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Periodontics DH 240

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LO 2. Discuss the initiation and progression of periodontal disease including its local and systemic contributing risk factors.

Analyze common periodontal indices used in the study of periodontal diseases in a population. Analyze epidemiological variables associated with periodontal disease. Explain historical and current theories on the initiation and progression of periodontal disease.

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Epidemiology of periodontal disease

Epidemiology

EPIDEMIOLOGY is the study of health and disease within the total population (rather than an individual) and the risk factors that influence health and disease.

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Risk Factors

Risk factors are characteristics that increase an individuals susceptibility to a disease. Risk factors are associated with a disease but do not necessarily cause the disease.

Examples of Risk Factors


Heredity Gender Physical environment Systemic factors Socioeconomic status Personal behavior

Epidemiologists study periodontal disease:

To determine its occurrence in the population To identify risk factors for periodontal disease

Disease Prevalence

It is the number of all cases of a disease (both old and new) that are identified in a specific population at a given point in time. For example, cancer prevalence is defined as the total number of people living with cancer at any point in time. It includes both people diagnosed with cancer in the past (who are still alive) as well as people recently diagnosed.

Prevalence vs. Incidence

Incidencethe number of new disease cases in a population that occur over a period of time. For example, cancer incidence is the number of new cases of cancer diagnosed in one year.

The prevalence of periodontal disease in the adult population is determined by performing clinical examinations on cross-sections of groups using indices.

Measuring Prevalence of Disease (check your book on page 84, may be tested on)

Examples of commonly used periodontal indices

CPITN

EIBI
GBI GI PSR

Community and periodontal index of treatment needs Eastman interdental bleeding index Gingival bleeding index Gingival index Periodontal screening and recording

Epidemiology and Periodontal Disease

A large percentage of the adult population has


periodontal disease.

Epidemiologic research provides current information about the methods and behaviors successful in

Treating periodontal disease Preventing periodontal disease

Variables Associated with PD


Gender Age Race Educational Level and SES Access to Dental Care

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1) Gender

Males have greater prevalence and severity of PD over females Causal? No more likely due to differences in other variables within the group such as oral hygiene practices, frequency of dental care etc.

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2) Age

Epidemiologic studies have shown that the incidence (number of NEW cases) of periodontal diseases increases with age.
Hypothesized that it is likely the result of cumulative effects of bacterial inflammation of the tissues over many years, or an increase in exposure to other risk factors, rather than a reduction in host resistance as a function of the aging process.

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As an individual lives longer, the chances increase that he or she will be exposed to additional risk factors for periodontal disease such as systemic illness, medications, and stress.

Evidence strongly suggests that periodontal health can be maintained throughout life if local etiologic factors are controlled.

Prevalence of Periodontal Disease in Various Age Groups

3) Race

Minority racial groups (non-Caucasians) have a higher prevalence of periodontal disease. Again causal? No could have genetic links or could be because of the other variables discussed ie: home care, access to care, etc.

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4) Socioeconomic Status and educational level

There is a greater incidence of periodontal disease in individuals with lower levels of income.
Underdeveloped countries have a higher incidence of chronic periodontitis. There is a greater incidence of periodontal disease in individuals with lower levels of education.

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5) Access to Dental Care

Individuals who desire or need dental care may not have access to care. Examples of barriers to dental care include transportation to a dental office and the financial expense of dental care. Is access to dental care an issue in Canada?

Difficulties in Measurement of Periodontal Disease

It is easier to evaluate a population for caries than periodontal disease.


Measuring caries is more objective. Development and disease progression is well known. Development and disease progression involves only the tooth structure.

Evaluation of periodontal disease is less specific. It has many different VARIABLES.

Periodontal disease involves hard and soft tissues. Multiple variables to consider are

Tissue color changes and swelling Loss of bone and supportive structures Degree of bleeding Probing depths

What Research Shows


Periodontal disease is one of the most widespread diseases in adults. Most individuals who have periodontal disease do not know that they have it. Periodontal disease is the leading cause of tooth loss in adults older than age 45 years.

23% of 65-74 year-olds have or have had severe periodontal disease. By age 60-69, less than half of all adults in the US have retained 21 teeth or more.

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Most adults 25 years of age or older have at least 2mm or more attachment loss. Severe periodontitis, with 6mm of attachment loss affects about 14% of adults ages 45 to 54.

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Control and Progression of Periodontal Disease

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Disease control of periodontitis


There, so far, have been 4 different theories on disease control of periodontitis. They are:
1. 2. 3.

4.

