ANDREA’S FILE VERY VERY IMPORTANT

Dear friends, these are remembered/repeated questions (RQs) and answers I have made from different files, I hope it helps you. I corrected and i think all is right but if yo find something wrong please let me know so we can have corrected file. Learn it, share it, and i hope you PASS. Good luck everyone!! God bless you..

“We must have perseverance and above all confidence in ourselves. We must believe that we are gifted for something and that this thing must be attained”

Marie Curie

1 ENDODONTICS

1)Diagnosgtics:

• Percussion—>presence of inflammation in PDL or not.

• Palpation—> spread of inflammation to perodotium from PDL or not. EPT-

Periodontal problem—-> pain to Lateral Percussion on a tooth with wide sulcular pocket.

• Pulp vitality—>necrosis or not.

Example: how do you distinguish acute apical absess and periodontal absess? Vitality

• Thermal test (hot & cold)—>PULP VITALITY (always most reliable). Hot (irrev), cold (rev)

• Transilumination—> to see cracked tooth (Craze line)

• Endo-perio: pulpal necrosis leading to a perio problem as pus drains from PDL.

• Perio-endo: infection from pocket spreads to pulp causing pulpal necrosis.

• To differentiate between endo-perio lesion—>1) EPT; 2) Percussion

2) Pulp Diagnostic:

• Normal Pulp - A normal pulp is symptom free and will normally be responsive to the electric pulp tester (EPT). When evaluated by thermal testing, the normal pulp produces a positive response that is mild and subsides immediately when the stimulus is removed. —>slight pain 1-2 sec.

2 • Reversible Pulpitis - clinical diagnostic indicating that the inflammation should resolve and pulp return to normal. The patient’s chief complaint is usually of an exaggerated response to thermal stimulus but once the stimulus is removed, the discomfort does NOT Linger. EPT results are responsive. —>Strong, momentary, painful response.

• Symptomathic Irreversible Pulpitis - If the inflammatory process progresses, irreversible pulpitis can develop. Patients may have a history of spontaneous pain and complain of an exaggerated response to hot or cold that LINGERS after the stimulus is removed. Removal of the cold causes return of symptoms and can be used as a diagnostic. —> Moderate to strong painful response. + to HEAT

• Asymptomathic Irreversible Pulpitis: clinical diagnostic indicating that that vital inflamed pulp is incapable if healing. No clinical symptoms but inframmation produced by caries, caries excavation, trauma.

• Pulpal Necrosis - Necrosis is a histologic term that denotes death of the pulp. Discolored tooth. Unstimulated night pain.. Teeth with total pulpal necrosis are usually asymptomatic unless inflammation has progressed to the periradicular tissues. The pulp will NOT respond to the EPT and if using a digital EPT, this result should be reported as NO response (NR) over 80. The pulp will NOT respond to thermal tests. The dental record entry for this pulpal diagnosis should be pulpal necrosis. PMN cells in Necrotic pulp. YES to palpation, YES to percussion.

• Pulpless Tooth - A tooth from which the pulp has been removed. For example, a tooth with previous pulpotomy/pulpectomy/root canal debridement or previous root canal therapy should be recorded as a pulpless tooth for the pulpal diagnosis. Previously Treated - A clinical diagnostic category indicating that the tooth has been endodontically treated and the canals are obturated with various filling materials, other that intracanal medicaments.

3 • Previously Initiated Therapy - A clinical diagnostic category indicating that the tooth has been previously treated by partial endodontic therapy (e.g. pulpotomy, pulpectomy).

• PreviouslyTreated- tooth that has been endodontically treated and canals are obtured with various fillings materials others than intracranial medications

4 3) Periradicular/PeriapicalConditions:

• Normal Periradicular Tissues - Normal periradicular tissues will be non- sensitive to percussion and palpation testing. Radiographically, periradicular tissues are normal with an intact lamina dura and a uniform periodontal ligament (PDL) space.

• Acute Periradicular Periodontitis or Sympthomatic apical Periodontitis- Acute periradicular periodontitis occurs when pulpal disease extends into the surrounding periradicular tissues and causes inflammation. However, acute periradicular periodontitis may also occur as the result of occlusal traumatism. The patient will generally complain of discomfort to biting or chewing. Sensitivity to percussion and palpation is a hallmark diagnostic test result of acute periradicular periodontitis. The PDL space may appear normal, widened, or there may or may not have apical radiolucency.

• Chronic Periradicular Periodontitis or Asymptomatic Apical Periodontitis - When bacteria or bacterial products from a necrotic pulp or pulpless tooth slowly ingress into the periradicular tissues, the patient’s immune system may become involved in a chronic conflict. The resultant inflammatory process causes periradicular bone resorption and DESTRUCTION that manifests as a periradicular radiolucency RL on the radiograph. Clinically, the patient is asymptomatic. Percussion and palpation testing produce non-sensitive responses.

• Acute Periradicular Abscess - In this situation, bacteria have progressed into the periradicular tissues and the patient’s immune response cannot defend against the invasion. It is characterized by rapid onset, spontaneous pain, pus formation, and often swelling of the associated tissues. Depending upon the location of the apices of the tooth and muscle attachments, a swelling will usually develop in the buccal vestibule, on the lingual/palatal, or as a fascial space infection. Percussion testing produces a response that is usually exquisitely sensitive. This exaggerated response can help differentiate between

5 acute periradicular periodontitis and the early stages of acute periradicular abscess. Palpation testing produces a sensitive response. Radiographically, the PDL space may be normal, slightly widened, or demonstrate a distinct radiolucency. SINUS TRACT—> HALLMARK. Must drain lesion.

