3/4: Etiology/Classification & Epidemiology of Periodontal Disease Flashcards
What TYPE of Gingivitis? Endocrine: Puberty, Pregnancy, Diabetes
Plaque-induced gingivitis-systemic factors
What TYPE of Gingivitis? Blood Dyscrasias - Leukemia
Plaque-induced gingivitis-systemic factors
What TYPE of Gingivitis? Drug Influenced Gingival Enlargements Anti-seizure medications-Dilantin Calcium channel blockers-Nifedipine Immunosuppressents-Cyclosporin
Plaque-Induced gingivitis-medications
What TYPE of Gingivitis? Drug-Influenced Gingivitis Oral contraceptives
Plaque-Induced gingivitis-medications
What are the 4 reasons for Plaque-incduced gingivitis?
- Dental Plaque 2.Modified Systemic Factors 3.Modified Medications 4.Modified Malnutrition
What TYPE of Gingivitis? Vitamin deficiencies, Scorbutic gingivitis “Scurvy”, Rare in the United States
Plaque-Induced gingivitis-malnutrition
What TYPE of Gingivitis? Specific Bacterial Origin, Viral Origin, Fungal Origin, Genetic Origin, Manifestation of Systemic Disease, Traumatic Lesions, Foreign Body Reactions
NON-plaque induced gingival diseases
What are the 7 causes of NON-plaque induced Gingivitis?
1.Specific Bacterial Origin 2.Viral Origin 3.Fungal Origin, 4.Genetic Origin 5.Manifestation of Systemic Disease, 6.Traumatic Lesions 7.Foreign Body Reactions
BIG QUESTION: What are the 3 medications (and what do they do?) involved in gingival overgrowth??
- Di-LAN-tin: anti-seizure 2.Ni-fed-i-pine:Calcium Channel Blocker (hypertension) 3.Cyclo-sporin (immunosuppressent-organ transplantaion)
What am I??? Before the disease manifests itself, the
pt has a factor that puts them at greater risk for
developing the disease.
Risk Factors
________ factors are risk factors that lower the probability of an event occuring.
Protective
______: The LIKELIHOOD a person will get a disease in a specified time period
Risk
_______: PROCESS of predicting an individual’s probability of disease.
Risk Assesment
Please name 5 bugs most associated with periodontitis.(YOU better start with the Rojo Complex!)
*1.Tannerella Forsythia *2. Porphomonas Gingivalis *3.Treponema Denticola 4.Aggregatibacter Actinomycetemcomitans 5.Prevotella intermedia
______: Bacterial populations adherent to each other or to surfaces and enclosed in a matrix.
Biofilm
Biofilm: Microorganisms in biofilm are resistant to ______, ___________ and the _________.
antibiotics, antimicrobials and the HOST RESPONSE!
Tooth Associated Subgingival Plaque: _______ adherent, biofilm
Densley
Tooth Associated Subgingival Plaque: G___ rods, cocci, filaments
G+
Tooth Associated Subgingival Plaque: Remove by ____, ____ virulent
S&RP….Less virulent
Tissue Associated Subgingival Plaque: ______ adherent.
Loosely adherent
Tissue Associated Subgingival Plaque: G__ motile anaerobes
G-
Tissue Associated Subgingival Plaque: Main type of bacterium-______… you have to remove by _______…it is _____ virulent
Spirochetes…remove by surgery…more virulent
Unattached Subgingival Plaque: “Free ______ ” in pocket
swimming
Unattached Subgingival Plaque: G___ motile anaerobes…type______
G-…Spirochetes
Unattached Subgingival Plaque: Remove by ______
Remove by flushing
Unattached Subgingival Plaque: ____ virulent
more!
HEALT—–>DISEASE: From G___ —–> G____….From _____ to ____ (& later spirochetes)……From ______ (movement) to _____(movement)……From _______ (Oxygen type) to________ (oxygen type)!!
From G+ to G-…….From cocci to rods (later spirochetes)…….From non-motile to motile……From facultative to obligate anaerobes
Calculus: Induces _______ to the tissues because it harbors bacterial plaque.
damage
Calculus: The _________ in calculus is greatly increased when compared to the tooth surface because of its surface roughness.
SURFACE AREA!!
Calculus: With increased surface roughness there is increased bacterial ______.
DENSITY
Calculus: “Mechanical _________” from calculus does NOT occur!!
irritation
What are the 5 important immune cells that show up for perio?