The CALCULUS theory. The NON-SPECIFIC plaque theory. The BACTERIAL SPECIFICITY theory. The HOST-BACTERIAL theory.

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1. The CALCULUS theory


Before 1960. Calculus is the primary risk factor, it was a MECHANICAL irritant to the tissue. Professional focus was on removal of calculus,debridement was scheduled every 6 months. Clients were told to brush 3 x daily to remove food particles.

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The Calculus Theory

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2. NON-SPECIFIC plaque theory

1965-1975 BACTERIAL plaque is the primary risk factor that causes periodontitis. All plaque was the same, it was TOO much plaque that caused the disease.
Treatment included professional debridement 2-3x per year and OHI was key Periodontitis was PREVENTABLE with good oral hygiene.
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NON-SPECIFIC plaque theory

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3. SPECIFIC BACTERIAL PLAQUE Theory


1975-1985. All plaque is NOT the same. Certain plaque is PATHOGENIC. Periodontitis results from SPECIFIC bacteria found in plaque that is different in composition from plaque found in health sites. Treatment: prof. debridement 2-3x per year The client was instructed in self-care to control plaque. Again, it was the clients FAULT if disease was not prevented.
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SPECIFIC BACTERIAL PLAQUE Theory

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4. The HOST-BACTERIAL interaction theory (Current Perspective)

It is the interaction of the HOST (client) with the PATHOGENIC bacteria that controls whether or not periodontitis is present. A BACTERIAL infection alone is insufficient to result in periodontitis.

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The HOST RESPONSE plays a critical role in the tissue destruction seen in periodontitis.

Some clients are at more risk than others.


RISK FACTORS (things that increase host susceptibility to perio disease) include local oral conditions, habits, systemic disease, and genetic factors.

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TREATMENT today consists of managing the BACTERIAL, LOCAL, and SYSTEMIC risk factors for periodontal disease. MAINTENANCE appointments are scheduled as frequently as needed to assist the client in controlling disease.

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TREATMENT not only consists of periodontal debridement of root surfaces and the pocket environment, but also
Antimicrobial therapy to reduce the bacterial load in the pocket. This therapy includes: antimicrobial mouthwashes, oral antibiotics, and controlled release local delivery drug devices.

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Also, when needed, referral to a physician for management of systemic disease. Client NEEDS to be educated about the role of bacterial plaque in periodontal disease and in plaque control techniques. The client is NOT at fault for their failure to control the disease, instead, risk factors are identified and eliminated or controlled whenever possible.

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The HOST-BACTERIAL interaction theory

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As we see periodontal diseases have many factors that contribute to its cause and progression!

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Progression of Periodontitis
It varies from: One individual to another. One site to another in the same persons mouth. One type of periodontal disease to another. There have been different theories too!

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1 . CONTINUOUS disease progression theory (historical, not believed anymore):


1.

2.

3.

states that periodontal disease progresses throughout the mouth in a slow and constant rate over the adult life of the client. All cases of untreated gingivitis lead to periodontitis. All cases of periodontitis progress at a slow and steady rate of tissue destruction.

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2. Intermittent Progression Theories


1. Periodontal disease is characterized by periods of disease activity (exacerbation) and inactivity (remission). 2. Tissue destruction is sporadic, with short periods of tissue destruction alternating with periods of disease inactivity. 3. Tissue destruction progresses at different rates throughout the mouth.
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4. Untreated gingivitis does not necessarily progress to periodontitis.

5. Susceptibility from person to person appears to be determined by HOST RESPONSE to periodontal pathogens.
6. The two theories of intermittent progression are: -Burst -Asynchronous Multiple Burst
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- Random Burst Theory:

This theory suggests that clients experience short periods of tissue destruction of about 4-7 months alternating with short periods of disease inactivity lasting for 4-7 months.

Occurring at RANDOM times and at RANDOM sites in the mouth. It is possible that some sites in the mouth have worsening bone loss while other sites remain the same.
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- Asynchronous Multiple Bursts theory:

1.

2.

This theory suggests that MULTIPLE bursts of disease activity occur over short periods of time followed by an indefinite period of remission. Most of the tissue destruction happens during a period of a few years.

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Implications

How does our understanding of the progression of PD affect the way we treat PDs?

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Etiology of periodontal disease

Multifactorial Etiology

ETIOLOGY is the study of ALL factors that may be involved in the development of a disease, including the nature of the disease agent, susceptibility of the client, and the way in which the agent invades the clients body. Multifactorial results from the interaction of many factors

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Multifactorial Etiology

Periodontitis has a MULTI-FACTORIAL etiology.


