Risk & risk factors By Dr. Abhishek Gaur (8741095005)
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Transcript of Risk & risk factors By Dr. Abhishek Gaur (8741095005)
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Risk & Risk FactorsFor
Periodontal Diseases
Guided By :
Dr. Balaji ManoharDr. Ravi Kiran N.Dr. NeemaDr. Aditi MathurDr. Barkha Makhijani
Presented By :Dr. Abhishek GaurPost-Graduate Student(Dept. of Periodontics)
SEMINAR ON :
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DEFINITIONSRisk is the probability that an individual will get a specific disease in a given period.
Risk factor is a characteristic, an aspect of behavior, or an environmental exposure that is associated with a disease.
Risk factors may be environmental, behavioral, or biologic factors that, when present, increase the likelihood that an individual will get the disease.
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Risk indicators are probable risk factors that have been identified in cross-sectional studies but not confirmed through longitudinal studies.
Risk predictors/markers although associated with increased risk for disease, do not cause the disease.
Risk determinant / background characteristic are the risk factors that cannot be modified.
Relative risk defined as the ratio of the risk of disease in the exposed group to the risk in the unexposed group. Obtained only from longitudinal studies.
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Cross-sectional study :In medical research and social science, a cross-sectional study (also known as a cross-sectional analysis, transversal study, prevalence study) is a type of observational study that involves the analysis of data collected from a population, or a representative subset, at one specific point in time.
Case-control study :Case-control studies typically include only individuals with a specific characteristic, with a sample, often a tiny minority, of the rest of the population. Cross-sectional studies are descriptive studies (neither longitudinal nor experimental). Unlike case-control studies, they can be used to describe, not only the odds ratio, but also absolute risks and relative risks from prevalence.
Longitudinal study :A longitudinal survey is a correlational research study that involves repeated observations of the same variables over long periods of time — often many decades. It is a type of observational study.
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Tobacco Smoking
Diabetes Occlusal forces
Pathologic Bacteria & Microbial Tooth
Deposits
RISK FACTORS
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Tobacco smoking is a well established risk factor for periodontitis. A direct relationship exists between smoking & the prevalence of periodontal disease. This association is independent of other factors, such as oral hygiene or age.
Berjstrom J. (1989) concluded that greater frequencies of periodontally involved teeth & diseased sites were found in smokers, indicating more severe disease among smokers as compared with non-smokers.
Cigarette smoking as a risk factor in chronic periodontal disease, Community Dent Oral Epidemiol 1989, Oct; 17 (5) : 245-7.
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Dr. Sreedhar & Dr. Shobha Prakash (2012) evaluated the influence of cigarette smoking on severity of periodontal disease and to quantify the strength of this influence in relationship to frequency & duration of smoking.
They concluded that, frequency & duration of cigarette smoking are directly proportional to periodontal disease severity indicating it as a risk factor.
Cigarette smoking as a risk factor for periodontal disease Severity, National Journal of Integrated Research in Medicine, 2012; 3 (2) : 132-135.
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An overwhelming body of data points to smoking as a major risk factor for increasing the prevalence and severity of periodontal destruction.
12,000 dentate individuals over the age of 18 years as part of the national health and nutrition examination survey. (NHANES III) were observed.
Smokers were 4 times as likely to have periodontitis as persons who had never smoked after adjusting for age, gender, race/ethnicity, education, and income/poverty ratio
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Papapanou (1996) A meta analysis of data
involving 2361 subjects indicated that current
smokers were nearly 3 times more likely to have
severe periodontitis.
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EFFECTS OF SMOKING ON THE ETIOLOGY AND PATHOGENESIS OF PERIODONTAL DISEASE
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Micro-Biology
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Studies have failed to demonstrate a difference in the rate of
plaque accumulation of smokers compared with
nonsmokers.
Bergstrom 1989 concluded that If an alteration in the
microbial challenge in smokers exists, it is due to a
qualitative rather than quantitative alteration in the plaque.
In 272 adult subjects… checker-board DNA-DNA
hybridization technology to screen for 29 different sub-
gingival species, it was found that members of the orange
and red complexes were significantly more prevalent in
current smokers than in nonsmokers and former smokers.
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Diabetes is a modifiable factor in the sense that though it cannot be cured, it can be controlled.
Studies that have examined the relationship between diabetes and periodontitis are heterogeneous in design and aim.
