Perio Therapy Test 1

Front 1

Systemic Antibiotics in Periodontics

Back 1

-for common forms of gingivitis and periodontitis, ScRP should always be carried out before antibiotics are administered
-development of resistant bacterial strains is a major concern in medicine

Front 2

Main Indications for systemic antibiotics in perio

Back 2

-refractory cases
-aggressive perio -medical conditions
-actue perio infections: perio abscess, NPD: NUG/NUP
-perio regeneration surgeries
-implant dentistry
-post-surgical infections

Front 3

Selection of antibiotics

Back 3

-travels easily to infection site
-concentration in GCF, gingiva and bone
-minimal side effects
-research showing efficacy

Front 4

Penicillin

Back 4

-beta-lactam, first antibiotic used in humans
-broad spectrum
-more than 90% of dose is absorbed
-bactericidal (inhibits synthesis of cell wall)
-useful in initial therapy, abscess, NUG and after periodontal surgery
-low toxicity, allergic reactions
-safe drug in general

Front 5

Tetracycline

Back 5

-most commonly prescribed adjunctiveagent in perio treatment
-broad spectrum/bacteriostatic
-GCF concentration 5-7 times more than serum
-gastrointestinal disturbance
-photosensitivity, discoloration of mucosa
-discoloration of children's teeth
-no mixture with calcium or metal ions
-candida super infection

Front 6

Minocycline

Back 6

-semisynthetic tetracycline

Front 7

Doxycycline

Back 7

-high compliance (single daily dose)
-useful after SCRP in severe perio cases such as aggressive and refractory perio

Front 8

Metronidazole

Back 8

-nitroimidazole, effective against anaerobic bacteria and parasites
-no effect on facultative and aerobic organisms
-side effects: metallic taste, headache, vertigo,peripheral neuritis, no alcohol: intestinal disturbance
-used in NUG/NUP
-used in combination therapy with other antibiotics

Front 9

Clindamycin

Back 9

-lincosamide, usually bacteriostatic
-bactericidal in high doses
-similar to erythromycin in terms of spectrum
-main feature: :bone penetration"
-recommended for patients allergic to penicillin
-side effects: diarrhea and gastric upset, pseudomembranous colitis (rare)

Front 10

Ciprofloxacin

Back 10

-fluoroquinolone
-seems to bebeneficial on refractory cases
-it may be combined with metronidazole
-adverse effects: GI upset, oral candidiasis, photosensitivity

Front 11

Azithromycin

Back 11

-macrolides family
-bacteriostatic
-used for upper and lower respiratory tract infections including oral infections such as periodontitis, perio abscesses and other acute oral infections
-it has better absorption than erythromycin due to high resistance to gastric acids
-achieves high oral soft andhard tissue concentrations

Front 12

Advantages of combination therapy

Back 12

-broadens antimicrobial range of the therapeutic regimen of a single antibiotic
-prevents emergence of resistant bacteria through overlapping antimicrobial mechanisms
-lowers the dose of individual antibiotics by exploiting possible synergy between two drugs

Front 13

Disadvantages of Combination therapy

Back 13

-may increase adverse reactions
-potential for antagonist drug interactions with improperly selected antibiotics

Front 14

CombinationTherapy

Back 14

-do not combine bactericidal with bacteriostatic
-amoxicillin and alvulanic acid-it protects amoxicillin from enzymatic degradation by penicillinase
-augmentin + doxycycline (sequential)
-amoxicillin or augmentin + metronidazole
-ciprofloxacin + metronidazole

Front 15

conclusions on systemic antibiotics

Back 15

-in perio, systemic antibiotics should be an exception rather than the rule
-if indicated, they should be used as adjunct to mechanical therapy
-they should not be used in cases of poor plaque control
-evidence has shown they offer little if any, adjunctive effect on smokers
-considered especially in refractory and aggressive cases of perio. In addition, they should be used in acute conditions and some medical situations
-there is a current trend favoring combined antibiotic therapy (e.g, amoxicillin and metronidazole)
-there is still lack of proper guidelines and decision remains empirical

Front 16

Rationale for using topical antimicrobial agents

Back 16

-pathogens may be unreachable: deep vertical defects, furcation, dentin tubules, biofilm
-sytemic antibiotics: adverse reactions, patient compliance

Front 17

Principles of topical antimicrobial agents

Back 17

local delivery
-pocket irrigation
-drug ointment/gel
-prolonged release

Front 18

Supragingival irrigation

Back 18

-will not reach deeper parts of pocket

Front 19

Subgingival irrigation

Back 19

-washed out rapidly by the GCF
-half-life of a non-binding drug is 1 minute
-levels don't reach the MIC (minimal inhibitory concentration) for oral microorganisms