• Subacute Periradicular Periodontitis - The patient will present with mild to moderate symptoms that may include spontaneous pain or discomfort on biting or chewing. The tooth may present with any pulpal diagnosis. Percussion testing produces a mild sensitive response and palpation testing may or may not be sensitive. Clinical symptoms are not as severe as acute periradicular periodontitis. Radiographically, the tooth will present anywhere from a normal periradicular appearance to a distinct radiolucency. These patients must receive endodontic treatment in a timely manner because the condition can quickly progress into acute periradicular periodontitis or an acute periradicular abscess.

• Chronic Periradicular or Apical Abscess (CAA) - An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort and intermittent discharge of pus through an associated sinus tract. Clinically, the patient is usually asymptomatic because the SINUS TRACT allows drainage of any exudate from the periradicular tissues (intermitent discharge PUS). EPT and thermal testing are non- responsive. Percussion and palpation testing usually produce non-sensitive responses. Radiographically, a periradicular lesion is associated with the involved tooth. This entity can also occur with a pulpless tooth that has been partially or definitely endodontically treated if continued bacterial contamination and/or leakage occurs. —> from granulomas and cysts (well defined RL)

• Focal Sclerosing Osteomeylitis (condensing osteitis) - This entity may be considered a true lesion of endodontic origin (LEO). The involved tooth will have an etiologic factor for low-grade, chronic inflammation such as a necrotic pulp, extensive restorative history or a crack. The patient may be asymptomatic or demonstrate a wide range of pulpal

6 symptoms. EPT and thermal tests may or may not be responsive. Percussion and palpation testing may or may not be sensitive. Radiographically, the involved tooth will present with increased radiodensity and opacity around one or more of the roots. Evidence supporting consideration as a LEO is that 85% of these periradicular radiodensities resolve after endodontic therapy if they have a pulpal diagnosis of irreversible pulpitis.

• Focal Osteopetrosis - This entity is not a LEO. The patient will be asymptomatic. EPT and thermal testing are responsive and normal. Percussion and palpation testing will typically be non-sensitive. The involved tooth is usually a virgin tooth or has a normal pulp. Radiographically, the tooth will present with increased radiodensity and opacity around one or more of the roots. No treatment is necessary and the tooth should simply be monitored at periodic recall.

• EPT------1-79 shows vital and 80 or over shows necrotic

Prognosis:

• Worst prognosis—-> lesion Perio-Endo

7 • Best prognosis—>lesion Endo-Perio

4) Endodontic Treatment:

• Endo (RCT) 1st

• Endo (SRP) 2nd

• Pulpotomy—>removal of coronal portion of Pulp. Caries more than 2/3 in dentin. Carious deciduous teeth or for permanent with undeveloped roots (open apex). Is an alternative to extraction when RCT is NOt possible. Emergency two. in permanent teeth with acute pulpitis. Pulpotomy in Fully Developed Permanent teeth are NOT successful (is temporary procedure). Formocresol—>90-98%, CAOH—>60% (succes rate).

• Pulpectomy—-> when irreversible pulpits, pulpal necrosis, hyperemic pulp, evidence of furcation or PA involvement seen on X-ray, spentneous pain, buccal or extraoral swelling and increased mobility.

• Pulp Capping—>accidental pulp exposure (mechanichally); pulp of young child. Not in primary teeth with caries exposures. In primary we do Pulpotomy.

• Direct Pulp Capping—>place a sedative antiseptic on exposed healthy pulp. Dycal (CAOH) (pintpoint)

• Indirect Pulp Capping—> Remove infected dentin. Place: 1) Apply Liner CAOH2 —>0.5-a.75 mm; then 2) GI (Resin modified glass Ionomer cement)—> as a base. Indications: for deep caribous lesions, no chronic pain, no Rx pathologic, vital pulp, normal tooth color, mobility.

8 5) Primary teeth:

• Radiolucency at furcation (1Primary molar)—> Necrotic Pulp—> Tx: EXT

• If it's a primary 2nd, YES furcation, but YES restorable—->PE

• If its any other primary tooth NO furcation—>PO

• NO furcation (1Primary molar)—> PO (pulpotomy)

• YES furcation (1Primary molar)—>EXT

• NO furcation NO restorable (1Primary molar)—> EXT

• NO furcation, YES restorable, YES root resorption—>EXT

• NO furcation, YES restorable, NO root resorption—>PE (pulperctomy)

• Percussion—-> for newly erupted teeth

• NO EPT—-> for traumatic tooth

9 6) Apexogenesis/ Apexification/Apicoectomy:

• Apexogenesis —->VITAL tooth/ open apex.

• Apexification—> NON-VITAL tooth/incomplete apex form.MTA. Example: irreversible pulpitis with open apex

• Apicoectomy—> root-end resection. Example: failing RCT, when an apical portion persistent apical pathology after RCT, apical fracture, overextension.

7) Root canal medications and irrigation:

• Calcium hydroxyde: a) preserve vitality and continue development, b) achieve apical closure. CONTRAINDICATED in a) pulpotomy in a child because it causes irritation leading to resorption in primary teeth and b) pulp symptomatic for the last month `

• MTA (mineral trioxide aggregate): MTA is an endodontic cement that is extremely biocompatible, capable of stimulating healing and osteogenesis, and is hydrophilic. Close apex with MTA. Least cytotoxicxic

• ZOE (Zinc Oxide Eugenol): used for pulpectomy. Apex not closed in primary teeth.

