2. Introduction
■ In most of the epidemiological studies , we seek to establish some
sort of causal relationship between a characteristic , behaviour or
exposure and the manifestation of a particular disease. Three types
of causations are generally identified:
Sufficient
cause
Necessary
cause
Risk
factor
3. ■ Risk indicators :
– They are probable and putative risk factors that have been identified in cross sectional
studies but not confirmed through longitudinal studies .
– They are not thought to be a part of causal chain.
■ Risk assessment :
– It is the process of determining the quantitative and qualitative likely of adverse events that
may result from exposure to specific health hazard or from the absence of beneficial
influences.
■ Risk factor :
– It is an environmental exposure ,aspect of behaviour or an inherent characteristic which is
associated with a disease.
– To be identified as a risk factor , the exposure must occur before disease onset.
■ Risk (Kleinbaum 1982):
– It is the probability that an individual will develop a given disease or exposure or
change in the health status in a given period.
4. ■ Risk markers or predictors:
These are characteristics having the ability to predict individuals at high
risk but they are not a part of causal chain . They may predict the future
course of the disease.
■ Risk determinants / background characteristic:
These forms sometimes substituted for the term risk factor should be
reserved for those risk factors that can not be modified , they are
probably not in the causal chain and not the targets for intervention.
5. The need for risk assessment :
Management
strategy
Creating
patient profile
Characterising
patients
Setting up
priorities
Effective
intervention
6. Risk assessment process:
Hill’s criteria for assessment of the risk
(1971):
Strength of the
association
Dose response
effect
Temporal
consistency
Consistency of
the findings
Biological
plausibility
Specificity of
the association
Coherence Experiments
Considerations
of alternate
explanations
7. Principles of risk assessment :
(Beck 1994)
identification
Multivariate risk assessment model
Assessment step
Targeting step
8. Major risk measures are :
“Absolute risk”
individuals probability to
develop a disease in a
given period of time
“Relative risk”
comparison of health risk
in btw two populationsie
one with exposure to
factors and other without
it.
“Odds ratio”
defined as odds of having
a disease if one is
exposed to a factor and if
one is not exposed to the
same factor.
“Attributable risk”
Difference in the
incidence rates of
occurrence of the disease
btw exposed and non
exposed populations
“Population attributable
risk”
used to express the
impact of exposure on the
outcome
“Prevalence rate ratio”
in cross sectional studies
prevalence is measured
not incidence.
9. Tobacco smoking:
■ It is a well established risk factor for periodontitis .
■ Smoking is strongly related to severity of diseases and to recurrent and refractory
diseases.
■ Numerous studies have shown the association of smoking with periodontitis and
they are as follows:
10. Authors Results
Haber et al 1993 Increased prevalence of periodontitis amongst smokers than non smokers
within both the diabetic(132) and non diabetic groups (99)
Bergstrom et al 1989 155 subjects were studied 56% were smokers and periodontal involvement was
seen higher in smokers .
Jette et al 1993 Studied lifelong use of tobacco products as a modifiable risk factor for poor
dental health using multiple regression analysis.
NHANES III 2000 >12000 dentates over 12 years were examined smokers had more than 4 times
periodontitis than nonsmokers.
Haffajee et al 2001 The major difference between the subgingival microbiota in subjects with
different smoking history was in the prevalence of species rather than counts or
proportions. The greater extent of colonization in smokers appeared to be due to
greater colonization at pocket depths <4 mm. Diferences in colonization
patterns between current and never smokers were greater in the maxilla than in
the mandible.
Silvia Sancilio et al 2016 The cytotoxicity exerted on HGFs by e-cigarettes fluids is not entirely ascribable
to nicotine. Since the e-cigarettes are advertised as a safer alternative to
traditional ones, especially for the possibility of “smoking” nicotine-free fluids,
further studies are necessary to clarify the mechanism involved in the
occurrence of cytotoxicity exerted by such compounds.
