1

CHRONIC

PERIODONTITIS

Presented By :

Dr. Vartika Srivastava 2

CONTENTS

Introduction

History

Classification

Prevalence

Clinical features

Symptom

Disease distribution

Disease severity

Disease progression

Risk factors

Pathogenesis

Diagnosis

Clinical

Radiographic

Prognosis

Treatment

Non surgical

Surgical

Conclusion

References

3

PART I PART II

Introduction

It is inflammatory disease of supporting tissues of teeth caused by specific micro-

organism or group of specific micro-organisms resulting in progressive destruction of

periodontal ligament and alveolar bone with pocket formation, recession or both.

“As an infectious disease resulting in inflammation within the supporting tissues of the

teeth , progressive attachment loss and bone loss” (Flemmig TF 1999)

4

• Chronic – (Greek – Kronos means time) long lasting

• Chronic periodontitis, formerly known as “adult periodontitis” or “chronic

adult periodontitis” is the most prevalent form of periodontitis.

• Most commonly seen in adults.

• Age associated but not age relate.

5

History

• Fauchard recognized the relationship

between oral hygiene and the etiology

of periodontal disease

John W. Riggs (1811-85) - periodontitis or alveolar

pyorrhea was known as ‘Riggs disease’ and he have

been first individual to limit his practice to

periodontics. 6

CLASSIFICATION

7

1977

• Juvenile Periodontitis

• Chronic Marginal Periodontitis

1986

• Juvenile Periodontitis

• A. Prepubertal

• B. Localized juvenile periodontitis

• C. Generalized juvenile periodontitis

• Adult Periodontitis• Necrotizing Ulcerative

• Gingivo-Periodontitis

• Refractory Periodontitis

1989

• Early-Onset Periodontitis

• A. Prepubertal periodontitis

• Localized

• Generalized

• B. Juvenile periodontitis

• Localized

• Generalized

• C. Rapidly progressive periodontitis

• Adult Periodontitis• Necrotizing Ulcerative

• Periodontitis Refractory

• Periodontitis PeriodontitisAssociated with Systemic Disease

8

AAP 1999

• Chronic periodontitis

Generalised

Localised

• Aggressive periodontitis-

Generalised

Localised

• Periodontitis as a manifestation of systemic diseases

9

Change in terminology……….?

(Wiebe et al 2000)

Age-dependent nature of the adult periodontitis designation was felt to be somewhat

arbitrary as similar bone loss patterns can also be seen in adolescents and even in the

primary dentition of children.

Another difficulty lay in the fact that the age at which a patient presents for treatment does

not necessarily reflect the age at which the disease began.

“Chronic” periodontitis refers to progression of the disease over time without treatment

and does not suggest that the disease is “untreatable

10

Prevalence

• NAHNES III (1988 – 1994) depends upon threshold chosen

eg. 1mm – 99%, 7mm – 7%

But for 3mm – 53.1%

Gupta(1962) Sample-800,

Russell’s Index, Bombay

Age 11 to 30 years- 90%PD

Age 30 years plus- 100% PD11

Clinical features

• Supra and subgingival plaque accumulation (frequently associated with calculus)

• Gingival inflammation

• Pocket formation

• Loss of periodontal attachment

• Occasional suppuration

• Poor oral hygiene – gingiva is typically may be slightly to moderately swollen 12

• Color- pale red to magenta

• Consistency – soft or firm

• Surface topography – loss of stippling

• Blunted or rolled gingival margin

• Flattened or cratered papillae.

• Furcation

• Tooth mobility

13

Attachment loss with and without deep PD

Pocket depths are variable, and both horizontal and vertical bone loss can be found14

• Furcation involvement in the molars

are common in advance cases of

chronic periodontitis.

• Tooth mobility often appears in

advanced cases when bone loss has

been considerable.

15

SYMPTOMS

Bleeding gums during brushing or eating

Increasing spacing between their teeth

Loose teeth

Usually painless, but sometimes localized dull pain radiating deep into the jaw

Sensitivity due to exposed roots

Food impaction

Halitosis

Gingival tenderness or itching16

DISEASE DISTRIBUTION

• Chronic periodontitis is considered a site-specific disease.

• The clinical sign of Chronic periodontitis , namely inflammation pocket

formation, attachment loss, and bone loss are considered to be due to the

direct, site specific effect of subginigival plaque accumulation.

