case Flashcards

1
Q

Marginal Ridge Discrepancies

A

a. Kepic/O’Leary – no correlation between marginal ridges and poorer perio parameters b. Pihlstrom - (looked at Mx first molars and found that un-even marginal ridges had more CAL (~0.5mm) and deeper PD than teeth w/ even marginal ridges

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2
Q

Male gender

A

Shiau 2010, systematic review and MA. Males have higher prevalence of periodontitis compared to females but not necessarily at greater risk for more rapid periodontal destruction. Sexual dimorphisms exist in immune function, involving both innate and acquired immunity. Men have higher levels of inflammatory cytokines, including interleukin‐1β and tumor necrosis factor‐α, than women, paralleling observed sex‐specific differences in periodontitis. Conclusion: Differential gene regulation, particularly in sex steroid–responsive genes, may contribute to a sexual dimorphism in susceptibility to destructive periodontal disease.

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3
Q

Interproximal plaque removal

A

KEIGER: RCT. proxabrush is more effective at removing interproximal plaque than floss in open interproximal spaces Kotsakis: Interdental brushes & waterjets are the best interproximal OH aid to decrease BOP. Flossing does not substantially decrease inflammation. However, no control over periodontal status (healthy vs reduced perio vs gingivitis)

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4
Q

How do you know that NST decreases inflammation?•

A

Caton: lack of sulcular epithelium ulceration, Less inflammatory infiltrate, More dense CT, Less perivascular edema at 4 weeks Caton developed interdental bleeding index - insert wooden pick interdentally, depressing papilla 1 -2 mm, repeated 4x, presence or absence of bleeding within 15 seconds Good index of epidemiological studies as it has high inter-examiner reliability

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5
Q

give evidence that it’s okay to retain hopeless teeth

A

Machtei - With (OFD), minimal detrimental effects; MT is key Wojcik – Treated and retained hopeless teeth can have no detrimental effect on alveolar bone levels on adjacent teeth at 8 years; MT is key

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6
Q

give evidence that you should EXT hopeless teeth

A

Machtei - Without perio tx, retained hopeless teeth caused 10x greater AL if you don’t treat them Grassi 1987 - Split mouth study involving SCRP and ext of hopeless tooth or retention og hopeless tooth. Found that Following extraction of hopeless teeth, the periodontal status of the adjacent teeth was more greatly improved that the contralateral side. In deep pockets (4-9mm), there was a 1.46mm PD decrease and 0.67mm CAL gain

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7
Q

what do you expect after SCRP

A

HUNG AND DOUGLASS META-ANAYLSIS: 4-6 mm =PD reduction of 1 mm, 0.5 mm CAL gain. 7+ mm = PD reduction of 2 mm, 1 mm CAL gain for deep initial periodontal probing depths

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8
Q

give me evidence that is it worthwhile to do reinstrumentation

A

Magnusson: patients whose hygiene did not drastically improve after first round of SRP showed significant benefits from additional round of SRP 16 weeks after initial instrumentation -Torfason: patients who were re-instrumented 4 weeks after initial therapy showed improved clinical gains compared to control (only instrumented at one visit) Rationale: patients with poor OH that can’t support surgery, initial instrumentation performed below office standard, inadequate response at all sites

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9
Q

why should you not re-instrument?

A

-Anderson 1996: Single episode of SCRP versus 3 rounds of SCRP. Second and third rounds of scaling were 24 hrs later. Residual calculus not removed after one episode of SCRP is not likely to be removed by repeated instrumentations. HOWEVER - THEY DID NOT ALLOW FOR SOFT TISSUE HEALING/SHRINKAGE WHICH MAY IMPROVE. Repeated episodes of SCRP does not eliminate the need for more invasive procedures (surgery). Badersten 1981: In single rooted teeth, a single initial episode of ultrasonic scaling is as effective as three episodes accomplished three months apart in the treatment.

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10
Q

How do you know that you are going to be better at local factor removal with surgery?

A

Caffese SCRP in molars- Brayer looked at single rooted teeth and found similar result)  how many surfaces were calculus free? • 1-3mm: 86% open vs. 86% closed • 4-6mm: 76% open vs. 43% closed • 7+mm: 50% open vs 32% closed

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11
Q

how do you know that an open contact is a local factor

A

Hancock – young male Naval recruits (17-19 yo) without much disease. Significant relationship between open contact and food impaction and food impaction causes increased PD, attachment loss, and BOP Assessed open contact with double strand of unwaxed floss Jernberg – older patient population (mean 43 yo) a) Open contacts/food impaction associated with increased PD (0.27 mm) and AL (0.48 mm) 1. Open contact = floss slipping through during mastication 2. Looked at open contact with contralateral closed contact 3. Food impactions associated with occlusal interferences

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12
Q

tell me about bone sounding

A

a. Ursell: bone sounding vs surgical measurements correlation coefficient 97% with mean 0.29 mm difference b. Mealey: Bone sounding in furcations is accurate within 1 mm 85% of the time. Average difference between bone sounding and surgical measurements was 0.5mm. Bone sounding increase diagnostic accuracy 10% clinical detection of furcation invasion.

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13
Q

buchanan

A

d. Buchanan: Radiographic Calculus – Sens 43%; Spec 92% a) PPV 92%; NPV 46%  Reported in text, Page 3 1. Sensitivity: w disease, how often test confirm presence 2. Specificity: w/o disease, how often test deny presence 3. PPV: test +, how often dx present 4. NPV: test -, how often dx non-present Hyer - a step of calculus greater than 0.5 mm more likely to be seen on radiograph. Greater than 30% of the root surface covered in calculus - more likely to be seen on radiograph. Altering the radiographs did not aid in its detection

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14
Q

calculus types

A

a) Four major crystalline forms 1. Hydroxyapatite (~ 58%) – major crystalline form in mature calculus 2. Magnesium whitlockite (~ 21%) 3. Octacalcium phosphate (~12%) 4. Brushite (~ 9%) – first crystalline form immature calculus

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15
Q

tooth proximity

A

Heins and Weider: Distance between roots and histology of bone a) 0-0.3 mm = no bone, direct PDL attachment between teeth b) 0.3-0.5 mm = Cortical bone only, no cancellous c) >0.5 mm = cortical and cancellous bone Hain Tal: distance between roots & defect type. *Correlates well w/ Sphere of Influence a) <2.5 mm = mostly horizontal bone loss b) 2.5 – 3.1 mm = possible to have single intra-bony defect c) > 3.1 mm = possible to have 2 intra-bony defects Waerhaug sphere of influence ranges from 0.5-2.7. mean 1.63mm Kim: Mand anterior teeth with <0.8mm inter-root distance 56% (RR = 1.56) more likely to lose ≥1mm bone over 10 years; evaluated on PAs and adjusted for confounders, like age and smoking

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16
Q

furcation classifications

A

i. Grade I incipient; pocket formation into flute; bone intact ii. Grade II moderate; pocket formation with loss of bone of varying depths; but not completely through iii. Grade III through and through; probable to opposite side with pocket formation iv. Grade IV exposed; furca is clearly visible due to loss of attachment and gingival recession • Hamp i. Degree I horizontal loss < 3mm ii. Degree II horizontal loss > 3mm but not all the way through iii. Degree III horizontal loss through and through • Tarnow and Fletcher (vertical component measured from ROOF of furca) i. Subclass A vertical loss 1-3mm ii. Subclass B vertical loss 4-6mm iii. Subclass C vertical loss > 7mm

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17
Q

maxillary 1st PM info why are furcations on this tooth significant?

