Classification and Etiology of Perio Diseases Flashcards

1
Q

What is gingivitis?

A

Inflammation of the Gingiva

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2
Q

Define Periodontitis…

A

Inflammation of the supporting tissues of the teeth. Usually a progressively destructive change leading to loss of bone and periodontal ligament. An extension of inflammation from gingiva into the adjacent bone and ligament.

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3
Q

What are the 8 Classifications of periodontal disease?

A
  • Gingival diseases
  • Chronic periodontitis
  • Aggressive periodontitis
  • Periodontitis as a manifestation of systemic diseases
  • Necrotizing periodontal diseases
  • Abscesses of the periodontium
  • Periodontitis associated with endodontic lesions
  • Developmental or acquired deformities and conditions
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4
Q

Describe dental plaque-induced gingival diseases…

A

Gingivitis associated with dental plaque only
Most common form of gingival diseases
Reversible once treated
Prevalence >90%
Characterized by the presence of clinical signs of inflammation confined to the gingiva

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5
Q

What are gingival diseases modified by medications?

A

Dental plaque-induced gingival diseases

Increasing in prevalence due to the increasing use of:
Anti-convulsant drug (50% of pts)s:
Phenytoin
Calcium channel blocker (25% of its)s:
Nifedipine, verapamil, diltiazem
Immunosuppressive drug (33% of its)s:
Cyclosporin A
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6
Q

What 3 origins contribute to nonplaque-induced gingival lesions?

A
Gingival diseases of:
Bacterial origin
Neisseria gonorrhea, Treponema pallidum
Viral origin
Herpes simplex viruses 1 & 2, Varicella zoster virus
Fungal origin
Candidasis, histoplasmosis
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7
Q

What are traumatic lesions of the gingiva?

A
Nonplaque-induced gingival lesions
Traumatic lesions
Factitial
Toothbrush trauma
Accidental
Damage through minor burns from hot food or drinks
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8
Q

What are 3 classifications of periodontitis?

A

Chronic periodontitis
Aggressive periodontitis
Periodontitis as a manifestation of systemic diseases

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9
Q

Describe Chronic Periodontitis…

A

Associated with plaque and calculus
irreversible
Generally slow to moderate rate of progression
Extent and severity may be increase with host-modifying factors
Diabetes, smoking, and stress

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10
Q

Chronic periodontitis descriptors according tot he AAP update in 2015…

A
Localized
< 30% of sites
Generalized
> 30% of sites
Severity
Slight, moderate, severe
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11
Q

2015 update

A

Generalized chronic periodontitis may be classified as periodontitis without a clear pattern of disease distribution of the affected teeth or >30% of teeth affected
age at detection be considered as a guideline in diagnosing aggressive periodontal diseases. The recommended age of younger than 25 years at the time of detection can be used, along with other diagnostic criteria.

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12
Q

Describe what slight periodontitis is according to the update in 2015?

A
Probing depths...>3 &amp; <5 mm
BOP...Y
Rad bone loss...Up to 15% of root length or
≥ 2mm &amp; ≤3 mm
CAL...1-2mm
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13
Q

Describe what moderate periodontitis is according to the update in 2015?

A

PD…≥5 & <7 mm
BOP…Y
Rad Bone Loss…16-30% or > 3mm & ≤5 mm
CAL…3-4mm

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14
Q

Describe what severe periodontitis is according to the update in 2015?

A

PD…≥7 mm
BOP…Y
Rad Bone Loss…>30% or > 5mm
CAL 5+mm

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15
Q

What is aggressive periodontitis?

A

Rapid attachment loss and bone destruction
Amount of microbial deposits inconsistent with disease severity
Familial aggregation of diseased individuals

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16
Q

Describe Localized Aggressive Periodontitis…

A

Circumpubertal onset
Specific, robust serum antibody response
Localized to first molar or incisor

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17
Q

Describe Generalized Aggressive Periodontitis…

A

Poor serum antibody response

Generalized proximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors

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18
Q

What 2 disease categories make up periodontitis as a manifestation of systemic diseases?

A

Hematologic disorders

Genetic Disease

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19
Q

What are some examples of Perio Hematologic Disorders?

A

Leukemia & Acquired Neutropenia

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20
Q

What are some examples of Perio Genetic Diseases?

A

Cyclic neutropenia, Down syndrome, Leukocyte adhesion deficiency

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21
Q

What are the 2 categories of necrotizing periodontal diseases?

