Porphyromonas gingivalis belongs to the phylum Bacteroidetes and is a nonmotile, Gram-negative, rod-shaped, anaerobic, pathogenic bacterium. It forms black colonies on blood agar.
It is found in the oral cavity, where it is implicated in certain forms of periodontal disease, as well as in the upper gastrointestinal tract, the respiratory tract, and the colon. It has also been isolated from women with bacterial vaginosis. Collagen degradation observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study that P. gingivalis can invade human gingival fibroblasts and can survive in them in the presence of considerable concentrations of antibiotics.P. gingivalis also invades gingival epithelial cells in high numbers, in which cases both bacteria and epithelial cells survive for extended periods of time. High levels of specific antibodies can be detected in patients harboring P. gingivalis. Dr Harshavardhan Patwal , explains the various enzymes enzyme peptidyl-arginine deiminase, which is involved in citrullination.[4] Patients with rheumatoid arthritis have an increased incidence of periodontal disease, and antibodies against the bacterium are significantly more common in these patients.
P. gingivalis is divided into K-serotypes based upon capsular antigenicity of the various types.
Systemic Peridoontology, link between systemic health and periodontology, diabetes and periodontology, Pregnancy and Peridotology,Nutrition and periodontology
Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.
Porphyromonas gingivalis belongs to the phylum Bacteroidetes and is a nonmotile, Gram-negative, rod-shaped, anaerobic, pathogenic bacterium. It forms black colonies on blood agar.
It is found in the oral cavity, where it is implicated in certain forms of periodontal disease, as well as in the upper gastrointestinal tract, the respiratory tract, and the colon. It has also been isolated from women with bacterial vaginosis. Collagen degradation observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study that P. gingivalis can invade human gingival fibroblasts and can survive in them in the presence of considerable concentrations of antibiotics.P. gingivalis also invades gingival epithelial cells in high numbers, in which cases both bacteria and epithelial cells survive for extended periods of time. High levels of specific antibodies can be detected in patients harboring P. gingivalis. Dr Harshavardhan Patwal , explains the various enzymes enzyme peptidyl-arginine deiminase, which is involved in citrullination.[4] Patients with rheumatoid arthritis have an increased incidence of periodontal disease, and antibodies against the bacterium are significantly more common in these patients.
P. gingivalis is divided into K-serotypes based upon capsular antigenicity of the various types.
Systemic Peridoontology, link between systemic health and periodontology, diabetes and periodontology, Pregnancy and Peridotology,Nutrition and periodontology
Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
Periodontal risk & making risk assessmentibrahimaziz15
Periodontal risk and risk assessment is very importnant in monitoring periodontally affected patients, this seminar will give you an idea about periodontal risk factors and how to make a periodontal risk assessment for patients.
Clinical risk assessment & diagnosis of periodontal diseaseRiad Mahmud
Prof. Dr. Md. Zahid Hossain, Division of Periodontology, Department of Preventive Dental Sciences, College of Dentistry, Najran University, Saudi Arabia.Former Professor of Periodontology, City Dental College, Dhaka
PERIODONTAL MEDICINE 1.pptx DIABETES DIABENitika588942
The term periodontal medicine, as first suggested by Offenbacher, that defines a rapidly emerging branch of periodontology focusing on the wealth of new data establishing a strong relationship between periodontal health or disease and systemic health or disease.
This means a two-way relationship in which periodontal disease in an individual may be a powerful influence on an individual’s systemic health or disease as well as the more customarily understood role that systemic disease may have in influencing an individual’s periodontal health or disease.It would be new diagnostic and treatment strategies that recognize the relationship between periodontal disease and systemic disease.
William Hunter, attesting to the influence of oral sepsis on systemic health and disease.
Recently scientists and clinicians have begun to provide an increasing body of scientific evidence suggesting that moderate untreated periodontitis may affect an individual systemically, and may contribute to cardiovascular disease, diabetes and pre-term low birth weight.This is important new information indeed. It appears that not just teeth are at stake in maintaining good oral health.
Rather, oral health is an important component of general health, and individuals with periodontitis may be at risk for other diseases as well.
Evidence has also shed light on the converse side of the relationship between systemic health and oral health: the potential effects of inflammatory periodontal diseases on a wide range of organ systems.Pathogenesis of periodontitis has changed remarkably over last 30 years.
The non-specific accumulation of bacterial plaque was once thought to be the cause of periodontal destruction, but it is now recognized that periodontitis is an infectious disease associated with a small number of predominantly gram-negative microorganisms that exist in a subgingival biofilm.
Furthermore, the importance of the host in disease initiation and progression is clearly recognized.
Although pathogenic bacteria are necessary for periodontal disease, they are not sufficient alone to cause the disease.
A susceptible host is also imperative. In a host who has relatively low susceptibility to disease, bacterial pathogens may have no clinical effect.
This may be due to a particularly effective host immunoinflammatory response that eliminates pathogenic organisms while minimizing destruction of native tissues.
Conversely, in a host with relatively high disease susceptibility, marked destruction of periodontal tissues may result.Acc. To William Hunter in 1900,
Oral microorganism- responsible for systemic conditions
Restoration instead of extraction, trapping of infectious agents
Gingivitis & periodontitis- foci of infection .Acc. To William Hunter in 1900,
Oral microorganism- responsible for systemic conditions
Restoration instead of extraction, trapping of infectious agents
Gingivitis & periodontitis- foci of infection
Acc. To William Hunter in 1900,
Oral microorganism
Risk assessment is the determination of quantitative or qualitative estimate of risk related to a well-defined situation and a recognized threat (also called hazard). Quantitative risk assessment requires calculations of two components of risk (R): the magnitude of the potential loss (L), and the probability (p) that the loss will occur. An acceptable risk is a risk that is understood and tolerated usually because the cost or difficulty of implementing an effective countermeasure for the associated vulnerability exceeds the expectation of loss."Health risk assessment" includes variations, such as risk as the type and severity of response, with or without a probabilistic context.