Thus, both positive and negative conclusions have been drawn with respect to the relationship between the two diseases.
In general no difference in impact has been determined between type 1 and type 2 diabetes mellitus.
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Diabetic parameters examined include glycemic control, duration of disease, presence of other diabetes-associated complications and population studied.
Periodontal parameters examined have included gingivitis, clinical attachment loss, and alveolar bone loss.
Tomar and Asma, 2000
A review of the literature by Kinane found considerable evidence to suggest that diabetes and periodontitis have a direct relationship.
Kinane and Chestnutt, 1997
Studies have shown a relationship between poor glycemic control and periodontal disease parameters.
Guzman et al., 2003; Tsai et al., 2002; Tervonen et al., 1994, Cutler et al., 1999
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Taylor et al. have suggested a bi-directional relationship between periodontal disease and glycemic control (Nishimura et al., 2003; Taylor, 2001) with each disease having a potential impact on the other.
Cross sectional studies on Pima Indians, a group displaying the highest prevalence of type 2 diabetes in the world, show an odds ratio of 2.8 to 3.4 for developing periodontal disease in type 2 diabetics compared to non-diabetics.
Emrich et al., 1991
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Similarly, longitudinal studies have shown increased risk of ongoing periodontal destruction in diabetics as compared to non-diabetics with an odds ratio of 4.2.
Finally, studies have been done which suggest that poorly controlled diabetics respond less successfully to periodontal therapy relative to well-controlled and non-diabetics.
Westfelt et al., 1996; Tervonan and Karjalainen, 1997
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Pathogenic Bacteria and
Microbial Tooth Deposits
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1996 World Workshop, limited their findings to three organisms: A.
actinomycetemcomitans, B. forsythia, and P. gingivalis.
Presumably because they met Socransky’ s modifications of Koch’s
postulates.
1. The organism must occur at higher numbers in disease-active sites than at
disease-inactive sites.
2. Elimination of the organism should arrest disease progression.
3. The organism should possess virulence factors relevant to the disease process.
4. The organism should elicit a humoral or cellular immune response.
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Ezzo & Cutler (2003) concluded that periodontal
pathogens as risk indicators are due to the fact that
the odds ratios between the presence of these
specific bacteria individually, and periodontitis are
not high enough to classify them as risk factors.
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A. actinomycetemcomitansTrue pathogen or high-risk organism.
Serotype b strains of A. actinomycetemcomitans, produce increased
amounts of leukotoxin, an important virulence factor, and are found
most often associated with periodontal disease.
The ability to evade the innate defenses and survive mechanical
periodontal therapy is its ability to invade gingival tissues and, in
particular, to invade epithelial cells.
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Bacteroides forsythia/ Tannerella forsythia
The least understood because it is the most difficult to cultivate in
vitro. Virulence traits including the production of a trypsin-like
protease and lipopolysaccharide.
Rudney JD, Chen R (2001) concluded that more recently its
ability to penetrate host cells or induce apoptosis has received
attention. Perhaps the most intriguing aspect of B. forsythia virulence
is its ability to induce apoptosis.
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Porphyromonas gingivalis
Three major virulence factors - fimbriae, gingipains and lipopolysaccharides.
The fimbriae mediate adherence to specific receptors on host cells, such as epithelial cells. Fimbriae also induce bacterial internalization by activating and mobilizing the epithelial cell cytoskeleton.
Gingipains are P. gingivalis proteases whose major function is nutrient acquisition through degradation of proteins into peptides.
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RISK DETERMINANTS / BACKGROUND CHARACTERISTICS
1. Genetic Factors
2. Age
3. Gender
4. Socioeconomic Status
5. Stress
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Genetic FactorsAlthough bacterial infection is the etiologic
agent in periodontal disease, studies of identical twins suggest 50% of susceptibility to periodontal disease is due to host factors.
Michalowicz et al., 2000
Similarly, indigenous and relatively isolated populations have been shown to develop distinct periodontal disease that differ from group to group.
Dowsett et al., 2001; Ronderos et al., 2001
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Kornman 1997 concluded that the familial
aggregation seen in localized and generalized
aggressive periodontitis also is indicative of genetic
involvement in these diseases.
A specific interleukin- 1 (IL-1) genotype has been
associated with severe chronic periodontitis.