A

Necrotizing ulcerative gingivitis (NUG)

Necrotizing ulcerative periodontitis (NUP)

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22
Q

Describe NUG, what 3 elements constitute a diagnosis?

A
Predisposing factors:
Stress, smoking, poor oral hygiene, &amp; immunosupression
Diagnosis based on three criteria:
1. Interproximal necrosis
2. Pain
3. Bleeding
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23
Q

Describe NUP…

A

Loss of attachment and bone
Ulceration and necrosis of gingival
Rapid destruction and exposure of underlying bone
Spontaneous bleeding and severe pain

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24
Q

What 4 clinical manifestations may come with an abscess?

A
Localized purulent infection
May exhibit one or more of the following:
Gingival swelling
Draining fistula
Pain on percussion
Increased mobility
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25
Common situations that predispose to abscess formation - can you think of 4?
Deep periodontal pockets Incomplete calculus removal Foreign body impaction Repeat antibiotic use
26
What are the 3 Abscesses of the Peridontium?
Gingival Periodontal Pericoronal
27
Describe what a Gingival Abscess is...
Involves interdental or marginal gingival Not associated with a periodontal pocket Typically does not involve the PDL
28
Describe what a Periodontal Abscess is...
Most frequently encountered of the 3 Arises from a preexisting pocket Bacterial etiology
29
Describe what a Pericoronal Abscess is...
Same as periodontal, though around a partially erupted tooth
30
Describe Periodontitis associated with endodontic lesions...
Combined lesions Infections of periapical tissues caused by pulpal death can locally join with separate infections from periodontal pockets
31
Order of TX for combined endo/perio lesions?
The endodontic infection should be controlled before beginning definitive periodontal therapy When regenerative or bone grafting techniques are planned
32
What are 4 categories of Developmental or acquired deformities and conditions?
- Tooth anatomical factors - Mucogingival deformities around teeth - Mucogingival Deformaties on edentulous ridges - Occlusal Trauma
33
What are some examples of tooth anatomical factors that can affect Perio?
cervical enamel projections, enamel pearls, furcation anatomy, tooth positions and proximity
34
What are some characteristics of mucogingival Deformaties around teeth?
Soft tissue recession, lack of keratinized tissue, gingival excess
35
What are some examples of Mucogingival Deformaties on edentulous ridges?
Ridge deficiencies, lack of keratinized tissue, aberrant frenum, muscle position
36
What are the 2 sub groups of occlusal trauma?
Primary | Secondary
37
Primary Etiology?
Microbiological | Host
38
What is secondary etiology
Environmental | Local Factors
39
What is dental plaque?
Primary Factor Organized mass adhering to teeth, prosthesis, and oral surfaces Classified as supragingival and subgingival
40
What is the composition of plaque?
80% water 20% solid Salivary glycoproteins, extracellular polysaccharides, proteins, lipids
41
Describe Supragingival Plaque...
Coronal to gingival margin Forms rapidly Aerobic > anaerobic
42
Describe Subgingival Plaque...
Apical to gingival margin Growth may be influenced by supragingival plaque Anaerobic > aerobic
43
Where does early plaque formation occur faster
In the mandibular arch Molar areas Buccal surfaces of the maxillary teeth Interdental regions compared to strict buccal or oral surfaces Tooth surfaces facing inflamed gingival margins
44
What is a Biofilm?
Organized Structure | Microcolonies of bacterial cells distributed in a shaped matrix or glycocalyx
45
What are the Organic Constituents of a Biofilm?
Polysaccharides, proteins, glycoproteins and lipid material
46
What are the Inorganic Constituents of a Biofilm?
Calcium, phosphorus, and trace minerals | As mineral content increases the plaque mass becomes calcified forming calculus
47
What are some unique features of Biofilm?
Protection-glycocalyx that encloses microbial community Nutrition-matrix is capable of trapping nutrients Quorum sensing-communication between bacteria
48
What are the 4 plaque development phases?
Adherence Lag Phase Rapid Growth Phase Steady State
49
What happens during the adherence phase?
Pellicle formation Glycoprotein Cell surface proteins Initial colonization gram + facultative bacteria
50
What happens during the lag phase?
Shift in genetic expression
51
What happens during the rapid growth phase?
Plaque maturation Co-aggregation/co-adhesion Quorum sensing
52
What happens during the steady state stage?
Internal transfer of nutrients Growth slows Tolerance Resistance
53
