Chronic periodontitis is an infectious disease resulting in inflammation with in supporting tissues of the teeth, progressive attachment loss and bone loss. With all emerging technologies, a successful diagnosis and treatment will only be achieved through open sharing of ideas, research findings and thorough testing .

1. CHRONIC
PERIODODONTITIS
Dr. Raina J. P. Khanam
Dept. Of Periodontics
2nd year PG
1

2. • Introduction
• Classification
• Clinical features
• Symptoms
• Disease distribution
• Radiographic features
• Disease severity
2

3. • Disease progression
• Prevalence
• Risk factors for disease
• Pathogenesis
• Diagnosis
• Treatment
• Conclusion
3

4.  Chronic periodontitis is defined as “An infectious
disease resulting in inflammation within the supporting
tissues of the teeth, progressive attachment loss and bone
loss.” (Flemmig TF 1999)
 Chronic periodontitis, formerly known as “adult
periodontitis” or “chronic adult periodontitis” is the most
prevalent form of periodontitis.
 It is generally considered to be a slowly progressing
disease.
INTRODUCT
ION 4

5. CLASSIFI
CATION1. Localized form (<30% of sites
involved)
2. Generalized form (>30% of sites
involved)
5

6. CLINICAL
FEATURES
1. Supra and subgingival plaque accumulation
(frequently associated with calculus)
2. Gingival inflammation
3. Pocket formation
4. Loss of periodontal attachment
5. Loss of alveolar bone
6. Occasional suppuration
6

7. In patients with poor oral hygiene, the gingiva typically may be
 slightly to moderately swollen
 Alterations in color ranging from pale red to magenta
 Loss of gingival stippling
 Changes in surface topography such as blunted or rolled gingival margins
 Flattened or cratered papillae
In advance cases of chronic periodontitis
 Furcation involvement
 Tooth mobility
7

8. SYMPTOMS
Bleeding gums during brushing or eating
Spacing between teeth as a result of tooth movement
Loosening of teeth
As chronic periodontitis is painless, patients are totally unaware that they have the disease
Sensitivity to exposed roots by heat, cold or both
Localized dull pain, sometimes radiating deep into the jaw
Gingival tenderness or itchiness
Food impaction may lead to discomfort
8

9. DISEASE
DISTRIBUTI
ONChronic periodontitis is considered a site-
specific disease.
For example, a proximal surface with chronic
plaque accumulation may have loss of
attachment, whereas the plaque free facial
surface of the same tooth may be free of the
disease.
Localized periodontitis:-
when less than 30% of
the sites are involved
demonstrating attachment
loss and bone loss.
Generalized periodontitis:-
when 30% or more of
the sites are involved
demonstrating attachment
loss and bone loss.
9

10. RADIOGR
APHIC
FEATURESRadiographically, pattern of bone
loss is observed :-
1. Vertical (angular) bone loss
2. Horizontal bone loss
Vertical bone loss:-
When attachment and bone
loss on one tooth surface is
greater than that on adjacent
surface.
 Associated with intrabony
pocket formation.
Horizontal bone loss:-
When attachment and
bone loss proceeds at a
uniform rate on the
majority of tooth
surfaces.
Associated with
suprabony pockets.
10

11. DISEASE
SEVERITYDisease severity may be described as
1. Slight
2. Moderate
3. Severe
Slight (mild) periodontitis:-
Periodontal destruction is generally considered slight
when not more than 1 to 2mm of clinical attachment loss
has occurred.
Moderate periodontitis:-
Periodontal destruction is generally considered moderate
when 3 to 4mm of clinical attachment loss has occurred.
Severe periodontitis:-
Periodontal destruction is considered severe when 5mm
or more of clinical attachment loss has occurred.
11

12. DISEASE
PROGRES
SIONThe rate of disease progression is
usually slow but may be modified by
systemic or environmental and
behavioral factors.
Because of its slow rate of
progression, chronic periodontitis
usually becomes clinically
significant in the mid-thirties or
later.
Chronic periodontitis does not progress at an
equal rate in all affected sites throughout the
mouth.
Some involved areas may remain static for long
periods, whereas others may progress more
rapidly.
More rapidly progressive lesions occur most
frequently in interproximal areas.
12