• Formocresol: most common medication for pulpectomy/pulpotomy

• NAOCl (Sodium Hypochlorite) —>NOT Chelator, Disolves ORGANIC tissue (necrotic). Desinfectant. Most common ittigant.

• EDTA (17%)—> YES Chelating agent, removes INORGANIC material and SMEAR LAYER.

10 8) Avulsed teeth:

• Most important factor of avulsed teeth—-> TIME

• HANK Solution—> best storage media for avulsed tooth

• Milk (PH 6.5-6.8)—>best to preserve PDL) or use Saliva, physiologic saline solution

• 90% Success rate—> before 15 min

• 50% Success rate—-> 30 min

• Splint avulsed teeth—-> 1-2 weeks / 7-10 days

• DO NOT replantation on avulse primary tooth.

Failure replantation of Avulsed teeth—> external resorption

9) SPLINT:

• Avulsion—>7-10 days Non Rigid Splint, antibiotics

• Horizontal root fractures—-> Rigid Splint, 3 months (12 weeks) . Dx: take multiple vertical X-rays.

• Extrusion—-> is a splint for 2-3 weeks

• Intrusion—>reposition and splint

10) Endodontic Lesions:

• PINK tooth—> internal resorption. Tx: RCT

• Replacement Resorption—> when tooth is ankylosed

11 • Vertical Root fracture—>RCT+ Crown + Pain—-> common in mandibular molars (mandibular 2nd followed by mandibular 1st and maxillary premolars are the most common affected). Most common cause is condensation of gutta percha. Isolated pocket depth. Is also called cracked tooth.

• Cracked tooth—> pain upon bitting. On MANDIBULAR 1st MOLARS.

• Occlusal Trauma—> Crown + sensitive to cold + sense to pressure

• Granuloma: RCT tooth, periapical lesion after apicoectomy, still sensitive, neutrophils, plasma cells NON-VITAL tooth. NO symptoms. Proceed by “ Chronic Apical Periodontitis”.

• Ameloblastoma—->benign, locally aggressive from odontogenic epithelium. Multilocular radiolucency cause root resorption. Most in mandible.

• Cyst—> inflammatory response of the period with develops from preexisting “Granuloma”. Central fluid- filled, epithet lined cavity. Chronically infected tooth. Rx: well-defined RL limited by RO border of bone sclerotic. Asymptomatic.

Granuloma and Cyst—>Only differentiated

• Cementoma (Periapical cementla dysplasia)—> ant. mand.RL- RO(Calcifies). Vital teeth

• Traumatic Bone Cyst—>not a true cyst, no epithelial lining. Young people, asymptomatic. RL appears arrows VITAL tooth.

• Globulomaxilary Cyst (developmental)—> Lat. incisors, canine roots. VITAL tooth.

• Lateral Periodontal Cyst—> VITAL

• Phoenix Abcess—> Acute exacerbation of a chronic apical periodontitis (ADECA)

12 11) Failure RCT:

• Cleaning of the canals

• Poorly filles canals (p

• Lack of seal

• Radiolucency and fistula due to—> incomplete RCT

• Inadequate disinfection

• Bacterial Infection (anaerobes)

12) Access to RCT:

• Maxillary Central incisor—> triangular

• Maxillary Lateral incisor, Canine and 2nd Premolar —> Oval

• Maxillary 1st Premolar—->Kidney shape

• Maxillary molars—-> triangular

• Mandibular molars —> trapezoid

13 OPERATIVE

1) Caries:

• Critical PH to develop caries—-> 5.5 (enamel starts to demineralized)

• Anticariogenic—> Fluoride

• Earliest sign in of carious lesion—> change in names opacity

• 3 factors caries initiation—-> a) substrate, b) bacteria, c) host susceptibility

• Caries Initiator—> S. mutans (acidogenic and cariogenic)

• Caries progression of the decay—> Lactobacilus

• Root caries—-> Latobacilus casei

• Most cariogenic—>Sucrose—> converting to—> Dextran (using envyme glucosyltransferase)

• Remineralized Enamel—> Harder and more resistant to acids, darker than surrounding, rougher than tooth structure

• Interproximal caries—> BELLOW the contact (apical to the proximal contact)

• Caries in children depend—>a) amount, b) consistency, c) time

• ECC (early childhood caries)—> Most on Max central an 1st molars, mandibular ulnafected because tongue blocks

• —->Age at which children develop dexterity and speech. (5 yrs speech 8 yrs dexterity).

14 2) Dx Caries:

• Exolorer catch

• DYFOTI—>Caries detection Class I, Class II and Class III

• DIAGNODENT—> Detects only Class I caries (occlusal caries)

DEFT—> for Kids

3) Most common caries:

• Most common caries —>Hispanic

• Most common Unrestored caries —->Black

• Most common caries in permanent teeth —->White females

• Most common location of caries —>Pits and fissures (2 cones) BOTH facing DEJ

4) Primary teeth Largest to Smallest:

• Largest primary teeth: Mandibular 2nd Molar

• Smallest primary teeth: Mandibular Lateral incisor

15 5) Permanent teeth Largest to Smallest:

• Largest permanent tooth: Maxillary 2nd Molar

• Smallest permanent tooth: Mandibular Central Incisor

6) Burs:

• Tungsten Carbide: cutting into dentin, metal crowns, amalgam. Cutting efficiency of carbide is more in dentin

• Diamond: for extracoronal prep

DO NOT use diamond on metal crown, generation of heat.