A

Gher & Verino: 78% of maxillary first premolars have a concavity on the palatal (furcal) surface of the buccal root Mesial deVELOPMENTAL GROOVE exjsts on single rooted max 1st PM - worsening prognosis Joseph - study done on 100 extracted maxillary 1st PMs: 37% of maxillary first premolars are bifurcated. 1/3 in cervical, 1/3 in middle, 1/3 in apical Mean root trunk length (CEJ to furcation) = 7.9mm 100% prevalence of mesial and distal root concavities, mesial is deeper -Root concavities retain plaque, complicate patient home care and worsen tooth prognosis if exposed; professional maintenance of these areas is crucial.

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18
Q

What evidence exist that lack of dental care can contribute to periodontal disease?

A

a. Loe and Anerud – Norwegians and Sri Lankans a) SL had 3x rate of interproximal LOA/yr b. Becker – patients who were not treated and not maintained had more tooth loss compared to patients who were treated and maintained and even patients who were treated (but not maintained) – treatment was ScRP and osseous surgery Treated and maintained – lost 0.11 teeth/yr Treated but not maintained – lost 0.22 teeth/yr Not treated and not maintained – lost 0.36 teeth/yr Axelsson and Lindhe –study where 180 patients received only symptomatic treatment and 375 received regular maintenance care – showed that preventative programs could resolve gingivitis and prevent periodontitis and tooth loss whereas patients without care deteriorated.

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19
Q

Recession classification

A

Miller a) Class 1: recession does not extend to mucogingival junction (MGJ), no interdental bone loss b) Class 2: Recession extends to or beyond MGJ but no interproximal bone loss c) Class 3: Recession extends to or beyond MGJ and some interproximal attachment loss or teeth malpositioning d) Class 4: recession extends to or beyond MGJ and severe bone/soft tissue loss in interdental area and/or severe tooth malpositioning. Cairo RT1: no interproximal loss, interproximal CEJs not clinically detectable RT2: interproximal loss, buccal attachment is apical or EQUAL ro interproximal attachment RT3: interproximal loss, buccal attachment is coronal to interproximal

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20
Q

Furcation entrance size

A

BOWER: furcation width of 200 ext mandibular and maxillary molars. 81% were less than 1mm. More than half were less than 0.75. Most could not fit the blade of a curette.

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21
Q

how deep can you clean

A

Stambaugh (7 posterior teeth included with 30 minutes spent cleaning each tooth) a) Average curette efficiency depth = 3.73 mm for plaque free b) Average curette limit = 5.52 mm where scratches evident c) Mesial sites cleaned the worst, DL sites were best

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22
Q

waerhaug #s

A

PD Non-surgical (plaque free surfaces) 0-3 89% 3-5 63% >5mm 11%

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23
Q

critical PD

A

Lindhe 2.9mm for NST (lose AL below it and gain AL if PD above this) b. 4.2mm for Surgical therapy c. 5.4mm where you will gain more attachment with surgical rather than NST

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24
Q

Give evidence of alcohol as a risk factor for periodontitis

A

Moderate alcohol drinking: 1-2 drinks/day for men (1/day for women) Heavy alcohol drinking: men >4 drinks/day; women >3 drinks/day Tezal: Used NHANES data Association between alcohol abuse and & CAL 5 drinks/week = O.R =1.2 for CAL 10 drinks/week = O.R. = 1.4 for CAL Alcohol consumption may be associated with increased severity of CAL in a dose-dependent fashion. Wang SR, MA Risk of periodontitis increased by 0.4% for each 1 g/day increment in alcohol consumption.

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25
Q

Mechanisms for alcohol use causing periodontitis

A

1) decreased complement, PMN function, altered T cell function 2) cytotoxic effects to cells by alcohol 3) altered clotting cascade, damage to liver and clotting factor production 4) nutritional and vitamin deficiencies

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26
Q

Modified Aldrete score

A

Aldrete Score: Activity: 2 - Able to move 4 extremities spontaneously on command 1 - able to move 2 extremities 0 - unable to move any extremities Respiration: 2 - breathe deeply and cough 1 - shallow dyspnea 0 - apnea Consciousness: 2 - fully awake 1 - arousable on calling 0 - non responsive Circulation: 2 - BP within 20 mmHg of original BP 1 - BP 20-50 mmHg of original BP 0 - BP 50 or more mmHg of original BP Color: 2 -Normal 1 -Pale, jaundiced, blotchy 0 - Cyanotic

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27
Q

BMI categories

A

BMI categories (high muscle density tends to be higher in number) Underweight <18.5 Normal weight 18.5-24.9 Overweight 25-29.9 Obese 30-34.9 Units are kg/m2

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28
Q

Effects of smoking on periodontium

A

-increased collagenase production (MMP-8) -decreases neutrophil qualitative function (decreases enzyme production, decreased chemotaxis) - changes in cytokine profile (e.g. increased IL-8) -suppression of OPG (which is protective) - decreased oxygen tension leading to increased gram negative bacteria - change in fibroblast wound healing (altered migration, root surface attachment) - decrease perfusion through blood vessels (but increased vessels) - direct cellular cytotoxicity of smoking - changes in IgG levels

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29
Q

how does smoking cessation affect periodontal disease risk

A

Fiorini: SR. Smoking cessation associated with decreased AL, PD and bone loss Rosa 2014: Prospective study. Patients got SCRP and then smoking cessation therapy afterwards and were follow up to 2 years. After 2 years, the subjects that quit smoking had significantly higher clinical attachment gain, reduction in PD and in the proportion of sites with CAL >3mm. Better response to non-surgical periodontal therapy results in patients who quit smoking. Bergstrom 2014: Sweden. A decline in smoking is related to a decrease in periodontal disease prevalence. Al-Harthi 2018: Used NHANES data from NHANES 2009-2010 and 2011-2012. Cross-sectional study. Each additional year of smoking cessation was associated with an additional 2.5-5.2% (3.4%) reduction in the odds of having periodontitis.

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30
Q

How do you know that smoking is risk factor for periodontal disease?