Kornman 1997
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Ageing is associated with an increased incidence of periodontal disease.
Grossi et al., 1994; Grossi et al., 1995
However it has been suggested that the increased level of periodontal destruction observed with aging is the result of cumulative destruction rather than a result of increased rates of destruction.
Thus aging is not a risk factor per se.Genco, 1996
Age
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Both the prevalence and severity of periodontal disease increases with age.
Papapanou 1998
Minimal loss of attachment in aging subjects enrolled in preventive programs throughout their lives.
Lindhe 1991
Intake of medications, decreased immune function, and Altered nutritional status interact…….
Loss of attachment may be of more consequence in younger patients.
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GenderGender plays an important role in periodontal disease.
United States national surveys conducted since 1960 demonstrate that
males have more loss of attachment than females.
Males have poorer oral hygiene than females, as evidenced by higher
levels of plaque and calculus.
Therefore it appears that gender differences in prevalence and
severity of periodontitis are related to preventive practices rather than
any genetic factor.
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RaceBeck and coworkers showed that blacks……….
More indicators related to socioeconomic……
P. intermedia was a risk factor for blacks but not for whites.
When blacks and whites belonged to the same socioeconomic
group, differences in periodontal disease often disappeared.
Grossi et al 1994, 1995
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Low Socioeconomic&
Educational StatusPeriodontal disease is more severe in individuals of lower
socioeconomic status and poorer education.
When adjusted for oral hygiene and smoking, the associations
between lower socioeconomic and educational status and severe
periodontal disease are not seen.
Thus socioeconomic and educational statuses do not appear to
directly affect the pathogenesis.
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Stress
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Defined as the psycho physiological response of an organism to perceived threat or challenge.
Emotional stress may interfere with normal immune function.
Haffajee AD, Socransky SS 1994
Bereavement and divorce appear to lead to a greater prevalence of periodontal disease.
Green 1986
An apparent association between psychosocial factors and risk behaviors such as smoking, poor oral hygiene, and chronic periodontitis. Individuals with financial strain, distress, depression, or inadequate coping mechanisms have more severe loss of attachment.
Genco 1999
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Corticosteroids have inhibitory effect on inflammatory cells i.e.,
macrophage & neutrophils.
Inhibition through suppression of cytokines such as IL-1, IL-6, TNF
and arachidonic acid metabolites.
Regulated at the level of gene expression by altering the messenger
RNA stability.
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Hypothalamus-pituitary-adrenal Cortex (HPA) Axis Is Stimulated
Anterior Hypothalamus Secretes Corticotrophin-releasing Factor
Which Act On The Hypophysis
The Pituitary Gland, Releases Adrenocorticotrophic Hormone
Which Acts On The Adrenal Cortex
Increases Production And Release Of Glucocorticoid Hormones
Which In Turn Stimulate The Immune Response
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General Adaptation SyndromeSelye’s classic work in the 1930s and 1940s describes the body's short-term
and long-term reaction to stress.
Stress is the cause of general adaptation syndrome and it can manifest as
fatigue, irritability, difficulty concentrating, and difficulty sleeping
Describes a three stage reaction to stress :
1. Alarm reaction
2. Stage of resistance
3. Stage of exhaustion
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Stage 1: Alarm reactionThe alarm reaction
Is the immediate reaction to a stressor
In the initial phase of stress, humans exhibit a "fight or flight"
response, which causes one to be ready for physical activity
However, this initial response can also decrease the effectiveness of
the immune system, making persons more susceptible to illness
during this phase
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Stage 2: Stage of resistance
Might also be named the stage of adaptation. If the stress continues,
the body adapts to the stressors it is exposed to.
Changes at many levels take place in order to reduce the effect of the
stressor.
E.g. if the stressor is starvation (possibly due to anorexia), the person
might experienced a reduced desire for physical activity to conserve
energy, and the absorption of nutrients from food might be
maximized.
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Stage 3: Stage of exhaustion
Stress has continued for some time. Body's resistance to the stress may
gradually be reduced, or may collapse quickly.
The immune system, and the body's ability to resist disease, may be
almost totally eliminated.
Patients who experience long-term stress may succumb to heart
attacks or severe infection due to their reduced immunity.
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RISK INDICATORS
Are probable risk factors that have been identified in cross-sectional
studies but not confirmed through longitudinal studies.