Front 20

Subgingival irrigation chlrohexidine and tetracycline

Back 20

-high substantivity
-unable to remain in pocket due to flushing of GCF

Front 21

Local delivery device

Back 21

-establish a drug reservoir
-have effective concentration
-be active for prolonged period of time

Front 22

advantagesof controlled-release local delivery

Back 22

-prolonged drug levels within therapeutic range
-minimization of harmful or systemic side effects
-protection of drugs with short in vivo half lives
-improvement of patient compliance

Front 23

perio controlled release delivery: problems

Back 23

-low volume of the prio pocket (.5 microliters) restricts size of the delivery system and total volume of drug-polymer applied
-high turnover rate of crevicular fluid (40 times/hr): participates not only in drug diffusion but also clearance

Front 24

Perio Treatment Summary

Back 24

-data reaffirm the overall effectiveness of ScRP as the standard of care
-evidence consistently demonstrates enhanced clinical improvements with adjunctive antimicrobials in patients with chronic perio: systemic, topical, controlled-release
-clinicians must assess overall patient risks and treatment goals in selecting cases for adjunctive antimicrobial treatment

Front 25

Gingivitis and mild perio

Back 25

-pockets 4-5mm
-are common possibly affecting a majority of the opulation

Front 26

Severe Perio

Back 26

-pockets >/= 6mm
-much less prevalent
-affecting 8% to 15% of adult populations in Western countries

Front 27

Perio disease

Back 27

-is not a natural consequence of aging
-is not necessarily correlated with plaque biofilm levels
-there are patients who are perio disease resistant and there are patients who are perio disease susceptible. Clearly, these two groups react differently to bacterial biofilm.

Front 28

Host Response

Back 28

-plaque bacteria are capable of causing direct damage to the perio tissues (release of H2S, butyric acid,other enzymes and mediators)
-great majority of the destructive events occurring in perio tissues result from activation of destructive processes due to host immune-inflammatory response to plaque bacteria
-the host response is essentially protective by intent but paradoxically can also result in tissue damage, including breakdown of connective tissue fibers in perio ligament and resorption of alveolar bone

Front 29

Host response continued..

Back 29

-the nature of host response to the presence of plaque is modified by genetic factors and systemic and environmental factors
-researchers are now trying to identify genetic traits that characterize individuals as "resistant" or "susceptible"
-researchers are also investigating host modulatory therapies which aim to modify or reduce destructive aspect s of the host response.
-a range of pharmeceuticals will ikely be devloped, targeting diffferent aspects of the host response as adjunctive treatments for perio disease

Front 30

Host modulation therapy

Back 30

-reduce tissue destruction
-stabilize or even regenerate the periodontium by modifying or downregulating destructive aspects of the host response and upregulating protective or regenerative responses
-delivered systemically or locally
-used as adjunct to conventional perio therapy always
-these pharmaceuticals do not "switch off" normal defense mechanisms or inflammation

Front 31

systemically administered agents

Back 31

-NSAIDS
-bisphosphonates
-subantimicrobial-dose doxycycline

Front 32

NSAIDS

Back 32

-inhibit prostaglandins (i.e PGE2) produced by neutrophils, macrophages, fibroblasts, and gingival epithelial cells in response to lipopolysachharide (LPS), a component of the cell wall of G-bacteria. PGE2 upregulates bone resorption by osteoclasts and inhibits fibroblast function
-NSAIDS are used to treat pain, acute and chronic inflammation
-NSAIDS: salicylates, indomethacin, ibuprofen, flurbiprofen and naproxen.

Front 33

NSAIDS continued

Back 33

-clinical studies have shown that NSAIDs significantly slow the rate of alveolar bone loss when compared to placebo
-long-term use of NSAIDs has significant side effects: gastrointestinal problems, hemmorhage, renal and hepatic impairment
-NSAIDs are not recommended for perio disease treatment and/or prevention

Front 34

Bisphosphonates

Back 34

-inhibitbone resorption by disrupting osteoclast activity
-inhibit collagenase
-animal and human studies suport the evidence of reduced alveolar bone resorption when taking this medication
-more recently, this drug has been associated with avascular necrosis of the jaws
-bisphosphonates are not recommended ofr perio disease treatment and/or revention

Front 35

subantimicrobial-dose doxycycline

Back 35

-20mg dose of doxycycline twice daily
-regimen time: 3-9 months
-used as an adjunct to SCRP inchronic perio patients
-inhibits enzymes, cytokines and osteoclasts
-it does not act as an antibiotic or antimicrobial
-it has been approved by the FDA and accepted by the ADA
-clinical studies show a modest but statistically significant effect regarding perio disease progression

Front 36

NSAIDS

Back 36

-topical mouthrinses (i.e. ketorolac) or locally delivered ketoprofenhave been investigated inthe past
-there is no current FDA approved-topical pharmacological agent used for periodontal host modulation