A

Tomar and Asma (NHANES III data) – OR of 4.0 for perio disease in smokers; cross-sectional data i. Dose dependent effect noted (OR 2.8 for <9 cig/day, OR 5.9 for >31 cig/day) ii. OLD THOUGHT: After 11 years of non-smoking, OR of perio prevalence returns to non-smoker levels Bergstrom: 3x more bone loss in smokers vs non smokers (10 year cohort)

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31
Q

types of maintenance

A
  1. Types of maintenance and indications a. Schallhorn/Snider, 1981 – Discuss different types of MT and breakdown of MT apt a) Preventative Periodontal MT – prevent occurrence of perio in periodontally healthy pt b) Trial MT – to maintain borderline cases and assess over time, the need for corrective therapy c) Compromised MT – to slow the progression of dz when surgical therapy not indicated due to Finances, Poor Hygiene, Lack of Restorative Plan, Medically Compromised d) Post- Treatment MT – prevent recurrence of active disease e) 52min average which included 28 minutes of polishing/flossing/ultrasonic/hand instrumentation
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32
Q

tell me about listerine

A

a. Listerine = essential oil a) Thymol, eucalyptol, methol, methysalicylate b) When used 2x daily, 34% reduction in gingival inflammation and plaque if used 2x daily c) Used as a preprocedureal rinse can reduce bacterial load by 94% d) MOA = cell wall disruption and inhibition of bacterial enzymes e) Negative = contains 21-27% alcohol which can cause patients irritation

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33
Q

Wilderman timeline

A

a. Immediate – clot formation and inflammatory response with PMN migration and polyband formation under the clot b. 1-2 days – epithelial migration begins at a rate roughly 0.5 mm per day beneath the polyband; mØ clean debris c. 3-4 days – a) fibroblastic activity increases and a disorganized CT matrix is forming b) Angiogenesis and vascular budding begins (requires 2 weeks for completion) c) Osteoclastic activity begins and peaks within first week d. 1-2 weeks – increasing collagen production and content, with osteoblastic activities beginning and osteoclastic activities decreasing e. 1 month – peak osteoblastic activity and completion of majority of collagen synthesis; collagen in parallel to root f. 6 months – maturation of CT and PDL insertion into the bone and root. New cementum formation. Periosteum formation. osseous surgery - average loss of crestal bone =0.8 mm (on buccal) - less bone is lost interproximally g. **** complete healing following osseous surgery required at least 6 months. Bone remodeling was seen out to 18 months. Collagen fibers were parallel to the long axis of the root until 5-6 months post-op, then they angled from an apical direction into and were attached to the root.  increase in mobility immediately after and might take 6 months to see improvement.

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34
Q

Suture design and flap adaptation

A

a. Nelson: no difference between interrupted sutures vs. continuous sling suture in perio parameters; all pts got coe pak b. Machtei – 12 subjects. Flap placed <3mm from the bone results in avg PD of 2.5 mm where sites with flap placed 4 mm or greater had average PD of 3.5 at 2 years PENNER: Bone sound and it is less than 3 there is a 94% chance that the probing depth will be less than 3 Bone sound >3 there is a 50% chance the probing depth will be less than 3 at the 6 month follow up Penner vs. Machtei R=.56; R=.43 Osseous; MWF Stent Used; No Stent 3-6 month follow up; 2 year follow up

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35
Q

would you use abx for chronic p?

A

NO Haffajee and Socransky: when used in conjunction with SRP b) WMD 0.24 mm additional gain for chronic periodontitis not clinically significant Borges: Adjunctive use of metronidazole and amoxicillin with SRP may increase the proportion of patients reaching a clinical endpoint of having ≤ 4 sites with PD ≥ 5mm. 14 days antibiotic regimen appears to have a greater effect compared to a seven days regimen. Sgolastra: in generalized aggressive patients specifically, SR, MA, Significant CAL gain and PD reduction were shown with FMSRP +AMX/MET compared to FMSRP alone.

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36
Q

tell me about chlorohexidine

A

• Cationic bisbiguanide that binds to proteins within pellicle. Gold standard. Adheres to soft and hard tissues and is released slowly over time = substantivity. Ruptures cell membranes. Has 6-8 hour effectiveness • Negative side effects = tooth stain, increased calculus formation (cell membranes form a pellicle, irregular taste_(dysgusia) • SLS and fluoride in toothpaste inactives it • CHX decreases plaque by 50-55% Van Strydonck - SR: Dose dependent, but not concentration dependent. As an adjunct to normal OH, CHX can lower plaque by 33% and gingivitis by 26%.

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37
Q

Is periodontal maintenance effective long term?

A

Hirschfield and Wasserman: 600 patients, 15 years recall. Based on response to therapy, pts were divided into 3 groups—well maintained (WM – lost 0-3 teeth): 83%, downhill (D – lost 4-9 teeth): 13%, and extreme downhill (ED – lost 10-23 teeth): 4%. Initial tx approach had little effect on tooth retention at 15 yrs. . Most frequently lost tooth =Maxillary 2nd molar Least likely to be lost = Mandibular first premolars and canines, even with a poor prognosis. Residual mobility did not lead to tooth loss (even Class 3 mobility). Tooth loss of teeth in “well maintained” group was typically molars with FI How prognostic is BOP in predicting future CAL? Lang showed that sites that had BOP at 4/4 maintenance visits only broke down 30% of the time BOP is better at determining prognosis of whole mouth as opposed to a single site

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38
Q

tell me about accessory canals

A

Gutman said that up to 28% of multirooted teeth have lateral canal in the floor of the furcation

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39
Q

steps of osseous sx

A

STEPS OF OSSEOUS SURGERY: 1) Bulk reduction of thick bone 2) Interdental fluting 3) Reduction of crater walls 4) Removal of radicular bone and widow’s peaks 5) Final shaping and smoothing

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40
Q

fremitus classification

A

FREMITUS CLASSIFICATION: INGERVAL: mobility in function, MIP, excursives (Functional tooth mobility) Class I: mild vibration Class II: palpable vibration, no visible movement Class III: movement visible to the naked eye

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41
Q

Re-evaluation: Why at 4-6 weeks?

A

a. Mosques- 42 days for bacteria to repopulate the sulcus b. Caton- least inflamed microvascular density in coronal tissues after 4 weeks (signs of repair) c. Best time to intervene hygiene

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42
Q

Overhangs

A

Lang - Cross-over study in periodontally healthy patients. Overhanging restorative margins alter the subgingival microflora to a more periodontopathic composition, directly increasing inflammation; and, demonstrating a potential mechanism for increased bone loss associated with iatrogenic restorative factors. How common are overhangs? Brunsvold – found 33% of patients, 25% of restored surfaces Jeffcoat - Effect of overhanging amalgam restorations on the alveolar bone height in patients with various degrees of severity of periodontal disease. 100 pts -The larger the overhang, the more bone loss. Small overhangs (<20% IP space), unlike med and large, did not result in a significantly greater amount of bone loss. Severity of bone loss increased with age and the longer the overhang was present Authors suggest that bone loss from overhanging restorations may be due to increased plaque/calculus accumulation from difficulty of OH rather than mechanical irritation with a notion of time, i.e. state of continuous inflammation over a prolonged period. Bone loss was found to be greater around teeth with overhangs in all periodontal disease types. Rodriguez-Ferrer - Effective oral hygiene is impeded in areas with overhangs. Removal of overhangs should be addressed during initial periodontal therapy. Wang - Molars with crowns or proximal restorations had a significantly higher percentage of furcation involvement. Mean probing periodontal attachment loss was greater for restored than non-restored molars

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43
Q

Miller mobility classification

A

Class 0 - Normal (physiologic) movement when force is applied. Class I – Tooth can be moved less than 1 mm in a BL or MD direction. Class II - Tooth can be moved 1mm or more in a lateral direction (buccolingual or mesiodistal). Inability to depress the tooth in a vertical direction (apicocoronal). Class III - Tooth can be moved 1mm or more in a lateral direction (buccolingual or mesiodistal). Ability to depress the tooth in a vertical direction (apicocoronal).

