Exam2 part 1 Flashcards
Describe phase 1 of the periodontal treatment phases
Phase 1: Initial (soft tissue) Therapy
- Scaling and Root Planing (SRP) - removal of accretions on the root
- Oral Hygiene Instruction (OHI)
When is the re-evaluation done in PD treatment and what is done at this time
4-6 weeks after initial therapy is completed
- Re-collect and analyze data
Describe phase 2 of the PD treatment phases
Phase 2: Surgical Therapy (hard tissue)
- Bony defects
- Grow bone back
What phase occurs during periodontal treatment after re-evaluation or of phase 2 if treatment has been successful
Maintenance phase
Calculation of attached ginigva
- AG=KG - Probing depth OR
2. AG = (GM to MGJ) - Probing depth
Calculation of CAL
CAL = PD + CEJ to GM (+ if apical, - if coronal)
Where does periodontal disease start in the mouth
Starts at most coronal part of interproximal tissue and migrates apically
What cells are found in gingiva
Squamous epithelium Keratinocytes Nonkeratinocytes - Melanocytes - pigment - Langerhan's cells - antigen presenting - Merkel Cells - free nerve endings
Name and define each of the ginigval fibers
Circular: Support & contour to free gingiva
Dentogingival: support of the gingiva
Dentoperiosteal: anchors tooth to bone
Alveologingival: attaches gingiva to alveolar bone
Transseptal: Keeps teeth in alignment and protects bone
What type of tissue characterizes the fiber groups
Type 1 and 3 collagen
Name and define each of the periodontal fibers
Alveolar Crest: Resists lateral movement
Horizontal: Opposes lateral forces
Oblique: absorbs occlusal forces (largest group)
Apical: Resists tipping of the tooth
Interradicular: Resists forces of luxation (pulling out) and tipping
Describe the MGJ (3)
- MGJ does not change, line is permanent
- Line of demarcation between alveolar mucosa and attached gingiva
- MGJ is point at which keratinized and non-keratinized epithelium meet
What is the relationship between smoking and GCF flow
There is immediate transient but marked increase
- Increased crevicular fluid at the smoking event
- Smoking has stunted inflammatory reaction
What is the role of GCF
It is a type of host defense mechanism
Is there a difference in GCF between healthy and unhealthy people
Healthy: Present in small amount
Diseased: Present in larger quantity in people with gingivitis causing tissue to look wet
Describe the composition of GCF
**IgG
Proteins, Ag, Ab (IgG), Enzymes, epithelial cells, leukocytes, electrolytes (K, Ca), Organic comp.
T or F, The GCF flow determines the permeability of the sulcular epithelium
True
What is the normal level of GCF
Normal = 0.43 to 1.56 uL (no gingivitis)
Levels of GCF increase with what 5 things
- Circadian rhythm: from 6 AM to 10 PM
- Inflammation: removes products
- Initial pathogenesis stage –> increase
- Female sex hormones
- Mechanical: chewing gum
- Immediate increase w/ smoking event
How do you test for GCF
Test with filter paper (threads or micropipette) at gingival sulcus and analyzed with Perioton
Is tetracycline higher or lower in GCF than in serum
Higher
Drug induced gingivitis begins where and spreads how?
Starts at interdental papilla extends to facial/lingual margins, can cover root surfaces
T or F, Drug induced gingivitis is only due to plaque specific association
False, may or may not be plaque-associated
What drugs are associated with drug induced gingivitis
- Anti-Convulsants/Anti-seizure (Dilantin)
- Ca Channel blockers (Nifedipine, Diltizen, Verpamil)
- Immunosuppressants (Cyclosporine, Tacrolimus)
- Oral contraceptives
Describe the action of drugs like Dilantin
Stimulates fibroblast proliferation, inactivation of collagenase
- Plaque induced
- Dose response is questionable
Describe action of drugs like Nifedipine, Diltizen, & Verpamil
Increase in cellular production and breakdown??