Others like zambon et al 1996 , tonetti et
al 1993
Trombelli et al 1997,lyder et al ,grossi et al & haffajee et al 1997 ,preber et al
1996
11. Diabetis mellitus
It’s a clear cut indication that it’s a risk factor for
periodontitis .
Epidemiological data demonstrate that the
prevalence and severity of periodontitis is
significantly higher in diabetics vs non diabetics.
12. Authors Results
Emrich et al 1991 He studied the relationship of NIDDM & periodontitis in 1342 Pima
Indians and found out the risk increases by 3 folds .
Trevonen et al 1994 This case study failed to demonstrate the association between DM and
Periodontitis . The subgingival microflora appears to be similar in both the
cases irrespective of severity of DM.
Hayden and Buckley 1989 No clear dose response and relation btw DM and Periodontal condition
severity could be documented .
Sefkam and Ainamo 1992 Patients with long term duration of poorly controlled DM appear to
experience more attachment and bone loss with good metabolic control.
Grossi et al 1996 Well controlled diabetis with good plaque control may respond favourably
to periodontal therapy in a manner similar to non diabetics .
13. Pathogenic bacteria and microbial tooth
deposits :
■ It is well documented that 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.
LOE H, Theilade E, Jensen SB: Experimental gingivitis in man. J Periodontol 1965; 36:177-187
■ Often, patients with severe loss of attachment have minimal levels of bacterial
plaque on the affected teeth, indicating that the quantity of plaque is not of major
importance in the disease process.
14. ■ However, although quantity may not indicate risk, there is evidence
that the composition, or quality, of the complex plaque biofilm is of
importance.
■ In terms of quality of plaque, three specific bacteria have been
identified as etiologic agents for periodontitis:
I. A. actinomycetemcomitans,
II. P. gingivalis,
III. Bacteroides forsythus.
15. ■ Cross-sectional and longitudinal studies support the delineation of these three bacteria
as risk factors for periodontal disease.
■ Additional evidence that they are causal agents include:
(1) Their elimination or suppression impacts the success of therapy,
(2) There is a host response to these pathogens,
(3) Virulence factors are associated with these pathogens and
(4) Inoculation of these bacteria into animal models induces periodontal disease.
Haffajee AD, Socransky SS: Microbial etiological agents of destructive periodontal diseases.
Periodontol 2000 1994; 5:78-111
■ Genco et al 1996 suggested that moderate evidence, athough not completely
supported by the criteria for causation, suggests that C rectus, E nodatum, F
nucleatum, P intermedia and T denticola are etiologic agents in periodontitis.Hence
quantity of plaque is not that important , it is the quality of plaque that determines risk
for periodontitis.
■ Various retrospective and prospective bacterial studies are done .
16. Authors Results
Wolf at al 1992
(similar results in studies by D zink
et al 1985 and Listgarten et al
1991)
Collected plaque from 6905 sites in 938 subjects , immunoassay was done to find out the presence
of Pg, Aa,Pi,Ec and Fn in each sample. High risk group had increased amount of Pg and Aa in
subgingival plaque and increased attachment loss at 6 and 58 months .low risk group had absence
of these microorganisms.
Skaar et al 1992 A.A presence was a microbial risk factor for progressive periodontitis in individuals with advanced
periodontitis .
Wennstrom and coworkers 1997 Absence of these indicator bacteria was a better predictor of no further loss of attachment than was
the presence of these for disease progression .
Haffajee and coworkers 1991 Increased P intermedia C. rectus , B forsythus, Peptostreptococcus micros in sites of progressive
adult periodontitis are suggestive of these bacteria to be risk factors of progressive periodontitis.Also
increased subgingival temperature , presence of existing disease and decreased levels of protective
species adds to the risk .
Papapanou et al 1997 Certain species ( Pg ,Td ,Bf ) in deep pockets 74% and progressing sites (66%). Colonization of these
species exceeding a certain threshold entails a significantly increased probability for an individual
subject to harbour deep pockets .
Page et al 1997 Presence of calculus serves as a reservoir for bacterial plaque as a risk factor for periodontitis.
Patients not receiving proper and regular care and poorly controlled diabetis results in negative
impact on periodontal health.
