This document discusses risk assessment in periodontal disease. It defines risk assessment as identifying populations at increased risk of developing periodontal disease and assessing their risk of current or future disease. Key risk factors discussed include tobacco smoking, diabetes, genetic factors, age, gender and socioeconomic status. Tobacco smoking is identified as a major risk factor, increasing the likelihood and severity of periodontal disease through effects on the immune system, blood vessels, bacterial microbiome and other physiological systems. The use of risk assessment tools to evaluate multiple risk factors can help with clinical decision making and reducing oral healthcare costs.

2. CONTENTS
• INTRODUCTION
•RISK ASSESSMENT
•THE CLINICAL PRACTICE OF RISK ASSESSMENT
• CATEGORIES OF RISK ELEMENTS FOR PERIODONTAL DISEASE
• RISK ASSESSMENT IN PERIODONTAL DISEASE
• TOBACCO SMOKING
• MECHANISMS UNDERLYING THE EFFECT OF SMOKING ON
PERIODONTITIS

3. • Clinical presentation of the periodontal patient who smokes
• DIABETES
• ANATOMIC FACTORS
• GENETIC FACTORS
• AGE
• GENDER
• SOCIOECONOMIC STATUS
• RISK ASSESSMENT IN PRACTICE
• PERIODONTAL RISK ASSESSMENT
• SCIENCE TRANSFER
• CONCLUSION

4. INTRODUCTION
• In today’s social environment, it is essential that rational and cost-
effective decisions be made for prevention and treatment of the
periodontal diseases.
• Our understanding of periodontal diseases has deepened, it has become
clear that certain risk factors are associated with disease development.
• The practice of risk assessment involves identifying populations at
increased risk of developing periodontal disease

5. • Assessing their risk of developing periodontal disease can have a
significant impact on clinical decision making.
• Risk assessment may reduce the need for complex periodontal therapy,
improve patient outcomes and ultimately reduce oral health care costs.
• It is a way of examining risks so that they may be avoided, reduced, or
managed. Risk can be identified in terms of risk factors, risk indicators,
or risk predictors

6. RISK ASSESSMENT
According to the American Academy of Periodontology, risk
assessment has been defined as the process by which qualitative or
quantitative assessments are made of the likelihood for adverse
events to occur as a result of exposure to specified health hazards or
by the absence of beneficial influences.

7. THE CLINICAL PRACTICE OF RISK
ASSESSMENT
• Most dentists and periodontists are not trained or experienced in risk
assessment nor in using interventions aimed at risk reduction in the
prevention and management of periodontal diseases.
• A computer-generated risk assessment model can aid in the identification of
patients at elevated risk of developing periodontal disease, and may help in
the selection of patients who require additional education or targeted
interventions

8. PERIODONTAL RISK CALCULATOR
• The PRC is a web-based tool that can be accessed through a dental
office computer.
• PRC calculated risk is for future periodontal disease for those
patients who do not yet have it and risk for future progression of
periodontal disease for those who already have it.
• A risk factor must have a scientific basis that is supported by
publication in refereed scientific journals.

9. • The application of risk assessment information through the
development of treatment recommendations to reduce risk must
occur.
• The calculation of risk is a multi-step process involving
mathematical algorithms that use nine risk factors, including:

10. • Patient age
• Smoking history
• Diagnosis of diabetes
• History of periodontal surgery
• Pocket depth
• Furcation involvements
• Restorations or calculus below the gingival margin
• Radiographic bone height
• Vertical bone lesions

11. GENETIC TESTS
• This test determines whether people possess a combination of alleles in two IL-1
genes.
• Studies have reported an increased frequency of a different IL-1 genotype in
people with advanced adult periodontitis compared with those with early or
moderate disease.

12. • Genetic testing for the specific IL-1 genotype may give indication
of increased susceptibility to tooth loss in periodontal
maintenance patients. .
• However, it may be concluded that genetic testing has potential
for the future, but more research is needed to evaluate its utility

13. • Risk is the probability that an individual will develop a specific disease in a
given period.
• Risk factors: environmental, behavioral, or biologic factors that, when
present, increase the likelihood that an individual will develop the disease.
• Exposure to a risk factor may occur at a single point in time; over
multiple, separate points in time; or continuously.

14. • Risk determinant/background characteristic, which is sometimes
substituted for the term risk factor, should be reserved for those risk
factors that cannot be modified.
it is biologically plausible as a causal agent for disease
it has been shown to precede the development of disease

15. • Risk indicators are probable or putative 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. These factors also are identified in
cross-sectional and longitudinal studies.

