Reviewer's Questions Flashcards
Eric: What is bulimia versus anorexia?
Bulimia nervosa: Eat larges amounts of food and then purges
Anorexia: Self-starvation
Eric: Different types of bulimia?
Which one has oral manifestations?
- Purging type: Self-induced vomiting, laxative abuse, diuretics or enemas (oral manifestations)
- Non-purging type: Excessive fasting, extreme dieting, or excessive exercise
Eric: BP of 114/74 is what blood pressure classification according to who?
Normal BP per American Heart Association
Normal: 120/ <80
Elevated: 120-130/<80
Stage 1: 130-139/80-89
Stage : 140+/90+
Hypertensive crisis: 180+/120+
Eric: Mechanism of fluorosis
What level of fluorosis does your patient have?
Excessive fluoride intake during enamel development (birth to 8 years)
- Disruption of ameloblast function (the ameloblasts don’t regulate mineral deposition properly)
- Hypomineralization of enamel (excess protein retention in enamel leading to porosity)
- Increased enamel porosity (retained enamel proteins trap water - leads to white lines)
She has mild - White striations
Eric: Differentiate mild/moderate/severe fluorisis
Mild: White striations or opaque areas
Moderate: More pronounced opacities with surface roughness
Sever: Brown staining, pitting, loss of enamel integrity
Eric: Normal ROM
What does clicking, popping, crepitus, or tenderness on palpation indicate?
40 to 50 mm
Clicking: Disk displacement with reduction (one click as it goes back onto disk)
Popping: Subluxation of the condyle (ligament laxity or joint instability)
Crepitis: Osteoarthritis (cartilage breakdown and bone-on-bone contact)
Tenderness: Capsulitis, synovitis, or myofascial pain)
Eric: Besides esthetic plane, what other planes are used to evaluate esthetics?
E-line (tip of nose to anterior point of chin): Upper lip slightly behind or touching and lower lip slightly behind
Ricketts Esthetic Plane (tip of nose to chin prominence): Upper lip 2 mm behind and lower lip 4 mm behind
Camper’s Plane (parallel to occlusal plane)
S-line (Steiner) - Line from chin to lower border of nose - lip should touch. If ahead, then protrusive and behind is concave
Eric: How did I test her saliva quality and quantity?
Quality: clear, watery - checked via mirror sticking to tongue or difficulty with gauze; patient report of dryness, dehydration
Quantity: Again, mirror stickiness or difficulty with gauze. Unstimulated test after 5 minutes should have .3 to .4 ml saliva
How did you evaluate the CO to MIP slide?
I evaluated the patient’s CO to MIP slide by guiding the mandible into an unstrained centric relation using bimanual manipulation (per Dawson).
Once in CO, I instructed the patient to gently close. It’s hard to
Eric - Who discussed long centric and freedom in centric?
Long centric: Gysi - 1.25
Freedom in Centric: Dawson - Less than 0.5
Achieved through a lingual concavity in maxillary anterior teeth
Eric - Why did you use cavity conditioner?
Why not etch with phosphoric acid?
Removes smear layer and debris for improved bonding
3% alumninum chloride hexahydrate seals dentin tubules
A systematic review showed it improved bond strength
Not phosphoric acid because those encourage hybridization within tubules and formation of resin tags. Glass ionomers react with the phosphate and calcium ions from hydroxyapatite, so you just need superficial cleaning like through PAA.
Besides fluorosis - what about amelogenesis imperfecta.
What is it?
What are the types (4)? Which is most common?
How would you diagnose?
- Amelogenesis imperfecta - Malfunction of proteins in the enamel resulting in abnormal enamel formation
Type 1: Hypoplastic (defective enamel formation - thin enamel and teeth, well mineralized)
Type 2: Hypomaturation (enamel formed/normal thickness - proteins don’t develop right, but it is soft, brittle, and prone to damage)
Type 3: most common Hypocalcified (Enamel formed/normal thickness, but not enough calcium - enamel is chalky and prone to tartar - enamel soft)
Type 4: Hypomaturation-hypoplasia with Taurodontism (teeth are small, thin enamel, large pulp chambers (taurodontism)
Diagnosis: Family history + clinical & radiographic findings + genetic testing
Treatment: Bonding, full coverage restorations,
Besides fluorosis - Dentinogenesis Imperfecta
What are the three types and which is most common?
Inherited disorder the affects dentin
Type 1 (OI-associated) - translucent, opalescent teeth that may appear yellow, brown, or blue-gray
- Teeth are weak/prone to fracture
Type II (Classic) - Most common
- Teeth are translucent, opalescent, blue-gray.
- Pulp chambers may be enlarged, leading to “shell teeth”
Type III (Brandywine)
- Teeth are translucent, opalescent, and often have a dark brown or black hue
- Mainly found in African Americans - dark brown/black hue (southern Maryland)
Driscoll: How can anti-anxiety and anti-depressants affect the patient? (4)
What are the types of drugs?