17. Neutrophil defects as risk factor for
periodontitis :
■ Many cases in periodontitis are best considered as the outcome of an
imbalance in the host parasite interaction .
Listgarten et al 1986.
■ studies of the host response in periodontal diseases show that PMN are
the key protective cell which undernormal circumstances limits the
pathology caused by periodontal microorganisms .
18.
19. Occlusal forces as a risk factor :
■ In 1917 and 1926 Stillman stated that excessive occlusal forces were the primary
cause of periodontal disease and the occlusal therapy was mandatory for control of
periodontal disease.
■ Orban and Weinman 1933 used histologic observation of human autopsy material
for evaluation of the effect of excessive occlusal forces on the periodontium.
■ Glickman and co-workers in 1950’s and 1960’s performed series of animal model
and human autopsy studies. Animal studies where high occlusal contact was
created by overcontouring a restoration were performed in dogs and monkeys.These
studies showed no evidence of occlusal contacts initiating periodontitis.
20. ■ Glickman and coworkers 1957 :
performed a series of studies using human autopsy material and said that occlusal
forces affected the attachment apparatus apical to bony defect Co-destructive
effect.
■ Waerhaug : His study was on morphology of bone pocket with plaque levels and
presence or absence of occlusal forces found that the plaque front was always in
close approximation with the epithelial attachment level . He concluded that bone
loss was always related to downgrowth of plaque and increased occlusal forces were
not related to vertical bone loss.
■ Polson and lindhe : concluded that bacterial plaque was the initiating factor and the
main cause for progression of PDL disease.
Thus it can be said that occlusal discrepencies were a significant risk factor contributing
to more rapid PDL destruction and the treatment os such will slow down the progress of
the destruction.
22. Genetic factors and heritable risk
factors in periodontal disease:
■ Highly sophisticated
DNA analysis
techniques have
recently demonstrated
that the transmission
among family members
can and does occur .
■ Its evidence comes
from three sources :
Association of adult
periodontitis with specific
genetically transmitted disease
traits
Twin studies for adult
periodontitis
Genetic analysis of families
with early onset periodontitis
23. Association of adult periodontitis with specific
genetically transmitted disease traits:
Enzyme and enzyme
inhibitor defects
Leukocyte defects
Inherited connective
tissue disorders and
others
Chromosomal
abnormalities
24. Minnesota twin registry
study 1991
Virginia twin registry
study
These studies are based on the fact that dizygotic twins share no more genes than non twin siblings, while the
genes in monozygotic twins are identical .
Thus if hereditary plays a significant role in periodontitis the probability of having the same disease in
monozygotic twins will be much higher than in dizygotic twins but the differences in the upbringing and
environments of twins complicate these studies .
25. Genetic analysis of families with early onset
periodontitis
Authors Results
Melnik et al 1976 Genetics of LAP suggested the likelihood of genetic basis for susceptibility
manifesting an X-linked dominant mode of transmission .
Boughman et al 1986
Hart et al
In the brandywine isolate of southern Maryland 70 patients were studied
belonging to five generations . The major locus was located on chromosome 4
which was similar for osteopontin , annexin III & IL-8.
--- controvertial to this study
Marzita et al 1994 100 patients were studied and with segregation analysis they demonstrated
the existence of autosomal dominant major locus for agg periodontitiswith 70
% affected population including blacks and non-blacks.
Kornmann et al 1997 Alterations in specific genes encoding the inflammatory cytokines IL-1α and IL-
1β were associated with severe chronic periodontitis in non smoker subjects.
Kinane et al 2003 He suggested that may be IL-1 gene alterations be a valid marker for
periodontitis but its usefulness as a genetic marker in general population may
be limited.
26. Age :
■ Both the prevalence and severity of periodontal disease increases with age . Papapanou et al.
demonstrated that the mean annual rate of bone loss among the initially 70-year-old subjects was
0.28mm compared to 0.07 on the 25-year-old individuals.