16. CATEGORIES OF RISK ELEMENTS FOR
PERIODONTAL DISEASE
Risk Factors
Tobacco smoking
Diabetes
Pathogenic bacteria
Microbial tooth
deposits
Risk Determinants
Genetic factors
Age
Gender
Socioeconomic status
Stress

17. Risk Indicators
HIV/AIDS
Osteoporosis
Infrequent dental
visits
Risk Markers/Predictors
Previous history of periodontal
disease
Bleeding on probing

18. TOBACCO SMOKING
• It’s a prevalent behavior with severe health consequences.
• A well-established risk factor for periodontitis.
• Heavy smokers may be up to five to seven times more likely to manifest or to
develop severe periodontitis than individuals who have never smoked

19. Haber et al conducted a study on subjects ranging in age from 19 to 40
years. Prevalence and severity of periodontitis were significantly higher
in current smokers than in those who had never smoked.
There is also evidence for a link between passive smoking and
periodontal disease
Haber J,Wattles J, Crowley M, Mandell R, Joshipura K, Kent R L. Evidence for cigarette smoking as a major risk
factor for periodontitis. J Periodontol 1993a 64:16-23.

20.  Nicotine (the addictive drug that produces the effects in the brain that
people are looking for)
 Hydrogen cyanide.
 Formaldehyde.
 Lead.
 Arsenic.
 Ammonia

21. Harmful effects result through systemic exposure following lung
absorption, in addition to the obvious absorption in the oral cavity
palmer et al. 1999

22. smoke is inhaled and absorbed through the alveoli or oral mucosa
facilitating neurotransmitter release
Dopamine and endorphins are released, which are often associated
with pleasure
it is absorbed rapidly into the pulmonary venous circulation. It then
enters the arterial circulation and moves quickly to the brain
Nicotine diffuses readily into brain tissue, where it binds to nAChRs.

23. The α4β2receptor subtype is believed to be the main receptor
mediating nicotine dependence.
Nicotine is a sympathomimetic drug
 increases heart rate ,cardiac contractility
 constricts cutaneous and coronary blood vessels
 transiently increases blood pressure
Nicotine also reduces sensitivity to insulin and may aggravate or
precipitate diabetes

24. EFFECTS OF SMOKING ON PERIODONTAL DISEASE
• Gingivitis ; ↓Gingival inflammation and bleeding on probing
PERIODONTITIS
↑Prevalence and severity of periodontal destruction
↑Pocket depth, attachment loss, and bone loss
↑Rate of periodontal destruction
↑Prevalence of severe periodontitis
↑Tooth loss
↑Prevalence with increased number of cigarettes smoked per da
↓Prevalence and severity with smoking cessatio

25. MICROBIOLOGY
• No effect on rate of plaque accumulation
• Qualitative rather than quantitative alteration in the plaque is seen.
• ↑Levels of periodontal pathogens in deep periodontal pockets
•Bacterial aggregation (bagaitkar et al.2011),promote
colonization with key periodontal pathogens

26. • Preber et al1980 - amount of plaque in smokers is higher compared to
non‐smokers
• Lie et al. 1998 - experimental gingivitis models the rate of plaque
formation was similar between smokers and non‐smokers
• Zambon et al. (1996) - higher prevalence of Aggregatibacter
actinomycetemcomitans, Tannerella forsythia, and P. gingivalis in current
and former smokers compared with never‐smokers.

27. • Haffajee and Socransky (2001)- found a higher prevalence of eight
bacterial species
• Gingival and periodontal ligament fibroblast recruitment and adhesion may
be negatively affected in smokers
• Collagen production is decreased while collagenolytic activity is increased

28. VASCULATURE
• Nicotine‐induced peripheral vasoconstriction as well as the
reduction in GCF
• Nicotine‐induced secretion of epinephrine resulting in gingival
vasoconstriction - influence tissue susceptibility - schwartz &
baumhammers 1972

29. IMMUNOLOGY
• ↑Tnf–α and PGE2 in gingival crevicular fluid (GCF)
• ↑Neutrophil collagenase and elastase in GCF
• Neutrophils express functional receptors for smoke components
• Numbers of nicotine receptors are increased in smokers (ackermann
et al. 1989)

30. • Neutrophil migration and chemotaxis and the oxidative burst in the
periodontal tissues are negatively affected in smokers (pabst et al.
1995).
• Smokers have depressed numbers of t‐helper lymphocytes,

31. PHYSIOLOGY
• ↓GCF flow and bleeding on probing with ↑ inflammation
• ↓subgingival temperature
• ↑Time needed to recover from local anesthesia
• In addition, the oxygen concentration in healthy gingival tissues appears
to be less.
• A single episode of smoking has been shown to produce a transient
increase in GCF volume (mclaughlin et al. 1993)