Front 37

Enamel Matrix Proteins (Emdogain), Growth Factors, and Bone Morphogenetic Proteins

Back 37

-surgical adjuncts may improve wound healing, perio regeneration and impact on host response
-the FDA has approved EMdogain as a host modulation agent besides a regenerationagent

Front 38

Periodontal Diseases
(Multifactorial Disease: Periodontal Pathogens, Host, & Environment)

Back 38

Initiation/Progression: Infection primarily by Gram negative anaerobic bacteria

Host Response: Defensive posture- inflammatory & immunologic changes to invading microbes, genetics

Modifying Factors: hygiene, smoking, stress, etc

Front 39

Genetic Factors in Health & Disease

Back 39

-Genetics is believed to play a role in almost every human disease, whether inherited or resulting from the body's response to environmental stresses (ex: viruses or toxins)
-Genetics is also implicated either in the susceptibility to infection or in the severity of the disease

Front 40

Genetic Factors in Health & Disease:
Single gene diseases (Mendelian)

Back 40

-Variations in a single gene are sufficient to cause expression of the disorder
-Predictable, recognizable inheritance patterns (such as autosomal dominant & X-linked recessive)
-Usually clinically evident in childhood
-Only individuals who carry a mutation in the causative gene are at risk for expressing the disorder
-Rare in the general population (Ex: sickle-cell disease, cystic fibrosis, & Duchenne muscular dystrophy)
Gene --> Disease

Front 41

Genetic Factors in Health & Disease:
Multifactorial diseases (Complex diseases)

Back 41

-In contrast, genetic factors alone are not sufficient to cause disease
-->Multifactorial diseases generally do not display the distinct inheritance patterns seen in Mendelian disorders
-Involves complex interactions among multiple genes & environmental factors
-Usually clinically evident later in line
--> Cardiovascular disease, diabetes, cancers, periodontal disease are common in the general population
Genes --> Disease <-- Environment

Front 42

Genetic Markers

Back 42

A genetic marker can be any type of biomolecule or assay that allows us to "read" inherited differences among individuals in their DNA sequences

These regions are said to contain "candidate genes" of high priority for further investigation
-Genes with known biological functions linked to disease
-Or, previous genome-wide surveys indicate strong statistical chances that disease susceptibility genes are located in certain regions of one or more chromosomes (gene function may not be known)

Types of variation include single nucleotide polymorphisms (SNPs)

Front 43

Genome Wide Association Study (GWAS)

Back 43

-Simultaneously investigates genetic variation across the entire genome
~Aim of identifying genetic associations related to a trait or disease of interest
~Has the potential to identify the genetic contributions to common diseases
-Analysis of the entire genome
~Not necessary to correctly guess which candidate genes are most interesting to evaluate
-A GWAS requires inclusion of well-characterized cases & controls study populations
~Large clinical sample sizes are required to reduce the likelihood of differences between cases & are simply due to chance

Front 44

Environment & Ethnicity Influence Susceptibility & Progression of Disease

Back 44

-Localized & generalized forms of aggressive periodontitis occur about 10X more frequently in African American compared to Caucasians
-Human racial & ethnic groups often differ dramatically in frequency of mutations at genes that have major effects on disease risk
~Ex: Cystic fibrosis is caused exclusively by recessive mutations in the CFTR gene
~Varies in frequency from 1 in 3,000 Caucasians to 1 in 15,000 African Americans in the US
~Only 1 in 350,000 Japanese are affected
-The environments of the populations may be dissimilar in important ways & contribute to observed differences could entirely explain the observed difference in frequency of disease between groups
~Variation in diet
~Exposure to pathogenic oral bacteria
-Unknown & unmeasured environmental factors

Front 45

Heritability of Disease: Twin Study

Back 45

All twins (whether identical or nonidentical) are expected to be more similar to their co-twin than to unrelated members of their local population
-However, if genetic variation plays an important role in determining the trait, then genetically identical twin pairs will be more similar to each other than nonidentical twin pairs (identical twins share 100% of the same genes; nonidentical twins share only 50% of their parents' genes)
-Typically raised in the same family environment (similar diet, microbial exposures, etc)

Front 46

Periodontal Findings in Adult Twins

Back 46

-Mean probing depth & attachment level scores were found to vary less in MZ twins reared together than DZ twins reared together.
-Discordance in the disease experience of MZ twins must be caused by environmental determinants as seen in twins reared apart.
-Statistically significant genetic variance was found for both the severity & extent of disease
--> a significant genetic component was identified for PD, attachment loss, & plaque.
-->38-82% of the population variance for periodontal disease may be attributed to genetic factors.