P. N. Papapanou and J. L. Wennstrom, “Radiographic and clinical assessments of destructive periodontal disease,” Journal of
Clinical Periodontology, vol. 16, no. 9, pp. 609–612, 1989.
■ The increased severity of periodontal disease and bone loss with age is probably related to the
length of time, where the periodontal tissues have been exposed to bacterial plaque, and is
considered to reflect individual’s cumulative oral history.
H. loe, A. Anerud, H. Boysen, and E. Morrison, “Natural history of periodontal disease in man. Rapid, moderate and no loss of
attachment in Sri Lankan laborers 14 to 46 years of age,” Journal of Clinical Periodontology, vol. 13, no. 5, pp. 431–445,
1986.
■ In support of this the studies further by Papapanou et al 1991 & 1992 enrolled old individuals with
preventive measures throughout their lives and noted minimal level of loss of attachment .thus we can say
that periodontal disease is not an inevitable consequence of aging . However it remains to be determined
whether changes related to aging process such as intake of medication , decreased immune function and
altered nutritional function interact with other well defined factors to increase the susceptibility to
periodontitis.
27. ■ Evidence of loss of attachment may be of more consequence in younger
patients .
■ The younger the patient the longer they have for exposure to causative factors
.therefore younger individuals with periodontitis may be at a higher risk for
continued disease as they age .
■ In a study of people over 70 years old, 86% had at least moderate
periodontitis or a severe form of periodontal disease, and over one fourth of
this 86% had lost their teeth.
■ The study also showed that the disease accounted for a majority of tooth
extractions in patients older than 35 years of age.
Khalaf F, AlShammari , Areej K, AlKhabbaz, Jassem M, AlAnsari, et al. Risk indicators for tooth loss due to periodontal
disease. J Periodontol. 2005;76:1910–18
28. Gender :
■ Gender plays an important role in periodontal diseases U.S National Survey
conducted since 1960 demonstrated that males have more loss of attachment
than females also males have more plaque and calculus as females due to
poorer oral hygiene.
U.S. Public Health Service, National Center for Health Statistics: Periodontal Disease in Adults, United States 1960-
1962
■ Therefore it appears that gender differences in prevalence and severity of
periodontitis are related to preventive practices rather than any genetic factor.
29. Race and ethinicity :
Authors Results
NHANES I survey Increased occurrence of periodontitis in blacks than in whites with pdl
index score of 1.28 and 0.76.
Albander et al 1997 14000 adolescent btw 9-12 grades were assessed for prevalence of
agg. and chr. periodontitis 10% adolescent blacks, 5% Hispanic and 1.3
% whites .
Mandall et al Increased periodontal treatment needs in children who are asians then
in whites.
Grossi et al Native Americans , Asians and pacific islanders were associated with
more bone loss
Albander et al 2003 Blacks had poor oral hygiene than Mexican Americans .
Schenkein et al Increased risk of periodontal diseases in blacks due to biological
predisposition where assessment of chemotactic response of
neutrophils was done in whites and blacks.
30. Socioeconomic status
■ Gingivitis and poor oral hygiene can be related to lower socioeconomic status (SES) .
■ This can most likely be attributed to decreased dental awareness and decreased frequency of
dental visits when 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.
U.S. Public Health Service, National Center for Health Statistics: Basic Data on Dental Examination Findings of Persons 1-74
years; United States 1971-1974
31. Risk indicators for periodontal
diseases:
HIV /AIDS
OSTEOPOROSIS
INFREQUENT DENTAL VISITS ORAL HYGIENE AND
COMPLIANCE
STRESS
32. 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.
Authors Results
Winkler et al 1992 Early reports on the periodontal status of patients with AIDS or individuals who
are HIV seropositive revealed that these patients often had severe periodontal
destruction characteristic of necrotizing ulcerative periodontitis.
Lamster et al 1994 Some reports have failed to demonstrate significant differences in the pdl
status of individuals with HIV infection and healthy controls
Mc Kaig et al Studied 316 dentate HIV infected subjects and assessed degree of
immunosuppression by measuring CD4 cell counts and clinical measures of
periodontal disease.