Risk Factors for Periodontitis:
1. 2. 3. 4.

Dental Plaque Biofilm (Primary risk factor) Host Response to Bacteria Local Contributing Factors Systemic Contributing Risk Factors

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Well discuss the 4 factors but with emphasis on local and systemic factors right now.

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1. Primary Risk Factor


Periodontal disease is a BACTERIAL INFECTION. BACTERIA need to be present for periodontal disease to occur. BACTERIA is a PRIMARY ETIOLOGICAL factor.

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2. Host Response

The way the body reacts to the pathogenic bacteria is the host response Complex interaction Later on we will get further into this risk factor. (biofilm and host response)

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3. Local Contributing Factors

local nearby in the mouth

Oral conditions that increase an individuals susceptibility to periodontal infection in specific sites. They do NOT initiate perio disease
Dental team should recognize in order to eliminate or minimize them.

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How do local contributing risk factors contribute to the disease process?

3 mechanisms of action:
A. B. C.

Increase plaque retention Increase plaque pathogenicity Cause direct damage to the periodontium

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A. Factors that increase plaque retention

Most often these decrease the effectiveness of self-care. Include:


Calculus Tooth morphology

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-Dental Calculus

Covered on its external surface by non-mineralized, living bacterial plaque Effects on the periodontium:

Irregular surface harbors plaque Creates ledges that are difficult or impossible for the client to self-clean

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-Tooth Morphology

Includes:

Overhanging restorations retains plaque and it difficult for the client to clean Untreated tooth decay the untreated defect acts as a harbor for plaque growth Tooth grooves or concavities on enamel or root surfaces naturally occurring.

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B. Factors that increase plaque pathogenicity:

Discussing the quality of the plaque not the quantity Mature plaque the older the plaque the more pathogenic the bacteria (we will discuss this in greater detail when we cover Biofilm) Genetics some people have more pathogenic bacteria than others.

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C. Factors that cause direct damage to the periodontium:

Includes:

Occlusal trauma Food impaction Patient habits (factitious) Faulty restorations or appliances

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-Occlusal Forces

Functional normal forces produced during mastication Parafunctional results from tooth-to-tooth contact when NOT eating (ie bruxing or clenching)

Treatment can include fabrication of an appliance or occlusal equilibration (adjustment)

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-Occlusal trauma

Occurs when excessive occlusal forces cause damage to the periodontium Can cause bone resorption allowing more rapid destruction of perio tissues in existing perio disease. Signs and Symptoms:

Clinical tooth mobility, pressure sensitivity, migration Radiographic widened PDL space, bone resorption

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-Food Impaction

Repeated food impaction can alter the gingival contour resulting in open embrassures that then lead to more food and/or plaque retention. Can be the result of restorations sometimes can be corrected with restorations.

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-Patient Habits

Tongue Thrusting (can cause excessive lateral pressure on the periodontium) Mouth Breathing (dries out the tissue) Improper use of dental aids (ie toothpicks)

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-Faulty Restorations or Appliances

Crown margins when placed too close to the crest of the bone it is called _________? Bulky crowns can encroach on the interdental space and cause damage to the papilla. Partial Denture clasps can impinge on the gingiva and retain plaque.

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4. Systemic Contributing Risk Factors

Increase the hosts susceptibility or amplify the host response to periodontal disease Include:
I. II. III. IV.

Tobacco use Diabetes mellitus Osteoporosis Hormone alteration medications

V. Stress VI. Genetic influences VII. AIDS VIII. Systemic

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I. Tobacco Use

One of the most important RFs in development AND progression of perio. Smokers are 2.6 - 6 times more likely to exhibit periodontal destruction 12-14 times more likely to have SEVERE attachment loss Smokers have more pathogenic bacteria present in their plaque biofilms AND form more calculus due the oral environment.
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Tobacco Use

Gingival inflammation and bleeding are often reduced or absent (heat and chemicals in cigarettes cause vasoconstriction) do NOT interpret as tissue health Studies show that due the importance of tobacco use as a risk factor for perio disease that for smokers, tobacco cessation counseling may prevent more perio disease than traditional OHI would. Healing is severely impeded with smokers perio treatment (surgical or non-surgical) will not be nearly as effective as for non-smokers.
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Effects of Smoking on Prevalence and Severity of Periodontal Disease

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II. Diabetes Mellitus

3 types

Type 1 insulin dependant 5-10% Type 2 adult onset 90-95% diet, exercise, medication/insulin controlled Gestational Diabetes only during pregnancy affects approx. 4% of pregnancies Burning tongue Xerostomia Candidiasis

Oral manifestations:

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Diabetes Mellitus

Only undiagnosed or poorly controlled diabetes is a risk factor for perio disease. Uncontrolled sugar levels can lead to increased sugar content in GC fluid bacteria feed on sugar. General immune/healing problems associated with uncontrolled diabetes would adversely affect the host response.

