red complex bacteria, are frequently
associated with ongoing attachment and bone
loss in chronic periodontitis.
• Periodontal pathogens like P. gingivalis may then
invade the periodontal tissue and therewith
induce further immune responses with
increasing concentrations of proinflammatory
mediators that may enhance periodontal
breakdown.

50. III. Local factors
• Microbial plaque is a crucial factor in the
inflammation of periodontal tissues, but the
progression of gingivitis to periodontitis is largely
governed by host-response and cumulative risk
factors that predispose an individual to periodontal
tissue destruction and attachment loss.
• Microbial biofilms of particular compositions will
initiate chronic periodontitis in certain individuals
whose host response and cumulative risk factors
predispose them to periodontal tissue destruction
and attachment loss.

51. Plaque retentive factors – calculus – most important
Others, subgingival and over hanging margins of restorations,
Subgingivally extending carious lesions,
Furcation involvements, cervical enamel projection.,
Crowded and mal-aligned teeth,
Root grooves and concavities

52. IV. Age
• CHRONIC PERIODONTITIS is AGE ASSOCIATED and not age related
disease.
• Both the prevalence and severity of periodontal disease increase
with age. It is possible that degenerative changes related to aging
may increase susceptibility to periodontitis.
• Early evidence demonstrates that both the prevalence and severity
of periodontitis increase with older age, suggesting that age may be
a marker for periodontal tissue support loss (van der Velden 1984,
1991; Johnson et al. 1989; Burt 1994).
• However, the concept of periodontitis as an inevitable consequence
of ageing has been challenged over the years and the alleged ‘age
effect’ likely represents the cumulative effect of prolonged
exposure to true risk factors (Papapanou et al. 1991).

53. V. Environmental factors
• The positive association exist between smoking and periodontitis
• Risk attributable to tobacco for chronic periodontitis is between 2.5
and 7.0. Also the response to periodontal therapy is impaired in
smokers.
• A further feature in smokers is that their signs and symptoms of both
gingivitis and chronic periodontitis, viz., gingival redness and bleeding
on probing (BoP), are masked by the dampening of inflammation
seen for smokers as compared to non-smokers
• Smoking has been shown to affect the vasculature, the humoral and
cellular immune responses, cell signalling processes, and tissue
homeostasis.

54. Effects of smoking on etiology and
pathogenesis of periodontal disease
Etiologic factor Impact of smoking
Microbiology No effect on the rate of plaque accumulation
Increased colonization of periodontopathic
microorganisms
Immunology Altered neutrophil functions
Increased GCF levels of TNF-a, PGE2, neutrophil
collagenase, and elastase
Physiology Decreased gingival blood vessels,
Decreased GCF flow and BoP,
Decreased subgingival temperature
Increased inflammatory mediators
Increased LA recovery time

55. • Smoking is a major risk factor for the development and
progression of generalized chronic periodontitis.
• Periodontitis is influenced by smoking in a dose
dependent manner. The intake of more than 10
cigarettes per day tremendously increases the risk of
disease progression when compared to nonsmokers and
former smokers, respectively.
• Compared to nonsmokers, the following features are
found in smokers:
• Increased periodontal pocket depth with more than 3 mm
• Increased attachment loss
• More recessions Increased loss of alveolar bone
• Increased tooth loss
• Fewer signs of gingivitis (less bleeding upon probing)
• A greater incidence of furcation involvement

56. VI. Systemic factors
• In several instances periodontitis is also associated with
other systemic disorders, such as Papillon–Lefèvre
syndrome, Ehlers–Danlos syndrome, Kindler syndrome,
and Cohen syndrome.
• Patients who suffer from diseases that impair host
immune responses (e.g., HIV/AIDS) may also show
periodontal destruction. it is also known that
osteoporosis, severe unbalanced diet, and stress, as well
as dermatologic, hematologic, and neoplastic factors,
interfere with periodontal inflammatory responses.