33. Patton et al Examined 570 HIV patients and found that administration of protease inhibitors
resulted in decreased prevalence of oral hairy leukoplakia and NUP.
Barr et al 1992 In a 20-month study of 114 homo- sexual and bisexual men, the relative risk of
longitudinal attachment loss >3 mm was 4.8 when CD4 counts were less than
400/mm3 and increased to 6.16 when CD4 counts were less than 200/mm3,
suggesting a correlation between the severity of periodontal disease and the
level of immunosuppression.
34. Other viruses :
■ Studies show that occurrence of human CMV and other Herpes virus infection in
periodontitis than in gingival lesions , deep pockets than shallow ones and in active CMV
replication occurs in PDL Defects.
■ Contreas et al : presence of HSV in subgingival sites was associated with a significantly
higher risk for severe chronic periodontitis and subgingival colonization of periodontopathic
bacteria..
■ Active CMV infections and Herpes virus infection are possible risk factors for destructive
periodontitis .
35. Osteoporosis :
■ Although 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 L, Whalen JP, Lesser GV, et al: Experimental studies on osteoporosis. Methods Achiev Exp Pathol 1975; 7:72-108
■ However, reports in humans are conflicting. In a study of 12 women with
osteoporosis and 14 healthy women, reported that the women with osteoporosis
had greater loss of attachment than the control subjects.
Van Wowern J, Klausen B, Kollerup G: Osteoporosis: a risk factor in periodontal disease. J Periodontol 1994; 65: 134.
■ Kribbs et al 1994 examined pdl status in osteoporotic and non osteoporotic females
although both the groups had varied results on bone mass still no differences in
periodontal status was found .
36. ■ Grodstein et al : conducted a prospective study on use of estrogen in osteoporotic
females and found significant reduction in risk of tooth loss.
■ Another 2 year prospective study had shown decreased gingival inflammation and
loss of attachment in post menopausal females with estradiol supplementation
within 5 years post menopause.
■ Aminobisphosphonates used in treatment of osteoporosis was examined in a study
on diabetic patients and resulted in improvement in pdl status and significantly
decresed alveolar bone loss.
■ Conclusion :
Women with osteoporosis and poor oral hygiene are at higher risk for developing
periodontal diseases over healthy women or osteoporotic women with good oral hygiene.
Also risk decreases with patients receiving estrogen replacement therapy.
However still future studies are needed to rule out whether it’s a true risk factor or not .
37. Infrequent dental visits ,oral hygiene
and compliance :
Identifying
failure to visit
the dentist
on a regular
basis as a
risk factor for
periodontitis
controversial.
Authors Results
Page RC, Beck JD: 1997 Study demonstrated an increased risk for severe periodontitis in
patients who had not visited the dentist for three or more years,
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.
Listgarten et al Study of adults with gingivitis found that 25 subjects out of 30
required recall intervals of 1-2 years in a 3 year study.
11 subjects who dint receive prophylaxis had similar results to those
who received prophylaxis every 6 months.
Bakdash et al 1994 Self reported cases for oral prophylaxis and clinical plaque scores
favoured oral hygiene practices as a possible risk factor for
periodontitis.
38. Stress
■ It has been strongly suggested that stress and related body distress
are important risk indicators for periodontal disease.
■ Genco et al 1994 suggested that individuals with financial distress ,
depression and inadequate coping mechanisms are having more
severe form of loss of attachment.
■ A study shows that people under physical or psychological stress are
prone to elevated biofilm plaque levels and increased gingivitis.
Hildebrand HC, Epstein J, Lorjova H. The influence of psychological stress on
periodontal disease. J West Soc Periodontol Periodontal Abstr. 2000;48:69–77
39. ■ The incidence of necrotizing ulcerative gingivitis
increases during periods of emotional and
physiologic stress, suggesting a link between the
two.
Shields WD: Acute necrotizing ulcerative gingivitis. A study of some of the contributing factors and
their validity in an Army population. J Periodontol 1977; 48:346-349.