• # 271 bur to start cavity prep

• To converge F & L walls—> bur 169 (tapered bur) if no 245

• Difference between 330 and 170 carbide burs (was asked)—> they both pear shaped with only difference in head lengths

• Bur 330–->2mm

• Bur 170/171—-> 4mm

• Difference between 245 and 330carbide burs—> Length.

• Bur 245 is longer

• Bur 245—> 3mm length, 0.8 mm diameter (pear and elongated bur)

• Bur 330—> 1.5 mm. (pear shape)

*More blades on Bur—> smoother, decreased cutting

*Less blades on Bur—> cut better but less smoother

16 7) Instruments:

• Spoon excavator—> remove caries and cave amalgams

• Chisels —-> cut enamel (Hatchet and GMT are chisels)

• Hatchet—>have a cutting edge in plane of handle. Not for bevel inlet prep.

• GMT (gingival marginal Trimmer)—> has curved blade and angled cutting edge. The advantage of using GMT instead of Enamel hatchet is angle of the blade.

8) Sterilization:

• Dry Heat—> DOES NOT cause corrosion to burs

• Steam Heat—> destructive to burs

9) Composite:

• Composite bond type—>Mechanical bond (micromechanical)

• Photo initiator for composite—-> Camphoroquinone

• The most radiopaque in composite is—-> Barium

• Microfill composites are —->more color stable than hybrid. Microfill have the smoothest finish compared to—> hybrids resins which are rougher. Rougher will pick up stain easier.

• Postoperative MOD composite pain, most likely—-> Hyperocclusion

• Composite Class 2 determined by—> caries extension

17 • Posterior composite failure mostly due to—> Polimerization Shrinkage in Margin , decay or microleakage

• Replace Post. composite due to—> a) Recurrent caries, b) Fracture

• Replace Ant. composite—-> staining

• Class 2 done without rubber dam will see microleakage —-> 2-4 weeks after

• Rubber Dam Holes TOO CLOSE——>hieghest chase of leakage

• HEMA composite—> cause Contact dermatitis

10) C- factor:

• Less Walls——-> Lower C Factor

• More Walls——> Higher C factor. Example= Class I

11) Amalgam:

• Axial pulp should be—> 0.5 into DEJ

• Retention grooves in axiobuccal/axiolingual walls—>for proximal resistance

• Gingivo-axial line angles—> Rounded

• All Walls—90 degree CAVOSURFACE MARGIN (external surface)

• Pulpal floor—> FLAT

• M and D walls of Class I amalgam—> must be DIVERGENT

18 • CLASS I amalgam—-> slight DIVERGE oclussal (M-D) only, CONVERGE B-L

• CLASS II amalgam —->CONVERGE B-L

• CLASS V amalgam—-> DIVERGE ALL walls

• RETENTION—> 1st= B-L Walls CONVERGE; 2nd= Retention Grooves/ occlusal devotail

• RESISTANCE—> 1st=Flat floors, ROUNDED angles (bevel in axiopulpal line angles)

• Minimal thickness—> Functional cusp= 2mm; Non- Functional cusp= 1.5 mm

• “Ideal” amount of dentin required between amalgam an pulp insulation—> 2 mm

• Spherical amalgam—> need to be condensed more

• Zinc in amalgam—-> deoxidizer (decrease oxidation)

• More corrosion in wich phase—> Gamma 2 Tin-Mercury

• Methyl Mercury (organic mercury)—> most toxic

• Amalgam if it is contaminated with water? loss of strength

• Overtrituration of amalgam—> Decreased setting time and decreased expansion and makes it stronger, will have “optimal strenght”

• Final polishing of amalgam—>at least 24-48 hours when amalgam is fully set

• Marginal leakage decreases as the —-> restoration ages

• Most for amalgam to fail—> outline cavity design, depth, poor condensation, inadequate cavity prep (especially the isthmus area)

19 12) Inlay/Onlay:

• Inlay—-> advantage over amalgam—> esthetics, less tooth reduction. The internal line angles are SHARP, but the axio-pulpal line angles are beveled or rounded. Prox. retention form is a rectangular box with a reverse bevel and a Reverse bevel not the gingival Wall.The Isthmus is the same for inlay and amalgam.Indicated= for LOW CARIES RISK. Inlay CAVOSURFACE —>40 degree

• Post-op sensitivity in direct Inlay—> Polymerization Shrinkage

• Onlay—>advantage of MOD only over amalgam—> better facial contour and Microleakage.

• Onlay Indicated—>when cuspal coverage is needed or when cusp undermined by Not enough dentin. Best indication for onlay—> LOW CARIES RISK.

• Cement for porcelain Onlay—> RESIN

• They are convergent. ONLY . WALL TO CONVERGE IN INLAY ONLAY = AXIAL WALL. But occlusal divergent

• When you include cusp into preparation, what is it called? Retention

*Removing cusp affects—> retention form

*Increasing intercuspal space affects —>resistance form

*Marginal ridges help with—> resistance form

*Loss of marginal ridge affects —>both resistance and retention

20 13) Gold:

• Malleability – deform (without fracture) under compressive strength; ability to form a thin sheet; gold is malleable

• Gold—>Greatest malleability and ductility

• Hardest metal (most rigid)—> Gold Type IV

• Only advantage of porcelain over gold—->esthetics.