13. Several models have been proposed to
describe the rate of disease progression.
(Socransky SS, Haffajee AD, Goodson
JM, et al)
In these models, progression is
measured by determining the amount of
attachment loss during a given period, as
follows:-
1. The Continuous Model
Its suggests that disease progression
is slow and continuous, with affected
sites showing a constantly
progressive rate of destruction
throughout the duration of disease.
13

14. 2. The random or episodic–burst model
It proposes that periodontal disease
progresses by sort bursts of
destruction followed by periods of no
destruction.
3. The asynchronous or multiple burst
model
It suggests that periodontal
destruction occurs around affected
teeth during defined periods of life.
14

15. PREVALENCE
 Chronic periodontitis increases in prevalence and severity with age,
generally affecting both genders equally.
 Periodontitis is an age associated, not age related, disease.
 In other words, it is not the age of the individual that causes the increase in
disease prevalence, but rather the length of the time that the periodontal
tissues are challenged by chronic plaque accumulation.
15

16. RISK
FACTORS
Risk - is the probability that an individual will get a specific
disease in a given period. The risk of developing the disease will
vary from individual to individual.
Risk factor - is a characteristic, an aspect of behavior, or an
environmental exposure that is associated with destructive
periodontitis.
16

17. RISK FACTORS FOR
DISEASE
 Prior History of Periodontitis
 Local Factors
 Systemic Factors
 Environmental and Behavioral Factors
 Genetic Factors
17

18. PRIOR HISTORY OF
PERIODONTITIS
 Although not a true risk factor for disease but rather a disease predictor, a
prior history of periodontal disease puts patients at greater risk for
developing loss of attachment and bone, given a challenge from bacterial
plaque accumulation.
 This means that a patient who presents with persistent gingivitis or
periodontitis with pocketing, attachment loss and bone loss may continue to
lose periodontal support if not successfully treated.
 In addition, a patient with chronic periodontitis who has been successfully
treated will develop continuing disease if plaque is allowed to accumulate.
18

19. LOCAL
FACTOR
S1. Plaque accumulation
2. Calculus
3. Overhanging
restorations
4. Carious lesions
extending subgingival
5. Furcation exposed
due to bone loss
6. Crowded and
malaligned teeth
7. Root grooves and
concavities
8. Microorganisms
19

20. ROLE OF
MICROORGANISMS
 Dental plaque is composed primarily of bacteria. One gram of plaque (wet weight)
contains approximately 10¹¹ bacteria.
 In a periodontal pocket,
Healthy crevice - 103 bacteria.
Deep pocket - 108 bacteria.
20

21. ROLE OF
BACTERIA
In chronic periodontitis, the bacteria most often detected at
high levels include
P. Gingivalis
T. Forsythia
P. Intermedia
T. Denticola
P. Nigrescens
C. Rectus
Eikenella cordens
F. Nucleatum
A. Actinomycetemcomitans
P. Micra
E. Nodatum
Leptotrichia buccalis
21

22. ROLE OF
VIRUSES
Recent studies have documented an association between
chronic periodontitis and viral micro organisms such as:-
Herpes virus
Epstein Barr virus (EBV-type 1)
Human cytomegalovirus (hCMV)
(Contreras & Slots 2000).
22

23. The identification and characterization of these and other pathogenic
microorganisms and their association with attachment and bone loss have led to
the specific plaque hypothesis for the development of chronic periodontitis.
This hypothesis states that only certain plaque is pathogenic and its
pathogenicity depends on the presence of or increase in specific
microorganisms. (Loesche WJ 1968)
This concept predicts that plaque harbouring specific bacterial pathogens
results in a periodontal disease because these organisms produce substances
that mediate the destruction of host tissues.
23

24. AGE
Both the prevalence and severity
of periodontal disease increases
with age.
(Burt 1994, Papapanou 1994,
1998).
Lindhe (1991, 1992) – minimal loss of
attachment in aging subjects enrolled in
preventive programs throughout their lives.
 Intake of medications,
 Decreased immune function, and
 Altered nutritional status interaction
24