• It may occur on one surface and other may be free of symptom.

17

In addition to being site specific, chronic periodontitis may be described as

being localized when few sites demonstrate attachment and bone loss or generalized

when many sites around the mouth are affected.

18

Disease Severity

• Slight (mild) periodontitis: Periodontal destruction is generally

considered slight when no more than 1 to 2 mm of clinical

attachment loss has occurred.

• Moderate periodontitis: Periodontal destruction is generally considered

moderate when 3 to 4 mm of clinical attachment loss has

occurred.

• Severe periodontitis: Periodontal destruction is considered severe when 5

mm or more of clinical attachment loss has occurred.

19

20

Disease Progression

• The rate of disease progression is usually slow but may be modified by

systemic and/or environmental and behavioral factors.

• Chronic periodontitis does not progress at an equal rate in all affected sites

throughout the mouth.

• Rapidly progressive lesions occur most frequently in interproximal areas' and

are usually associated with areas of greater plaque accumulation and

inaccessibility to plaque control measures (e.g., furcation areas, overhanging

margins, sites of malposed teeth, or areas of food impaction).

21

22

• Several models have been proposed to describe the rate of disease

progression.

• In these models, progression is measured by determining the amount of

attachment loss during a given period, as follows-

1. The Continuous Model.( SOCRANSKY et al 1984)

2. The Random Model or Episodic Burst Model.

3. The Asynchronous, Multiple-Burst Model.23

24

Continuous model ( Socransky et

al 1984)

Rapid burst model

Multiple burst model

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

25

RISK FACTORS FOR DISEASE

• Prior History of Periodontitis

• Local Factors

• Systemic Factors

• Environmental and Behavioral Factors

• Genetic Factors

26

Prior History Of Periodontitis

Although not a true risk factor for disease but rather a disease predictor, a

prior history of periodontitis puts patients at greater risk for developing further

loss of attachment and bone, given a challenge from bacterial plaque

accumulation.

27

Local factor

Plaque retentive factors: calculus28

Overhanging restorations29

Trauma from occlusion Micro-organism

30

ROLE OF MICROBES

• 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.

• Nonbacterial microorganisms that are found in plaque include Mycoplasma species,

yeasts, protozoa, and viruses.31

Significance Of Microbial Community

These include:

(a) A broader habitat range for growth.

(b) An increased metabolic diversity and efficiency.

(c) An enhanced resistance to environmental stress, antimicrobial agents and the

host defenses.

Shapiro (1998), Marsh & Bowden (2000).

32

33

SOCRANSKY ,HAFFAJEE 1998

World Workshop in Periodontology consensus

report 1996

Designated as A .A comitans , P. gingivalis & B. forsythus as

periodontal pathogens.

34

ROLE OF VIRUSES

• More recently, viruses including cytomegalo , Epstein Barr, Papilloma and

herpes simplex have been proposed to play a role in the etiology of

periodontal diseases, possibly by changing the host response to the local

subgingival microbiota.

(Contreras & Slots 2000).

35

ROLE OF FUNGI

• Hannula J, Dogan B, Slots (2001) showed geographical differences in the

subgingival distribution of C. albicans serotypes and genotypes and suggested

geographic clustering of C. albicans clones in Subgingival samples of Chronic

Periodontitis patients.

36

Systemic and environmental risk factors

Uncontrolled diabetes mellitus (types I and II)

Smoking

Emotional stress

Oral hygiene habit

Environmental factor and Nutrition

Osteoporosis

HIV 37

38

DIABETES

• Diabetes mellitus is a disease of metabolic dysregulation.

• About 37-40million Indians have diabetes and is expected to double

by 2025. India is having maximum number of diabetic patients.

39

Microvascular changes

HyperglycemiaGlycosylation of

basement membrane proteins

Thickening of basement membrane

Altered structural and physical

properties of BM

Disruption of collagen fibers in BM, swelling of

endothelium

Impedes oxygen diffusion, metabolic waste elimination,

PMN migration diffusion of serum factor including antibodies

Susceptible to infection

Brownlee et al 1994

40

Hyperglycemia + collagen

AGEs

Increases cross

linking between collagen molecule

s

Reduced solubility

and turnover

of collagen

Failure in periodontal repair

and regenerat

ion

(Brownlee 1994)

41

SMOKING

• Undoubtedly one of the main and most prevalent, risk factors for

chronic periodontitis, risk calculations suggesting 40% of the cases of

chronic periodontitis may be attributable to smoking.