■ Emotional stress may interfere with normal immune
function and may result in increased levels of
circulating hormones that can have an impact on
the periodontium.
Haffajee AD, Socransky SS: Microbial etiological agents of destructive periodontal diseases.
Periodontol 2000 1994; 5:78-111.
Rose RM: Endocrine responses to stressful psychological events. Psychiatr Clin N Am 1980;
3:251-276
40. ■ Stress diminishes saliva flow and increases dental plaque formation. Emotional
stress modifies the saliva pH and its chemical composition like the IgA
secretion .
Reners M, Breex M. Stress and periodontal disease. Int J Dent Hygiene 2007; 5:
199–204.
■ A series of studies made by Deinzer et al., examine the impact of academic
stress by students at university during their examination period on
periodontal health. Academic stress was shown to be a risk factor for gingival
inflammation with increasing crevicular interleukin-1b levels and a diminution of
the quality of the oral hygiene .
Deinzer R, Ruttermen S, Mo bes O, Herforth A. Increase in gingival inflammation
under academic stress. J Clin Periodontol 1998; 25:431–433.
41. Risk markers / predictors for
periodontal disease:
Previous history
of periodontal
diseases.
Bleeding on
probing
42. Previous history of periodontal disease:
■ Individuals who have the
most severe disease at
the initial examination
are at greatest risk of
future disease.
■ Conversely patients
currently free of
periodontitis have
decreased risk of
developing loss of
attachment than who
currently have
periodontitis.
Authors Results
Listgarten 1991 Risk of future pdl deterioration is strongly associated with the
presence and severity of disease at baseline .
Grabic et al 1991 Suggested that probability of future pdl deterioration
increases with increasing pocket depth and clinical
attachment loss at baseline
43. Bleeding on probing :
■ Best clinical indicator of gingival inflammation.
■ Increased bleeding on probing frequency at sequential periodontal maintenance
and examination periods support the well accepted clinical observation that
longitudinal bleeding on probing is a risk factor for future attachment loss.
Authors Results
Lang and kal dahl et al Absence of BOP may be associated more often with areas exhibiting
in disease progression.
Claffey et al Suggested that the combination of increasing pocket depths and
frequent BOP is more likely to lead to future attachment loss.. 90%
of the pockets with BOP will be associated with future attachment
loss over a 42 month period.
45. ■ Risk assessment in periodontal
disease is that the diseases are
multifactorial and assessment
should therefore be at multiple
levels.
■ The presence of pathogenic
bacteria alone is not sufficient to
cause the disease.
■ In simple terms, there are four
levels to consider:
45
The patient
level Perform at
initial
examination
The whole
mouth level
Perform at
initial
examination
and post initial
therapy
The tooth level
Perform post-
initial/definitive
therapy and
maintenance
The site level
Perform post
definitive
therapy and
during
maintenance
48. In periodontology, current methods to assess periodontal
risk factors include:
Periodontal
risk calculator
(PRC),
Health
information
suite (OHIS),
the Previser
risk calculator
TM
The
hexagonal
risk diagram
for
periodontal
risk
assessment
(PRA),
The
periodontal
risk
assessment
model
developed by
Chandra
The simplified
method
(UniFe) (Union
of European
railway
industries) for
periodontal
risk
assessment.
48
Douglass CW. Risk assessment and management of periodontal disease. J Am Dent Assoc. 2006;137:275–315
49. The Periodontal Risk Calculator (PRC)
■ Page et al. developed a computer-based risk assessment tool, the PRC, for
objective, quantitative assessment of risk.
■ The PRC is a web based tool that can be accessed through a dental office
computer.
Page RC, Krall EA, Martin J, Mancl L, Garcia RI. Validity and accuracy of a risk calculator in predicting periodontal disease. J Am
Dent Assoc. 2002;133: 569-576.
49
50. The calculation of risk using this model is based on mathematically
derived algorithms that assign relative weights to nine factors
including
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 and vertical
bone
lesions
50
51. ■ A three point scale is used to document pocket depth and radiographic bone
height.
■ The PRC assigns the individual a level of risk on a scale from 1 (lowest risk) to
5 (highest risk).