- Xerostomia, altered taste, bruxism, oral bleeding
- SSRI and Tricyclic antidepressants
Driscoll: How does Estradiol affect the patient in terms of oral health?
Can promote wound healing but also can lead to inflammation
Driscoll: What does flattening of the condyle indicate?
Degenerative joint disease (osteoarthritis)
Temporomandibular disorders
Condylar Remodeling
Condylar Resorption
Patrick: Wetselaar/Lobbezoo TWES
Treatment Module: Primary criteria:
- Grade 0/1 indicates what when it’s on what surfaces?
- Grade 2 indicates what when it’s on what surfaces?
- Grade 3/4 indicates what when it’s on what surfaces?
0/1 - Occlusion/articulation surfaces or non-occlusal: Counseling/preventive measures/monitoring
2: Non-occlusal/non incisal surface: Treatment must be considered
3/4: Occlusion/articulation surface: Treatment must be considered
Patrick: Wetselaar/Lobbezoo TWES
Secondary criteria (3) for treatment?
- Speed of tooth wear process (slow: Monitor / fast: restore)
- Age (younger the patient, sooner you treat
- Etiological factors (the more and more difficult to eliminate, you should treat)
Patrick: Wetselaar/Lobbezoo TWES
Quanitification module:
What is the 5 point scale used for occlusal and incisal grading?
What about the palatal?
Difference between this system and the Basic Erosive Wear Examination?
0: No (visible) wear
1: Visible wear w/in enamel
2: Visible wear w/ dentin exposure and loss of clinical crown height <1/3
3: Loss of clinical crown height 1/3 < x < 2/3
- Loss of clinical crown height >2/3
Palatal:
0: No wear
1: Wear in enamel only
2: Wear w/ exposed dentin
Difference: TWES isn’t summated, but BEWE is
Patrick: TWES
What modules are in the TWES? (9)
- Qualification
2: Quantification, screening module (each sextant + max ant palate gets one score)
- Quantification: Clinical crown length (quick/easy to do)
- Quantification, finer-grained measurements (each individual tooth - 8 point scale for incisal/occlusal and 3 point for non-occlusal)
- Questionaires
- Salivary analysis
- Treatment - complaints of patient versus clinical reasons
- Treatment - When to start treatment (Amount of wear, which teeth, number of teeth; Speed of wear, age, etiological factors)
- Level of difficulty
Patrick: Tooth Wear Evaluation System
Clinical signs of erosion (10)
- Occlusal cupping, incisal grooving/cratering, rounding of cusps and grooves
- Wear on non-occluding surfaces
- Raised restorations
- Broad concavities within smooth surface enamel, convex areas flatten, or concavities become present
- Increased incisal translucency
- Clean, non-tarnished appearance of amalgams
- Presentation of enamel “cuff” in gingival crevice
- No plaque, discoloration, or tartar
- Hypersensitivity
- Smooth silky-shining, silky-glazed appearance, sometimes dull surface
Patrick: Tooth Wear Evaluation System (TWES) by Wetselaar & Lobbezoo
Clinical signs of attrition (5)
Clinical signs of abrasion (3)
AT1: Shiny facets, flat and glossy
2: Enamel and dentin wear at same rate
3. Matching wear on occluding surfaces
4. Possible fracture of cusps/restorations
5. Impressions in cheek, tongue, and/or lip
AB1: Usually at cervical areas of teeth
2. Lesions are more wide than deep
3. Premolars and cuspids affected
Patrick: What classification systems exist for Tooth Wear?
- Verrett
- Smith & Knight Tooth Wear Index
- Basic Erosive Wear Examination (Barlett 2008)
- Tooth Wear Evaluation System (Peter Wetsalaar and Lobbezoo 2017))
Patrick: What amount of wear for the molar and premolars is thought to be physiological a year?
Molars: 29 um/year
Premolars: 15 um/year
1989 article by Lambrechts on Quantitiave in vivo wear of human enamel
Patrick: Basic Erosive Wear Exam (Barlett)
- What’s the four point criteria breakdown for erosive wear?
- Why isn’t dentin clearly mentioned in the breakdown?
- What are the risk level breakdowns? At which risk level were restorations acceptable?
0: No erosive wear
1: Initial loss of surface texture
2: Distinct defect, hard tissue loss <50% of surface area
3: Hard tissue loss >50%
*Dentin often involved in 2/3
- Authors argue differentiating enamel/dentin loss is difficult.
- Risk:
None: 0-2
Low: 3-8
Medium: 9-13
High: 14+ (avoid restorations, but cases of severe progression may consider special care that may involve restorations)
Patrick: Bruxism definition article
Why should bruxism not be labeled purely as “parafunction”?
There are positive roles too:
- Prevent upper airway collapse during sleep and thereby obstructive sleep apnea.