• It has been estimated that there are 1.1 billlion are smokers worldwide

and 182 million (16.6%) of them live in India.

42

• The International Classification of Disease (ICD-10) has

recognized that “Tobacco Dependence” is a disease .

• The negative effect of cigarette smoking on the

Periodontium is Cumulative and Dose dependent. (Sreedhar,

Shobha P 2006)

43

MECHANISMVascular alterations

Altered neutrophil function

Decreased IgG production

Decreased lymphocyte proliferation

Increased prevalence of periopathogens

Altered fibroblast attachment and function

Difficulty in eliminating pathogens by mechanical therapy

Negative local effects on cytokine and growth factor products44

Psychophysiological

response of the organism

to a perceived challenge or

threat.” (Breivik et al 1996)

45

46

NUTRITION

Vitamin C or ascorbic acid is essential for the formation of collagen and intercellular

material, bone and teeth.

Anti oxidant that reduces free radicals that cause DNA damage to immune cells.

↓ phagocytic function of neutrophils and macrophages

↓ antibody response

↓ cytotoxic T-cell activity

47

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 48

GENDER

• United States national surveys..

• Abdellatif et al (1987) have shown that males have poorer oral hygiene…

• Gender differences in prevalence and severity of chronic periodontitis are

related to preventive practices rather than any genetic factor.

49

RACE

• In USA – prevalence, severity and extent of chronic periodontitis is more in

Black, intermediate in Mexican African and least in Whites.

CAL

• Whites – more on facial aspect and associated with gingival recession.

• Blacks – interproximal areas

50

OSTEOPOROSIS

• It is a disease characterized by low bone mass and deterioration of bone

structure that causes bone fragility and increases the risk of fracture.

• A direct association between skeletal and mandibular osteopenia and

destructive periodontal disease as measured by loss of interproximal

alveolar bone in postmenopausal women has been reported.

(Wactawski-Wende and coworkers 1996)51

• Studies in animal models indicate that osteoporosis does not initiate

periodontitis, there is evidence that the reduced bone mass seen in

osteoporosis may aggravate periodontal disease progression

(Krook 1975, Aufdemorte 1993).

• Both osteoporosis and periodontal diseases are bone resorptive

diseases……hypothesized that osteoporosis could be a risk factor for the

progression of chronic periodontal disease.

52

HIV

AIDS epidemics in US suggests HIV positive patients

especially those with AIDS and low count of T

Lymphocytes(CD4 <200 cells/ml) were at increased risk

of chronic periodontitis.

Recent – HIV infection alone does not increases the risk

for periodontitis.

(Smith et al 1995) 53

GENETICS • Multifactorial disease………………..?

• Twin studies – it has familial component but transmission of bacteria among

family members and due to common environmental factors it is difficult to

interpret.

• Polymorphism in genes encoding for IL-1alpha and beta is associated with

aggressive form of chronic periodontitis in Northen America.

(Korman1998)54

Effect of chronic

periodontitis on systemic

disease

55

56

Chronic periodo

ntitis

Diabetes

Renal disease

Respiratory

disease

Preterm birth

Cardiovascular disease

Stroke

PATHOGENESIS

CP is initiated and sustained by bacterial plaque, but host

defense mechanism plays an integral role on its pathogenesis.

57

58

59

60

CHRONIC

PERIODONTITIS

Part II61

CONTENT

Diagnosis

A. Clinical

B. Radiographic

Prognosis

Treatment

A. Non surgical

B. Surgical

Conclusion

References

62

DIAGNOSIS

Clinical Radiograp

-hic

63

Clinical diagnosis

• Clinical parameters, such as pocket probing depths, bleeding on probing

(BOP) and suppuration (Badersten et al. 1985) or micro- biological

parameters using dark-field microscopy (Listgarten & Levin 1981, Listgarten

& Schifter 1982) with or without adjunctive culturing techniques (Rosling et

al. 1984) as indicator tests for disease "activity".

64

DISEASE ACTIVITY

Consistent with the view of periodontitis as a highly localized infection of the

periodontium, disease activity is perceived as the condition under which

periodontal attachment loss increases abruptly at discrete sites over a relatively

short period of time in a small percentage of sites (Socransky et al 1984).