25. SYSTE
MIC
FACTO
RS
The rate of progression of
chronic periodontitis is
generally slow.
However, when chronic
periodontitis occurs in a
patient who also has a
systemic disease that
influences the effectiveness
of the host response, the rate
of periodontal destruction
may be significantly
increased.
Diabetes (Type 1 and Type 2) is
a systemic condition that can
increase the severity and extent
of periodontal disease.
The synergistic effect of plaque
accumulation and modulation
of an effective host response
through the effects of diabetes
can lead to severe and extensive
periodontal destruction that
may be difficult to manage with
standard clinical techniques
without controlling the systemic
condition.
25

26. 26

27. ENVIRON
MENTAL
AND
BEHAVIOR
AL
FACTORS
Smoking has been shown to
increase the severity and
extent of periodontal disease.
When combined with
plaque-induced chronic
periodontitis, an increase in
the rate of periodontal
destruction may be observed
in patients who smoke and
have chronic periodontitis.
As a result, smokers with chronic periodontitis have more attachment and
bone loss, more furcation involvement and deeper pockets.
There is appearance of more supragingival and less subgingival calculus
and demonstrate less bleeding on probing than non smokers.
27

28. 28

29. Emotional stress has
previously been
associated with
necrotizing ulcerative
disease, perhaps because
of the effects of stress on
immune function.
Increasing evidence
suggests that emotional
stress also may influence
the extent and severity of
chronic periodontitis.
29

30. NUTRITION
Vitamin C or ascorbic acid is essential for the formation of collagen and intercellular
material, bone and teeth.
Low levels of ascorbic acid influence the metabolism of collagen within the
periodontium, thereby affecting the ability of the tissue to regenerate and repair itself.
Ascorbic acid deficiency interferes with bone formation, leading to loss of periodontal
bone.
Ascorbic acid deficiency increases the permeability of the oral mucosa to titrated
endotoxin and titrated inulin.
30

31. GENE
TIC
FACT
ORS
Periodontal destruction is
frequently seen among family
members and across different
generations within a family,
suggesting a genetic basis for the
susceptibility to periodontal
disease.
A study of monozygotic twins
suggest a genetic component to
chronic periodontitis, but the
influences of bacterial
transmission among family
members and environmental
effects make it difficult to
interpret a complex interaction.
Although no clear genetic determinants have been described for patients
with chronic periodontitis, a genetic predisposition to more aggressive
periodontal breakdown in response to plaque and calculus accumulation
may exist.
31

32. PATHOGENESIS
OF
PERIODONTITIS
(Page RC, Kornman KS
1997)
32

33. CLINICAL
DIAGNOSI
S
1. Probing pocket depth
Periodontal probing is done on all surfaces of
every tooth in the dentition.
During probing, a thin periodontal probe should
be used with gentle pressure and it should be
‘‘walked’’ around the entire circumference of
each tooth.
2. Clinical attachment loss
It is the distance from the cemento-enamel junction to the
apical extent of the pocket and represents the best clinical
measure of disease severity in terms of loss of support for the
teeth.
Ramfjord et al. proposed that loss of attachment was
considered the best measure of disease progression.
3. Bleeding on Probing
Gingival bleeding has universally been considered an
indicator of gingival inflammation and by some investigation,
an indicator of disease activity (Polson 1985).
Lang NP and Joss A et al (1986) reported Bleeding on
probing is a predictor for the progression of periodontal
disease. They reported that pockets with a probing depth of >
5 mm had a significantly higher incidence of BOP.
33

34. 4. Gingival recession is recorded during periodontal probing as the
distance of the free gingival margin to the cemento-enamel
junction .
Miller’s classification is widely accepted classification to
determine the gingival recession:
 Class I: Recession that does not extend to the mucogingival
junction and is not associated with loss of bone or gingival
tissue in the interdental area;
 Class II: Recession that extends to the mucogingival junction
and is not associated with loss of bone or soft tissue in the
interdental area.
 Class III: Recession that extends to or beyond the mucogingival
junction with loss of bone or soft tissue in the interdental area.
 Class IV :Recession extending to or beyond the mucogingival
junction with severe loss of inter- dental bone and/or soft tissue
and/or severe tooth malposition.
34

35. 5. Mobility
 Tooth mobility is a clinical expression of periodontitis.
 Many attempts have been made to develop mechanical or electronic
devices for the precise measurement of tooth mobility.
 Mobility is graded clinically by holding the tooth firmly between the
handles of two metallic instruments or with one metallic instrument and
a finger.
Mobility is graded according to the ease and extent of tooth movement as
follows:
 Normal mobility
 Grade I: Slightly more than normal.
 Grade II: Moderately more than normal.
 Grade III: Severe mobility faciolingually and/or mesiodistally,
combined with vertical displacement.
35