External modifying factors of periodontal diseasesMonika
Terminologies
Periodontitis
Risk indicator, risk factor & risk predictor
Socioecological model of periodontal diseases
Introduction
External modifying factors
a. Role of tobacco products
Evidence from cross sectional studies
Evidence from longitudinal studies involving periodontal attachment loss & periodontal healing
Role of low socioeconomic status
Evidence from cross sectional studies
Evidence from longitudinal studies
c. Role of lifestyle & dental care habits
Evidence from cross sectional studies
Evidence from longitudinal studies
Role of Acquired Systemic & Infectious disease
Role of psychosocial stress
Effect of Allergies
Effect of epilepsy & phenytoin therapy
Effect of Human immunodeficiency virus
e. Conclusion
f. References.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
3. INTRODUCTION
Periodontitis – one of the most ubiquitous diseases
Destruction of tissue and loss of bone support following inflammatory host response
Severe: 5-20% of most adult populations worldwide (Haynes et al., 2006; Zhang et al.,
2009)
Multifactorial etiology– mixed microbial infections
Periodontal disease as an infection, and the overall role and definition of periodontal
risk factors
Old concept (1960s)– all individuals were equally susceptible to periodontal disease--
misconception
3
4. INTRODUCTION
o 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 part of a causal chain
о RISK ASSESSMENT:
- It is the process of determining the quantitative and qualitative likeliness of adverse events that may
result from exposure to specific health hazard or from the absence of beneficial influences
o RISK FACTOR:
- It is an environmental exposure, aspect of behavior or an inherent characteristic which is associated
with a disease
- To be identified as a risk factor, the exposure must occur before the disease onset 4
5. INTRODUCTION
o RISK (Kleinbaum, 1982):
- It is the probability that an individual will develop a given disease or exposure or change the
health status in a given period.
RISK MARKERS or PREDICTORS: these are characteristics having the ability to predict individuals
at high risk but they are not part of a causal chain. They may predict the future course of the
disease.
RISK DETERMINANTS/ BACKGROUND CHARACTERISTIC: these terms sometimes substitute 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
6. NEED TO IDENTIFY RISK FACTORS
Recommendations of risk-factor modification as a
PUBLIC HEALTH MEASURE
Strength of evidence– contribution to the body of
epidemiologic evidence
Stringent criteria to establish causality
Extent to which any risk factor contributes to
periodontal disease (ATTRIBUTABLE RISK)
Currently only available for some risk factors– future
studies are necessary to determine and prioritize risk
factors for management of periodontal disease
6
8. RISK CHARACTERISTICS
Several studies throughout literature points to the fact
Loe et al., 1986: 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.
More studies carried out in some of the developed countries show changing
patterns of periodontal disease progression (P.D. Miller, 1987; R Teles, 2018)
AGE
8
9. RISK CHARACTERISTICS
Multiple studies point to a higher rate of periodontal destruction in males as compared
to the female population. (Grossi, 1995; Slade, 1995; Genco, 1997)
Related to ignorance of oral hygiene seen in males.
Men could potentially benefit from being preferentially targeted for preventive
measures and more aggressive interventions. (Periodontology 2000, Genco 2013)
GENDER
9
11. RISK CHARACTERISTICS
Periodontal disease has a reciprocal relationship with educational level.
Several studies involve different racial populations in relation to different expression for
periodontal disease
Race– not modifiable
EDUCATION and RACE
11
12. RISK CHARACTERISTICS
Studies show genetic risk factors associated with periodontitis [Hart, 1994].
Composite IL-1 genotype is significantly associated with the severity of adult periodontitis. Also confirmed
that both IL-1 genotyping and smoking history provide objective risk factors for periodontal disease in a
private practice environment [McDevitt et al., 2000].
Risk for periodontitis is not shared equally by the population. It is clear that periodontitis severely affects a
high-risk group representing around 10–15% of the population, in whom the disease quickly progresses
from chronic gingivitis to destructive periodontitis [Johnson et al, 1988].
Aggregation within families strongly suggests a genetic predisposition. [Benjamin-Baer, 1967; Marazita et
al., 1994; Hassell and Harris, 1995].
Familial patterns may reflect exposure to common environmental factors within these families.
The problems associated with the clinical differentiation of periodontal disease are not uncommon in
medical genetics, since similar problems arise in the study of other delayed onset hereditary traits
[Boughman, 1988]
GENETICS
RISK FACTORS
Polymorphisms in–
IL-1α, IL-1β, IL-6, IL-10,
MMP-3 (chronic form),
and MMP-9 (chronic
form)
12
13. RISK CHARACTERISTICS
Familial aggregation and twin studies
Virginia Twin Registry study, 1970s
Minnesota Twin Registry, 1991
Marazita et al., 1994
Rapp et al., 2011
Meng et al., 2011
GENETICS
13
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 heredity 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 their upbringing and
environments of twins complicated these
studies
14. RISK CHARACTERISTICS
Growing interest in connection with cardiovascular risk and periodontitis.
In a study by Ebersole et al. (1997), they reported significantly higher levels of CRP among those with
adult periodontitis, especially among those having more active sites
Studies report elevated CRP levels among those with periodontitis [Noack, 2001; Pitiphat et al., 2008].
The participants of the MI Life Study [Noack] also reported positive association between elevated
levels of CRP (>3mg/L) and severity of periodontitis.
Bacterial infections may often provide a strong stimulus for a systemic acute phase response that
may result in increased production of acute-phase proteins like CRP, macroglobulin, and serum
amyloid.
In a recent study, it was found that the concentrations of hs-CRP and IL-6 were significantly higher in
the sera of patients with periodontitis and periodontal treatment decreased the levels of serum hs-
CRP and IL-6 [Nakajima, 2010].