1. Human Immunodeficiency Virus / AIDS
2. Osteoporosis
3. Infrequent Dental Visits
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HIV / AIDS Early reports by Winkler 1992 ………patients often had
severe periodontal destruction characteristic of necrotizing
ulcerative periodontitis.
More recent reports by Lamster 1994 , Swango 1991, have
failed to demonstrate significant differences in the
periodontal status of individuals with HIV infection and
healthy controls.
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The relative risk of longitudinal attachment loss correlated
with the CD-4 levels suggesting a correlation between the
severity of periodontal disease and the level of
immunosuppression.
Barr 1992
Studied individuals with HIV, AIDS individuals who were
HIV seronegative & found no significant differences in
BOP, PD.
Scheutz 1997, Papapanou 1998
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OsteoporosisOsteopenia and osteoporosis are systemic skeletal diseases characterized by :
Low Bone Mass Micro-architectural Deterioration
Increase In Bone Fragility & Susceptibility To Fracture
WHO….osteoporosis is considered to be present when BMD is 2.5 standard deviations below the young normal.
Osteopenia is defined as bone density levels between 1 SD and 2.5 SD below normal Bone Mineral Density.
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Both osteoporosis and periodontal diseases are bone
resorptive diseases……hypothesized that osteoporosis
could be a risk factor for the progression of periodontal
disease.
Aufdemorte 1993 conducted 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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Von Wowern et al 1994 reported that the women with osteoporosis had greater loss of attachment than the control subjects.
Kribbs 1990 examined pocket depth, bleeding on probing, and gingival recession in women with and without osteoporosis; the two groups had significant differences in bone mass, no differences in periodontal status were noted.
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Infrequent Dental VisitsAs a risk factor for periodontitis is controversial.
Page 1997
One study demonstrated an increased risk for severe
periodontitis in patients who had not visited the dentist for three or
more years.
Korman et al. 1998
Whereas another demonstrated that there was no more loss of
attachment or bone loss in individuals who did not seek dental care
when compared with those that did over a 6-year period.
Topayi et al. 1999
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RISK MARKERS / PREDICTORS
1. Previous History of Periodontal Disease.
2. Bleeding on Probing
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A history of previous periodontal disease is a good clinical predictor
of risk for future disease.
Page 1997
Patients with the most severe existing loss of attachment are at the
greatest risk for future loss of attachment.
Conversely, patients currently free of periodontitis have decreased
risk for developing loss of attachment than those who currently have
periodontitis.
Previous History Of Periodontal Disease
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Bleeding on ProbingBleeding on probing is the best clinical indicator of gingival
inflammation.
Page 1997
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.
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CLINICAL RISK ASSESSMENT FOR
PERIODONTAL DISEASE
Demographic data
Medical history
Dental history
Clinical examination
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Conclusion
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Risk Assessment involves identifying elements that may predispose a patient to developing disease or may influence the progression of disease that already exists.
In either case, these patients may require modifications of their prognosis & treatment plan.
In addition to an evaluation of the factors contributory to their risk, these patients should be educated concerning their risk, and when appropriate, suitable intervention strategies should be implemented.
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In the case of localized aggressive periodontitis the defect may be relatively benign. In more severe conditions of neutrophil dysfunction, the incidence may be so low or the disease so debilitating as to preclude rigorous analysis of periodontal relationships.
Future studies will likely be focused on understanding the relationship between genetic and environmental factors and also on the rapid and practical identification of at-risk individuals, and will allow us to tailor therapy to more closely suit the needs of our patients as individuals and thus achieve better results.
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References1. Carranza Clinical Periodontology, 10th Edition.
2. Jan Lindhe, Clinical Periodontology & Implant Dentistry, 5th Edition.
3. Acquired immune suppression and other risk factors/indicators for periodontal disease progression, Periodontology 2000, Vol. 32, 2003, 118–135.
4. Finding genetic risk factors for periodontal diseases : is the climb worth the view?, Periodontology 2000, Vol. 30, 2002, 79–90.
5. Global risk factors and risk indicators for periodontal diseases, Periodontology 2000, Vol. 29, 2002, 177–206.
6. Risk factors for periodontal disease progression among elderly people, J Clin Periodontol 2002: 29: 592–597.
7. Risk factors for tooth loss in an adult population: a radiographic study, J Clin Periodontol 2008; 35: 1059–1065.
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