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Periodontal Disease and Diabetes


Elevated blood sugar levels suppress the hosts immune response and results in: Poor wound healing Susceptibility to recurrent infections

Periodontal disease is often considered the 6th complication of diabetes and may place the individual at risk for future diabetic complications

*From The Amer Acad of Periodontology, pamphlet

III. Osteoporosis

Loss of bone density


Postmenopausal lack of estrogen Long term steroid treatments or marked lack of activity

Can exacerbate bone resorption

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A quick word on Bisphosphonates

Bisphosphonate medications are primarily used to treat cancer (intravenous [IV] administration) and osteoporosis (oral administration). They act by inhibiting osteoclastic activity, which leads to less bone resorption, less bone remodeling, and less bone turnover. In the treatment of osteoporosis, the goal is to harness osteoclastic activity to minimize or prevent bone loss and in many cases, to increase bone mass by creating an advantage for osteoblastic activity. There is an association between bisphosphonates and osteonecrosis of the jaws in some patients.
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Osteonecrosis presents as exposed alveolar bone occurring spontaneously or after a dental procedure. The sites may be painful with surrounding soft tissue induration and inflammation. Infection with drainage may be present.

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IV. Hormone Alteration


Most obviously in puberty, pregnancy and menopause. Strong hormone fluctuations can alter the host response to plaque biofilm producing an exagerated inflammatory response. Definitely still a secondary RF (cannot occur in the absence of plaque) Should stress the importance of proper self-care. Menopause can cause decreased hormones and result in xerostomia, altered taste and burning sensations.

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V. Stress (psychosocial)

May be the result of behavior changes:

Poor home care Poor diet Increase in parafunctional habits such as smoking or bruxism.

Stress can also alter the host immune response increasing the susceptibility to periodontal infections.

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VI. Genetics

Could be related to:


Genetically more pathogenic bacteria (Downs Syndrome) Genetically determined immune response Genetically defective immune cells (PMNs)

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VII. AIDS

Immunodeficiency Could include other immunodeficiency diseases (ie: Lupus, or medication induced immunosuppression) High risk of: NUG, NUP and LGE

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VIII. Systemic medications

Possible Effects
1.

2. 3.

Alteration of plaque composition (ie increase sugar or PH) Effect on gingival tissues (ie hyperplasia) Effect on salivary flow (saliva is antimicrobial, reparative, and physically cleansing)

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Cyclosporine-Influenced Gingival Overgrowth

Nutritional Deficiencies

They exacerbate the severity or extent of periodontal disease. Good nutrition results in:

Increased resistance to infection. Strengthened epithelial barrier. Ability to repair damaged tissue.

The lower the calcium intake, the more severe the periodontal disease.

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Summary

Periodontitis has a multifactorial etiology. Bacterial plaque is the primary etiological risk factor, but other risk factors increase a clients susceptibility to periodontal disease. These other risk factors are:

Local risk factors Systemic risk factors

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Scenario

Two individuals who have exactly the same level of plaque control and exactly the same amount of plaque accumulation do not necessarily develop the same severity of periodontal disease. How do you explain this fact?

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Scenario

A new client presents in the office. After initial assessment, the following is noted: The client has poor plaque control, generalized calculus deposits, poorly controlled diabetes, a history of smoking cigarettes, and inadequate dietary intake of calcium. How would you characterize the likelihood that the client will develop periodontitis in the future? What might you tell the client about their situation?

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Review

What are the 4 theories of the etiology of periodontal disease? What are the 3 perspectives on periodontal disease progression?

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Review

What are the 4 main risk factors that make up the MULTIFACTORIAL etiology of periodontal disease? Which one is PRIMARY? What does that mean?

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Review

What does a widened PDL space mean? What could be the cause of a burning tongue sensation? List the adverse affects that smoking has on the periodontium.

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Resources

Nield-Gehrig, Jill S. (2008) Foundations of Periodontics for the Dental Hygienist (2nd ed.). Baltimore, Philadelphia: Lippincott Williams and Wilkins.
Weinberg, Westphal, Froum and Palat (2006). Comprehensive Periodontics for the Dental Hygienist (2nd Edition). Pearson Prentice Hall.

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