32. • Less is known about the mechanisms underlying the effects of passive
smoking on the periodontium.
• Increased levels of salivary cotinine (a nicotine metabolite),
• Higher levels of a number of inflammatory mediators
• Increased proportion of phagocytic cells in gingival lesions possibly
indicating an altered host response to the bacterial challenge

33. CLINICAL PRESENTATION OFTHE
PERIODONTAL PATIENTWHO SMOKES
• Clinically and radiographically with signs of increased bone,
attachment, and tooth loss .
• Deeper pockets in anterior and maxillary palatal sites
• Fibrotic gingiva and limited gingival erythema and edema relative to
the amount of plaque and the severity of the underlying bone loss
(scott & singer 2004).

34. • Bleeding on probing is reduced in a dose‐dependent manner in
smokers compared to non‐smokers with similar levels of plaque
(Bergstrom & Bostrom 2001)

35. EFFECTS OF SMOKINGON RESPONSETO
PERIODONTALTHERAPY
Nonsurgical
• ↓Clinical response to scaling and root planing
• ↓Reduction in pocket depth
• ↓Gain in clinical attachment levels
• ↓Negative impact of smoking with ↑level of plaque control
• negative effects on healing following non‐surgical and surgical
periodontal therapy

36. • Response to therapy is compromised in smokers, with current smokers
exhibiting less probing depth reduction and/or attachment gain
compared to former or never smokers.

37. SURGICALTHERAPY AND IMPLANTS
• Heavy defined as ≥20 cigarettes/day; light defined as ≤19
cigarettes/day
• Less pocket reduction and less gain in clinical attachment levels than
nonsmokers or former smokers.
• These differences began immediately after the completion of therapy
and continued throughout 7 years of supportive periodontal therapy.

38. • A negative effect of smoking on longterm implant success, patients
should be informed and advised of it.
• Smoking cessation should be recommended before implants
• Deterioration of furcation areas was greater in heavy and light smokers
than in former smokers and nonsmokers.
• Negative impact on the outcomes of guided tissue regeneration
(gtr)and the treatment of intrabony defects by bone allografts.

39. MAINTENANCE PHASE
• ↑Pocket depth during maintenance therapy
• ↓Gain in clinical attachment levels
• ↑Recurrent/refractory disease in smokers
• ↑Need for re-treatment in smokers

40. • ↑Need for antibiotics in smokers to control the negative effects of
periodontal infection on surgical outcomes
• ↑Tooth loss in smokers after surgical therapy

41. PATIENT MANAGEMENT
• Inform of their enhanced risk for limited or delayed treatment responses.
• Improved patient oral health, overall health, and quality of life.
• Smoking cessation has been shown in longitudinal studies to have
beneficial effects on the periodontal status (bolin et al. 1993; rosa et al.
2011),

42. • Smoking cessation alone or in conjunction with non‐surgical
periodontal therapy appears to result in a subgingival microbiota
that comprises higher levels of health‐associated species and
lower levels of pathogens (fullmer et al. 2009; delima et al. 20

43. • The effects of smoking on the host are reversible with smoking cessation
• Smoking cessation programs should be an integral component of
periodontal education and therapy
• Several tobacco intervention approaches can be used in helping the
patient deal with the nicotine withdrawal symptoms and psychologic
factors associated with smoking cessation.

44. • Ask: Ask about smoking behavior directly and document status
• Advise: Advise patient to quit
• Assess: Assess the patient’s readiness and motivation to quit
• Assist: Assist the patient willing to make a quit attempt by providing a
structured plan for quitting.
• Arrange: Arrange follow‐up, including behavioral support and telephone
contact/counseling. The first week of cessation is especially critical

45. • Pharmacologic treatment options include nicotine replacement therapy,
sustained‐release bupropion, and varenicline (aubin et al. 2011).
• Nicotine replacement therapy - use of products that provide low doses
of nicotine, but do not contain the toxins found in smoke.
• To relieve cravings for nicotine and ease the withdrawal symptoms.