• Gold crown is —> MORE CONSERVATIVE

• Gold—>Functional cuss=1.5 mm; Non-Functional cusp=1 mm

• Bevel edge of Gold—> for marginal stability and better adaptation

• Gold inlay/onlay—> divergent walls (2-5 degrees per wall), 30 degree bevel margins for better fit, skirt – extend beyond line angle

• Gold MOD Onlay—> the axial pulp walls are—> Converging

• Zinc Phosphate—> can be used for gold

• Base metal indicated over gold alloy—> FPD

Metal=0.5mm; Porcelain= 1-1.5mm; Tooth cutting=1.5-2mm

• Use base metal apposed to gold—> long span bridges

• Most accurate pulpal test to determine vitality of a tooth with a full- gold crown—> THERMAL TEST

• “Galvanic Shock”—-> gold on upper tooth, lower amalgam, patient has severe pain

21

14) Glass Ionomer:

• Can be Used to—> cement a bridge and fill a cervical lesion

• Base for CAOH—>Glass ionomer, Zinc Phosphate, Resin Gals ionomer

• Place GI as a LINER—> OVER—>CAOH =for pulp capping to protect the pulp (put 2mm)

• GI —-> forms IONIC BOND

• GI —> is brittle= high compressive, low tonsil strength

• Acid in GI—-> silicate glass powder & polyacrilic acid

• Cool Glass slab—>to mixciment—>to incur orate more powder into liquid as possible

• GI as a cement—-> Low PH, can cause sensitivity, pulp irruptability, least erosive

22 • GI as a restorative material—->Release Fluor, Low solubility, thermal increase, chemical adhesion, biocompatible.

• GI used in—> low stress baring areas, root caries, Class V

15) Veneers:

• Veneers reduction—>incisal 0.7; middle 0.5 and gingival 0.3mm

• Most technique sensitive part of placing veneers—> Preparation

• Need—>2 appointments

• Cement—>Resin cement

• Repair sequence—> a) Microetch, b) Etch, c) Silinate, and d) Bonding

*Etchant—>create microspores, micromechanical retention, NOT chemical

• Order of bleaching and veneering process —>Bleach, wait 2 weeks, prep tooth and cement

• Sodium Fluoride (NAFl)—> do NoT stain veneers

23 16) Porcelain:

• Only advantage of porcelain over—> done in one appointment

• Porcelain is—> strongest under compression

• Porcelain cement with —> Resin

• Porosity in PFM—> inadequate condensation

• Porcelain and veneer—> rounded internal

• Most lab complain—> tooth under reduced

• Cooper stain porcelain—> Green (cervical third)

• Silver turns porcelain—> Green (other parts of the teeth)

• Best material to oppose porcelain crown—> porcelain

• Weakest porcelain—> Feldspastic

• Crown—> 1st=check esthetics (shade); 2nd=Interproximal contact

• Reason for functional cusp bevel—> Resistance, structural durability, prevent cusp fracture

• PFM (Porcelain Fused to Metal)—>margin should be subgingivally and have 2mm of incised reduction.

• Junction of PFM—> right angle, not round

*Thickness Metal structure= 0.5 mm

*Porcelain Thickness= 1-1.5 mm

*Porcelain occlusal= not less than 1.5 mm

*Tooth reduction for PFM= 1.5- 2.0 mm

24 *Labial shoulder=1.5 mm

• If you see opaque parcelain—> Inadequate reduction of Inciso facial (1/3 incised PFM)

• Anterior PFM, incised 3rd was radioopaque—> Improper second plane of reduction

17) Modified Bridge Lap Pontic:

• Barely touch gum

• Minimaly ridge contact (residual ridge)

• Oclussal gingival dimension—> is the most important

• Worst cantaliver—> Lateral abutment+ central pontic—> NO

18) Shade:

• Hue: Color. Hue should be selected 1st. Least important. Wavelength

• Chroma: saturation

• Value: Lightness. Is the most important in shade selection. Can’t be incresed. From 0-100

-Orange —> change Hue

-Yelow—> increase the chroma

-Violet—-> reduce de value

-Staining on porcelain------reduce the value, increases metamerism and loss of floursence. Increase Chroma.

25 • Prevent Metamerism by—> shade under multiple light sources

19) Bleaching:

• Office bleaching————superoxol (35% hydrogen peroxide)

• Walking bleaching------sodium perborate.(10% carbamide hydrogen peroxide)

• Internal Bleaching————superoxol——side effect: Cervical Root resorption (CRR)

• Worst response for—> gray stain (tetracyclines)

• Most successful teeth for bleaching—> aged yellow staining

20) Bevel termination:

• All ceramic or porcelain jacket crowns—> shoulder

• Metal ceramic with porcelain (PFM) extended to marginal edge —> shoulder

• Metal ceramic with metal collars—> shoulder with bevel or chanfer

• Full gold crown —> bevel (feather edge) or chanfer

21) Visible- Light Curing Unit (Dual):

• Hold the light as close as possible to resin—> within 2 mm

• Increasing layers of —->1.5 to 2 mm at a time

• Cure longer—-> with darker shades resin; Cure Light intensity—-> 400

26 PROSTHODONTICS

1) RDP

• Rest------mostly premolar and canine

• Anti rotational device——rest/connector

• Indirect retainer------rest should be placed away from distal extension as possible

• Retention—> retentive arm of clasps (direct retainer)....against vertical occlusal forces and resistance of metal deformation

• Support—> rest (indirect retainer) ....against vertical forces

• Stability....> alveolar ridge + harmonious occlusion ...against horizontal forces *Reciprocation (cross-arch stabilization).....> rest + minor connector + reciprocal clasp arm.

