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RISK FACTORS FOR PERIODONTAL DISEASE

Dr. Soundarya Singh

Lecturer

Department of Periodontology

Subharti Dental College and Hospital

Meerut

INTRODUCTION

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• Periodontitis - multifactorial disease with microbial dental plaque as the initiator.

• Periodontitis - increases the risk for certain systemic diseases such as heart disease, low birth weight, respiratory diseases and possibly other conditions.

TERMINOLIGIES

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Risk is the probability that an individual will develop a specific disease in a given period.

The risk for developing the disease will vary from individual to individual.

Risk factors environmental,

behavioral,

biologic

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• Risk factors - Identified through:

Longitudnal studies.

• A risk factor that cannot be modified is often referred to as risk determinant/background characterstics.

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• Risk indicator is used to describe a putative (or potential) risk factor identified to be associated with disease from case control or cross-sectional studies, but not yet confirmed in longitudinal or interventional studies.

• A risk predictor/marker although associated with increased risk for disease, do not cause the disease.

RISK FACTORS

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MICROBIAL TOOTH DEPOSITS

RISK DETERMINANTS/BACKGROUND CHARACTERISTICS

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GENETIC FACTORS

AGE

GENDER SOCIOECONOMIC

STATUS

RISK INDICATORS

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INFREQUENT

DENTAL

VISITS

RISK PREDICTOR/MARKERS

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PREVIOUS HISTORY

OF PERIODONTAL

DISEASE

BLEEDING ON

PROBING

TOBACCO SMOKING

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• A direct relationship between smoking and prevelance of periodontal disease.

• greater - clinical attachment loss

- disease progression

- loss of alveolar bone

The average number of bleeding sites are found to be lower in smokers

• Non surgical therapy is found to be less effective in smokers

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Biologic phenomena

Smoking attachment loss

• Vasoconstrictive effect on gingival blood vessels.

(Baab & Oberg 1987)

• Smoking functional activity of leukocytes and

macrophages, as well as chemotaxis and

phagocytosis of PMNs. (Palmer 1988)

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• Tobacco Nicotine

Cotinine

Detected in

saliva and crevicular fluid (Langone et al 1973)

serum and urine (McGuire et al 1989)

Root surfaces of periodontally involved teeth of smokers

(Cuff et al 1989)

Presence of cotinine on root surface: impair wound

healing and alter the host response

DIABETES MELLITUS

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DIABETES MELLITUS

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Complex metabolic disease characterized by chronic hyperglycemia

Diminished insulin production, impaired insulin action, or a combination of both

CLASSIFICATION:

Type I: insulin-dependent;juvenile diabetes

Type II:non-insulin-dependent;adult onset diabetes

Gestational diabetes(pregnancy diabetes)

Other type:

•Genetic defects affecting -cell function

•Pancreatic diseases/injuries

•Infections

•Drug induced diabetes

•Endocrine disorders

•Other genetic syndromes

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TYPES OF DIABETES

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Type 1

“Juvenile”

Type 2

“adult-onset”

Caused by cell médiate auto-

immune destruction of insulin

producing islet cell

Caused by peripheral resistance to

insulin action, impaired insulin

secretion & increased glucose

production in liver

Results in insulin deficiency Insulin producing beta cells are not

destroyed

Marked tendency towards

ketosis and coma

Not prone to ketosis

Type 1 Type 2

Thought to be genetic in origin Associated with obesity and

inactivity

May be triggered by childhood

infection (e.g. mumps)

Most common seen in 90- 95%

of all cases

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Periodontitis – sixth complication of

diabetes [ Löe H. 1993]

ORAL MANIFESTATIONS OF DIABETES

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Mucosal drying and cracking

Burning mouth and tongue

Diminished salivary flow

Alterations in the flora of the oral cavity, with greater predominance of Candida albicans, hemolytic streptococci, and staphylococci.

Increased rate of dental caries

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Enlarged gingiva

Sessile or pedunculated gingival polyps

Polypoid gingival proliferations

Abscess formation

Periodontitis

Loosened teeth

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Mechanisms of interaction :

1. Changes in subgingival environment

2. Altered microbiota : Shift to a flora predominated my G-ve rods and filaments.

3. Altered tissue hemostasis and wound healing

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• Hyperglycemic state- ADVANCED GLYCATION END PRODUCTS

(AGES).

AGE-enriched gingival tissue has greater vascular permeability,

experiences greater breakdown of collagen fibres and shows

accelerated destruction of both nonmineralized connective tissue and

bone

Lalla E & Dambrosio J 2001

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Diabetics have higher than normal levels

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Diabetic patients, concentration of oral microbial flora is

increased due to higher concentration of glucose in saliva

and crevicular fluid.