- Verapamil + cyclosporine given to kidney transplant patients in combination
T or f, Immunosuppresants that are involved in drug-induced gingivitis are dose related
true
Describe the 3 main categories involved in plaque induced disease
- Systemic factors (Endocrine, Blood dyscrasias)
- Drugs
- Malnutrition (Vit. deficiency, Scurvy)
What 5 main categories involved in Non-plaque induced disease
- Microorganism (Bacteria, Virus, Fungal)
- Systemic disease (benign mucous membrane pemphigoid)
- Trauma (toothbrush abrasion)
- Foreign body reactions (popcorn kernal, ortho)
- Genetic (hereditary gingival fibromatosis)
Chronic gingivitis classification:
- localized or generalized
- Severity
Localized: 30% of sites involved
- Diffuse: GM + AG + Papilla
Severity of CAL = soft tissues, bone loss, probing
Slight: 1 or 2 mm CAL
Moderate: 3 to 4 mm CAL
Severe: 5+ mm CAL
When we speak about a percentage of sites being either localized or generalized, what sites are used to count percentage
Each tooth has 6 sites, so, total # of teeth x 6.
Sites= Mesial buccal, Straight buccal, Distal buccal, Distal palate, Straight palate, Mesial palate
T or F, Aggressive gingivitis is most prevalent in adults but can occur in children or adults
False, Chronic gingivitis
Describe clinical presentation of Chronic Gingivitis
Plaque & calculus present
Redness
BOP (bleeding on probing)
T or F, Chronic gingivitis mainly occurs in younger patients who are otherwise healthy
False, Acute/Agressive gingivitis
Describe difference betwen localized and generalized in Acute/Aggressive gingivitis:
Localized: Molars/Incisors
Generalized: Molars/Incisors/and other teeth
What bacteria plays a significant role in Acute/Aggressive gingivitis
A. actinomycetemcomitans
In which race is Acute/Aggressive gingivitis more prevalent
African Americans
Define gingival abscess
A localized purulent infection that involves the marginal gingiva and interdental papilla
Describe the 3 main points of the clinical features of gingival abscesses
- Localized swelling - marginal or interdental
- Red, smooth, shiny surface
- May present purulent exudate (not firm)
Describe the etiology of gingival abscesses
- Bacteria carried into gingival tissue
- Foreign body
- Popcorn hull
- Toothbrush bristle
- Fingernail
- Dental materials
Treatment of gingival abscess
- If fluctuant, establish drainage
- Debridement (removing gross debris)
- Rinse (saline or CHX)
- Follow-up
T or F, Gingival abscesses are not cysts, not encapsulated but tend to cause bone loss and pocket formation
False, All true except that they do not cause bone loss or pocket formation
Clinical features of periodontal abscesses (6)
- Localized purulent inflammation in periodontal tissues
- Dull, constant pain, recent origin
- Edematous, erythematous, smooth, shiny surface
- Discharge of pus with probe or pressure
- Mobility
- Rapid pocket formation
Describe the etiology of periodontal abscess
- Extension from infected pocket
- Incomplete removal of calculus
- Root fracture
- Multiple abscesses
- Think systemic disorder (diabetes, immunosuppression)
Describe microscopically periodontal abscess
Localized accumulation of viable and non-viable PMNs within the pocket wall
Describe microbiologically periodontal abscess
Gram negative MO, fusiforms and spirochetes
Pericoronal (periodontal abscess)
Over a partially erupted tooth (over the crown)
What type of gingivits is pregnancy gingivitis classified as
Plaque induced gingivitis
- Including (prevotella intermedia) - uses steroids as growth factor
How is pregnancy gingivitis distributed throughout the mouth
Marginal and generalized
Prevention of pregnancy associated gingivitis
Plaque control
T or F, pregnancy associated gingivitis causes a decrease in GCF
False, an increase
How long will pregnancy associated gingivitis last
Goes away after pregnancy
Name 4 risk factor for PD
Microbial –> specific organism, total microbial burden, biofilm pathogenicity
Systemic –> diabetes (DM), genetics, sex, race, HIV
Behavioral –> tobacco use, patient compliance
Local –> restorations, tooth anatomy, malocclusion