What is the Non-specific plaque hypothesis?
Disease results from “elaboration of noxious products by the entire plaque flora” It is not the specific bacterial but the entire microbial community Control of disease depends upon amount of plaque accumulation
54
What is the Specific plaque hypothesis?
Only certain plaque is pathogenic | Pathogenicity depends on presence of or increase in specific microorganisms
55
What factors contribute to bacterial pathogenicity?
Virulence factors Influence attachment Provide protection Provide mechanism for penetration of host tissue Fimbria, capsule, glycocalyx, endotoxin, proteolytic enzymes
56
What type of bacteria are generally found in the Microbiota of periodontal health?
Gram-positive, Streptococcusand Actinomyces
57
What type of bacteria are generally found in Chronic Periodontal disease Microbiota?
Gram-negative, P. gingivalis and T. forsythia
58
What Microbiota are found in Localized Aggressive Periodontitis?
A. actinomycetemcomitans, Eubacterium, A. naeslundii, F. nucleatum, C. rectus
59
What Microbiota are found in Generalized Aggressive Periodontitis?
P. gingivalis, T. forsythia, A. actinomycetemcomitans, Campylobacter species
60
Periodontitist complexes
Blue, Purple, green, yellow, orange, red
61
Red Complex
Porphyromonas gingivalis Tannerella forsythensis Treponema denticola
62
Is there a Genetic Component to chronic periodontitis? If so, what percent?
Heritability for Chronic Perio=50% | IL-1β gene polymorphism
63
What are contributing factors for calculus?
``` Calculus Smoking Diabetes mellitus Age Anatomical factors Other ```
64
What is calculus?
Consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prostheses Classified as supragingival and subgingival Can form in as little as 48 hrs
65
What is Supragingival calculus?
Coronal to gingival margin and visible in the oral cavity Hard with claylike consistency, easily detached from the tooth surface Heterogeneous, filamentous microorganisms Mineralized from Saliva
66
What is Subgingival calculus?
Located below the crest of the marginal gingiva Typically hard and dense, may appear dark brown or greenish black Homogenous, microorganisms are cocci, filaments and rods Mineralied by GCF
67
How does calculus attach to a tooth?
Organic pellicle on enamel Mechanical locking into surface irregularities or undercuts Resorption bays, cemental tears, root gouging/caries Intimate adaptation of calculus to cementum
68
How does one detect calculus clinically?
Probing | 58% of surfaces thought to be clean had calculus (Sherman et al. 1991)
69
Calculus detection radiographically....
Radiographically Sensitivity = 43.8% Specificity = 92.5%
70
What are some stats regarding calculus removal efficacy based on PD?
``` 1-3mm = 83% effective 3-5mm = 39% >5mm = 11% ```
71
How does calculus play a role in dental disease?
Promotes the retention of dental plaque and may increase the rate of plaque formation Porosity can serve as a reservoir for pathogens and can retain noxious bacterial components Delay healing up to 120 days if left on surgically treated teeth
72
Smoking effects on: | Local flora
No differences in bacterial counts between smokers and non-smokers(Preber and Bergstrom 1992) Subjects positive for Aa, Tf, and Pgwas significantly higher in current smokers(Zambon et al. 1996)
73
How does smoking effect vasculature?
Peripheral vasoconstriction | Local ischemia
74
Smoking effects on surgical therapy? Non surgical therapy?
Non-surgical Less favorable pocket depth reduction, less gain in CAL(Preber and Bergstrom 1985; Preber et al. 1995; Grossi et al. 1997) Surgical Less PD reduction and greater attachment loss(Ah et al. 1994)
75
How does smoking effect fibroblasts?
Fibroblast effects Reduction in fibroblast secretion, with dose-dependent inhibition of proliferation(Tipton et al. 1995) Altered attachment of fibroblasts to teeth(Raulin et al. 1988)
76
How does smoking affect PMN?
Decreased mobility and phagocytosis (Kenney et al. 1975)
77
How does smoking effect macrophages?
Decreased functional activity of macrophages
78
What are some general statistics in the US regarding Diabetes?
6-7% of the United States population has diabetes mellitus 40-50% of the people are unaware that they have the disease Blacks and Hispanics have a higher prevalence
79
How does diabetes affect the periodontium?
``` Vascular changes Increased collagen breakdown Altered oral microbial flora Advanced glycogen endproducts (AGEs) Altered gingival crevicular fluid glucose Altered defense mechanisms ```
80
How does diabetes effect periodontal therapy?
Non-surgical No difference in clinical, microbiological and immunological response after 4 months(Christgau et al. 1998) Surgical and maintenance Patients with diabetes respond well to treatment and remain successful with adequate