46. • Nicotine supplements come in different forms: transdermal patch,
gum, lozenges, nasal spray, and inhaler.
• Sustained‐release bupropion inhibits the neuronal uptake of
norepinephrine and dopamine.
• Control nicotine withdrawal symptoms and may also help patients
manage associated anxiety and depression

47. • Should be initiated 1–2 weeks before the quit date, since 1 week is
necessary to achieve steady‐state blood levels
• Treatment usually lasts for 2–3 months, but it can continue safely for
maintenance for up to 6 months.
• The use of bupropion is contraindicated for patients with a history of
seizures, eating disorders,

48. • Complex patients such as those suffering from psychiatric illness or medical
co‐morbidities should be referred to smoking cessation specialists/clinics
where comprehensive treatment can be offered.
• “Brief intervention” approach may be a useful model. The dental team can
give patients educational brochures to take home and also provide some
encouragement and support by relating tobacco use to medical and oral
health risk

49. • Varenicline is the newest drug for smoking cessation.
• Structure similar to that of nicotine and thus it can antagonize nicotine
binding to its receptor sites.
• Treatment starts 1 week before the quit date and continues for 3
months; maintenance treatment, if needed, may be for up to 6 months

50. DIABETES
• Diabetes mellitus is the term used to describe a group of metabolic
disorders distinguished by altered glucose tolerance and impaired
carbohydrate metabolism (American Diabetes Association, 2001)
• Chronic hyperglycemia is associated with long-term dysfunction and
damage to numerous end-organs, with marked effects on the eyes,
kidneys, heart, nerves, and blood vessels

51. • Epidemiological data confirm that diabetes is a major risk factor for
periodontitis; susceptibility to periodontitis is increased by
approximately threefold in people with diabetes.
• existence of a two-way relationship between diabetes and
periodontitis, with diabetes increasing the risk for periodontitis, and
periodontal inflammation negatively affecting glycaemic control

52. • Oral and periodontal health should be promoted as integral
components of diabetes management.
• In the early 1990s periodontitis was sometimes referred to as the
‘sixth complication of diabetes’
• Periodontal disease had not been included in the complications list
for diabetes, but rather as a comorbidity of the two diseases.

53. • The majority of research has focused on type 2 diabetes mellitus as
a risk factor for periodontitis, probably because both diseases have
historically tended to develop in patients in their 40s and 50s.
• Including xerostomia and candidal infections as well as periodontitis.

55. ASSOCIATIONS BETWEEN OBESITY
AND PERIODONTITIS
• Adiposity can be regarded as a systemic disease that predisposes individuals
to a variety of comorbidities and complications, and a number of studies
have reported associations between obesity and periodontitis
• with a BMI of ≥27 kg/m2 ,were in the highest quartile for insulin resistance
had a significantly increased risk of severe periodontitis compared with
those in the lowest quartile

56. • The impact of periodontitis on changes in hba1c was assessed in a
prospective 5 year study of 2,973 non-diabetic individuals.
• Those participants with the most advanced periodontitis
demonstrated an approximately fivefold greater absolute increase in
hba1c with those with no periodontitis at baseline

57. • Periodontitis predicts the progression of hba1c among diabetes-
free individuals and it is continuing to identify whether these
subclinical changes in hba1c may translate into an increased risk of
incident diabetes at 10 years

58. ‘TWO-WAY’ RELATIONSHIP
• Not only is diabetes a risk factor for periodontitis, but periodontitis
could have a negative effect on glycaemic control.
• Inflammation is a central feature of the pathogenesis of diabetes and
periodontitis
• The inflammatory response is characterised by dysregulated secretion
of host-derived mediators of inflammation and tissue breakdown

59. • Diabetes may result in general impaired inflammatory and
immune responses as well as impaired healing, while periodontitis
is characterized by an unbalanced inflammatory and immune
response to the dysbiotic flora

62. ORAL MICROBIOTAAND DIABETES
• Study of young japanese individuals with type 1 diabetes mellitus, a
greater proportion of participants with periodontitis harboured P.
Gingivalis and P. Intermedia than those who were periodontally
healthy
• In 2013, in patients with type 1 diabetes also being affected by
chronic periodontitis, aemaimanan et al examined the presence of
selected periodontal pathogens and their association with glycemic
control.

63. • In periodontitis sites they found a higher quantity of Porphyromonas
gingivalis (but not Treponema denticola, Tannerella forsythia, and A.
actinomycetemcomitans) in patients with poorly controlled glycemia
compared with patients with well‐controlled glycemia

64. PERIODONTALTREATMENT IS ASSOCIATED
WITH IMPROVED GLYCAEMIC CONTROL
• Several meta-analyses have confirmed that effective periodontal
therapy can result in reduced hba1c
• Patients who received at least one episode of periodontal surgery
had hba1c levels that were 0.25% lower than patients who did not
undergo periodontal surgery

65. • Relate to reduced systemic inflammation (e.g. Reduced serum levels of
mediators such as tnf-α and IL-6) following the treatment and resolution
of periodontal inflammation.
• Katagiri et al found that gingival inflammation improved with an
improvement in blood glucose control through diabetes treatment.
However, they reported no improvement in the depth of periodontal
pockets or attachment level.