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44
Q

waerhaug sphere of influence

A

0.5 - 2.7 mm. avg = 1.6 mm

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45
Q

root proximity to sinus

A

Sharan & Madjar: superior curvature of sinus floor, ext of 2nd molar or multiple molars and root proximity to sinus all lead to increased sinus pneumatization

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46
Q

Talk about suture material

A

chromic gut = multifilament absorbable suture made from collagen from intestine;. dissolved by enzymatic degradation, treatment with chromic acid salts to slow down degradation. maintains strength for 10-14 days. Moderate tissue reaction. Leknes - Placement of sutures in gingival tissues elicits an inflammatory reaction and that the magnitude of this reaction may vary with the suture material used. Braided silk sutures apparently cause a more extensive inflammatory tissue reaction in an environment characterized by moisture and infectious potential than ePTFE PTFE suture = monofilament polytetrafluoroethylene, chemical inertness. non-absorbable less risk of colonization by microorganisms of monofilament sutures vs braided. PGA - multifilament

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47
Q

CAMBRA

A

Caries Management by Risk Assessment why is this patient moderate? this patient is moderate because he only has conditions that out him in the moderate risk category high risk category examples: sugary foods or drinks for prolonged time period between meals, chemo/radiation, teeth missing due to caries in past 36 months, 3 or more carious lesions in past 36 months moderate risk category examples: 1 or 2 caries lesions/restorations in past 26 months, visible plaque, tooth morphology that compromises OH, exposred root surfaces, open contacts, medications that reduce salivary flow

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48
Q

When are you going to get the best oral hygiene in your patients?

A

At the re-eval. Edith Morrision showed that the very best oral hygiene you’re gonna get is at the re-eval

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49
Q

What factors contribute to clinical mobility?

A

o Attachment loss o Excessive occlusal forces

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50
Q

Tell me about furcation arrows

A

Deas/Mealey: Furcation Arrow – Sens 39%; Spec 92%; PPV 72%; NPV 75% An additional 120 uninvolved furcations were included as controls. The involved maxillary molars were radiographed with standard periapical radiographic techniques. Projected radiographs were evaluated independently by six dentists who determined whether there was a triangular radiographic shadow (“furcation arrow”) over the mesial and distal proximal areas. The association of the furcation arrow image with Degree 2 or 3 furcation involvement was significant when compared with uninvolved furcations. The image was equally apparent over mesial or distal furcations and was not affected by the existence of a buccal furcation involvement. The incidence of the image over both uninvolved proximal furcations and proximal furcations with Degree 1 involvement was low and did not differ significantly. Because the furcation arrow seldom appears over uninvolved furcations, the appearance of the image indicates that there is proximal bony furcation involvement. However, absence of the furcation arrow image does not necessarily mean absence of a bony furcation involvement because the arrow was not seen in a large number of furcations with Degree 2 or 3 involvement. Hardkopf: Dry skull study. Correlation between degree 2 or 3 furcation and furcation arrow.

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51
Q

tell me about maintenance after surgery

A
  1. Westfelt: Surgical tx patients with MT intervals of 2w, 4w, or 12w following therapy for first 6 months, then at 6 months all patient put on maintenance every 3 months a. Attachment loss was inversely proportional to maintenance interval i. Higher the interval; less the AL ii. Most critical within first year of tx
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52
Q

how do you get patients to increase compliance, what are traits that make a patient more/less compliant?

A

Wilson – compliance decreases with increase in number of years since active therapy and shorter intervals of maintenance; compliance increases if pt had surgery How to increase compliance  when did below =patient compliance increase 16% to 32% 1) Accommodate patients schedules 2) Make appointments before pt leaves office 3) Appointment reminders via telephone 4) Allow pt to see general dentist hygienist if it is easier for them factors that have decreased compliance 1) Smokers (Ramseir) 2) Male (Novaes) 3) Younger (Novaes) 4) Increase years since surgery (Wilson) 5) Shorter intervals (Wilson) 6) Stressfull life events, neurotic (Umaki)

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53
Q

root caries

A

Reiker – 82% patients had at least one root surface with caries and/or a root filling; plaque scores = most important factor associated with root caries

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54
Q

blood pressure classification

A

Normal= <120/<80 Elevated: 120-129/<80 Stage 1: 130-139/80-89 Stage 2: 140+/90+ Hypertensive crisis is 180/120 Target for patients with diagnosed hypertension: <130/<80

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55
Q

discuss staging in perio dz

A

first look at severity: stage 1: 1 to 2 mm interdental CAL, RBL in coronal third (less than 15%); and no tooth loss due to periodontitis. Max probing depth less than or equal to 4 mm. stage 2: 3 to 4 mm of CAL, RBL in coronal third (15 to 33%); and no tooth loss due to periodontitis. Max probing depth less than or equal to 5 mm. stage 3: 5 mm or greater of interdental CAL and bone loss extending to middle third of root and beyond. 4 teeth or less lost due to periodontal disease. Probing depth greater than or equal to 6 mm. Vertical bone loss greater than or equal to 3 mm. Furcation involvement class II or III. Moderate ridge defects. stage 4: 5 mm or greater of interdental CAL, bone loss extending to middle third of root and beyond. 5 or more teeth loss due to periodontal dz. In addition to stage III complexity: -Masticatory dysfunction -Secondary occlusal trauma -Severe ridge defects -Bite collapse, drifting, flaring -Less than 20 teeth remaining

56
Q

Complexity factors associated with staging

A

Stage 1: max PD of 4 mm or less Stage 2: max PD of 5 mm or less Stage 3: PD 6 mm or greater, vertical bone loss greater than 3 mm, furcation grade 2 or 3 Stage 4: masticatory dysfunction, secondary occlusal trauma (tooth mobility >2), severe ridge defect, bite collapse, flaring, drifting, less than 20 remaining opposing teeth

57
Q

Grading

A

primary criteria = direct evidence of progression = RBL or CAL. indirect evidence of progression = RBL divided by age and case phenotype Grade A = no RBL or CAL over 5 years. slow rate of progression, bone loss/age is less than 0.25, heavy biofilm deposits with low level of destruction. Non smoker. No diabetes. Grade B = less than 2 mm of RBL or CAL over 5 years. moderate rate of progression, bone loss/age is 0.25 to 1.0. destruction commensurate w/ biofilm deposits. Less than 10 cigarettes a day. A1c less than 7%. Grade C = rapid rate of progression, 2 mm interdental CAL over 5 years, destruction exceeds expectation given biofilm deposits, clinical patterns suggestive of periods of rapid perio progression and or early onset disease. 10+ cigarettes a day. A1c 7% or greater. Grade modifiers = smoking, A1c (glycemic control)1

58
Q

1999 armitage classification

A

CDC/AAP Severe = 2+ interproximal sites with 6+ mm CAL AND 1+ interproximal site with 5+ mm PD Moderate = 2+ interproximal sites with AL 4+ mm OR 2+ interproximal sites with PD 5+ mm) Mild = 2+ interproximal sties with AL 3+ mm AND 2+ interproximal sites with PD 4+mm (not on same tooth) OR one site with PD 5+ mm

59
Q

Give dr mealey the evidence that you can have regeneration w/o placing a bone graft?