Shane: What does aluminum oxide do to zirconia?
It cleans and roughens the surface to increase surface energy and wettability - enhancing the micro mechanical
Shane: What is tertiary dentin?
What is secondary dentin? When is it produced? How is it distinguished from 1º dentin?
It is reparative dentin secreted by odotonblast-like cells subject to strong stimuli like trauma or caries.
2º: Dentin produced after root completion. Slower and more intermittent deposition of dentin throughout life. Results in reduction of pulp chamber size. Distinguished from primary dentin by random arrangement and reduction of dentinal tubules.
Shane: How did you assess the teritary dentin and why did you leave it?
I assessed with my explorer, spoon, and caries detecting solution.
I choose to leave it as it was not soft or leathery, it was away from the enamel and primary dentin at the margin, and I could seal the tooth properly with an indirect restoration. Saw no need to remove further material, risk opening an entry way into the obturation and risk compromising the obturation.
Shane: Per Schwendicke, what are the three groups of caries removal:
- Non-selective caries removal (to hard dentin)
- Selective cases removal (to firm or soft dentin)
- Stepwise caries removal (in two visits)
Shane: Caries detector die
- How does it work?
- Does it differentiate between infected and affected dentin?
- Any concern about carcinogens?
- It is the sole means to determine presence of caries?
- The agents (made from acid red 52 solution in a propylene glycol base) reliably stain only the dentin that is infected with bacteria and irreversibly demineralized. They stain the collagen fibers exposed by the bacteria during the demineralization process. They do not stain bacteria.
- In a way - They stain the organic matrix of less mineralized dentin or loose/degraded collagen.
- Yes, we don’t use fuchsin solution anymore because of that.
- No, optical assessment and tactile feel are key as dye staining and bacterial penetration are independent phenoma.
Shane: Caries Detecting Dye - if you get a false positive, where is it commonly observed?
What about the “intensity” of the stain?
False positives ae observed at the DEJ and circumpulpal dentin due to their change in collagen levels.
Darker, intense stains can be removed and leaving the lightly stained areas.
Shane: What causes bilateral linea alba?
What are differentials?
Chronic friction or pressure from teeth against the buccal mucosa. It’s a thickening of the oral mucosa.
Leukoplakia, hairy leukoplakia (from viral )
Shane: What is the process of gingival inflammation:
- At 2-4 days (initial lesion)?
- 4 to 7 days (early lesion)?
- 2 to 3 weeks (established lesion)
- Advanced lesions (variable timeframe)
- 2-4 days: Bacteria accumulate in gingival sulcus and inflammatory response occurs (increase blood flow, fluid, neutrophils)
- Early signs of gingival redness (increased blood flow, breakdown of collagen fibers)
- Redness, swelling, bleeding upon probing, further breakdown of collagen fibers. Junctional epithelium may migrate apically to form deepened sulcus.
- Progression into periodontitis (irreversible damage of periodontal tissues)
Shane: Is there any change in shear bond strength for zirconia when bonding to dentin with resin or RMGI?
Yes, one paper showed resin cements achieved 6 MPa (Panavia) and 4.79 (RelyX) versus 1.6 MPa for Fujicem
Shane: Why do you think it’s minor salivary gland?
What differential besides minor salivary glands?
- No minor glands on anterior hard palate. Punch biopsy confirmed inflamed salivary gland.
Telangiectasia (small red blood vessels - much more red)
Palatal petechiae from: strep throat, infectious mono, viral infections or bacterial infections.
Trauma
GERD reflux irritation
Irritation from smoking
Patrick: Is air particle abrasion necessary for zirconia bonding?
Does particle size matter?
What bond strength of zirconia relative to lithium disilicate?
- 2015 study by Pereira found APA had two fold increase in bond
- Some articles say particle size does not matter
- Relative bond strength is 39 to 65% that of lithium disilicate
Why zirconia and not lithium disilicate?
- High flexural strength (900-1200+ MPa versus 300-500 MPa)
- Fracture resistance ( 5-10 MPa·m½ versus 2-3.5 MPa·m½(
- Can be more conservative with reduction
- Zirconia is very tissue friendly and biocompatible
- Ease to fabricate and ability to replicate intimate details due to 23% shrinkage
Shane: What does GERD do in the short term (8) and long term to the throat (9) and palate (3)?
Short term: Inflammation, irritation, sore throat, sour/bitter taste, globus sensation, increased saliva, scratches of throat, gag reflex changes
Long Term Throat: Inflammation, tissue damage or ulceration, vocal cord issues, difficulty swallowing, increased mucus production, dental problems, risk of Barrett’s esophagus, swollen parotid glands, esophageal cancer
Long Term Palate: Irritation/redness, sores, altered taste perception
Shane: Difference between affected and infected dentin
Affected: Hard, leathery, resists removal with spoon, may be demineralized
Infected: Soft, demineralized, easily deformed, carious