■ An algorithm was developed to quantify disease severity from pocket depth and
bone height values.
51
52. ■ The base risk score is calculated using an algorithm that correlates disease
severity with age
■ The risk score is increased if there is a positive history of periodontal surgery
and if the patient smokes more than 10 cigarettes per day, or the patient has
diabetes that is poorly controlled.
■ The existence of furcation involvements, vertical bone lesions or sub-gingival
restorations or calculus increase risk when the risk score is otherwise less
than four.
52
53. Oral Health information suite (OHIS),
Previser risk calculator TM
■ The OHIS is an information system that compiles, analyzes and quantifies
clinical information about factors like current oral health status, interventions
needed and treatment outcomes, be they beneficial or detrimental, that are
attributable to treatment and behavioral decisions.
■ The OHIS satisfies the need for a quantitative way to assess risk for
periodontitis, as well as providing, for the first time, quantification of
periodontal status and changes in status over time.
Page RC, Martin JA, Loeb CF. The Oral Health Information Suite (OHIS): its use in the management of periodontal disease.
J Dent Educ. 2005;69:509–20
53
54. ■ The Periodontal Assessment Tool (PAT) is an integral part of the Oral Health
Information Suite (OHIS)TM
(PreViser, Inc., Mount Vernon, WA; www.previser. com) and is considered as a
modification of the PRC method.
■ Following the input of only twenty-three items taken from a routine
periodontal examination, the system generates linguistic and numeric
periodontal diagnoses and a risk score for future disease, and prepares a
report in two versions; one for the dentist’s clinical documentation and
another for the patient.
54
55.
56. The hexagonal risk diagram for
Periodontal Risk Assessment (PRA)
■ Lang and Tonetti described a functional diagram based on six parameters for use
in estimating an individuals’ risk for progression of periodontitis.
Lang NP, Tonetti MS. Periodontal risk assessment (PRA) for patients in supportive periodontal therapy (SPT). Oral Health Prev
Dent. 2003;1:7-16.
■ The PRA model consists of an assessment of :
56
Percentage of
bleeding on
probing,
Prevalence of
residual
pockets
greater than
4 mm (³ 5
mm),
Loss of teeth
from a total of
28 teeth,
Loss of
periodontal
support in
relation to the
patient's age,
Systemic and
genetic
conditions,
and
Environmenta
l factors, such
as cigarette
smoking.
57. CALCULATING THE PATIENT'S INDIVIDUAL
PERIODONTAL RISK ASSESSMENT (PRA)
■ Based on the six parameters
specified above, a multi-
functional diagram is
constructed for the PRA.
■ In this diagram, the vectors
have been formed on the basis
of the scientific evidence
available.
57
58. A low PRA
patient has
all
parameters
within the
low-risk
categories or
at the most
one
parameter in
the
moderate-risk
category
58
59. A moderate
PRA patient
has at least
two
parameters
in the
moderate
category,
but at most
one
parameter
in the high-
risk
category
59
60. A high PRA
patient has
at least two
parameters
in the high-
risk
category
60
61. ■ In a high-risk patient who yields high BOP
percentages and high numbers of residual
pockets, the patient's risk for disease
progression may be reduced into the
moderate category if further periodontal
therapy is provided.
■ These two parameters (BOP and residual
pockets) are easily affected by therapy,
while other parameters, such as numbers
of missing teeth or systemic and genetic
factors are either irreversible and cannot
be reduced or may only be affected with
great additional efforts (smoking
cessation).
61
62. The periodontal risk assessment model
developed by Chandra
■ In 2007, Chandra evaluated a novel periodontal risk assessment model in
patients presenting for dental care.