Elevation of CRP levels among those with periodontitis indicates that periodontitis may also have
systemic cytokine mediated effects that may in turn participate in atherogenesis.
CRP (Aljehani et al., 2014)
14
15. MODIFIABLE RISK FACTORS
Over 400 microbial phylotypes in subgingival plaque (Berezow, 2011)
Dominated by G- anaerobic rods and spirochetes
Presence of these putative pathogens– necessary but not sufficient
alone.
Only one species– not a risk factor (Ezzo & Cutler, 2003)
STRONG EVIDENCE– P.gingivalis (Kou et al., 2008) and
A.actinomycetemcomitans (Dogan et al., 2008) in relation to
pathogenesis of periodontitis
i. B. forsythus (Huang et al., 2005)
ii. P. intermedia (Lovegrove, 2004)
iii. P. micros (Tanabe et al., 2007)
iv. F. nucleatum (Saito et al., 2008)
MICRO-ORGANISMS
P .gingivalis
A. a
T.
forsythia
15
16. MODIFIABLE RISK FACTORS
- There is accumulating evidence for a higher level of periodontal disease among smokers [Kubota et
al 2011, Vouros et al, 2009].
- Tobacco smoking exerts a substantial destructive effect on the periodontal tissues and increases the
rate of periodontal disease progression [Zini, 2011].
- Risk factors including tobacco smoking modify the host response to the challenge of bacteria in
microbial dental plaque [Ozcaka 2011, Kumar et al].
- Smokers with periodontal disease seem to show less signs of clinical inflammation and gingival
bleeding compared to nonsmokers [Bergstrom, 1990].
- That could be explained by the fact that nicotine exerts local vasoconstriction, reducing blood flow,
edema, and clinical signs of inflammation [Jensen et al, 1991].
- Nicotine acetylcholine receptor has been found to play an important role in the development of
nicotine related periodontitis [Wang et al, 2010].
SMOKING
16
17. MODIFIABLE RISK FACTORS
SMOKING AS A RISK FACTOR FOR PERIODONTAL DISEASE—
Cigarette smoking has long been associated with periodontal disease and tooth loss
Source of more than 4,000 toxins
Major risk factor for all cause mortality, cardiovascular disease, various cancers, and several chronic diseases.
The finding that smoking is associated with periodontal disease suggests that it is probably a major risk factor for
subsequent tooth loss.
An association between acute necrotizing ulcerative gingivitis and tobacco smoking was reported in 1947 (Pickup,
2004).
Bergstrom & Preber (1994). Most of the studies showed poorer oral hygiene in smokers compared with nonsmokers,
and this probably accounts for the prevailing concept at the time, that smoking was not a risk factor for periodontitis
and that oral hygiene alone would account for the differences in the levels of periodontal disease between smokers
and nonsmokers.
Erie County Study (Grossi, 1994&1995) when adjustments for confounding and correlations were made, smoking was
one of the major risk factors, both for periodontal attachment loss as well as for alveolar crest bone loss.
SMOKING
17
18. ANALYSIS OF EPIDEMIOLOGIC STUDIES IMPLICATING SMOKING AS A RISK FACTOR FOR PERIODONTAL
DISEASE-
The importance of cigarette smoking as a risk factor for periodontal disease is supported by:
(i) consistency of results across many studies;
(ii) strength of the association;
(iii) dose–response of the association;
(iv) temporal sequence of smoking and periodontal disease; and
(v) biologic plausibility
- There is a need for long-term follow-up of nonsmokers and those who have quit smoking to determine
clearly the effects of smoking cessation on the periodontium.
- However, existing studies of smoking cessation, or of nonsmokers vs. smokers, strongly suggest that part of
the management of periodontal disease should involve an attempt at smoking cessation
MODIFIABLE RISK FACTORS
SMOKING
18
19. SMOKING AS A RISK FACTOR FOR PERIODONTAL DISEASE: PATHOGENIC MECHANISMS–
- Cigarette smoke contains more than 4,000 reported toxic substances, such as carbon monoxide, oxidizing
carcinogens (such as nitrosamine) and nicotine.
- Adverse effects fall into several categories regarding the effect of cigarette smoking on—
• Microbiology (microbiota/periodontal pathogens)
• Gingival blood flow
• PMNL phagocytosis
• Cytokine production
• CD3, CD4 and CD8+ T-cell subsets
• Periodontal healing
MODIFIABLE RISK FACTORS
SMOKING
- shift toward a more pathogenic subgingival flora
- reduced microcirculation
- dysfunction of neutrophils
- production of proinflammatory cytokines
- increased levels of pathogenic T-cells
19
20. MODIFIABLE RISK FACTORS
Patients with undiagnosed or poorly controlled diabetes mellitus type 1 or type 2 are at higher risk
for periodontal disease. [Stegeman, 2005; Meng, 2007]
More rapid progression of periodontitis in poorly controlled diabetics
Despite discrepancy regarding this issue in the scientific literature, it seems that the effect of
glycemic control is related to the mode of periodontal therapy [Grossi & Genco, 1998]
DIABETES
DIABETES MELLITUS AS A RISK FACTOR FOR PERIODONTAL DISEASE–
o The abnormal glucose metabolism results from defects in insulin action or in insulin production
(or in both in severe cases).
o The prevalence of diabetes increases sharply after age 45. For example, among seniors over 65
years of age, the prevalence of diabetes is about 27%.
o growing public health concern globally
o leads to significant mortality and morbidity
o associated with its major complications, such as cardiovascular disease and end-stage renal
disease.
o Diabetes is also the leading cause of loss of limbs and new cases of blindness in the USA (CDC,
2011).
o Diabetes mellitus and periodontal disease are both chronic, common diseases in the population,
especially in those over 65 years of age, and are related.