A
  1. FROUM & STAHL a. OFD  ~2mm recession, 1.4mm gain in attachment, 1.2mm radiographic bone fill, and 0.8mm crestal resorption; LJE healing; plaque control enhances gains
60
Q

what are tooth and patient levels factors that influence tooth loss?

A

Pretzl: Factors that influence tooth loss at the patient level were: non-compliant periodontal maintenance, plaque index and age. Factors at the tooth level were: interproximal bone loss, furcation involvement, and abutment type.

61
Q

how important is maintenance when it comes to tooth loss

A

Wilson - in study of 162 patients, none of the compliant patients lost teeth, all tooth loss was in erratic compliers

62
Q

Goldman

A

Furcation-involved teeth are most frequently lost. Mandibular canines are rarely lost.

63
Q

What is the proposed mechanism for occlusion causing periodontal destruction?

A

Proposed mechanisms: history of vertical defect formation via human necropsy Glickman: “Theory of Co-destruction” – occlusal trauma causes reorganization of the transeptal fiber bundles and damages vessels, which directs inflammation into the periodontal ligament space to cause intrabony defects. a) Above transeptal fibers: zone of irritation, plaque-induced inflam ONLY b) Below transeptal fibers: zone of co-destruction, plaque OR occlusal-induced inflammation Waerhaug: DISPROVED THEORY OF CODESTRUCTION. Histologically showed that intrabony defects are associated with a downgrowth of plaque. There was NO correlation between clinical signs of occlusal trauma and defect formation. a) Sphere of influence of plaque found to be 0.5-2.7 mm; average of 1.6mm c. Signs of Occlusal Trauma a) widened PDL, fremitus/mobility, crestal bone loss/funneling, wear facets, tooth migration, tooth fracture

64
Q

Does mobility affect perio therapy?

A

YES Flezar (Michigan studies) – SRP, MWF, Osseous therapy all produced significantly better results on non-mobile teeth. Worse outcomes for mobile teeth. Even some AL w/ Class 3 Cortellini: greater mobility at baseline, sig smaller CAL gain at 1 year for regeneration Wang HL: mobile molar teeth lost significantly more attachment over time when compared to non-mobile controls NO Trejo/Weltman: Found that Miller 1 or 2 mobility had no impact on regenerative therapy Schulz: mobile teeth with bone graft – splinted teeth responded better to therapy

65
Q

what is a sign that a tooth might lose attachment in maintenance

A

claffey - BL: Persistent BOP combined with either a deep residual probing depth or increase in PD may be useful in identification of sites at risk for progression of periodontal disease. BOP alone is not as predictive of LOA.

66
Q

why should we brush teeth 2x daily what should we use to brush our teeth

A

. De Freitas - brushing and flossing q48h results in higher levels of gingival inflammation compared to q24h or q12h, which are both equivalent. Tritten - standard and manual TB are capable of removing supragingival plaque and reducing signs of gingival inflammation. However, the sonic toothbrush was statistically superior in removal of plaque from hard to reach areas such as interproximal regions.

67
Q

where do we leave calculus

A

Jones & O’Leary 1978: Scaling alone is not as effective, Root planing is necessary to render diseased root surfaces as free of detectable endotoxin as healthy root surfaces. Areas where the residual calculus was found were: 1) at CEJ, 2) in root flutes and 3) at line angles.

68
Q

• What does gingival phenotype tell you about the bone underneath that?

A

o Name articles (Dr. Cook) found that the thicker the bone the thicker the gingival phenotype

69
Q

Is there a relationship between occlusal discrepancies and periodontitis?

A

YES Youdelis and Mann: Non-working contacts were found to be associated with increased bone loss and PD (WEAKNESS: study utilized only charts and models, retrospective). Found that 53% of MOLARS had nonworking contacts NO Shefter and McFall: Non-working contacts were not found to be associated with any increased PD (56% of subjects had nonworking contacts) Bernhardt: largest cross sectional study to date. Pomerania– significant difference in PD and CAL in teeth with NW contacts (0.13, 0.14 mm) but magnitude of effect is small

70
Q

What is the significance of root groove?

A

Leknes - found a relationship between root grooves and attachment loss. Surface with root grooves tended to have greater AL.

71
Q

Why did you select Kwok and Caton?

A

Kwok and Caton based their prognostic system on the stability of bone and attachment, instead of tooth mortality. Survival and stability are separate. Teeth are typically maintained until dentist extracts them Prognostic system includes patient and tooth level factors

72
Q

Compare and contrast McGuire & Nunn and Kwok and Caton

A

McGuire & Nunn - use tooth loss as an endpoint Kwok & Caton - based on periodontal stability and conaiders patient related factors such as compliance, smoking, diabetes, in addition to tooth related factors`

73
Q

What are tooth related factors that are associated with tooth loss?

A

McGuire & Nunn - Initial probing depth, initial furcation involvement, initial mobility, initial crown-to-root ratio, and initial root form were all associated with tooth loss.

74
Q

why is giving a prognosis important for patient communication?

A

Important to meet patient wishes: Are my teeth worth it— what are my chances? How likely will I suffer an adverse outcome? Over what time frame might this occur? Do my chances change with time?

75
Q

What evidence exists that would support the idea that patients can maintain their treatment results even with poor OH?

A

Ramfjord - AL and PD 1 year after therapy can be maintained over 7 years with maintenance every 3 months, regardless of variations in the efficacy of the patient’s plaque control. (however plaque control overall in this group was good) Morrison - There is no consistent relationship between the severity of gingivitis and variations in PD and AL when patients are on a 3-month recall

76
Q

Where is the furcation entrance of the maxillary first molar?

A

Bower: Mesial: 3.6 mm apical to CEJ B: 4.2 mm apical to CEJ D: 4.8 mm apical to CEJ

77
Q

Once you have lost all of the attachment to the root trunk, what percentage of overall attachment have you lost for a maxillary first molar?

A

Herman: root trunk: 32% P: 24% MB: 25% DB: 19% chen - linear estimation overestimates supported ratios and makes remaining tooth support seem better than it actually is

78
Q

Larato

A

Mexican dry skulls 1) Average number of furcation involvements increases with age. 2) 1st permanent molars are most commonly involved. 3) In the maxilla, the buccal aspect is the most common, followed by the mesial. 4) In the mandible, the buccal aspect is most common. 5) Maxillary bicuspids show the lowest incidence of all multirooted teeth. 6) Incidence of furcation involvement decreases the more posterior the tooth in the arch.

79
Q

What evidence suggests that maxilary molars with furcation invasion will affect the premolars?