• *Bracing....> clasps in non-undercut area ( occlusal rest-minor connector junction should be acute < 90 degree for max. bracing.

2) Working and Balancing side:

• Working side —> the contact is between lingual inclines of facial cusps on maxillary teeth and buccal inclines of facial cusps of mandibular teeth.

27 • When you are moving towards working side it means the cusp slope of maxillary buccal cusp is higher, that's why there is no contact on balancing side.

• So reduce the facial cusp of maxillary working side in order to provide balancing side contact.???

• Centric glide or interferences —>movement of the mandible while in centric relation, from the initial occlusal contact into maximum intercuspation. There is premature contact between mesial inclines of max teeth and distal inclines of mand. teeth. CORRECTION: A centric interference (forward slide) can be corrected by grinding the mesial inclines of maxillary teeth and distal inclines of mandibular teeth.

• Protrusive interference —>anterior movement of the mandible from max intercuspation towards the incisal edges. -occurs when distal facing inclines of max posterior teeth contact mesial inclines of mand. posterior teeth during a protrusive movement. CORRECTION: distal of upper and mesial of lower (DUML).

• Retrusive is opposite of protrusive.

• Working side interference —>occurs when there is contact between max. and mand. posterior teeth on the same side of the arch in the direction the mandible moved causing disoclusion of teeth. - Working side interferences generally occur on the inner aspects of the lingual cusps of maxillary molars.) CORRECTION: Buccal upper-Lingual lower (BULL RULE).

• Non-working side interference(balancing side)—>occlusal contact between max. and mand. teeth on the side opposite the direction the mand. has moved. - results when there is contact between max. buccal facing inclines of

28 palatal cusp and mand. lingual inclines of buccal cusp on the non- working side

CORRECTION: Grind the secondary centric holding cusps( Grind the inner inclines of the mandibular buccal cusp) Never grind the maxillary lingual cusps (primary centric holding cusps)..(LUBL) For the National Board Exam questions, you can reduce the maxillary lingual cusp if it is high in centric as well as other occlusal positions -> in reality, you should not. (Dental decks)

Reference crown #30=

***Inclines to the RIGHT—-> L inclines of B cusp

***Inclines to the LEFT—-> B inclines of L cusp

29

30 31 3) Impression Material:

• Additional Silicones—-> MOST STABLE impression elastic impression moisture environment ,Gets affected by latex.

LEAST distorted by water—> additional silicones or condensation silicones better answer if available

• Condensation Silicones—-> releases alcoholic

• Poliether—> Most Rigid impression, sticks to the teeth, hard to remove

• Polisulfide—> best for tear strength, but would NOT use for a single crown

• Irreversible Hydrocoloid (ALGINATE)—> NO for final FPD impression, NO for crown impressions, DO NOT use for casting impressions

• Reversible Hydrocoloid—>

4) TMJ:

• Inferior Compartment—> Art. disc + condyle—>HINGE type

• Superior Compartment—>Mand. fossa + art. disc—> TRANSLATION

• Bennet movement—> working side

• Bennet angle—> Non- working condyle

• Dislocation of condyle—> mandible deviates the OPPOSITE

• Subcondylar Fractures Dx—> deviation of mandible to the SAME side of the fracture.

32 • Condylar Hyperplasia—> malocclusion, chin deviate AWAY from the affected side, slowly elongation of the face

33 PEDIATRIC DENTISTRY

• Calcification of primary teeth——> ADBCE (14,15,16,17,18 weeks)

• Calcification of permanent teeth —>1st molar at birth , all anterior teeth except max lateral incisor 6months, lateral incisor 12months, 1st PM 18months, 2nd PM 24months and 2nd Molar 30months

• Calcification of primary teeth begins —>in 2nd trimester and complete in 3-4 years

• LEEWAY space—> in maxilla 1.mm and mandible 3.1mm

• Until the establishment of contact—->no need for bitewing radiograph in child

• At the age 6 —->1st OPG

• Most common retained primary tooth —->primary mandibular 2nd molar

• At birth child can`t differentiate b/w sour bitter and sweet.

• Transverse ridge------mb-ml------separates the mesial portion from rest of crown and in primary mandibular 1st molar

• Primary Mandibular 1st molar------longest cusp MB and sharpest cusp ML. no central fossa.

• Primary mandibular 2nd molar----resemble permanent mandibular 1st molar---same outline cavity design for amalgam but MB.DB and D on primary are equal size while in perm 1st molar distal is shorter

• Primary molar —->has more prominent facial crest of contour

• Prim teeth greatest FL diameter------of mand 2nd molar

34 • Ant tooth having shorter inciso cervical height than MD width is prim max CI.

• Cusp of prim max canine is longer and sharper than perm max canine and also MCR is longer than DCR (opposite is true for perm canine)

• Primary Maxillary 1st molar occlusal pit and grove pattern is H shaped.------varies from any other tooth in arc Pulp therapy is contraindicated in children who have serious illness like leukemia and cancer pts

• SUCCESS of pulpotomy depends upon vitality of radicular pulp

• Calcification of pulp------pulpotmy contra indicate

• Formocresol------19% formaldehyde+ 35% cresol and 15% glycerin and water

• Formocresol causes fixation of pulp and degeneration of odontoblasts. Pulpotomy------formocresol brown, glutryladehyde pink and ferric sulfate dark red.