20
21. MODIFIABLE RISK FACTORS
MECHANISMS TO EXPLAIN THE ROLE OF D. MELLITUS IN PERIODONTITIS-
DIABETES
AGE- RAGE Altered wound healing
Altered native immune response Effect of periodontitis
21
22. MODIFIABLE RISK FACTORS
TWO-WAY RELATIONSHIP BETWEEN DIABETES AND PERIODONTAL DISEASE-
- First evidence– late 1990s (reported by Genco et al., 2005)
- Bidirectional nature of relationship (Papapanou et al., 2011)
Effects of diabetes on periodontal disease
Evidence of effect
Effect of periodontal treatment in controlling diabetes
DIABETES
22
23. MODIFIABLE RISK FACTORS
- TWO-WAY RELATIONSHIP BETWEEN DIABETES AND PERIODONTAL DISEASE-
a. CROSS-SECTIONAL STUDIES
b. LONGITUDINAL STUDIES
DIABETES
23
24. MODIFIABLE RISK FACTORS
o PRE-DIABETES AS A RISK FACTOR FOR PERIODONTAL DISEASE –
- More undiagnosed than diagnosed
- At high risk for diabetes
- Associated with major risk factors for CVD and other diabetic complications (Cowie et al.,
2009)
- This longitudinal study confirmed that the incidence of periodontal disease was associated
with elevated baseline levels of glycated hemoglobin.
- In conclusion, there is evidence for hyperglycemia (elevated glucose level) being a risk
factor for developing periodontal disease
DIABETES
24
25. MODIFIABLE RISK FACTORS
GESTATIONAL DIABETES AS A RISK FACTOR FOR PERIODONTAL DISEASE-
- Several studies show a strong relationship
- Reports on NHANES III data– over 4000 women in USA
- Nonsurgical periodontal treatment of pregnant women is probably safe for both the
mother and the child (Newnham, 2009)
- Hence, management of periodontal disease during pregnancy may be an option to
modify the increased risk of worsening periodontal disease in pregnant women.
DIABETES
25
26. MODIFIABLE RISK FACTORS
o EFFECTS OF PERIODONTAL DISEASE ON THE INCIDENCE OF DIABETES MELLITUS –
DIABETES
26
27. MODIFIABLE RISK FACTORS
o PERIODONTAL TREATMENT AND GLYCEMIC CONTROL-
o Considerable evidence existing
o Further studies required.
DIABETES
[Genco & Borgnakke, 2013]
27
28. MODIFIABLE RISK FACTORS
Mechanisms:
High concentrations of cholesterol
Action of oral bacteria in the process of atherosclerosis
Participation of acute-phase proteins that may increase in chronic periodontitis (Kamil et al,
2011)
Periodontitis can elicit a systemic inflammatory response– deserves attention (Mattila et al,
2002)
Rich source of subgingival microbiota and host response predisposes to vascular diseases
(Kinane & Lowe, 2002)
Bacteremia from periodontitis primary cause of infective endocarditis (Nakamura et al.,
2011)
Putative and independent risk factor for cerebrovascular disease– ischemic stroke. (Wu et al.,
2000)
CARDIOVASCULAR DISEASES
28
29. MODIFIABLE RISK FACTORS
Mechanisms:
- Decreased salivary flow-- Xerostomia is a concern because saliva plays a major antimicrobial
role in protecting both the soft and hard oral tissues.
- Altered pH and composition of plaque– more adherent to tooth surfaces
- Agents affecting diagnoses
- DIGO
DRUG-INDUCED DISORDERS
29
30. MODIFIABLE RISK FACTORS
- Patients with inadequate stress behavior strategies (defensive coping) are at greater risk for severe
periodontal disease [Johansson 2007, Aimetti 2007].
- Stress is associated with poor oral hygiene, increased glucocorticoid secretion that can depress
immune function, increased insulin resistance, and potentially increased risk of periodontitis
[Merchant et al, 2003].
- Men who reported being angry on a daily basis had a 43% higher risk of developing periodontitis
compared with men who reported being angry seldom
- Studies have found some periodontal disease indicators such as tooth loss and gingival bleeding
to be associated with work stress [Marcenes & Sheiham, 1992] and financial strains [Moss et al,
1996].
STRESS
Association between severity of periodontal attachment loss and alveolar bone loss in those
reporting financial strain and different coping behaviors, adjusted for age, gender and
smoking.
High problem-focused coping is considered to be effective, and the risk for financial strain on
periodontal disease is nullified in this group. [Genco et al., 1999]
30
31. MODIFIABLE RISK FACTORS
Passive coping strategies resulted in
more pronounced periodontal disease
Active coping strategies (presumably a
more effective form of coping) had a
milder disease level and more favorable
course of treatment.
STRESS
- Exposure to psychological stresses may affect the host immune response as well as encourage unhealthy
behaviors.
- Exposure to stress release of noradrenaline through SNS by activation of the adrenal medulla
immunosuppressive effects (Seiffert et al, 2002).
- Such immunosuppressive effect can enhance periodontal tissue destruction (Breivik, 2011).
- Stress can:
Promote production of corticotropin-releasing hormone by the pituitary gland
Production of glucocorticoid hormones from the adrenal cortex
Lead to decreased production of proinflammatory cytokines as a result of the release of
neuropeptides from sensory nerve fibers. (neuropeptides– immune system modulators enhanced
tissue destruction.)
modify behaviors that are harmful to periodontal health
- poor oral hygiene
- increased smoking
- fewer dental visits
- changes in eating habits.
31
33. MODIFIABLE RISK FACTORS
OBESITY
Important risk factor for periodontal disease (Suvan et al, 2011)
Variations in diet patterns
OBESITY AS A RISK FACTOR FOR PERIODONTAL DISEASE –
- Effects on general health – insulin resistance, chronic systemic inflammation (Kopelman,
2007)
- Hypothesis: association of obesity with chronic diseases, including periodontal diseases
result of chronic systemic inflammation associated with obesity.