-Study indicates that both genetics & environmental factors influence disease

Front 47

Using Genotype Frequencies to Predict Disease

Back 47

-Genotype frequencies of an inherited DNA variant for a group of periodontitis cases are statistically compared to the frequencies of the variant in a matched group of periodontally healthy control subjects.
-If the genotype frequencies differ so greatly that the results are very unlikely to occur by chance, then we conclude that the genotype that is more common in the cases compared to the controls is "associated" with increased disease risk

Front 48

Using Genotype Frequencies to Predict Disease
(Considerations)

Back 48

-Races & ethnic groups sometimes differ dramatically in genotype frequencies (Historic isolation in different geographic regions & Differences in environment, diet, etc)
-Cases & healthy controls should be "matched" as closely as possible (race, ethnicity, smoking behavior, age, gender, etc)
-When properly controlled, observed differences in genotype frequency are likely to be caused by real biologic effects on disease development or progression rather than as artifacts of some kind.

Front 49

Genetic Factors in Health & Disease
(BRCA1 & BRCA2 and Cancer)

Back 49

-A woman's lifetime risk of developing breast and/or ovarian cancer is greatly increased if she inherits a harmful mutation in BRCA1 or BRCA2
-But, NOT EVERY woman who has a harmful BRCA1 or BRCA2 mutation will develop breast and/or ovarian cancer
-Risk factors: age, BCP, hormone replacement therapy, dietary fat, obesity, alcohol consumption, etc

Front 50

Identification of Shared Genetic Susceptibility Gene for Coronary Heart Disease & Periodontitis

Back 50

-CHD is the leading cause of death worldwide (has a strong genetic basis)
-Similar to perio disease; it is propagated by several environmental & behavioral risk factors (both diseases share smoking as a major environmental risk factor & relate to diabetes mellitus, obesity, & gender)
-Association between presence of CHD & periodontitis, which is dependent on the severity of periodontal disease
-Similarities in the spectrum of bacteria in the oral cavity & in coronary plaques
-Both diseases are characterized by an imbalanced immune reaction & a chronic inflammatory process
-Periodontitis is also associated with elevated C-reactive protein levels (A common genetic risk factor for perio & atherosclerosis)
-These findings indicate a possible mutual genetic basis underlying both diseases

Front 51

Identification of Shared Genetic Susceptibility Gene for Coronary Heart Disease & Periodontitis
(Study Findings)

Back 51

-The study identified a shared associated of the CHD high-risk locus on chromosome 9 with AgP.
--> Mapped to the ANRIL loci
--> ANRIL function not clear
-The study demonstrates that CHD & perio MAY be genetically related by at least 1 susceptibility locus

Front 52

Identifying Genetic Markers in Perio Disease
(IL-1 Genotype)

Back 52

-IL-1 genotype is a strong predictor of severe disease in NON-smoking Caucasians between ages 40-60 with an odds ratio of 18.90.
-In NON-smoking Caucasians, there was a strong association between severity of perio & the composite genotype
-86% of the severe perio subjects were either smokers or were positive for the IL-1 genotype
-Many studies on the IL-1 gene polymorphisms indicate that genetic variation at these loci may be associated with only a modest effect on disease risk
-"Huynh-Ba et al (2007) --> "there is insufficient evidence to establish if a positive IL-1 genotype status contributes to progression of perio and/or treatment outcomes"
-Similar lack of supporting evidence for use of IL-1 genetic testing to predict implant success has also been reported.

Front 53

Genetic Associations
(Limitations)

Back 53

-Most genetic association findings have been drastically underpowered.
-The majority (66%) of these association reports for chronic & aggressive perio are based on samples of 100 cases or less, and 41% are based on less than 60 cases
--> Need Large, Well defined study populations to make a strong conclusion
-With few exceptions, there are just as many or more reports with no significant association was found for the gene as there are positive findings (the negative studies may differ in terms of the racial or ethnic composition of the subjects)
-Different clinical definitions or sources of information
--> Clinical attachment loss vs bone loss measured from radiographs
-->Other various quantitative measures might be employed
-->Apart from small study populations, standardization of study protocol is a problem

Front 54

Genetic Disorders Associated with Periodontal Disease
(Syndromes)

Back 54

A number of extremely rare conditions consistently include periodontitis among the array of clinical manifestations that define a syndrome:
-Down's syndrome
-Chronic granulomatous disease
-Leukocyte adhesion deficiency syndrome
-Pappillon-Lefevre
-Hypophosphotasia
-Ehlers-Danlos syndrome
-Glycogen storage disease 1b
-Cohen's syndrome

However, a number of syndroms, such as fetal alcohol syndrome, are purely environmental in origin

Front 55

Genetic Disorders Associated with Periodontal Disease
(Clinical Manifestations)

Back 55

Clinical manifestations (periodontitis) are caused by mutations in specifric genes
Ex: Mutations in the cathepsin C gene
-Papillon-Lefevre
-Haim-Munk syndromes
-Some forms of nonsyndromic prepubertal periodontitis
-Possibly associated with risk of aggressive periodontitis

Front 56

Genetic Disorders Associated with Periodontal Disease
(Leukocyte Adhesion Deficiency)

Back 56

-CD18 deficiency
-Absent of severely reduced levels of Beta 2 integrin molecule
-Patients suffer from recurrent infections
-Severe periodontal disease

Front 57

Influence of Genetics & Host Factors on Periodontal Disease

Back 57

1 out of 2 adults have had, currently have, or will have some type of perio issue.