• Formocresol is fastest of all apply only 15 seconds while glutryl for 4 min and form for 5min

• IAN block success ratio is more in children and antpost position of mandibular foramen is about the same or distal in children.

• Most commonly used anesthetics in children—> are lidocoine and mupivacaine

• Primary teeth------class 2------no need for gingival bevel-----bcz enamel rods occlusally

• SS crown in child------oclusal reduction----1-1.5mm and buccal reducation 1-1.5mm

• Primary teeth are more mineralized as compare to permanent teeth.

35 • Most injuries to primary teeth 1.5-2.5 years

• Avulsed primary tooth not replanted.

Fluoride:

• Rule of 6 for fluoride...

• Fluoride in 1 liter of water at 1 ppm —> 1 mg/L=1ppm

• Fluoride replace in hydroxylappatite—-> HYDROXYL

• LEAST soluble—>Fluorapatite (insoluble)

• Fluoride DOES NOT—> Increase the strength of collagen

• Neutral sodium fluoride tray on teeth—>4 min

• MOST BENEFICIAL Fluoride —> anyone but most beneficial to Children

• Fluoride—> BREAKSDOWN collagen, is bacteriocidal, fluoroapetite is more resistant to acid attack, decreases solubility of enamel, excreted by kidneys, helps remineralize.

• Fluoride is localized in—> Outer EnameL

36 • Fluoride stored—-> skeletal tissues

• WORKS BEST—-> SMOOTH SURFACES

• Interproximal caries—> Decresed (-) due to fluoride

• PH=====APF (acidulated fluoride) ————3.0-3.5 (Not in toothpaste). NO for porcelain crowns, will wear away GI (glass ionomer)

• Sodium fluoride—————PH 9.2—> BEST for CHILDREN

• Stanous fluoride—> may stain (IN toothpaste)

• ADA recommends to apply apply in office fluoride for—-> 4 minutes (if a child vomit than 2min +1min)

• Risk of fluorosis------excess of 3ppm

• Toxic dose of Fluoride—> 5-10 mg/Kg

• If water fluoried is —>more than 0.6pp—> NO fluoride supplementation

• The new recommended level—> is 0.7 ppm.

• The optima; range of fluoride in the community water—> 0.7 and 1.2 ppm

• EPA highest concentration of natural fluoride in drinking water—>4 mg/L

• Community fluoride—>0.2% / week in udnerprivelaged areas

• Percentage of fluoride water in US —>85% (should be 65-70%)

• Effectiveness of Water fluoridation in the U.S. is—> 20%-40% (40%)

• How do they administer Fluoride in schools? —>0.2% fluoride rinse 1x week

37 • If the age of child is less than 6 months or more than 16 years------no fluoride supplementation

Examples:

*4 year old 0.4 ppm fluoride —-> gives 0.25 mg/L supplement

* 4 year old lives in a community with 0.28 ppm—> give systemic supplement.

* 2 year old takes 20 mg fluoride pill—> nausea

* 7 years old patient has no fluoride in drinking water—> give systemically 1 mg

* 7 years old patient living in an area with 0.2 ppm fluoridated water—> supplement 1.0 ppm

* Supplementation for 10 year old with no other fluoride source—> 1 mg every day

38 PATHOLOGY

1)Most common:

• Most common impacted anterior tooth —maxillary canine

• Most common impacted tooth —lower 3rd molar then upper 3rd molar and maxillary canine then mnd 2nd pm

• Most common supernumerary tooth — mesiodens

• Most common ectopically erupted tooth — maxillary permanent first molar followed by canines - Man: canine & 2 pm

• Most common malignancy of oral cavity—squamous cell carcinoma

• Most common benign tumor of oral cavity — fibroma

• Most common retained tooth – primary mandibular second molar

• Most common recurring cyst— odontogenic keratocyst (OKC)

• Most common cyst in oral cavity— Periapical cyst

• Most common odontogenic cyst— Radicular cyst

• Most common non-odontogenic cyst— Nasopalatine cyst (NC)

• Most common epithelial odontogenic tumor— Ameloblastoma

• Most common odontogenic tumor— Odontoma

• Most common non odontogenic tumor—osteosarcoma

• Most common lichen planus —reticular lichen planus

• Most common dermatosis to affect oral cavity — lichen planus

39 • Most common chemical burn in oral cavity —aspirin burn

• Most common topical fluoride in adults — stannous fluoride

• Most common topical fluoride in children—1.23 APF gel.

• Most common brushing technique- scrub technique

• Most common developments cyst —nasopalatine cyst

• Most common complication of GA (op) —nausea

• Most common used drug for petit-mal epilepsy—Ethosuximide

• Most common used drug for grand-mal - Phenytoil

• Most common drug used for temporal epilepsy —Carbomezepine

• Most common treatment for cyst – enucleation

• Most common used clasp—simple circlet clasp

• Most common used face bow in fpd— kinematic

• Most common complication of RA involves TMJ—fibrous ankylosis

• Most common salivary malignancy minor salivary glands and in children —mucoepidermoid carcinoma (MEC)

• Most common salivary malignancy in palate area— Adenoid Cystic Carcinoma (ACC) (2nd most common)

• Most common type of haemophilia— haemophilia A

• Most common type of gingivitis in children--- eruption gingivitis

• Most common type of cerebral palsy is – athetoid/ spastic

40 • Most common nerve involved in C sinus thrombosis – abducent

• nerve

• Most common type of impaction —-mesoangular

• Most common benign epithelial tumor---- papilloma

• Most common complication of surgical extraction of lower third molar — loss of blood clot

• Most common used instrument grasp — pen grasp

• Most common susceptible tooth for caries— mandibular first molar

• Most common contrast media - iodine in oil

• Most common cause of light radiographs — exhausted developer

• Most common cause of failure of RCT— inadequate cleaning and shaping-debridement

• Most common isolated yeast strain from RCT— Candida

• Most common bacteria found in root canals — gram positive

• Most common part of oral cavity affected by L planus –buccal mucosa.