33
35. MODIFIABLE RISK FACTORS
ROLE OF THE IMMUNE AND INFLAMMATORY RESPONSE IN PERIODONTAL DISEASE SEEN IN OBESE AND
OVERWEIGHT INDIVIDUALS-
- Obese individuals develop infections of various types (including postoperative and nosocomial infections) more often
than do people of normal weight (Falagas 2006).
- The mechanisms by which obese people are predisposed to infection include the participation of adipose tissue in
inflammation and immunity. A variety of proinflammatory and anti-inflammatory factors are produced by adipose
tissue (Fantuzzi 2005).
- A heightened inflammatory response is regularly observed in individuals in who are obese (Shoelson 2006).
- The adipocytes in centrally located adipose tissue act as critical sites for the generation of inflammatory responses
and mediators. In addition, careful examination of adipose tissue during obesity reveals the presence of increased
numbers of macrophages, which may also contribute to the inflammatory mediators produced by adipose tissue
(Hotamisligil 2006).
- There is evidence suggesting that changes in the proinflammatory and immune responses associated with obesity
may contribute to their increased susceptibility to periodontal disease.
- Further studies required.
OBESITY
35
36. MODIFIABLE RISK FACTORS
METABOLIC SYNDROME AS A RISK FACTOR FOR PERIODONTAL DISEASE-
- Metabolic syndrome: cluster of disorders-- ↑BP, ↑plasma glucose, ↑body fat around waist and upper
abdomen, altered cholesterol levels
- Increased risk of heart disease, stroke and diabetes
- Cause– unknown. Probably associated with insulin resistance
- Itself risk factor for type 2 DM, CVD and periodontal disease
- Increases total mortality (Grundy , 2005)
METABOLIC SYNDROME
36
37. MODIFIABLE RISK FACTORS
EVIDENCE FOR THE ASSOCIATION OF METABOLIC SYNDROME WITH PERIODONTAL DISEASE—
- There appears then to be a reciprocal relationship between periodontal disease and metabolic
syndrome; however confirmatory studies in other populations, and studies to explain the mechanisms
of these effects, are needed.
- There is also an unanswered question of which of the multiple components of metabolic syndrome are
more strongly associated with periodontal disease.
- It is reasonable to expect that obesity and diabetes or prediabetes would affect periodontal disease as
there is strong, independent evidence for the association of both factors with a greater risk for
periodontal disease.
- However, although the roles of elevated blood pressure, dyslipidemia involving elevated triglycerides,
and lower high-density lipoprotein cholesterol, are of great interest, it is less clear as to how they may
affect periodontal disease.
METABOLIC SYNDROME
37
38. MODIFIABLE RISK FACTORS
MECHANISMS TO EXPLAIN THE ASSOCIATION BETWEEN PERIODONTAL DISEASE AND
METABOLIC SYNDROME—
- Heightened chronic systemic inflammatory response
- Hyperglycemia
- Reduced high-density lipoprotein cholesterol
- Obesity
- Elevated cytokines: interleukin-6, interleukin- 1b and the acute-phase proteins, C-reactive protein,
and fibrinogen.
- Elevated systemic inflammatory response greater tissue destruction
METABOLIC SYNDROME
38
39. MODIFIABLE RISK FACTORS
INTERVENTION TRIALS—
- 1st study: Jenszch et al, 2009
- Intervention to reduce the components of metabolic syndrome in patients with both metabolic
syndrome and periodontal disease
- Resulted in reduction of the concentration of interleukin-1b and interleukin-6 in GCF. There was
also a reduction in gingival inflammation and pocket depth.
- Reducing periodontal inflammation significantly reduces C-reactive protein levels, as well as
fibrinogen
- In addition, if it turns out that metabolic syndrome is indeed a risk factor for periodontal disease, or
there is a two-way relationship, testing the effects of intervention by modifying metabolic syndrome
on the periodontal status is needed to justify incorporation of modification of metabolic syndrome
as a goal of risk reduction for periodontal disease [Genco & Borgnakke, 2013]
METABOLIC SYNDROME
39
40. NON-MODIFIABLE RISK FACTORS
OSTEOPOROSIS AS A RISK FACTOR FOR PERIODONTAL DISEASE —
- Several studies suggest a relationship between skeletal osteoporosis and bone loss
- Post-menopausal osteoporosis in women– may result in dental osteopenia involving mandible (Suresh et al.,
2010)
- Direct association between skeletal and mandibular osteopenia and loss of alveolar crestal height and tooth
loss in postmenopausal women (Khader et al, 2010)
- Periodontitis and osteopenia may have common etiological agents that may either directly influence or
modulate both disease processes (Cashman et al., 2007)
- POSSIBLE MECHANISM: main risk factor for osteoporosis in women is menopause, which is associated with
reduced estrogen production that results in increased bone resorption . In addition, there is also a decrease in
calcium absorption and an increase in calcium excretion, which increases the calcium requirement. This process
has a significant impact on mortality and morbidity. (Genco, 2013)
- Also, because menopause is associated with increased bone resorption, other disease processes that involve
bone loss, including periodontal disease and tooth loss, are probably affected.