A

Ehnevid: Periodontal status (deeper PDs) and response to non surgical therapy (0.5 mm less PD reduction) are negatively influenced by proximal furcation invasion of degree 2 or degree 3. The presence of a deeper furcation invasion is a risk factor adjacent tooth periodontal breakdown

80
Q

can molars with furcation invasion be maintained?

A

Roos & Thompson: 88% teeth were functioning after 5-24 yrs, despite the fact that many of these teeth had at least one root that had 50% or less bone support prior to treatment. had OFD only.

81
Q

Why did you choose osseous and not regeneration?

A

for regeneration - need coronally advanced flap versus apically positioned flap doesn’t allow for me to decrease PDs w/ coronally advanced flap - goes against tx objective defect has wide root divergence interproximal bone level is equal to the crest of bone

82
Q

How do you explain the fact that some studies show no difference between surgery and non-surgery?

A

Success of therapy rests upon gaining access to the subgingival environment, by whatever means, and altering that environment significantly enough to favor the host. Studies have shown that the ability to thoroughly debride the root surface depends upon depth of the pocket and the operator’s level of experience. Most of the studies indicated that for sites > 7 mm surgical access resulted in better reduction in PD. Maintenance has been shown to have a great impact on the long term results of therapy. Nyman (1977) reported that in the absence of recall at 6 months OH returned to baseline with a resultant increase in PD and attachment loss regardless of treatment. Another aspect affecting the results of these studies revolves around the statistical analysis used. The use of mean values for small numbers of patients can result in a few extremes distorting the overall conclusions drawn from the results. Since buccal and lingual initial pockets are usually more shallow than interproximal pockets, the meaning of this information distorts the findings.

83
Q

\how do local anesthetics work?

A

Local anesthetics are weak bases. Lipid solubility: determines, potency, plasma protein binding and duration of action of local anesthetics Local anesthetics with lower pK have a more rapid onset of action (more uncharged form more rapid diffusion to cytoplasmic side of Na+ channel) Cationic form of anesthetic binds at inner surface of Na+ channel – preventing Na+ influx (rising phase of membrane potential) which initiates AP → blockade of nerve impulses (e.g., those mediating pain)

84
Q

What evidence do you have that osseous surgery supports your tx goals?

A

Olsen & Ammons - osseous vs OFD. Osseous surgery cases at the 5-year follow-up resulted in fewer residual pockets and less inflammation than flap curettage, especially in 5-8mm pockets. Kaldahl (Nebraska) - The largest amount of PD reduction at the deepest sites was accomplished by osseous, which was maintained over 7 years versus

85
Q

Who would propose that you not treat this patient surgically?

A

Becker - longitudinal study comparing SRP, osseous, MWF - 5 year follow up - no significant difference between treatment1`

86
Q

Can you do full mouth SRP in one day in all patients?

A

Insurance will not pay for one day full mouth SRP Lafaurie - 81% of patients had anaerobic bacteremia after SRP (reconsider in joint patients or artificial valve patients)

87
Q

What is another way you can clean furcations besides ultrasonic or hand isntruments?

A

Parashis- The use of a rotary diamond bur was the most effective method of calculus removal in the furcation area compared to hand instrumentation.

88
Q

Why did you do full mouth disinfection?

A

De Soete - Patient’s treated with full-mouth disinfection had a greater shift towards healthier bacteria than the traditional SRP. In deep pockets, FMD has been shown to have a greater effect on CAL than traditional SRP

89
Q

Describe healing OF THE DENTOGINGIVAL Unit after srp versus sx

A

REPAIR, wherein damaged tissues are replaced by tissues that do not duplicate the function of the original tissues. occurs by the formation of a long junctional epithelial attachment to the root surface and by limited areas of C.T. attachment at the apical extent of the lesion. AFTER SRP: Separation of the dentogingival junction from the tooth surface: initial cellular reattachment by poorly differentiated hemidesmosomes in the apical third of the junctional epithelium, by 5 days it was totally restored. When the junctional epithelilum has been disrupted but not removed, final healing is probably similar to normal turnover, whereby new cells originating at the apical end of the junctional epithelium displace older cells coronally. AFTER SX: Essentially complete removal of the junctional epithelium by extensive root planing/curettage or surgical resection. Studies in dogs, monkeys, and rats have shown that after removal of the epithelial attachment, new junctional epithelium originates from the cut edge of oral epithelium. Migrating sheets of epithelium originating from the basal layer of oral epithelium at the wound edge were visible 1 to 2 days after. The connective tissue was rapidly covered with regenerated JE within 5 to 12 days.

90
Q

tell me about metronidazole

A

bactericidal against anaerobic bacteria including bacteriodes, fusobacteria, and treponemes. Aerobic, facultative and microaerophilic organisms are likely unaffected by metronidazole.

91
Q

how often should you replace your toothbrush?

A

Schmickler - The continuous use of the toothbrush for six months did show a reduction in the effectiveness according to an increase in gingival inflammation and plaque accumulation, which occurred at 4 months.

92
Q

What anticalculus agent do you recommend?

A

Stannous flouride has been show to inhibit crytsal formation pyrophosphates (can cause hypersensitivity rxn) copolymers

93
Q

WHy did you splint your pts teeth?

A

Cortellini found that in teeth receiving generative therapy - mobility negatively affected CAL gain Schulz - teeth splinted before bone grafts had better PD reduction/CAL gain than nonsplinted Prevent further tipping or drifting of teeth and provide patient comfort

94
Q

why do you believe your pt has aggressive perio?

A

Both chronic and aggressive periodontal disease occur in susceptible hosts and are caused by dental biofilms. Patients suffering from either disease have no known medical conditions that contribute to the development of their periodontitis. · Patients w/ generalized aggressive or chronic periodontitis have relatively intense gingival inflammation (this difference is likely due to the microbial biomass that form on the tooth surface over time). · Generalized aggressive periodontitis may be advanced chronic periodontitis in a young person with high susceptibility (would explain shared histopathology/immunopathology) MICHAWOLICZ STUDY - QUOTE THIS - THERE IS A GENETIC COMPONNENT = AGGRESSIVE PERIODONTITIS MAY EVEN HAVE A STRONGER GENETIC COMPONENET INCLUDING SEVERAL GENES

95
Q

Discuss pathologic migration

A

Greenstein: Migration of maxillary anterior teeth occurs when force vectors exceed the resistance of the periodontium. - Potential vectors of force include the following: occlusal trauma, posterior bite collapse, occlusal habits prevalence = 33% if flared teeth have normal bone levels and do not occlude with opposing teeth during centric occlusion or excursive movements, then the clinician knows the flaring was caused by something other than occlusion Brunsvold: Author cites prevalence of PTM can range from 30.3% to 55.8%. Tooth migration is often the motivation for patients to seek periodontal therapy.