66. EFFECT OF PREDIABETES ON PERIODONTITIS
• Prediabetes is the subclinical disease stage at which blood sugar is above
the accepted cut‐off value, but without the presence of other diabetes
symptoms.
• Abduljabbar et al showed that subjects with prediabetes exhib‐ited
higher periodontal parameters (plaque percentage, bleeding on probing,
probing pocket depth, bone loss, and missing teeth) compared with
nondiabetes controls

67. MICROBIAL DEPOSITS AND ORAL HYGIENE STATUS
.
• Accumulation of bacterial plaque at the gingival margin results in the
development of gingivitis and that the gingivitis can be reversed with the
implementation of oral hygiene measures.
• Studies demonstrate a causal relationship between accumulation of
bacterial plaque and gingival inflammation

68. • Increase certain species of pathogenic bacteria associated with
more severe forms of periodontal disease.
• Lack of plaque control interferes with resolution of inflammation
and control of periodontitis

69. • Complete control of supragingival plaque with or without subgingival
instrumentation is reported to be effective following surgical or
nonsurgical therapy
• Many studies have demonstrated significant reductions in probing pocket
depths, attachment gains and, of course, in gingival inflammation, with
improvements in oral hygiene alone.

70. • In terms of quality of plaque, three specific bacteria have been identified
as etiologic agents for periodontitis.
• A.actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella
forsythia (formerly Bacteroides forsythus).
• P. gingivalis and T. forsythia are often found in chronic periodontitis,
whereas A. actinomycetemcomitans is often associated with aggressive
perodontitis.

71. • Their elimination or suppression impacts the success of therapy.
• There is a host response to these pathogens.
• Virulence factors are associated with these pathogens.
• Inoculation of these bacteria into animal models induces
periodontal disease.

72. • Although not completely supported by these criteria for causation,
moderate evidence also suggests that Campylobacter rectus,
Eubacterium nodatum, Fusobacterium nucleatum, Prevotella
intermedia, Peptostreptococcus micros, Streptococcus intermedius, are
etiologic factors in periodontitis (Genco et al, 1996)

73. P GINGIVALIS
• One of the prime etiological agents in the pathogenesis and progression
of the inflammatory events of periodontal disease (hajishengallis et al.,
2012).
• This periodontopathic bacterium was found in 85.75% of subgingival
plaque samples from patients with chronic periodontitis (datta et al.,
2008)

74. • A study by bodet et al. (2006) demonstrated that this asaccharolytic
bacterium is associated with T. Denticola and T. Forsythia to form
the red bacterial complex which is highly recognized in advanced
periodontal lesions
• Number of P. Gingivalis has been shown to increase substantially in
sites with periodontitis and lower or non-detectable in sites with
subgingival health or plaque-associated gingivitis (schmidt et al.,
2014)

75. • P. Gingivalis is known to produce virulence factors that could
penetrate the gingivae and cause tissue destruction.
• Fimbriae, capsules, lipopolysaccharide (lps), lipoteichoic acids,
haemagglutinins, gingipains, outer membrane proteins, and outer
membrane vesicles

76. A. ACTINOMYCETEMCOMITANS
• The primary etiologic agent of LAGP and has also been implicated in
chronic periodontitis and severe non-oral infections
• The ability of the bacterium to express a leukotoxin (ltxa) is
considered to be an important virulence property.

77. • Kills white blood cells in a variety of ways, and leukocyte destruction
is essential for subsequent bacterial growth and stimulation of the
host inflammatory response
• Leukotoxicity is substantially correlated with attachment loss in
adolescents

78. TANNERELLA FORSYTHIA
• An anaerobic gram-negative member of the cytophaga-bacteroides family
which was initially described as bacteroides forsythus by tanner et al. And
later reclassified as tannerella forsythia
• The pathogenic potential of T. Forsythia was enhanced in the presence of
other bacteria.
• T. Forsythia is a pathogenic organism which might play synergistic roles in
inflammation along with other periodontal pathogens.