Environmental/Host Factors:
-Plaque quantity/composition
-Smoking status
-Oral hygiene
-Systemic health
-Occlusion
-Iatrogenic factors

Front 58

Influence of Genetics & Host Factors on Periodontal Disease
(Plaque)

Back 58

-Although bacterial plaque is essential for the initiation of periodontitis, the amount of plaque does not necessarily correlate with onset of disease or its severity
-Each person has an individual dose-response curve that impacts host susceptibility to periodontitis:
--> Heredity modifications
--> Microbial exposures
--> Attitudes & behaviors
--> Environmental exposures

Front 59

Influence of Genetics & Host Factors on Periodontal Disease
(Environment)

Back 59

-In the majority of cases, it is likely that the development of periodontitis depends on the collective presence of a number of environmental risk factors in conjunction with a number of genetic risk factors at a given time point during life (it's not just hygiene)
-It is important for both clinicians & patients to recognize the influence of genetics, exposures & behaviors on: 1) Disease susceptibility, 2) Progression, & 3) Response to therapy

Front 60

Influence of Genetics & Host Factors on Periodontal Disease
(Genetic Risk Factors)

Back 60

-The more genetic risk factors an individual has inherited, the greater the genetic predisposition & the higher the chance of early development of periodontitis
-Environmental risk factors will influence genetic factors
-However, individual risk factors alone are not typically sufficient to cause disease
-Periodontitis is a multifactorial disease with significant genetic, behavioral & environmental components similar to other chronic diseases

Front 61

Periodontitis Conclusions --> Current Risk Factors Include:

Back 61

1. Etiologic agents/periodontal flora
2. Genetic susceptibility
3. Medical conditions
4. Behavior
5. Access to care
6. Background
7. Exposures (smoking, medication, etc)
-Evaluation of ALL the risk factors significantly enhance the clinician's ability to choose the appropriate intervention at the individual level & make accurate predictions of treatment outcomes.

Front 62

Host Modulation and Comprehensive Perio management

Back 62

-patient needs to well informed
-rationale for using host-modulation must be given
-patient should have ownership of their condition management
i.e. cost, compliance, research data validating its use

Front 63

Periostat

Back 63

-doxycycline
-inhibits connective tissue breakdown
-downregulation of destructive events (like cytokines IL-1,6, and TNF alpha and PGE2)
-inhibits production of reactive oxydations species by PMNs etc.
-reduces osteoclast activity and bone resoption
-blocks osteoclast MMPS
-stimulates osteoblast activity and bone formation

Front 64

Emerging host modulatory therapies

Back 64

-chemically modified tetracyclines
-novel anticytokine drugs (i.e. anti TNF-alpha
-IL-1 receptor antagonists
-Drug combination such as subantimicrobial dose doxycyclineand bisphosphonates (animal studies have shown benefit)

Front 65

Subantimicrobial dose doxycycline

Back 65

-is the ONLY currently approved drug in the US market for periodontal host modulation
-in future, a range of host modulation therapeutic agents may be available to specifically target different aspects of the destructive cascade of breakdown.

Front 66

Etiology of Furcation

Back 66

Primary Factor: Bacterial plaque
Other factors:
-Anatomic: root trunk length, root morphology
-local developmental anomalies: cervical enamel projections
Prevalence and severity of furcation involvement increase with age
Dental caries and pulpal necrosis may affect the furcation area

Front 67

Challenges of furcation

Back 67

-patient cannot maintain a plaque free furcation
-complex anatomic area to be reached during periodontal instrumentation
-furcation involvement leads to less favorable periodontal prognosis

Front 68

Diagnosis & Classification

Back 68

Clinical: Nabers probe (furcation is not always accessible without an open gingival flap)
Radiographic: Radiolucency (not always seen)
Furcation Entrance Dimensions:
-81% with orifice of </= 1mm
-58% with </= .75mm

Front 69

Local Anatomic Factors for furcation

Back 69

-root trunk length
-root length
-root form
-interradicular dimension
-anatomy of furcation
-cervical enamel projections

Front 70

The shorter the root trunk the more likely ...

Back 70

the patient will have furcation

Front 71

Which entrance to furcation is more narrow on a max molar?

Back 71

buccal

Front 72

Whats important about palatal root of max molar?