OSTEOPOROSIS, DIETARY CALCIUM and VIT. D
40
41. NON-MODIFIABLE RISK FACTORS
DIETARY CALCIUM & VIT. D AS A RISK FACTOR FOR PERIODONTAL DISEASE —
- Inverse relationship between dietary calcium and periodontal disease throughout literature
- Individuals (especially women) with a low intake of dietary calcium had more severe periodontal disease
(Nishida et al., NHANES III data, 2000; Al-Zahrani et al., 2006; Shimazaki et al., 2008)
- Bisphosphonates -- effective in reducing alveolar bone loss in those patients who had low baseline bone
mineral density (Jeffcoat et al., 2007; Cetinkaya et al, 2008)
- Cause for concern: association of bisphosphonates I.V. with oral osteonecrosis (Hellstein, 2011)
- Limited evidence to indicate that altered bone biology leading to osteoporosis has effects on tooth loss
and possibly periodontal status
- Negative role of osteoporosis in risk for implant failure
OSTEOPOROSIS, DIETARY CALCIUM and VIT. D
41
“TERIPARATIDE”
42. NON-MODIFIABLE RISK FACTORS
- Hemorrhagic gingival overgrowth with or without necrosis is a common early manifestation of
acute leukemia [Genco and Loe, 1993].
- Patients with chronic leukemia may experience similar but less severe periodontal changes.
- Chemotherapy or therapy associated with bone marrow transplantation may also adversely
affect the gingival health [Tiemann et al., 2007].
HEMATOLOGICAL DISORDERS
42
43. NON-MODIFIABLE RISK FACTORS
- Chronic periodontitis involves complex interactions between microbial factors and susceptible hosts [Bureau,1996; Offenbacher, 1997].
- Bacterial components: lipopolysaccharides and cytokines activate the macrophages to produce cytokines such as interleukin(IL)-1
and tumor necrosis factor (TNF) [Radvar et al 2010].
- These cytokines activate the fibroblasts that reside in the periodontal tissues to the matrix metalloproteinases (MMPs), a plasminogen activator, which
can activate plasmin.
- Plasmin, in turn, can activate some other types of latent MMPs, while tissue inhibitors of metalloproteinases (TIMPs) can inactivate the active MMPs
- This induce the enhanced degradation of collagen
- MMP-8 and -9 are released from the polymorphonuclear leukocytes (PMN) and are responsible for a substantial part of the destruction caused by the
host response.
- MMP-13 also facilitates bone resorption by degrading the collagenous matrix of the bone after the bone is demineralized by osteoclasts
- Increased plasma levels of MMP-8 and MMP-9 in chronic periodontitis patients and emphasized the importance of periodontal
treatment to avoid elevated MMP-8 and -9 levels which are associated with many systemic diseases, particularly cardiovascular
disorders [Marcaccini et al, 2009].
- A recent review on the modifiable risk factors concluded that smoking and excess caloric intake contribute to increases in systemic
markers of inflammation and can modify gene regulation through a variety of biologic mechanisms [Reynolds 2014].
HOST RESPONSE
43
44. NON-MODIFIABLE RISK FACTORS
Hormonal fluctuations in the female patient may alter the status of periodontal health [Lopez-Marcos et
al, 2005].
Such changes may occur during puberty, the menstrual cycle, pregnancy, or menopause.
Changes may also be associated with the use of oral contraceptives. The most pronounced periodontal
changes occur during pregnancy, as a significant proportion of pregnant women suffer from pregnancy
gingivitis.
Women on hormonal replacement therapy(HRT) and oral contraceptives experience increased gingival
inflammation [Soory et al, 2010].
With oral contraceptives, this increase in gingival inflammation is mainly related to the duration of use as
it has been suggested that prolonged use of oral contraceptives may detrimentally affect the
periodontium.
FEMALE HORMONAL ALTERATIONS
44
45. NON-MODIFIABLE RISK FACTORS
Offenbacher et al [1996] found significantly more periodontal attachment loss among mothers of PLBW
infants compared with mothers of normal-term infants.
Studies have suggested an adverse influence of periodontal disease on the course of pregnancy
[Baskaradoss et al, 2011]
Periodontal disease may increase the risk of having preterm low birth weight (PLBW) infants
Effect of biologic mediators of inflammatory processes such as prostaglandins E2 and TNF.
Bacterial LPS also may have a triggering role in adverse change of the course of pregnancy. [Gazolla et
al, 2007]
FEMALE HORMONAL ALTERATIONS– PREGNANCY
45
47. PREVIOUS HISTORY OF PERIODONTAL DISEASE
47
Individuals who have the
most severe disease at the
initial examination are at
the greatest risk of future
disease.
Conversely, patients
currently free of
periodontitis have a
decreased risk of
developing loss of
attachment than who
currently have periodontitis.
AUTHORS RESULTS
Listgarten, 1991 Risk of future periodontal
deterioration is strongly associated
with the presence and severity of
disease at baseline.
Grabic et al., 1991 Suggested that probability of future
periodontal deterioration increases
with increasing pocket depth and
clinical attachment loss at baseline.
48. BLEEDING ON PROBING
48
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 & Kaldahl et al, 1996 Absence of BoP may be associated more often
with areas exhibiting in disease progression
Claffey et al, 1990 Suggested that the combination of increasing
pocket depths and frequent BoP is more likely
lead to future attachment loss. 90% of the
pockets with BoP will be associated with future
attachment loss over the next 42 months.
49. CLINICAL APPLICATIONS: RISK ASSESSMENT
“Risk assessment is defined as the process by which qualitative or quantitative assessments
are made of the likelihood for adverse event to occur as a result of exposure to specified
health hazards or by absence of beneficial influences.”
American Academy of Periodontology, 2008
49
50. CLINICAL APPLICATIONS: RISK ASSESSMENT
PATIENT LEVEL
Performed at initial
examination
WHOLE MOUTH
LEVEL
Performed at initial
examination and
post-initial therapy
TOOTH LEVEL
Performed post-
initial/definitve
therapy and
maintenance
SITE LEVEL
Performed post-
definitve therapy
and during
maintenance
50
Risk assessment in periodontal disease is that
the disease is 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 4 levels to consider:
51. CLINICAL APPLICATIONS: RISK ASSESSMENT
51
Patient-
level risk
assessment
Mouth-level
risk
assessment
Tooth-level
risk
assessment
Site-level
risk
assessment
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.