81
How does controlled vs. non controlled diabetes differ in periodontal treatment? 
The level of control seems to play a role in the level of gingival inflammation and attachment loss (Cohen et al. 1970) Poorly controlled diabetic patients had more gingival bleeding than well to moderately-controlled diabetic patients (Ervasti et al. 1985)
82
Age effects on: Periodontium... 
Decreased cellularity Increased collagen fiber coarseness Decreased collagen turnover Gradual breakdown of the peridontium with age Epithelium becomes thinner Connective tissue becomes denser PDL shows less fiber and cellular content and becomes irregular
83
Age effects on: | Treatment
No difference between healing responses of three age groups <40, 40-49, >49(Lindhe et al. 1985) More frequent recall appointments due to recession and greater amounts of exposed cementum(Robinson 1979)
84
What are Cervical Enamel Projections? What are the 3 grades?
Prevalence 90% of isolated furcation involvements are associated with CEPs Grade 1: Distinct change in the CEJ Grade 2: Enamel projection approaching the furcation Grade 3: Enamel projection extending into the furcation
85
Where are enamel pearls usually found?
Prevalence Most common in the furcation region, particularly on third molars They range in size from small to large with large pearls having underlying dentin and possibly pulp
86
What is an Intermediate bifurcation ridge?
Convex excrescence of cementum that runs longitudinally between the mesial and distal roots of mandibular molars Prevalence Found more frequently on first molars Irregular contours make plaque and calculus removal difficult
87
What 2 teeth typically present with palatoradicular grooves?
Prevalence 8.5% of patients 4.6% (centrals 3.4%, laterals 5.6%) 47% terminated > 5 mm on the root surface
88
How can close root proximity effect periodontal treatment?
Areas of tight root proximity are difficult to treat and more vulnerable to breakdown
89
What age group typically presents with cementum tears?
Prevalence | More common in older patients
90
Accessory canals...
Prevalence Occur in approximately 25-50% of molars Tend to occur more frequently in first molars than second molars(Gutman 1978)
91
What restorative defects can greatly hinder periodontal treatment?
Overhangs Act to extend the sphere of influence of plaque apically Removal should be completed during initial therapy Margin location Biologic width invasion
92
What is Factitial injury?
Self-inflicted injuries can be difficult to diagnose Injuries are produced in a variety of ways Picking the gingiva with a fingernail Improper use of toothpicks or other oral hygiene devices Most often once identified pt can be instructed to avoid the injurious behavior
93
Why have a classification system?
Sets the stage for context for treatment planning Helps in estimating outcomes Communication with colleagues and patients Allows researchers to study the same disease
94
Chronic Periodontal Prevalence
46% of adults over 30 years have chronic periodontitis 8.9% severe chronic periodontitis 37.1% non-severe chronic periodontitis Likelihood of periodontitis increases with age
95
2 Forms of bacteria in Mouth
Planktonic/free flotation | Plaque/biofilm
96
Experimental Gingivitis in Man
``` Gingivitis in 10-21 days Increase quantity of plaque Increased quality of plaque Resolution within seven days of OH Bacterial plaque causes gingivitis Loe 1965 ```
97
Natural History of Periodontitis in Man
``` 480 male Sri Lankan tea laborers No conventional OH or dental care Three subpopulations Rapid progression –8% Moderate progression –81% No progression -11% ```
98
CEP's
28.6% on buccal of mandibular molars 17% on buccal of maxillary molars 90% of isolated mandibular furcation involvements
99
What are the squealae of Marginal ridge discrepancies?
May lead to food impaction Inflammation Bone loss Attachment loss
100
What are signs and symptoms of occlusal trauma?
``` Signs and symptoms of occlusal trauma Occlusal wear Fremitus Widened PDL Local angular defect Furcation bone loss Pain Fractured/chipped teeth ```
101
Define primary occlusal trauma...
Excessive occlusal forces to a tooth or teeth with normal support
102
Define secondary occlusal trauma
Normal or excessive occlusal forces applied to a tooth or teeth with a reduced periodontium
103
traumatogenicocclusion
Any occlusion that produces forces that cause an injury to the attachment apparatus
104
What are some long term complications of Diabetes?
``` Long-term complications Retinopathy Neuropathy Nephropathy Macrovascular disease Altered wound healing Periodontitis ```