RISK FACTORS FOR PERIODONTAL DISEASEdental.subharti.org/periodonotics/e-lectures/Dr. Soundarya-...
Transcript of RISK FACTORS FOR PERIODONTAL DISEASEdental.subharti.org/periodonotics/e-lectures/Dr. Soundarya-...
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RISK FACTORS FOR PERIODONTAL DISEASE
Dr. Soundarya Singh
Lecturer
Department of Periodontology
Subharti Dental College and Hospital
Meerut
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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.
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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.
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RISK FACTORS
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MICROBIAL TOOTH DEPOSITS
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RISK DETERMINANTS/BACKGROUND CHARACTERISTICS
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GENETIC FACTORS
AGE
GENDER SOCIOECONOMIC
STATUS
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RISK INDICATORS
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INFREQUENT
DENTAL
VISITS
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RISK PREDICTOR/MARKERS
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PREVIOUS HISTORY
OF PERIODONTAL
DISEASE
BLEEDING ON
PROBING
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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
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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
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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
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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]
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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
.
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
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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
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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
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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.
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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
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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
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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
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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
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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.
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STRESS HYPOTHESIZED AS A COMMON
PATHWAY FOR SEVERAL RELATED CHRONIC
DISEASES OF MAN
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0
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RISK INDICATORS 42
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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.
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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
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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.
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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.
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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