79. ANATOMIC FACTORS
• Anatomic factors, such as furcations, root concavities,
developmental grooves, cervical enamel projections, enamel pearls,
and bifurcation ridges, may predispose the periodontium to disease
as a result of their potential to harbor bacterial plaque and present a
challenge to the clinician during instrumentation

80. CERVICO ENAMEL PROJECTIONS
• Cervical enamel projections are flat, ectopic deposits of enamel
apical to the normal cemento-enamel junction (CEJ) level in molar
furcation areas (Masters et al, 1964)
• These enamel deposits usually have a triangular shape and a
tapering form, extending apically into furcation areas

82. ENAMEL PEARLS
•Enamel pearls are larger, spheroid-shaped, ectopic
deposits of enamel that can also be located at furcation
or other root surfaces of molars (Moskow et al, 1990)
• The nature of the attachment of the periodontal ligament to the
enamel pearls has not been show n. Kerr8 postulates that the
fiber of the periodontal ligament could have no true attachment
to the tooth in the area of the cervicoenamel projection or the
enamel pearls

84. PALATOGINGIVAL GROOVE IN MAXILLARY
INCISORS
• Groove starts in a hollow region coronally to the cingulum and p
roceeds distoapically, interrupting the continuity between the
distal marginal ridge and the cingulum. It may then continue for
variable distances along the length of the distolingual aspect of the
root
• The epithelial attachment in this area is normally diseased, forming
a ready pathway for the ingress of bacterial endotoxin and the
formation of an infrabony periodontal pocket.

86. GENETIC FACTORS
• Periodontitis, especially the early onset forms, aggregates in families
• Inherited and chromosomal disorders in which increased susceptibility
to periodontal disease
Acatalasia
 Congenital erythropoietic porphyria,
Ehlers-danlos syndrome

87. • Michalowicz et al found that roughly 50 per cent of the population
variance for susceptibility to severe periodontitis was due to heredity
alone
• Genetic factors influence clinical measures of gingivitis, probing pocket
depth, attachment loss, and interpoximal bone height.

88. • The familial aggregation seen in localized and generalized aggressive
periodontitis also is indicative of genetic involvement in these diseases
• Kornman et al.demonstrated that alterations in specific genes encoding
the inflammatory cytokines interleukin-1α and interleukin-1β (IL-1α, IL-
1β) were associated with severe chronic periodontitis in non-smoking

89. • Changes in the IL-1 genes may be only one of several genetic
changes involved in the risk for chronic periodontitis.
• Alteration in the il-1 genes may be a valid marker for periodontitis in
defined populations
• In addition, genetics plays a role in regulating the titer of the
protective immunoglobulin G2 (igg2) antibody response to A.
Actinomycetemcomitans in patients with aggressive periodontitis

90. • Immunologic alterations, such as neutrophil abnormalities, monocytic
hyperresponsiveness to lipopolysaccharide stimulation in patients with
localized aggressive periodontitis, and alterations in the
monocyte/macrophage receptors for the fc portion of antibody,also
appear to be under genetic control

91. Age
• Both the prevalence and the severity of periodontal disease increase
with degenerative changes related to aging may increase
susceptibility to periodontitis.
• attachment loss and bone loss seen in older individuals are the result
of prolonged exposure to other risk factors over a person's life,
creating a cumulative effect over time.

92. • Aging alone does not increase disease susceptibility.
• Evidence of loss of attachment may be of more consequence in
younger patients., Aggressive periodontitis in young individuals often
is associated with an unmodifiable risk factor, such as a genetic
predisposition to disease.
• Young individuals with periodontal disease may be at greater risk for
continued disease as they age.

93. GENDER
• National U.S. surveys conducted since 1960 demonstrate that men have
more loss of attachement than women.
• In addition, men have poorer oral hygiene than women, as evidenced by
higher levels of plaque and calculus.
• Therefore, gender differences in prevalence and severity of periodontitis
appear to be are related to preventive practices rather than any genetic
factor.

94. STRESS
• The incidence of necrotizing ulcerative gingivitis increases during
periods of emotional and physiologic stress,
• Emotional stress may interfere with normal immune function and may
result in increased levels of circulating hormones, which can affect the
• Adult patients with periodontitis who are resistant to therapy are more
stressed than those who respond to therapy.

95. • Individuals with financial strain, distress, depression, or
inadequate coping mechanisms have more severe loss of
attachment. Although epidemiologic data on the relationship
between stress and periodontal disease are limited, stress may be
a putative risk factor for periodontitis.

96. • Gingivitis and poor oral hygiene can be related to lower
socioeconomic status
• This can most likely be attributed to decreased dental awareness
and decreased frequency of dental visits compared with more
educated individuals of higher SES.
• After adjusting for other risk factors, such as smoking and poor oral
hygiene, lower SES alone does not result in increased risk for
periodontitis

97. HUMAN IMMUNODEFICIENCYVIRUS
• Human Immunodeficiency Virus/Acquired Immunodeficiency
Syndrome It has been hypothesized that the immune dysfunction
associated with human immunodeficiency virus (HIV) infection and
acquired immunodeficiency syndrome (AIDS) increases susceptibility
to periodontal disease.
• These patients often had severe periodontal destruction
characteristic of necrotizing ulcerative periodontitis.