Back 72

the divergence between it and the other roots leading to a potential wide area for furcation on mesial and distal furcation entrance

Front 73

Root trunk & furcation invasion

Back 73

probing depth & attachment level not always correlate with presence or absence of furcation involvement

Front 74

Root Form & furcation invasion

Back 74

-root form influences furcation involvement

Front 75

Mesial furcation on max molar is measured from

Back 75

from the palatal

Front 76

Max Molars

Back 76

-1st molar has a shorter root trunk than 2nd
-distances between CEJ and furcation entrances are:
Mesial: 3mm
Buccal: 3.5
Distal: 5mm
(3,4,5 is easy to remember)
-buccal furcation entrance is narrower than distal and mesial counterparts
(KNOW THIS ON EXAM)

Front 77

Max Premolars

Back 77

-40% of first max premolars have two root cones
-furcation is usually in the middle or apical third of the root complex
-mean distance from CEJ to the furcation entrance is approximately 8mm
-the width of the furcation entrance is approximately .7mm

Front 78

Mandibular Molars

Back 78

-1st molar has a shorter root trunk than 2nd
-distances between CEJ and furcation entrances are approximately
lingual >4mm
buccal >3mm
-buccal furcation entrance is often <.75mm wide while the lingual entrance is >.75mm in most cases
***average curette = .75-1.1mm

Front 79

Enamel Projections & Pearls

Back 79

-cervical enamel projections (CEPs) are reported to occur on 8.6% to 28.6% of molars
-the prevalence is highest for second molars (mandibular and maxillary)
-these projections can affect plaque removal, can complicate SCRP and may be a local factor in the development of gingivitis and periodontitis
-CEPs should be consider for removal in oder to facilitate periodontal maintenance

Front 80

Classification of Furcation Involvement

Back 80

Degree I- horizontal loss of periodontal support not exceeding 1/3 width of the tooth
Degree II- horizontal loss exceeding 1/3 of the width of the tooth. Not encompassing total width of the furcation area
Degree III- horizontal through and through

Front 81

Treatment of Furcation: Non-surgical

Back 81

-Oral Hygiene Procedures
-Scaling and Root Planing

Front 82

Treatment of furcation: Surgical

Back 82

-Osseous Resection
-Root Resection
-Regeneration
-Hemisection
-Extraction

Front 83

Therapy for Class I Furcation

Back 83

-OHI
-SCRP
-Consider furcation "plasty"

Front 84

Therapy for Class II Furcation

Back 84

-OHI
-SCRP
-consider furcation "plasty"
-periodontal regeneration
-root resection/separation (possible)
-tunnel preparation (possible)
-extraction (possible)

Front 85

Therapy for Class III Furcation

Back 85

-OHI
-SCRP
-Consider furcation "plasty"
-Periodontal regeneration
-root resection/separation
-tunnel preparation
-extraction

Front 86

Prognosis for furcations

Back 86

-furcation problems are not as severe a complication as originally suspected
-caries prevention in the furca is very critical
-teeth with furcation involvement may last longer than expected

Front 87

Keys for Long-Term Success

Back 87

-thorough diagnosis
-selection of patients with overall good compliance
-excellence in non-surgical therapy
-careful surgical and restorative management

Front 88

Factors that Influence Rate and Severity of Perio Disease

Back 88

-Biological Factors (genetics, systemic disease, innate immune response.
-Behavioral Factors: oral hygiene, smoking, stress
-a polymicrobial infection (strain dependent)

Front 89

Perio Disease: Dual Challenge

Back 89

-Bacteria
-Host response

Front 90

Juvenile Periodontitis Types in 1986

Back 90

-Pre-pubertal perio
-localized juvenile perio
-generalized juvenile perio

Front 91

AAP Perio Types in 1986

Back 91

-Juvenile Perio
-Adult Perio
-Necrotizing Ulcerative Gingivo-Perio
-Refractory Perio

Front 92

World Workshop Perio Types 1977

Back 92

-Juvenile Perio
-Chronic Marginal Perio

Front 93

World Workshop 1989 Perio Types

Back 93

-Adult perio
-Early Onset Perio (Pre pubertal perio, Juvenile Perio, Rapidly Progressing Perio)
-Periodontitis Associated with Systemic Disease
Necrotizing Ulcerative Perio
-Refractory Perio

Front 94

International Workshop 1999 Perio Types

Back 94

-Gingival Diseases
-chronic perio
-aggressive perio
-periodontitis as a manifestation of systemic disease
-necrotizing perio diseases
-Abscesses of periodontium
-periodontitis associated with Endo lesions
-Developmental or acquired deformities and conditions

Front 95

Rational for New Classification

Back 95

-Perio diseases are not age dependent: see same diseases in adolescents as seen in adults, see highly destructive disease in >35yr olds
-Cannot define age of onset: juvenile/post juvenile
-all forms of perio can be refractory
-NUG/NUP combined -separate diseases?