57. • In addition to defined syndromes,
periodontitis is also associated with severe
systemic diseases, such as diabetes
mellitus, cardiovascular disorders, stroke,
and lung disorders.
• In the context of diabetes mellitus, a
number of patients exhibit an increased
body weight (obesity), which also
correlates with the prevalence and
severity of periodontal attachment and
bone loss.

58. Diabetes mellitus
• Periodontitis is now considered as the sixth complication of diabetes
mellitus. For diabetes mellitus and periodontitis, there is a known
interaction during which both diseases mutually correlate to each
other.
• Patients with diabetes mellitus exhibit a higher risk to develop
periodontitis, and the periodontal infection/inflammation may
negatively interfere with the glycemic control of the diabetic patient
• The diabetic state is associated with:
• Decreased collagen synthesis
• Increased collagenase activity
• Altered neutrophil function
• Elevated blood sugar levels suppress the host’s immune response
and results in:
• Poor wound healing
• Susceptibility to recurrent infections

59. HIV- AIDS
• (AIDS) is an infection-driven impairment of the immune
system and is caused by the human immunodeficiency virus
(HIV).
• HIV-positive individuals are more likely to experience chronic
periodontitis than the general population-- do not take into
account the level of oral hygiene, the presence of preexisting
gingivitis, poor diet, the age of the patient, smoking, other
periodontal disease risk factors, the degree of
immunodeficiency.
• Ceballos-Salobrena and colleagues reported a 30% decrease in
the prevalence of chronic periodontitis among patients with
AIDS who were receiving HAART

60. Nutritional deficiencies
• In animal studies, it is shown to affect the periodontal tissues
but Epidemiologic data does not support this suggestion.
• Nutritional influences on inflammation are now accepted and
actively being researched (Kinane and Ritchie 2005)
• Gingival bleeding – vitamin C deficiency.
• Evidence suggests that avitaminosis – C may aggravate
established chronic periodontitis.
• Vitamin D deficiency.
• Calcium deficiency.

61. VII. Immunologic Factors
• Chronic periodontitis is a disease induced by bacteria
organized in the dental biofilm. Onset, progression, and
severity of the disease depend, however, on the
individual host immune response.
• Patients may show alterations of peripheral monocytes,
which relate to reduced reactivity of lymphocytes or
enhanced B-cell response.
• Not only B cells and macrophages, but also periodontal
ligament cells, gingival fibroblasts, and epithelial cells
synthesize pro-inflammatory mediators—such as
interleukin-1 beta (IL-1 beta), IL-6, IL-8, prostaglandin-E2
(PGE2), tumor-necrosis factor alpha (TNF-alpha), and
many others—that modify innate and adaptive immune
responses at periodontal sites

62. VIII. Behavioral factors and stress
• Influence physiologic systems like the endocrine and immune
system, leading to health changes. , inflammatory conditions
and impaired wound healing.
• The association between stress and disease is particularly
strong for infectious diseases, inflammatory conditions and
impaired wound healing.
• Specific periodontal conditions associated with psychosocial
variables, including chronic periodontitis, NUG , chronic and
experimental gingivitis.
• Patients with periodontitis often report the experience of
family- or work-related stress. Positive correlations between
cortisol levels and periodontal indices (plaque index, gingival
index), bone loss, and missing teeth were recorded

63. • Stress and Periodontal Disease: Potential
Mechanisms
1. Immunosuppression via cortisol secretion
2. Poor oral hygiene compliance in patients with
chronic stress
3. Patients with stress are less likely to seek
professional care
4. Patients with stress may smoke more frequently

64. IX. Genetic factors
• There is convincing evidence from twin studies for a
genetic predisposition to the periodontal diseases.
Indicated that risk of chronic periodontitis has a high
inherited component.
• Much attention has been focused on polymorphisms
associated with genes involved in cytokines
production.
• Patients with the IL-1 genotype increased the risk for
tooth loss by 2.7 times
• The combined effect of the IL-1 genotype & smoking
increased the risk of tooth loss by 7.7 times.