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
- Presence of removable prosthesis
- Levels of recession
- Gingival inflammation and depth of pockets.
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. Part of this assessment includes:
- Individual tooth mobility (mobility index)
- Tooth movement or drifting of periodontally compromised teeth
- Residual tooth support (radiographically). The extent of residual
radio graphic bone support helps determine long-term prognosis.
- Presence, location and extent of furcation lesions
- Individual tooth anatomy - Presence of "talon cusps" or bulbous
crowns
- Anatomy of tooth embrasures and contact points
- Presence of ledges or deficiencies on restorations
- Individual occlusal contacts – Prematurities
- Soft tissue contours
- Subgingival calculus.
Site-level risk assessment would include:
- 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.
52. CLINICAL APPLICATIONS: RISK ASSESSMENT
RISK ASSESSMENT TOOLS:
1. The oral health information suite (OHIS)
2. Periodontal Risk Calculator(PRC)
3. Hexagonal risk diagram for periodontal assessment (PRA)
4. Modified Periodontal risk assessment model [developed by Chandra]
5. UniFe(Union of European Railway Industries) for periodontal risk assessment
6. AAP risk assessment Tool
7. Dentorisk
8. Risk Assesment-Based Individualized Treatment (RABIT)
9. Cronin/Stassen BEDS CHASM Scale 52
53. CLINICAL APPLICATIONS: RISK ASSESSMENT
Medical history
Dental history
Periodontal examination
53
Risk factor/ risk determinant
identification
NSPT and SPT
Positive response Negative response
Appropriate
periodontal
maintenance
Reassess risk
factors/
determinants
Tobacco smoking
Cessation strategies
Diabetes
Physician consultation
Monitor glycemic control
Microbial tooth deposits/pathogenic bacteria
Microbial sampling
Antibiotic susceptibility testing
Genetic factors
Determine family history of disease
IL-1 genotype assessment
Age
Length of exposure to risk elements
Evidence of aggressive disease
Postmenopausal women
Gender
Male
Postmenopausal women
Socioeconomic status
Frequency of dental visits
Dental awareness
Stress
Life events
Coping mechanisms
54. CLINICAL APPLICATIONS: RISK ASSESSMENT
AAP SELF-ASSESSMENT TOOL
How old are you?
Are you female or male?
Do your gums ever bleed?
Are your teeth loose?
Have your gums receded, or do your teeth look
longer?
Do you smoke or use tobacco products?
Have you seen a dentist in the last two years?
How often do you floss?
Do you currently have any of the following
health conditions? i.e. heart disease,
osteoporosis, osteopenia, high stress, or
diabetes
Have you ever been told that you have gum
problems, gum infection or gum inflammation?
Have you had any adult teeth extracted?
Have any of your family members had gum
disease?
54
A systematic review found that one good self report measure was
actually the simple question:
“Has any dentist ⁄ hygienist told you that you have deep pockets?”
It had a sensitivity of 55%, a specificity of 90%, a positive predictive
value of 77% and a negative predictive value of 75%, which were all
calculated using actual clinical pocket depth as measured by clinicians.
(Blicher et al 2005)
55. CLINICAL APPLICATIONS: RISK ASSESSMENT
Health Improvement in Dental Practice Model (HIDEP) [Fors & Sandberg (2001),Sweden]
Computerized tool that uses predefined risk groups for selecting and managing individual
treatment and prevention schemes.
Tool designed to assess the risk of other aspects of oral health in addition to periodontal status
OBJECTIVE
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.
Consists of 5 risk and 4 disease categories for both caries and periodontal diseases. Scores
assigned according to 14 parameters. Final result places patients on a health-disease scale and
low or high risk for disease scale for both caries and periodontal disease
55
Parameters utilized in tool
• Total number of teeth
• Total number of intact teeth (teeth without restorations, caries, or crowns, number of caries
lesions (initial lesions included)
• caries experience
• fluoride exposure
• saliva diagnostics (including secretion, buffering capacity, lactobacilli criteria, and streptococcus
mutans)
• sugar intake frequency
• oral hygiene screening
• professional risk estimation for caries and periodontitis
• gingival bleeding
• probing of periodontal pockets
• radiographic examination, registration of tartar and/or overhang
56. CLINICAL APPLICATIONS: RISK ASSESSMENT
ORAL HEALTH INFORMATION SUITE (OHIS)– PreViser Risk Calculator [Page & co-workers (2003),USA]
- A component of the Oral Health Information Suite.
- The PRC is a web‐based tool that can be accessed through a dental office computer.
- The risk calculation is a multi‐step process involving mathematical algorithms
OBJECTIVE
- To provide a risk score of a patients’ susceptibility for periodontal progression on a scale of 1 (lowest risk) to
5 (highest risk).
56
PARAMETERS
9 risk factors which include:
• 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
57. CLINICAL APPLICATIONS: RISK ASSESSMENT
Periodontal Risk Assessment Model (PRA) [Lang & Tonetti (2003), Switzerland]
A functional diagram (spider web shape) formulated based upon the combination of various
parameters that have been proposed in scientific literature as impacting the patient risk for further
disease progression.
- Hexagonal risk diagram
OBJECTIVE
To classify patients as low, medium or high risk for periodontal disease progression.
57
PARAMETERS
1. Percentage of bleeding on probing
2. Prevalence of residual pockets greater than 4 mm
3. Loss of teeth from a total of 28 teeth
4. Loss of periodontal support in relation to the patient's
age
5. Systemic and genetic conditions
6. Environmental factors, such as cigarette smoking.
58. CLINICAL APPLICATIONS: RISK ASSESSMENT
Modified Periodontal Risk Assessment Model (Modified PRA) [Chandra (2007), India]
A new periodontal risk assessment model based on periodontal risk assessment (PRA) model by
Lang and Tonetti that was targeted to be:
1. Easier to generate and use
2. Would assess diabetes on an individual radius
3. Would incorporate dental factors include “others factors” such as stress and socio-economic
factors
DIFFERENCES FROM PRA
environmental factors, systemic and genetic factors are specifically defined as diabetes status and
interplay of dental systemic factors that accounts for dental factors.