Front 96

Periodontal Therapy Methods

Back 96

-Behavioral modificiation
-occlusal therapy
-pre-prosthetic surgery
-perio-systemic relationships
-implant therapy
-perio-plastics
-Host modulation
-Regenerative surgery
-resective therapy
-Antimicrobial therapy
-Scaling and root planing

Front 97

Adjuncts to Mechanical Therapy

Back 97

-Systemic antibiotics
-Local antimicrobial therapy
-Host modulatory therapy

Front 98

Primary Etiology of Perio Disease

Back 98

-PLAQUE!

Front 99

Non-specific Plaque hypothesis

Back 99

-Any bacteria in plaque will cause disease
-This hypothesis is incorrect

Front 100

Specific Plaque Hypothesis

Back 100

- The kind of bacteria populating the plaque is important not just quantity, this hypothesis is about quality of plaque

Front 101

Pathogens of Perio

Back 101

-Actinobacillus actinomycetemcomitans
-Porphyromonas gingivalis
-Prevotella intermedia
-Bacteroides forsythus
-Campylobacter rect
-Treponema Species
-Eikenella corrodens
-Micromonas (Peptosteptococcus) micros
-Fusobacterium nucleatum
-Selemonas species
-Eubacteria species
-Enteric rods and Pseudomonas species

Front 102

Aggressive Perio Localized and Generalized

Back 102

-Clinically healthy
-Rapid bone destruction
-Familial aggregation
* Can spontaneously arrest but also can progress to the generalized form, want to get retrospective radiographs to determine how disease has progressed

Front 103

Aggressive Perio Secondary Features

Back 103

-Microbial deposits not consistent with extent of destruction
-Preponderence of AA (especially in Localized form); elevated P. gingivalis in some populations
-Phagocyte abnormalities
-Hyper-responsive macrophage
-Disease may arrest on its own

Front 104

Localized Aggressive Perio

Back 104

-Puberty
-Robust serum antibody response to infecting agents
-First molars/central incisors (first teeth to erupt and are colonized earlier)
-Preponderance of AA
-Chief complaint of patients will be esthetics of teeth because they are flaring out due to bone loss.

Front 105

A. actinomycetemcomitans virulence factors

Back 105

-surface mannans
-LPS
-Leukotoxin
-Surface vesicles
-Chemotaxis inhibiting factor
-alters lymphocyte function
-catalase production
-fibroblast inhibiting factor
-epitheliotoxin
-collagenase
-bone resorbing factor
-invades epithelial cells
*NOT ALL AA are equal pathogens

Front 106

Host Response in Localized Aggressive Perio

Back 106

-75% dysfunctional neutrophils
-decreased chemotactic response
-Elevated antibodies to AA

Front 107

Generalized Aggressive Perio

Back 107

-Usually <30 years old
-destruction in episodic
-affects at least 3 permanent teeth other than 1st molars/central incisors

Front 108

Host Response in Generalized Aggressive Perio

Back 108

-Poor Serum antibody response
-Diverse microbial pattern; bacteria similar to that associated with chronic perio
-Defects in either neutrophils or monocytes

Front 109

Aggressive Perio: Modifying Factors

Back 109

-Smoking
-Stress
-Drugs
-Hormones

Front 110

Genetics of Localized Aggressive and Generalized Aggressive Perio

Back 110

-Heritable variants of same disorder
-Both forms of the disease frequently occur in the same family

Front 111

Suggested Protocol for Aggressive Perio

Back 111

-Ascertain Family history
-Microbiologic testing
-Home care reviewed
-Scaling and root planing with antibiotics
-Medical consultation/evaluation
-Reevaluation
-Place on short term maintenance (q 2-3 mo) to evaluate further response after initial therapy
-Repeat reevaluation in 6 mo for need for additional active therapy (ie Surgery)

Front 112

Antimicrobials

Back 112

-Topical (rinses and irrigants)
-Local Delivery (fibers, gels, root surface therapy)
-Systemic
-Innate

Front 113

Advantages of Systemic Antibiotics

Back 113

-reaches bacteria deep in pockets
-treats entire mouth vs. site specific (including mucosal tissue, tongue which are both reservoirs and GCF and saliva)
-Supported in literature as beneficial for refractory pts and pts with aggressive perio

Front 114

Bacterial Culture and Antibiotic Sensitivity Testing

Back 114

-Total Cell counts
-Relative proportions of pathogens
-Detects unusual pathogens
-Antibiotic sensitivity testing
-Requires viable organisms
-Costs $120-125

Front 115

Microbial Testing Indications

Back 115

-Aggressive Perio (<35 y/o with rapid bone loss)
-Refractory perio
-Perio complicated by systemic disease (ie: diabetes)