36. Device to check mobility – Periotest
Ranges:
-8 to +9 : Clinically firm tooth
10-19 : Palpable mobility
20-29: Visible mobility
30-50 : Mobility in response to lip & tongue movements
36

37. 6. Furcation
 It is important to document furcation involvement
because teeth with periodontal pockets in furcation have
been shown to have increased loss of attachment and a
poorer prognosis following periodontal therapy than
teeth without furcation involvement. (McGuire MK, J
Periodontol 1996)
 Furcation can be probed with naber’s probe to determine
extension of pockets into areas between roots.
 Grade I involves incipient bone loss
 Grade II involves partial bone loss (cul-de-sac)
 Grade III involves total bone loss with a through-and-
through opening of the furcation.
37

38. 7. Pathological tooth migration
 Pathological tooth migration is a characteristic
sign of an advanced form of chronic
periodontitis.
 Microbial plaque-induced periodontal
infection is considered to be the most common
causative factor. (Kim et al. 2012)
38

39. RADIO
GRAPHICAL
DIAGNOSISWidening of PDL space
Loss of interdental crestal margin
Localized or generalized loss of alveolar
supporting bone.
Blunting of the alveolar crest due to
beginning of bone resorption
Bone loss may be either horizontal or
vertical.
39

40. TREATMENT
PLANING
Successful periodontal therapy is dependent on anti-
infective procedures aimed at eliminating pathogenic
organisms found in dental plaque associated with the
tooth surface and within other niches in the oral cavity.
Slots J. Subgingival microflora and periodontal disease. J
Clin Periodontol 1979: 6: 351–382
40

41. Mechanical therapy consists of debridement of the roots by the meticulous use
of hand or power-driven scalers to remove plaque, endotoxins, calculus and
other plaque-retentive local factors.
The term mechanical therapy refers to both supra-gingival and sub-gingival
scaling as well as root planing.
Numerous studies since the 1950’s have indicated that manual instrumentation
in general takes from 20% to 50% longer to achieve the same clinical end-
points than that of sonic and/or ultrasonic scalers (Badersten A et al 1981).
The American Academy of Periodontology 1996 World Workshop consensus
report states that ultrasonic and sonic instrumentation have shown similar
clinical effects as manual scaling and root planing.
MECHANICALAPPROACH
41

42. CHEMICAL APPROACH
 Chemotherapeutic approaches include topical application of antiseptics or
sustained-release local drug delivery agents that are designed to prevent plaque
accumulation and to disinfect the root surfaces and adjacent periodontal tissues.
Vandekerckhove et al. were among the first to report a new innovative treatment for
periodontal infections using a partial-mouth disinfection protocol that consisted of a
thorough supragingival and subgingival chlorhexidine application (rinses, irrigation and
tongue brush) followed by four quadrants of scaling and root planing within 24 hours.
42

43. In disease sites that are more difficult to control, local drug delivery devices
such as chlorhexidine chips (PerioChipTM) or 10% doxycycline gel
(AtridoxTM) may be placed directly adjacent to the infected site.
Radvar et al. and Kinane et al. compared three types of local delivery devices,
tetracycline fiber, metronidazole gel and minocycline gel in combination with
scaling and root planing, to scaling and root planing alone. All treatments
improved attachment levels over the 6-month testing period, but there were no
significant differences between treatment.
Another new nonsurgical approach includes using a systemic sub-anti-
microbial dose of doxycycline (PeriostatA) that targets tissue breakdown by
blocking bacterial and host-derived enzymes associated with loss of alveolar
bone and connective tissue .
43

44. SURGICAL
THERAPY
Surgical techniques includes
Gingivectomy
Undisplaced flap
Modified Widman flap with and without osseous re-contouring
Apically positioned flap with and without osseous re-contouring
44

45. CONCLUSION
Chronic periodontitis is an infectious disease resulting in
inflammation with in supporting tissues of the teeth,
progressive attachment loss and bone loss. With all
emerging technologies, a successful diagnosis and
treatment will only be achieved through open sharing of
ideas, research findings and thorough testing .
45

46. 46