65

How to Diagnose ?

66

Probing pocket depth– walking of probe.

G.V.Black was first to describe systematic use of probe to explore periodontal

pocket.

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.

67

• Increased probing depth and loss of clinical attachment are pathognomonic

for periodontitis.

• Therefore, pocket probing is a crucial and mandatory procedure in

diagnosing periodontitis and evaluating periodontal therapy.

• Reduction of pocket depth and gain of clinical attachment are the major

clinical outcome measurements used to determine success of treatment.

68

• Although recent increases in probing depth and clinical attachment loss are

evidence of disease activity in the recent past, but not necessarily of on

going disease, they are highly indicative of diseased pockets, active lesions,

and further loss of attachment.

69

Clinical attachment loss

• Clinical attachment loss 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.

• Clinical attachment level greater than 1 mm should be considered in

establishment of periodontitis.

• Ramfjord et al. proposed that loss of attachment was considered the best

measure of disease progression.

70

• Gingival recession is recorded during periodontal probing as thedistance of the free gingival margin to the cemento-enamel junction .

• Miller’s classification is widely accepted classification to determine thegingival recession:

• Class I: Recession that does not extend to the mucogingival junctionand is not associated with loss of bone or gingival tissue in theinterdental area;

• Class II: Recession that extends to the mucogingival junction and isnot associated with loss of bone or soft tissue in the interdental area;

• Class III: Recession that extends to or beyond the mucogingivaljunction with loss of bone or soft tissue in the interdental area; and

• Class IV :Recession extending to or beyond the mucogingivaljunction with severe loss of inter- dental bone and/or soft tissueand/or severe tooth malposition.

71

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).

• Although bleeding on probing alone …………may serve as

an excellent predictor for future loss of attachment.

• Lack of bleeding on probing does appear to serve as an

excellent indicator of periodontal health.

72

• 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.

• They conclude that BOP is a limited but yet useful prognostic indicator in

clinical diagnosis for patients in periodontal maintenance phase.

73

SUPPURATION

• Gingival suppuration : weak predictor of active periodontal destruction, but

better than bleeding.

• Suppuration upon probing is associated with probing attachment loss.(Anita

Bmjersten 1985)

Journal of Clinical Periodontology 1985: 12: 432-4074

• A strong association with the risk of disease progression was reported by

Armitage et al (1994).

• The sites with suppuration at baseline (25% of the total sites) were at a

threefold higher risk of further bone loss during the following 6 months.

75J Periodontol.1994 Feb;65

SUBGINGIVAL TEMPERATURE

• Elevated temperature is one of 4 cardinal inflammatory signs.

• Subgingival temperature is thought to directly reflect the subgingival

inflammatory state (Hoithius et al. 1981)

• In a study by Fedi and Killoy (1992), the temperature of pockets more than

5mm deep with bleeding on probing was 1.00C to 1.80C higher than that of

pockets less than 3mm deep without bleeding.

76

• Haffajee et al used this probe to asses its predictability in identifying loss of

attachment, concluding that sites with a red (higher) temperature indication

had more than twice the risk for future attachment loss than did those with a

green indication.

• Subgingival temperature like other signs of inflammation has good specifity

but poor sensitivity when considered as marker for progressive periodontitis

77

MOBILITY

• Tooth mobility is a clinical expression of periodontitis.

• Many attempts have been made to develop mechanical or electronicdevices for the precise measurement of tooth mobility.

• Mobility is graded clinically by holding the tooth firmly between thehandles of two metallic instruments or with one metallic instrumentand one.

• An effort then is made to move it in all directions. Abnormal mobilitymost often occurs facio-lingually.

78

Mobility is graded according to the ease and extent of tooth movement asfollows:

• Normal mobility

• Grade I: Slightly more than normal.

• Grade II: Moderately more than normal.

• Grade III: Severe mobility faciolingually and/or mesiodistally, combinedwith vertical displacement

79

• 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

80

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.

81

Pathological tooth migration

82

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., In 2012.

He observed that no single factor is associated with

PTM, but the primary factor is periodontal bone loss.

Radio graphical Diagnosis

Widening of PDL space

Loss of corticated interdental crestal margin

Localised 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.83

84

• Numerous cross sectional and longitudinal epidemiologic studies have used

radiographs as the principal method of determining the presence or absence

of periodontal destruction.