98. • Some studies support that as the degree of immunosuppression
increases in adults with AIDS, periodontal pocket formation and loss
of clinical attachment also increase.
• Evidence also suggests that AIDS-affected individuals who practice
good preventive oral health measures, including effective home
care and seeking appropriate professional therapy, can maintain
periodontal health.

99. OSTEOPOROSIS
• Osteoporosis has been suggested as another risk factor for periodontitis.
• Although studies in animal models indicate that osteoporosis does not
initiate periodontitis, evidence indicates that the reduced bone mass
seen in osteoporosis may aggravate periodontal disease progression.
• However, reports in humans are conflicting. In a study of 12 women
with osteoporosis and 14 healthy women, von wowern et al reported
that the women with osteoporosis had greater loss of attachment than
the control subjects.

100. • In contrast, kribbs examined pocket depth, bleeding on probing, and
gingival recession in women with and without osteoporosis.
• Although the two groups had significant differences in bone mass, no
differences in periodontal status were noted.
• However, it appears that a link may exist between osteoporosis and
periodontitis, and additional studies may need to be conducted to
determine if osteoporosis is a true risk factor for periodontal disease

101. • One study demonstrated an increased risk for severe periodontitis in
patients who had not visited the dentist for 3 or more years
• another demonstrated that there was no more loss of attachment or
bone loss in individuals who did not seek dental care compared with
those who did over a 6-year period.
• However, differences in the ages of the subjects in these two studies
may explain the different results. Additional longitudinal and
intervention studies are necessary to determine if infrequency of dental
visits is a risk factor for periodontal disease.

102. Previous History of Periodontal Disease
• 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.
• Conversely, patients currently free of periodontitis have a decreased risk
for developing loss of attachment compared with those who currently
have periodontitis

103. BLEEDING ON PROBING
• Bleeding on probing is the best clinical indicator of gingival
inflammation.
• Although this indicator 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.

107. The principles of the risk assessment process were discussed by Beck
(1994) and should consist of the following four steps
1)The identification of one or several individual factors that appear to
be associated with the disease.
2)In case of multiple factors, a multi-variate risk assessment model
must be developed that discloses which combination of factors does
most effectively discriminate between health and disease.

108. 3)The assessment step, in which new populations are screened for
this particular combination of factors, with a subsequent
comparison of the level of the disease assessed with the one
predicted by the model.
4)The targeting step, in which exposure to the identified factors is
modified by prevention or intervention and the effectiveness of the
approach in suppressing the incidenceof the disease is evaluated

109. RISK ASSESSMENT IN PERIODONTAL DISEASE
•Periodontal disease is multifactorial and assessment should
therefore be at multiple levels.
• PATIENT LEVEL
• MOUTH-LEVEL RISK ASSESSMENT
• TOOTH-LEVEL RISK ASSESSMENT
• SITE-LEVEL

110. • Patient-level risk assessment can be determined at the initial
consultation by performing the following:
Family history for hereditary, inborn or genetic risk factors. Take a
detailed history of gum disease or early tooth loss in the family.
• Medical history for systemic diseases, e.g. diabetes mellitus,
cardiovascular diseases, osteoporosis
• Present dental history - Assess motivation to oral hygiene.
• Social history, which includes smoking - current or former smoker,Habits
like bruxism

111. Mouth-level risk assessment
• would be performed at the initial examination, after a basic
periodontal examination, and would include:
Examination of attachment loss relative to age
• Occlusal examination in static relationship
• Occlusal examination in dynamic relationship
• Examination of levels of oral hygiene
• Examination of levels of plaque-retentive factors

112. • Presence of removable prosthesis
• Levels of recession
• Gingival inflammation and depth of pockets

113. • Tooth-level risk assessment may or may not be carried out at the
initial examination.
• A detailed periodontal chart and radiographic assessment
should be performed.

114. Individual tooth mobility (mobility index)
Tooth movement or drifting of periodontally compromised teeth
Residual tooth support (radiographically).
Presence, location and extent of furcation lesions
Individual tooth anatomy - Presence of "talon cusps" or bulbous
crowns
Anatomy of tooth embrasures and contact points

115. SITE-LEVEL RISK ASSESSMENT
• Bleeding on probing
• Exudation from periodontal pockets
• Local root grooves or root concavities
• Individual probing pocket depth
• Attachment levels
• Other anatomical factors like enamel pearls, root grooves.