96
Q

Glipizide

A

Sulfonylurea - oral Adjunctive or alternative monotherapy for patients who have suboptimal response to or cannot take metformin. Sulfonylureas have a relatively high risk of hypoglycemia when compared to other noninsulin antidiabetic agents due to their mechanism of action. Risk for stress-induced hypoglycemia moa - Stimulates insulin release from the pancreatic beta cells; reduces glucose output from the liver; insulin sensitivity is increased at peripheral target sites

97
Q

Discuss moa and prevalence and symptoms of diabetes mellitus

A

symptoms of diabetes = polyuria, dolydypsia, polyphagia purpose of insulin = allows glucose from the blood to enter cells of insulin-dependent tissues in 2018 - 10.5% of population had diabetes type 2 diabetes - peripheral resistance to insulin, impaired insulin secretion. strong genetic predisposition. more common in hispanics.

98
Q

How can you diagnose DM?

A

HbA1c > 6.5% (a normal is less than 5.7%) Fasting glucose of 126 mg/dL or more (normal is less than 100) fasting is defined as no caloric intake for at least 8 hrs 2-hr post prandial glucose of 200+ for oral glucose tolerance test. oral glucose tolerance test is a glucose load of 75g of glucose disolved in water (normal is less than 140) symptoms of diabetes and a casual blood glucose of 200+

99
Q

what is an A1c

A

glycated hemoglobin assay measures glycosylation of hemoglobin A in RBCs over past 3 months (lifespan of RBC)

100
Q

what is a target A1c

A

less than 7%

101
Q

give the estimated average glucose value for certain A1c

A

6% = 126 6.5% = 140 7% = 154

102
Q

definition of hypoglycemia what are symptoms of hypoglycemia etiology of hypoglycemia

A

lower limit for glucose level = 70 mg symptoms usually hit at less than 50-60 mg etiology: overadministration of glipizide, presence of infection, insufficient intake of food Symptoms: can manifest as depression or stimulation of nervous system: hunger, nausea, sweating, anxiety, nervousness, tremor, palpations, tachycardia, hyperventilation, HTN Severe hypoglycemia can cause seizure and unconsciousness tighter glycemic control has greater risk for hypoglycemia

103
Q

how do you manage hypoglycemia

A
  • check blood glucose to confirm hypoglycemia (to rule out syncope) - if patient is awake, administer 15g of carbohydrate via juice each gram of carbohydrate raises blood glucose 5 mg/dL (since she weighs more, likely 2.5 mg/dL). 15 g of carb would raise her 35-75 mg -if patient is unconscious and has IV > administer 30 mL of 50% dextrose > will give you 15 g of dextrose intravenously. this will raise her 35-75 mg if pt is unconscious without IV > administer 1 mg of glucagon intramuscularly > glucagon releases stored glucose from the liver by breaking down glycogen
104
Q

oral manifestations of uncontrolled diabetes

A

xerostomia, periodontitis, periapical/periodontal abscessess especially multiple, painful burning mucosa

105
Q

what are some dental management considerations for patients with DM

A

before every appt: did they take medicvation, have they eaten, how are they feeling, have they taken their blood glucose that morning if they are less than 150 mg and they are not NPO consider giving them juice check throughout procedure to see how patient feels

106
Q

what are you doing for pain for your patient on sulfonylureas

A

NSAIDs can enhance efficacy of sulfonylureas - use with caution

107
Q

are you giving your diabetic patients steroids

A

potentially can cause them significant hyoerglycemia - for up to days to weeks

108
Q

diabetes insipidus

A

large amounts of dilute urine and increase thirst lacks of ADH or kidneys do not respond to ADH

109
Q

what is occlusal trauma?

A

histologic term describing injury resulting in tissue changes within the attachment apparatus as a result of occlusal forces

110
Q

what is an occlusal interference?

A

any contact that inhibits the remaining occluding surfaces from achieving stable and harmonious contacts

111
Q

what is secondary occlusal trauma?

A

injury resulting from normal or traumatic occlusal forces applied to a tooth with reduced attachment

112
Q

what is happening in the bone and PDL when her teeth are migrating (pathologic migration)

A

compression zone = compression of PDL, rupture of vessels, bone resorption tension zone = tearing of PDL fibers, bone apposition

113
Q

What is the effect of traumatic occlusal forces on an inflamed peridontium

A

Lindhe found that TOF applied to an inflamed periodontium lead to a progressive increase in mobility and did not reach physiologic adaptation like the noninflamed sites lindhe found that in dogs with periodontitis and TOF - the teeth with TOF had 3x greater loss of CT attachment than those without TOF polsom disagreed and found that monkeys with periodontitis and TOF did not have an increased loss of CT attachment

114
Q

Does mobility itself increase the rate of periodontitis?

A

not in a plaque -free enviroment. Lindhe found mobile teeth that were plaque free had similar CT attachment loss to nonmobile teeth

115
Q

if you remove the TOF in a combined lesion (perio + TOF) but don’t treat the perio what happens? what happens when you resolve the perio but not the TOF?

A

1 - no improvement in CT 2 - increase in bone volume and decrease in mobility but no improvement in CT attachment level

116
Q

what is the effect of TOF in a healthy periodontium?

A

increased mobility and PDL width, loss of bone height, no loss of CT attachment completely reversible

117
Q

When do you decide to do an occlusal adjustment?

A

Occlusal adjustment - should be reserved for definite diagnosis of traumatic lesion, not when you notice an occlusal discrepancy Treatment studies: Do occlusal adjustments provide any long-term benefit? NO h. Burgett/Ramjford: Patients with adjustment gained 0.4 mm more attachment @ 2 years (not clinically significant); no difference in PD or mobility Harell & Nunn: group of treated perio pts either with or without correction of occlusal discrepancies during therapy; significant difference of 0.167 mm increase in PD/year (not clinically significant) in the untreated group DEAS and MEALEY: argue that only occlusal discrepancies that show signs of occlusal trauma should be adjusted; those discrepancies that do not show signs of occlusal trauma should not be adjusted. Indications: progressively increasing mobility, discomfort, traumatic injuries, don’t adjust if inflammation isn’t controlled

118
Q

How do AGEs affect collagen?

A

advanced glycation end products can glycosylate collagen decreasing its turnover (impaired wound healing) pts with diabetes have increased collagenase which degrades newly sysntheszied collagen

119
Q

Does periodontal tx reduce patients A1c?

A

Sgolstra - SR, found that SRP reduces A1c by 0.65%

120
Q

what is the significance of patient missing her spleen?

A

located in upper left quadrant similar to large lymph node Removes RBCs holds reserve of blood participates in humoral and cell mediated immunity pts missing spleen have a greater susceptibility to infection. significantly diminished frequency of memory b cells

121
Q

what are symptoms of generalized anxiety disorder

A

most frequent psychiatric disorder persistent diffuse form of anxiety with autonomic hyperactivity and apprehension and excessive worry considerations: detect anxiery by physical apperance, speech, pt with GAD could have panic attack sudden overwhelming feeling of terror with palpations, dizziness, faintness, swaeting, tingling, chest pain, lasts about 30 mins

122
Q

fluoexetine (prozac)

A

selective serotonin reuptake inhibitor 14% of patients taking Prozac have xerostomia Problems with SSRI-induced bruxism have been reported Fluoxetine may impair platelet aggregation due to platelet serotonin depletion, possibly increasing the risk of a bleeding complication. The risk of a bleeding complication can be increased by coadministration of other antiplatelet agents such as NSAIDs and aspirin. Monitor patients closely for signs of serotonin syndrome such as mental status changes (eg, agitation, hallucinations, delirium, coma); autonomic instability (eg, tachycardia, labile BP, diaphoresis); neuromuscular changes (eg, tremor, rigidity, myoclonus); GI symptoms (eg, nausea, vomiting, diarrhea); and/or seizures. Discontinue treatment (and any concomitant serotonergic agent) immediately if signs/symptoms arise.