• The primary criterion for bone loss in these studies was the distance from

the cementoenamel junction (CEJ) to the alveolar crest, The threshold

distance of bone loss has varied from 1 mm to 3 mm, although most of the

studies have used > 2 mm as the criterion for bone loss.

85

CHAIR SIDE DIAGNOSTIC KITS

86

87

Quantitative.

Highly sensitive method capable of analyzing a single periodontal site in health as well as disease.

Reproducible.

Highly specific.

Simple to perform.

A rapid, one or two stage procedure.

Non-invasive.

Versatile in terms of sample handling, storage and transport.

Amendable to chairside use.

Economical.

THE IDEAL DIAGNOSTIC TEST SHOULD BE

Chairside periodontal test kits can be categorized as

88

Microbiological test kits

Biochemical test kits Genetic kits

Various chair side kits

PERIOSCAN

(Perioscan requires a plaque sample to detect the presence

of enzymes capable of degrading N-benzoyl-DL-arginine-

2-naphthylamide (BANA) from relatively few anaerobic

periodontal pathogens)

89

• POCKET- WATCH (Periodontal Tissue Monitor System)

The Pocket Watch detects elevated levels (>1200IU) of Aspartate

Aminotransferase (AST) in GCF and is used as an objective, biochemical test

for diagnosing & monitoring the disease activity, to determine when to treat,

and also to evaluate the treatment effectiveness.

• PERIOCHECK

This system (Pro Dentec Bates ville) detects the presence of neutral proteinases

such as collagenase in GCF

90

• PROGNOSTIK [Dentsply]

It detects the presence of serine proteinase and elastase in GCF samples.

• PERIOGARD [Colgate]

It detects the presence of Aspartate Aminotransferase in GCF sample.

• EVALUSITE

This chair side immunoassay detects periodontal pathogens such as Aa commitans , P gingivalis , P intermedia .

91

• CRP LATEX KIT

C- Reactive Protein (CRP) latex slide test (Serology kit) is

used for the qualitative and semi-quantitative measurement

of C-reactive protein (CRP) in human serum.

• Topas- I (Toxicity Pre Screening Assay)

• Introduced to detect two markers of infection:

Increased levels of bacterial toxins.

Increased levels of human inflammatory proteins &bacterial proteins

92

• PERIODONTAL SUSCEPTIBILITY

TEST, IL GENETICS INC.

WALTHAM.MASS

Detects the presence of a specific form of 2 IL

genes; Allele 2 at IL1A+4845 & IL1B+3954.

Test also used to correlate the IL-1 production

with other clinical parameters; BOP, Bone &

attachment loss and tooth & implant loss.

93

• BIOLISE

Recently a software has been made Biolise [SLT-Lab instruments, Craitsheim,

Germany] which is used to detect the elastase activity in GCF.

[Hermann et al 2001].

• GLUCOMETER

It is used for Blood glucose measurements using gingival crevicular blood.

94

PROGNOSIS

• Slight-to-moderate periodontitis, the prognosis is generally good, provided

the inflammation can be controlled through good oral hygiene and the

removal of local plaque-retentive factors .

• In patients with more severe periodontitis, as evidenced by furcation

involvement and increasing clinical mobility, or in patients who are

noncompliant with oral hygiene practices, the prognosis may be downgraded

to fair to poor.

95

TREATMENT PLANNING

96

Treatment for periodontitis generally falls into twocategories:

1) Procedures designed to halt the progression of disease.

2) Procedures designed to regenerate structures destroyedby disease.

Pihlstrom BL, Committee of the American Academy of Periodontology. J Periodontol 1997: 68

Non surgical

Surgical

97

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.

98

Slots J. Subgingival microflora and periodontal disease. J Clin Periodontol 1979: 6: 351–382

• Since periodontal disease is a plaque-induced infection and most patients are

not skilled in mechanical plaque removal, professional cleaning is almost

universally indicated to sustain long-term stability of the periodontium .

• Anti-infective therapy includes both mechanical and chemotherapeutic

approaches to minimize or eliminate microbial biofilm (bacterial plaque), the

primary etiology of gingivitis and periodontitis..

99

MECHANICAL

APPROACH

100

• Mechanical therapy consists of debridement of the roots by the meticulous

use of hand or power-driven scalers to remove plaque, endotoxin, 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.