116. Periodontal Risk Assessment

119. SCIENCETRANSFER
• Risk factors, when present, increase the probability of having
disease and is of prime importance to assess and record it .
• Maintenance therapy without considering the risk factors is of no
effect.

120. CONCLUSION
• Risk assessment is an important part of modern day periodontal
practice
• It is an integral part of the information upon which a plan of
treatment and maintenance is based.
• The treatment plan should focus on efforts to lower the level of risk.
• The awareness of risk factors also helps with the identification and
treatment of co-morbidities in the general population as many
periodontal disease risk factors are common to other chronic
diseases such as diabetes, cardiovascular diseases and stroke

121. E-cigarettes
• E-cigarettes have the potential to benefit adults who smoke and who are
not pregnant if used as a complete substitute for regular cigarettes and
other smoked tobacco products.
• E-cigarettes come in many shapes and sizes. Most have a battery, a
heating element, and a place to hold a liquid.
• E-cigarettes produce an aerosol by heating a liquid that usually contains
nicotine
• E-cigarettes are known by many different names. They are sometimes
called “e-cigs,” “e-hookahs,” and “electronic nicotine delivery systems
(ENDS).”
• e-cigarette aerosol generally contains fewer harmful chemicals than
smoke from burned tobacco products.

122. HbA1c
• Glycosylated haemoglobin count (Hb A molecules)a form of the
haemoglobin compound is used to identify the average level of plasma
glucose concentration over an extended period of time.
• In the process called glycosylation,the haemoglobin’s normal exposure to
high blood sugar levels usually takes place in a controlled environment i.e
it is overseen by enzymes
• But A1c subtype of Hb is formed in non enzymatic pathway (in the
absence of these enzymes) – non enzymatic glycosylation or glycation.
• Not all Hb is converted to HbA1c
• Conversion rate depends on concentration of glucose that the Hb is
exposed.

123. SmokelessTobacco
• Can cause tissue injury on account of their carcinogenic properties
• Among smokeless tobacco users, there is an increased gingival recession
with exposure of tooth root surface, periodontal pocket formation, plaque
and calculus accumulation which leads to periodontitis. The gingival
recession is more prominent in the anterior teeth region.
• The main categories of smokeless or chewing tobacco-induced oral
mucosal soft-tissue lesions reported are: oral squamous cell carcinoma
(scc) and verrucous carcinoma.
• Products are available such as betel quid with tobacco, zarda, gutka ,mawa
and khaini

124. Classification of cervical enamel projection
• Grade I: The enamel projection extends from the CEJ of
the tooth toward the furcation entrance.
• Grade II: The enamel projection approaches the entrance
to the furcation. It does not enter the furcation and
therefore no horizontal component is present.
• Grade III: The enamel projection extends horizontally
into the furcation.

125. Coaggregation
• Coaggregation is the result of cell-to-cell recognition between distinct cell
types. Macroscopically, the phenomenon can usually be detected as
clumping when the different cell types are mixed. Microscopically, the
clumps of cells formed consist of a network of interacting cell types.
• The structure of coaggregates is dependent on the shape of the cell types
and the ratio of the coaggregating partners.
• Fusobacterium nucleatum is mixed with an excess of spherical cells like
Streptococcus, corn cob-shaped coaggregates can be detected where the
central fusobacterial cell is surrounded by streptococci

126. STRESS

127. COVID -19
• Viral replication in host cells leads to activation of the NLRP3
inflammasome, resulting in release of proinflammatory cytokines
• This inflammatory response is further enhanced by release of
damage associated molecular patterns (DAMPs) following cell
death.
• One of which is the fact that its symptoms seem to be related to a
‘cytokine storm’ which exhibits itself as elevated serum levels of
IL-6, IL-1b, IL-8, and TNF-alpha.

128. REFERENCES
• Michael g. Newman, Henry h.Takei, Perry r. Klokkevold, Fermin a. Carranza.
Carranza’s clinical periodontology tenth edition
• Elizabeth Koshi, S. Rajesh , Philip Koshi , P. R. Arunima. Risk assessment for
periodontal disease. Journal of Indian Society of Periodontology. 2012; -Vol 16,
Issue 3
• Roy C. PageWashington,James D. Beck Chapel Hill. Risk assessment for
periodontal diseases. International Dental Journal.1997; 47, 61-87
• David Polak,Terukazu Sanui, Fusanori Nishimura, Lior Shapira. Diabetes as a risk
factor for periodontal disease—plausible mechanisms. Periodontology 2000.
2020;83:46–58