123
Q

Torsade de pointes

A

Fluoxetine is one of the drugs confirmed to prolong the QT interval and is accepted as having a risk of causing torsade de pointes Prolongation of the QT interval can increase a person’s risk of developing this abnormal heart rhythm. Specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics Most episodes will revert spontaneously to a normal sinus rhythm.[2] Symptoms and consequences include palpitations, dizziness, lightheadedness (during shorter episodes), fainting (during longer episodes), and sudden cardiac death. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate into ventricular fibrillation, leading to sudden death in the absence of prompt medical intervention.

124
Q

What do you do if you think your pt is having a seizure?

A

Seizure - Prevent injury, remove objects from mouth, gently restrain - Verify patent airway during/after - Benzodiazepine IM or IV at 5 minute mark o Midazolam 5mg IM - Apply pulse oximeter - Oxygen - Diabetic? Consider Hypoglycemia - Beware of hypoxia during/after - Risk of hypoventilation post-seizure

125
Q

What do you do if your patient is having a hypoglycemic event?

A

Symptoms: - Altered mental status, feeling of impending doom, confusion, sweating - Blood sugar <70mg/dl (normal BS=70-110) - Conscious: give oral sugar (soda, juice, cake icing) - Semi-conscious: avoid oral liquids (cake icing) - Unconscious: cake icing or parenteral agent o 50% dextrose IV o 1mg glucagon IM o 0.3mg EPI IM - Oxygen (nasal cannula) wait 15-30 min - Seizure may occur - EMS if not resolved Note: make sure to monitor pt’s blood sugar throughout the appointment.

126
Q

What is a seizure?

A

Abnormal electrical activity in the brain in most people it is idiopathic phases of tonic-clonic seizure: prodrome: appearance of aura, epleptic cry, increased HR and BP ictal: convulsive phase, mouth frothing post-ictal: consciousness returns

127
Q

Syncope

A

most common emergency in dental office preceding symptoms: lightheadedness, palpations, nausea, sweating, impaired vision, inability to think vasovagal reaction: sudden severe emotional stress, anxiety, caused by peripheral vasodilation with drop in blood flow to brain and loss of consciousness placing patient in trendelenbtug will restore conscioussness if do not regain consciousness, activate EMS

128
Q

Atorvastatin

A

Inhibitor of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis Decrease levels of high-sensitivity C-reactive protein, inhibition of platelet aggregation, and anticoagulant effects

129
Q

How does obesity relate to periodontal disease?

A

Obesity causes elevated systemic inflammation. Elevated systemic inflammation can cause • increased insulin resistance • Elevated liver-derived acute phase proteins such as **CRP and fibrinogen*** o CRP activates complement and stimulates neutrophil chemotaxis to propagate inflammation o Il-6 causes hepatic CRP production  CRP = complement reactive protein – binds to damaged cells and activates neutrophil chemotaxis  Increased levels of CRP are associated with increased likeliness of cardiovascular incident as well as obesity and periodontal disease o Periodontal disease is chronic inflammation and an increase in systemic mediators of inflammation can contribute to periodontal destruction • Obesity is related to elevate serum levels of pro-inflammatory cytokines (Il-1, TNFalpha, and IL-6) o Adipocytes secrete these mediators as adipocytes are highly metabolically active o Adipocytes are also filled with macrophages and macrophages secrete pro-inflammatory cytokines as well • These proinflammatory cytokines contribute to the propagation of periodontal disease

130
Q

Does periodontitis have systemic effects? Is the periodontitis affecting Jerry’s obesity and diabetes?

A

• Biofilm places bacterial pathogens and their production in direct contact with the blood stream • Patients with severe periodontitis have a greater incidence of bacteremia and endotoxemia which may have a direct effect on target organs • Periodontium is a reservoir of pro-inflammatory cytokines that dump systemically • Periodontitis may elicit production of acute phase proteins • SO, yes the local chronic inflammation in the oral cavity can have systemic effects on the inflammatory processes in the body

131
Q

Please speak specifically about the association between obesity and periodontal disease

A

OBESITY = BMI> 30 kg/m2 – THERE IS A MODEST POSITIVE ASSOCIATION BETWEEN OBESITY AND PERIODONTAL DISEASE SUVAN - SR & MA - OBESE PATIENTS ARE 1.8 TIMES MORE LIKELY TO HAVE PERIODONTAL DISEASE THAN A NON-OBESE PERSON NASCIMENTO - Incident weight gain as a risk factor for incident periodontitis in Brazilian cohort. As weight gain goes up, the risk of periodontitis goes up, RR of 1.33

132
Q

DOES THIS PATIENT HAVE METABOLIC SYNDROME?

A
  1. Waist circumference (35F, 40M) 2. Fasting glucose >100mg/dl 3. Triglycerides above 150mg/dl 4. HDL <40 (or medicated) 5. BP >130 sys or >85 dia (or medicated)
133
Q

PLEASE DESCRIBE THE RELATIONSHIP BETWEEN METABOLIC SYNDROME AND PERIODONTITIS

A

NIBALI – SR & MA. OR - PATIENTS W/METS ARE 2 TIMES MORE LIKELY TO HAVE PERIODONTAL DISEASE THAN A NON METS PERSON KIM, KOREAN NHANES: Hip to waist circumference ratio is a better indicator of obesity than BMI; measurement of waist circumference >40 is considered obese Mechanisms – in overweight/obese – adipose tissue is a proinflammatory reservoir and primes the system for inflammation GENCO: (NHANES III study)-more adipose tissue produces TNF-a and has more metabolically active macrophages (IL-6). This creates a pro-inflammatory environment ****ADA code for chairside diabetes is D0411

134
Q

Does periodontal disease affect glycemic control?

A

Taylor - Type 2 diabetics with severe perio were more likely to have worsening glycemic control compared to patients without perio

135
Q

Does glycemic control affect diabetes?

A

Tsai - NHANES - poorly controlled DM were 3x more likely to have severe perio

136
Q

Is periodontitis a sign of early diabetes?

A

Yes Teeuw - 18% of severe periodontitis patients had A1c > 6.5 and had not been diagnosed with diabetes

137
Q

Does the treatment of periodontal disease improve the patient’s diabetic status?

A

Sgolstra - MA - SCRP was associated with reduction in A1c of .65% Engebretson - MA - SCRP was associated with 0.36% reduction in A1c Engebretson - did the largest RCT of type 2 DM subjects w/ perio - mostly moderate perio and well controlled DM (7-9%) no significant change in A1c Calabrese - intensive periodontal tx - type 2 subjects had a decrease in A1c of approximately 0.95%