65. HERITABILITY OF GINGIVITIS
• It is feasible that genes implicated in the regulation of
inflammatory process of periodontal tissues associated with
plaque accumulation may play a role in explaining the
individual variability in the severity of both plaque-induced
gingivitis and destructive periodontitis (Dashash et al. 2007).
• Periodontal disease development and progression can be
caused by MMPs produced by both infiltrating and resident
cells of the periodontium.
• One of the most important MMPs, MMP-9 (also known as
gelatinase B or 92-kD type IV collagenase), is active against
collagens and proteoglycans.
• The coding gene is located on chromosome 20q11.2- q13.1,
and several polymorphisms have been detected in the MMP-9
gene (Vokurka et al. 2009).

66. GENES ASSOCIATED WITH
GINGIVITIS RISK:
• IL-1 cluster, IL-6,10, 12,18
• MMP-9
• TNF
• Fibrinogen
• LT-A.

67. HERITABILITY OF
AGGRESSIVE PERIODONTITIS
• Some types of aggressive periodontitis seem
to be inherited in a Mendelian manner, and
both autosomal modes and X-linked
transmission have been proposed.
• The results in different sets of families are
consistent with both autosomal-dominant
and autosomal recessive inheritance, as well
as X-linked dominant inheritance, but no
single inheritance mode that would include
all families has been established (Meng et al
2011)

68. GENES ASSOCIATED WITH AP
RISK:
• IL-1 cluster, IL-
4,6,10,12,13,18
• TNF-a
• TGF-b
• Vit D receptor
• Estrogen receptor
• LF
• RANK/RANKL/OPG,
• MMP 1,2,3,9,
• TIMP
• CD14
• Cathepsin C, IFN-gamma
Polymorphisms in genes of :
• Cell-surface receptors for
immunoglobulins (Fc)
• Formyl-methionyl-leucyl-
phenylalanine (FMLP)
• Human leukocytic antigen
(HLA)
• Vitamin D Are promising
candidates for susceptibility
assessment of aggressive
peridontitis. (Yoshie et al.
2007).

69. HERITABILITY OF CHRONIC
PERIODONTITIS
• In contrast to aggressive periodontitis, chronic periodontitis does
not typically follow a simple pattern of familial transmission or
distribution. The twin study is probably the most popular method
that supports the genetic aspects of chronic periodontitis
• Michalowicz et al. (1991) examined the relative contribution of
environmental and host genetic factors to clinical measures of
periodontal disease through the study of twins reared together and
monozygous twins reared apart. Heritability estimates indicated
that between 38 and 82% of the population variance for these
periodontal measures of disease may be attributed to genetic
factors.
• Adult periodontitis was estimated to have approx 50% heritability,
which was unaltered following adjustments for behavioral
variables,including smoking.
• Corey et al. (1993) revealed that approximately half of the variance
in disease in the population is attributed to genetic variance.

70. CANDIDATE GENES FOR
CHRONIC PERIODONTITIS
• Interleukin-1, 2, 4, 6, 10
• Fc gamma receptor
• TNF
• Vitamin D receptor

71. TREATMENT

74. Periodontal Evaluation
Comprehensive periodontal examination
Diagnosis and prognosis
Patient education
• Clinical findings and disease status
• Disease pathogenesis and prevention
• Personalized oral hygiene instruction
Reduction of systemic and environmental risk
factors
• Physician consultation
• Smoking cessation
Periodontal treatment plan
• Oral hygiene assessment and education
• Nonsurgical therapy
• Periodontal reevaluation
• Periodontal supportive maintenance

75. Nonsurgical Therapy
Oral hygiene assessment and education
Infection control
• Nonsurgical periodontal therapy
• Supra-gingival and sub-gingival scaling and
root planing
• Extraction of hopeless teeth
Reduction of local risk factors
• Removal or reshaping of overhangs and
over contoured restorations
• Restoration of carious lesions
• Restoration of open contacts