Front 116

Microbial Testing Contraindications

Back 116

-Inactive, clinically stable perio
-Perio health of gingivitis (with exception of family member of aggressive perio patients)

Front 117

Contraindications for Systemic antibiotics

Back 117

-Inactive, clinically stable
-Gingivitis

Front 118

Perio Initial Therapy

Back 118

-ID patients at risk
-aggressive perio pts
-refractory pts
-perio associated with sytemic disease

Front 119

Re-evaluation

Back 119

-test for elimination of pathogens
-poor response to initial therapy in spite of good compliance

Front 120

Surgical Therapy

Back 120

-optimize antibiotics with regeneration

Front 121

Maintenance

Back 121

-test for elimination of pathogens
-suspect recurrence of disease-test for reappearance of pathogens
-suspect refractory disease

Front 122

Patients with Diabetes

Back 122

-adjunctive antibiotics may enhance results of SRP

Front 123

Antibiotics used in tx of Perio

Back 123

-Amoxicillin or Augmentin
-Metronidazole
-Ciprofloxacin
-Azithromycin
-Clindamycin
-Tetracycline or Doxycycline

Front 124

Antibiotic Therapy in Perio

Back 124

-More use of combination therapy: Amoxicillin + Metronidazole
-Want synergistic and not antagonistic, do not use static and cidal together

Front 125

Systemic Antibiotic Side Effects

Back 125

-GI problems
-Superinfections
-Hypersensitivity
-Drug interactions
-Resistance!!

Front 126

Lack of Response to Initial Therapy

Back 126

-Repeat microbial testing
-Evaluate for underlying systemic disorder
-Place on short term maintenance (q 2mo)
-Consider host modulation therapy

Front 127

Refractory Perio Definition

Back 127

-Continued progression of disease in spite of excellent patient compliance and perio therapy which has been successful in most patients
-Can be identified in chronic or aggressive perio pts, can be localized or generalized

Front 128

What is NOT Refractory

Back 128

-incomplete or inadequate conventional therapy
- systemic condition contributing to disease process
-Rapid attachment loss due to non perio modifying factors
-Recurrence of disease after several years of successful maintenance therapy

Front 129

Refractory Perio: Contributing Factors

Back 129

-smoking
-diagnosis of advanced or aggressive disease prior to therapy
-Perio pathogens
-altered host response
-Genetics
-Reduced PMN chemotaxis and phagocytosis
-Altered CD4+, CD8+ cells and or ratio, upregulation of IL-1
-Elevated cytokines in GCF
-Upregulation of genes
-Systemic disease
-Stress

Front 130

Refractory Perio: Suggested Protocol

Back 130

- Short maintenance intervals (every 2 months)
-Controlling risk factors (smoking, home care and stress)
-Local and/or systemic antibiotics (with bacterial sampling)
-Host modulation therapy
-Refractory disease: not a homogeneous group therefore require individualized tx protocols

Front 131

Treatment of Refractory Perio Disease

Back 131

-Scaling and Root planing to decrease biomass
-Local delivery >/= 4mm to decrease bacterial load in pocket
-Systemic antibiotics to decrease bacterial load in oral cavity and invasive bacteria
- Professional supragingival plaque removal weekly for 3 months, control supragingival flora
-maintenance every 3 months
-controlled for 2 years

Front 132

Local Delivery of Antimicrobials

Back 132

-High GCF concentration
-Decreased chance of resistance
-minimal side effects
-patient compliance

Front 133

Reasons for Local Delivery

Back 133

-localized persistence or recurrent PD in chronic perio pts (re-eval and maintenance)
-Adjunct to ScRP
-Refractory sites/pts in combination with systemic antibiotics
-aggressive pts?

Front 134

Local Delivery Contraindications

Back 134

-Replacement for ScRP in initial therapy or maintence
-as replacement for surgery
-in pts with multiple areas requiring tx
-as a substitute for systemic antibiotics but may be used in combo
* Not a replacement when systemic antibiotics are needed, surgery preferred options for generalized and deep PD

Front 135

Surgery indications

Back 135

- PD 5-6mm, with BOP
->1-2 sites per quad or >4-5 sites in mouth
->/= 7mm PD

Front 136

Periostat

Back 136

-20mg doxycycline hyclate
-inhibits collagenase
-anti inflammatory agent
-NOT ANTIMICROBIAL
-adjunct to ScRP and 3 month recall
-when used for 6-9 months with ScRP reduced pockets more than just ScRP alone
-used during maintenance therapy in refractory perio, smokers, severe generalized chronic perio

Front 137

Periostat Precautions

Back 137

-Controlled clinical trials are needed to confirm use in refractory pts
-studies of long term effects have potential for bacterial resistance
-Tx strategies have not been evaluated
*suppression of bacteria and subsequent reduction in host response is still the best way to control perio disease!