Deshpande K 2010

Prevotella intermedia, Prevotella melaninogenica, Bacteroides gracilis, Eikenella

corrodens, Fusobacterium nucleatum and Campylobacter rectus

PATHOGENIC BACTERIA AND MICROBIAL TOOTH

DEPOSITS

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• Relationship between accumulation of bacterial plaque and gingival

inflammation.

• Quantity of plaque is not of major importance but quality, of the

complex plaque biofilm is of importance.

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Specific bacteria have been identified as etiologic agents for

periodontitis:

• Aggregatebacter actinomycetemcomitans,

• Porphyromonas gingivalis,

• Bacteroides forsythus.

• P. gingivalis and B. forsythus in chronic periodontitis,

• A. actinomycetemcomitans is often associated with aggressive

periodontitis.

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Anatomic factors :

• furcations, root concavities, developmental grooves,

cervical enamel projections, enamel pearls, and

bifurcation ridges

• the presence of subgingival and/or overhanging

margins

• calculus

RISK DETERMINANTS

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GENETIC FACTORS

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• Studies conducted in twins have shown that genetic factors

influence clinical measures of gingivitis, probing pocket depth,

attachment loss, and interproximal bone height.

• The familial aggregation is seen in localized and generalized

aggressive periodontitis

• A specific interleukin- 1 (IL-1) genotype has been associated

with severe chronic periodontitis

AGE

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• The attachment loss and bone loss seen in older

individuals is a result of prolonged exposure to other

risk factors over a person's life, creating a

cumulative effect over time.

GINGIVAL EPITHELIUM

• Thinning and decreased keratinization

• Increase in epithelial permeability to bacterial agents

• Decreased resistance to functional trauma

• Flattening of retepegs and altered cell density

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GINGIVAL EPITHELIUM

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• Effect on the location of the junctional epithelium

• No effect

• Gingival recession

• Increase in the width of attached gingiva

GINGIVAL CONNECTIVE TISSUE

• Coarser and more dense gingival connective tissue

• Qualitative and quantitative changes in collagen

• Increased insoluble collagen and increased

mechanical strength

• A greater collagen content

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PERIODONTAL LIGAMENT

• Decreased no. of fibroblasts

• Irregular structure

• Decreased organic matrix production and epithelial cell rests

• Increased amount of elastic fibers

• Conflicting reports regarding changes in the width

– May be more dependent on the function

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CEMENTUM

• Increase in cemental width

• 5 to 10 times

• Greater apically and lingually

• Increased surface irregularity

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ALVEOLAR BONE

• More irregular periodontal surface of bone and

less regular insertion of periodontal fibers

• Age is a risk factor for alveolar mass reduction in

osteoporosis.

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•Socket healing independent of age

•Implant union - age independent

•Bone graft from donors more than 50 years of age

have less osteogenic potential

GENDER

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• males have more loss of attachment than females.

• males have poorer oral hygiene than females.

• Hormonal and other physiological and behavioural

differences may also contribute to the higher risk for

periodontal diseases in males than in females

SOCIOECONOMIC STATUS

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• Gingivitis and poor oral hygiene can be related

to lower socioeconomic status.

• Decreased dental awareness and decreased

frequency of dental visits.

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STRESS AND

PERIODONTIUM

STRESS

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• Emotional stress may interfere with normal immune

function and may result in increased levels of circulating

hormones.

• Apparent association between psychosocial factors and

risk behaviors such as smoking, poor oral hygiene, and

chronic periodontitis.

STRESS HYPOTHESIZED AS A COMMON

PATHWAY FOR SEVERAL RELATED CHRONIC

DISEASES OF MAN

4

0

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RISK INDICATORS 42

AIDS/HIV

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• Reports on the periodontal status of patients with AIDS or individuals

who are HIV seropositive

severe periodontal destruction characteristic of necrotizing ulcerative

periodontitis.

OSTEOPOROSIS

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• 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

INFREQUENT DENTAL VISITS

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• Identifying failure to visit the dentist on a regular basis as

a risk factor for periodontitis is controversial.

PREVIOUS HISTORY OF PERIODONTAL

DISEASE

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• A history of previous periodontal disease is a good clinical

predictor of risk for future disease .

• Patients with the most severe existing loss of attachment

are at the greatest risk for future loss of attachment.

BLEEDING ON PROBING

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• Best clinical indicator of gingival inflammation.

• Although bleeding on probing alone does not serve as a

predictor for loss of attachment, bleeding on probing

coupled with increasing pocket depth 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.

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THANK YOU