58
PARAMETERS UTILIZED IN TOOL
Additional factors are re-defined or included:
1. Diabetic status, age, dental status-systemic factors interplay and other background
characteristics.
2. Bone loss/age is replaced with attachment level/age
3. Other background factors are included to include estimated socio-economic or stress
factors.
4. The scores on each trajectory ranged between 1 and 5 based on a color coding
59. CLINICAL APPLICATIONS: RISK ASSESSMENT
University of Ferrara (UniFe) [Trombelli et al. (2009), Italy]
A proposed simplified method for periodontal risk assessment based upon five parameters derived
from patient medical history and clinical recordings.
- Each parameter assessed is allocated a parameter score according to defined criteria.
- The algebraic sum of the parameter scores is calculated and relates to a risk score between 1 and
5.
59
PARAMETERS
The UniFe tool uses five parameters:
1. Smoking status
2. Diabetes status
3. Number of sites with PD ≥ 5mm
4. Number of sites with bleeding on probing (BOP)
5. Bone loss/age to assign risk categories to patients.
60. CLINICAL APPLICATIONS: RISK ASSESSMENT
DRS, a patient risk score (DRS dentition) or a tooth risk score (DRS tooth, DentoRisk). [Lindskog et al.
(2010), Sweden]
A Web-based analytic tool that calculates chronic periodontitis risk for the dentition (Level I) and, if an
elevated risk is found, prognosticates disease progression tooth by tooth (Level II).
OBJECTIVE
To provide a dentition (patient level) risk score based upon systemic and local predictors. It allows for
further risk assessment at the tooth level if patient-level risk is found to be elevated
60
PARAMETERS UTILIZED IN TOOL
Systemic predictors:
- Age
- Family history of periodontitis
- Systemic disease
- Skin test result (assesses patient’s inflammatory
reactivity)
- Patient compliance and disease awareness
- Socioeconomic status
- Smoking habits and
- Therapist’s experience with periodontal care
61. CLINICAL APPLICATIONS: RISK ASSESSMENT
Risk Assessment-Based Individualized Treatment (RABIT) [Teich (2013), USA]
Advocates a modified approach that supports individualized risk-based recall schedules not only
after active therapy is completed but also during the course of treatment. Approach assesses risk of
other aspects of oral health in addition to periodontal status
OBJECTIVE
To classify patients as low, medium or high risk for periodontal disease progression or caries risk with
accompanying recommendation for maintenance visit interval
61
Parameters utilized in tool
Computer system assigns a risk level based upon caries risk assessment and periodontal risk
assessment. The specific parameters used to generate the level of risk are not reported in the paper
(reported as developed according to existing evidence)
62. CLINICAL APPLICATIONS: RISK ASSESSMENT
Cronin/Stassen BEDS CHASM Scale [Cronin (2008), UK]
- This represents a four step risk assessment model.
- The BEDS CHASM model uses a scoring system that can be
compared with average scores to estimate an odds ratio
- The calculated Odds ratio helps to standardize risk
assessment, allowing factors to be easily compared with the
standard numerical index
62
PARAMETER SCORE
B- BMI 2
E- Ethnicity 1.5
D- Diabetic 2.5
S- Stressed 2
C- College 2.5
H- Hygiene 2
A- Age 65+ 3.5
S- Smoker 1.5
M- Male 1.5
The total score of 19 indicates the highest risk.14
63. LIMITATIONS AND ISSUES OF RISK ASSESSMENT
Which one the most accepted??
- PRC and PRA seem well suited to satisfy the goals proposed with patient-based risk assessment (Tonetti 1998).
- It appears, however, particularly important to emphasize that risk segmentation of recall populations with PRA or its modifications have been validated
in multiple populations and settings around the world (Brazil, China, France, Germany, India, Sweden and Switzer- land), increasing the generalizability
and external validity of the tool and therefore the potential applicability to clinical practice.
Limitations
- Beyond their value in patient education, is it clear that risk calculators can truly aid clinicians in making better diagnoses and prognoses?
- Is a computer-aided mathematical tool, such as the PreViser Risk Calculator, better diagnostic aid than the clinicians approach?
Issues in Risk Assessment
Diagnosis :
- A diagnostic test is either highly specific or highly sensitive.
- Diagnostic tests differentiate whether or not a person has a specific disease at that time. Risk is the likelihood that people without disease who are
exposed to certain factors (risk factors) will get the disease within a specified time interval.
Risk factors:
- Removal of a risk factor does not necessarily cure the disease
- Reducing a risk factor in a condition that has multiple risk factors only reduces a proportion of the risk.
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64. CONCLUSION
Overgrowth of biofilms, especially in the subgingival area, with the emergence of periodontal pathogens is a necessary, but
often insufficient, condition for the development of periodontal disease.
Risk factors work to change the susceptibility or resistance of individuals to the disease. It is reasonable to talk of ‘‘eliminating’’
or modifying these risk factors as part of the management of periodontal disease.
Identification of periodontal risk factors has contributed vastly to our understanding of the pathogenesis of periodontitis. This
has opened promising new avenues for periodontal therapy as well as for periodontal disease prevention. However, the
utility of such risk factors to predict disease incidence, progression and treatment outcomes at an individual patient level
remains limited.
In conclusion, it is imperative that the clinician looks beyond the oral cavity for factors of which to potentially recommend
modification in order to help their patients reach their common goal of prevention or management of periodontal disease –
and thereby possibly improve general health as well.
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