101

• The term periodontal debridement was suggested by Smart et al. to describe

the light overlapping strokes used for instrumenting the root with a sonic or

ultrasonic scaler.

• The endpoint of all periodontal debridement is to produce a root that is

biologically acceptable for a healthy attachment.

102

• Numerous studies since the 1950’s have indicated that manual instrument

tation 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).

• When manual instrumentation or sonic/ultra- sonic scalers are used for the

treatment of the sub- gingival pockets, profound shifts in the composition

of the microbial flora are observed (Bollen CML et al 1998)

103

• Mechanical therapy is usually the first mode of treatment recommended for

most periodontal infections (Cobb CM.1996)

• 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.

104

• According to recent systematic reviews (Tunkel et al. 2002, van der Weijden

& Timmerman 2002, Hallmon & Rees 2003), there is no major difference in

the efficacy of debridement techniques using hand or power-driven

instruments in terms of pocket reduction and gain in clinical attachment.

• While Tunkel et al. (2002) concluded, based on their systematic review, that

the use of ultrasonic/sonic devices requires less treatment time than manual

instrumentation,

105

• The traditional modality as an initial periodontal treatment phase has been to

perform scaling and root planing by jaw quadrant (Q-SRP) at a series of

appointments (Badersten et al. 1984).

• More recently, Quirynen et al. (1995) advocated the benefit of performing

full- mouth SRP within 24h in order to prevent re-infection of the treated

sites from the remaining untreated periodontal pockets.

106

CHEMICAL

APPROACH

107

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.

108

Rationale for adjunctive topical or systemic

antimicrobial agents

Mechanical therapy alone may not effectively control infection, particularly in deeppockets.

Poor plaque control increases the rate of reinfection of the pocket

Root surface, tongue, tonsils and within other niches in the oral mucosa harborpathogenic bacteria that recolonize the periodontal pocket and can act as sources forreinfection

Actinobacillus actinomycetemcomitans and other tissue-invasive organisms are not easilyirradicated without concomitant antibiotic therapy

109

• 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.

110

• Antimicrobial products such as mouthrinses containing essential oils,

triclosan or chlorhexidine are also useful adjuncts to brushing and flossing in

gingivitis and periodontitis patients and can reduce plaque accumulation and

gingivitis by 0–75% .

111

• In disease sites that are more difficult to control, local drug delivery devices

such as chlorhexidine chips (PerioChipTM) or 10% doxycycline gel (Atri-

doxTM) may be placed directly adjacent to the infected site.

• By placing an antibiotic or antiseptic in direct contact with the root surface,

pathogenic organisms that were not accessible to mechanical removal by

hand or power-driven instruments can be reduced or eliminated.

112

• 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.

113

• Another new nonsurgical approach includes using a systemic

subantimicrobial dose of doxycycline (PeriostatA) that targets tissue

breakdown by blocking bacterial and host-derived enzymes associated with

loss of alveolar bone and connective tissue .

• Ashley has reported in a summary of several studies that as an adjunct to

either scaling or root planing or supra-gingival scaling and dental prophylaxis,

subantimicrobial doses of doxycycline were shown to reduce collagenase

levels in both gingival crevicular fluid and gingival biopsies.

114

SURGICAL THERAPY

115

• Nonsurgical therapy is performed prior to surgical treatment for periodontitis.Surgery is indicated where nonsurgical methods fail.

• Advantages of periodontal surgery :

Improved visualization of the root surface

More accurate determination of prognosis

Improved pocket reduction or elimination

Improved regeneration of lost periodontal structures

An improved environment for restorative dentistry

Improved access for oral hygiene and supportive periodontal treatment

116

• Pocket elimination procedures gave the greatest probing depth

reduction.

• Pocket elimination was defined as gingivectomy or a flap

procedure with or without osseous re-contouring.

117

Surgical techniques includes

Gingivectomy

Undisplaced flap

Modified Widman flap with and without osseous re- contouring

Apically positioned flap with and without osseous re-contouring

118

CONCLUSION

• Chronic periodontitis 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 .

119

REFERENCES

Carranza. Clinical periodontology 9th , 10th and 11th edition

Outline of periodontics Manson, Eley, 4th edition.

Relationship between periodontal disease and systemic health Periodontology 2000, Vol. 25, 2001, 21–36

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