76. Periodontal Reevaluation
Inquiry of new concerns or problems
Inquiry of changes in patient's medical
and oral health status
Oral hygiene assessment and education
Comprehensive periodontal examination
Assessment of outcome of nonsurgical
therapy
Determination of required additional
nonsurgical and
adjunctive therapy

77. Surgical Therapy
Adjunct to nonsurgical therapy
Should only occur once patient demonstrates proficient biofilm control
Objectives:
• Primary: Access for root instrumentation
• Secondary: Pocket reduction through soft tissue resection, osseous
resection, or periodontal regeneration
Periodontal access surgery
• Resective
• Regenerative
Extraction of hopeless teeth
Periodontal plastic surgery
• Muco-gingival surgery
• Aesthetic crown lengthening
Pre-prosthetic surgery
• Prosthetic crown lengthening
• Implant site preparation and implant placement

78. Periodontal Maintenance Therapy
Inquiry of new concerns or problems
Inquiry of changes in patient's medical and
oral health status
Oral hygiene assessment and education
Comprehensive periodontal examination
Professional maintenance care
• Supragingival and subgingival biofilm and calculus
removal
• Selective scaling and root planing
Assessment of recall interval and plan for
next visit

79. Bibliography
• Carranza And Newmann’s Clinical Periodontology 13th Edition.
• Jan Lindhe. Clinical Periodontology And Implant Dentistry, 6th Edition.
• T. F. Flemming. Periodontitis. Annals. 1991. 4. 1.32.
• Zhuang LF, Watt RM, Mattheos N, et al: Periodontal and peri-implant
microbiota in patients with healthy and inflamed periodontal and peri-
implant tissues, Clin Oral Implants Res 27:13, 2016.
• Shaju jp, zade rm, das m (2011) prevalence of periodontitis in the Indian
population: a literature review. J Indian soc periodontology 15: 29-30
• Periodontal disease and diabetes: A two-way street; Brian L. Mealey,
DDS, MS; JADA, Vol. 137 October 2006
• Global burden of severe periodontitis in 1990-2010: A systematic review
and meta-regression. J Dent Res. 2014;93:1045–1053.
• Ceballos-Salobrena A, Gaitain-Cepeda LA, Ceballos-Garcia L, et al: Oral
lesions in HIV/AIDS patients undergoing highly active antiretroviral
treatment including protease inhibitors: a new face of oral AIDS?, AIDS
Patient Care STDS 14:627–635, 2000.

80. • Schatzle M, Faddy MJ, Cullinan MP, Seymour GJ, Lang NP, Burgin W,
Anerud A, Boysen H, Loe H. The clinical course of chronic
periodontitis: V. Predictive factors in periodontal disease. J Clin
Periodontol 2009; 36: 365–371.
• Socransky SS, Haffajee AD, Goodson JM, et al: New concepts of
destructive periodontal disease, J Clin Periodontol 11:21, 1984
• Slots J: Herpesviral-bacterial interactions in periodontal diseases,
Periodontol 2000 52:117, 2010.
• Genco RJ, Ho AW et al. models to evaluate the role of stress in
periodontal disease. Ann Periodontol 1998;3:288-303.
• Heitz-Mayfield LJA, Schatzle M, Loe H, Burgin W, Anerud A, Boysen
H, Lang NP: Clinical course of chronic periodontitis. II. Incidence,
characteristics and time of occurrence of the initial periodontal
lesion. J Clin Periodontol 2003; 30: 902–908.
• Chronic Periodontitis And Aggressive Periodontitis, A Comparison.
Periodontology 2000 Vol 53.2010
• Martha Nunn. Understanding the etiology of periodontitis; an
overview of periodontal risk factors. Perio 2000 Vol. 32. 2003
• Ishikawa. Host responses in periodontal diseases: a preview. Perio
2000. 43 . 2007.9-13.