■ This new model based on the periodontal risk assessment model by Lang and
Tonetti where the following parameters are recorded:
Chandra RV. Evaluation of a novel periodontal risk assessment model in patients presenting for dental care. Oral Health Prev Dent. 2007;5:39-48
62
other risk
determina
nts.
dental
status,
smoking
status,
diabetic
attachme
nt
loss/age
ratio,
number of
teeth lost,
number of
sites with
pocket
depths ≥
5mm,
% of sites
with
bleeding
on
probing,
63. ■ It is a continuous multilevel risk
assessment model that
incorporates subjective tooth
and site risk assessments and
generates a functional diagram,
and depending on the area of
the polygon categorizes the
patient into low-, medium- and
high-risk categories.
63
64.
65. The simplified method (UniFe) for
periodontal risk assessment
■ In 2009, Trombelli and co-workers proposed a new objective method (UniFe)
(Union of European Railway Industries) in order to simplify the risk assessment
procedures.
■ Risk assessment according to UniFe method is based on five parameters,
derived from the patient medical history and clinical recordings.
Trombelli L, Farina R, Ferrari S, Pasetti P, Calura G. Comparison between two methods for periodontal risk assessment. Minerva Stomatol.
2009;58:277-287
65
68. Various models for risk assessment
Author(country) study type Risk assessment tool description Objective
Fors & Sandberg (2001)
(Sweden)
Health Improvement in Dental
Practice Model(HIDEP)
To create and evaluate a
computerized tool capable of
creating overviews of the oral
health situation as well as
identifying risk factors and at- risk
patients.
Page et al. (2003)
(USA)
Periodontal Risk Calculator (PRC) To provide a risk score of a patients
susceptibility for periodontal
progression on a scale of 1(lowest
risk) to 5(highest risk).
68
69. Author(country) study type Risk assessment tool description Objective
Lang & Tonetti (2003) (Switzerland) Periodontal Risk Assessment Model
(PRA)
To classify patients a slow, medium
or high risk for periodontal disease
progression
Chandra(2007) (India) Modified Periodontal Risk
Assessment Model (Modified PRA)
To classify individuals a slow,
medium or high risk for periodontal
disease progression
Trombelli et al. (2009) (Italy) University of Ferrara (UniFe) To provide a risk score of a patients’
susceptibility for periodontal
progression on a scale of 1(lowest
risk) to 5 (highest risk)
Lindskog et al. (2010) (Sweden) DRS a patient risk score(DRS
dentition) or tooth risk score(DRS
tooth).
To provide a dentition (patient level)
risk score based upon systemic and
local predictors .
69
70. Author(country) study type Risk assessment tool description Objective
Teich (2013) (USA) Risk Assessment-Based
Individualized Treatment(RABIT)
To classify patients as low, medium
or high risk for periodontal disease
progression or caries risk with
accompanying recommendation for
maintenance visit interval
L€uetal.(2013) (China) PRA(as proposed by Lang & Tonetti
2003):
To classify patients as low, medium
or high risk for periodontal disease
progression.
Busby et al. (2014) (UK) Oral Health Status(OHS) as part of
Den Plan Excel/ Previsor Patient
Assessment(DEPPA)
To provide patient-level risk scores
for periodontal disease, caries and
oral cancer.
70
71. References :
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as risk factors for periodontal disease and tooth loss. Journal of Periodontology
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■ Alpagot T, Wolff LF, Smith QT, Trao SD. Risk indicators for periodontal disease in a racially
diverse urban population. Journal of Clinical Periodontology 1996;23:982–988.
■ Bergstrom J. Cigarette smoking as risk factor in chronic periodontal disease. Community
Dentistry and Oral Epidemiology 1989;17:245–247. [PubMed: 2791514]
■ Bergstrom J. Tobacco smoking and supragingival dental calculus. Journal of Clinical
Periodontology 1999;26:541–547. [PubMed: 10450815]
72. ■ Page RC, Martin JA, Loeb CF. The Oral Health Information Suite (OHIS): its use in the
management of periodontal disease. J Dent Educ. 2005;69:509–20.
■ Douglass CW. Risk assessment and management of periodontal disease. J Am Dent
Assoc. 2006;137:275–315.
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diseases. Periodontol 2000 1994; 5:78-111.
■ Rose RM: Endocrine responses to stressful psychological events. Psychiatr Clin N
Am 1980; 3:251-276
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