1.PMNs 2.Mast Cells 3.Macrophage 4.T-Lymphocytes 5.B-Lymphocytes
_______ – 1st responder, migrates into sulcus / pocket
PMNs – 1st responder, migrates into sulcus / pocket
________– releases amines, increases vascular permeability
Mast Cell – releases amines, increases vascular permeability
_________ – present antigen to T-cells
Macrophage – present antigen to T-cells
_________– lymphokines and delayed
hypersensitivity
T-lymphocytes
__________–may differentiate into plasma cells – active in antibody formation
B-lymphocytes–maydifferentiateintoplasma cells – active in antibody formation
PAGE & SCHRODER GRAFTS!!! Intial Stage: ____clinical, no ______, _______ flow of gingival crevicular flow
SUBclinical…NO GINGIVITIS(you got that wrong, idiot)….INCREASED
PAGE & SCHRODER GRAFTS!!! Which Stage: Acute inflammation: Vasculitis, PMNs, Macrophages
Initial
PAGE & SCHRODER GRAFTS!!! How long is the INITIAL stage?
2 -4 days
PAGE & SCHRODER GRAFTS!!! Early Stage: Clinical signs of ________: Redness, bleeding, edema
GINGIVITS (you got that wrong, idiot)
PAGE & SCHRODER GRAFTS!!! Which Stage: T-cell lesion
Early
PAGE & SCHRODER GRAFTS!!! How long is the EARLY stage?
4-7 days
PAGE & SCHRODER GRAFTS!!! Which stage: Chronic gingivitis
Established
PAGE & SCHRODER GRAFTS!!! Which stage: B-cell lesion: Plasma Cells
Established
PAGE & SCHRODER GRAFTS!!! How long is the ESTABLISHED stage?
2-3 weeks
PAGE & SCHRODER GRAFTS!!! Which Stage: Periodontitis
ADVANCED
PAGE & SCHRODER GRAFTS!!! Which Stage: Alveolar bone loss, pocket formation, B-cell lesion
ADVANCED
PAGE & SCHRODER GRAFTS!!! How long does it take to reach the advanced stage?
UNDETERMINED!
What are the three important Cytokines?
IL-1ß….MMP (1&8)…..TNF-alpha
Cytokine: bone resorption
IL-1Beta
Cytokine: connective tissue breakdown
MMP (1&8)
Cytokine: bone resorption (with PGE2)
TNFalpha
________ DECREASES the clinical expression
of inflammation.
Smoking
Smokers have _____ clinical inflammation than non-smokers with similar local factors.
LESS
Current Smokers= ___ times as much periodontal disease
4X
Is the damage caused by smoking reversible?
Yes
Smoking and Microbiology: ____ effect – rate of plaque accumulation….._______ pathogens in shallow pockets…… ________ pathogens in deep pockets….. Mixed results on _______ microorganisms

NO effect….INCREASES….increases…..specific
Smoking and Immunology: _______ Immune response to challenge….._______ PMN chemotaxis and phagocytosis….. ________ TNF-ά, PGE2, MMP-8
Decreased…..decreased….increased
Smoking Effects on Recurrent disease: Periodontitis either _______ or never ______Refractory….Consider addition of ________ to treatment…. Overall, more ______ loss in smokers

Comes back (Recurrent)…..goes away (refractory)…..antibiotics…tooth
______ such as collagenase produce collagen breakdown………._________: Produce bone resorption……_________: Produce bone resorption
MMPs…..Prostaglandins…osteoclasts
What are the three ways we can modify host response?
1.Systemic TetraCyclene to decrease MMPs 2.Systemic NSAIDS to reduce Prostaglandins 3.Systemic Bisphosphanates—reduce osteoclasts
What is the most important DATA we collect on a Perio exam? What DATA is going to tell us an increase in disease?
CAL…increase in CAL/probing depths
What is the Primary Etiologic Fator for PerioDiesase? (2 factors please)
PLAQUE! & a susceptible host
Diagnosis Extent: _______ when ≤ 30% of sites involved.
Localized
Diagnosis Extent: ________ when >30% of sites involved.
Generalized
Diagnosis Severity: Slight = ___ or ____ mm CAL
1 or 2 mm of CAL
Diagnosis Severity: Moderate = ___ or ___ mm CAL
3 or 4 mm of CAL
Diagnosis Severity: Severe = ____ or more mm CAL
5 mm or more o’ CAL