• Most common isolated yeast strain from RCT— Candida

• Most common bacteria found in root canals --- gram positive

• Most common part of oral cavity affected by L planus –buccal

• Most common site for Kaposis sarcoma —palate

• Most common melanoma — superficial spreading

41 • Most common malignancy affecting skeletal bone—metastatic carcinoma

• Most aggressive salivary gland tumor— adenocarcinomakijuhybggf

• The most common cause of Bells Palsy is—> Herpes simplex

• Cleft palate more in females and cleft lip more in males

• Caucasians have more lip cancer while African american have more oropharyngeal carcinoma.

• Most common neoplasm—> Basal Cell Carcinoma

• 2nd most common neoplasm—> Saquamous Cell Carcinoma (SCC)

2) Least Common:

• Least common melanoma— acral

• Least common site for SCC —-Cancer of nasopharynx

• Least common neoplasm —> Malignant Melanoma (MM) (epithelial cell tumor)

3) Rx appearance:

-“Ground Glass appearance”--> Fibrous dysplasia, Albright’s Syndrome, Hyperthyroidism

-“Punched out radiolucencies”-->Multiple Myeloma Hand Schüller Christian, Histiocitosis X, Letterer Siwe, Eosinophilic granuloma

-“Cotton Wool Appearance"-->Paget's Disease

42 - “Tooth Floating in Air”-->Eosinophilic Granuloma

-"Snow Appearance” or “Snow flake”--> Calcifying Epithelial Odontogenic Tumor (CEOT)/ Pindborg

-“Honey Comb Appearance”--> Odontogentic Myxoma

-“Soap Bubble Appearance"--> Aneurysmal Bone Cyst, Cherubism

-“Scooped out radiolucencies at mid root level”--> Histiocytosis X (langerhans cell histiocytosis) Hand Schuller- Christian triad

-“Scalloped radiolucencies around the roots of teeth”--> Simple Bone Cyst aka Traumatic Bone Cyst

-“Dead Space”—> traumatic bone cyst

-“Beaten Metal appearance on the skull”-->Crouzon Syndrome

-“Enlarged marrow spaces”--> Sickle Cell Anemia

-“Widened PDL with dissolving bone"--> Non-Hodgkin lymphoma

-"Moth-Eaten radiolucency”--> External Resorption, Ewing’s Sarcoma

-“Salt and pepper appearance radio-graphically”-->COC

-“Onion skin appearance”—> Garre’s Osteomyelitis

-“Swiss cheese pattern” —> Adenoid Cystic Carcinoma

-“Sunburst”—> Osteosarcoma

-“Starry Sky”—> Burkit’s Lymphoma

-“Heart Shaped”—-> Nasopalatine duct cyst

“Teardrop shape or Inverted Pear shape”—> Globulomaxilary Cyst

“Sausage like” appearance—> Sialodenitis

43 -“Radiopaque”—> Focal diffused Sclerosing Osteomyelitis

4) Location:

• Cemento-osseous dysplasia---lower anterior

• Traumatic bone cyst--- mandibular between canine and molar region

• Primordial cyst--- mandibular 3rd 4th molar region

• Dentigerous --- mostly mandibular 3rd molar and maxi canine region

• Stafne bone cyst--- below mandibular canal

• Lateal periodaontal cyst--- mandibular canine, premolar area

• Bohn’s nodule---- newborn gingiva

• Epstein pearl--- midline of palate of newborn

• Cementoblastoma--- mandible molar area, grows on roots

• OKC--- mandibular molar and ramus

• Nasopalatine duct cyst-- between roots of maxi central incisors

• Globulomaxillary cyst--- between maxi lateral and canine

• Thyroglossal duct cyst-- midline of neck

• Dermoid cyst--- FOM or upper neck

• Brachial cyst--- anterior to sternocleidomastoid

• Ossyfiying fibroma--- premolar area

44 5) Stadistics:

• Highest DMFT = White (caucasian) (highest amount of restored teeth)

• Highest Untreated primary teeth = Hispanic Highest

• Highest untreated perm teeth = Black (African American)

• Highest Moderate periodontitis = Black males ( African American)

• Highest Class II caries = Whites (caucasian)

• Highest Class III caries = Blacks (African American)

• Highest Cleft lip/palate w/ Class III occlusion = Native American

• Highest Cleft lip alone = Asian

• Highest Cleft lip in USA = 1:700 to 1:800

• Highest class 2 malocclusion = whites of northern European descent

• Highest class 3 malocclusion = Asian Caucasians

• Cancer =Asian Caucasian have more lip cancer while African american have more oropharyngeal carcinoma.

• Highest anterior open bite = African American(blacks)

• Highest deep bite = cuacasian( whites)

• Highest cemento osseous dysplasia = black middle aged women

6) Reverse General things:

• Reverse overjet.—> Class III MO

• Reverse polarity —> ameloblastoma

45 • Reverse bevel —> Class II, gold, inlay

• Reverse bevel incision —> in undisplaced flap when the incision is done coronal to the sulcus

• Reverse occlusal plane —> in panoramic radiograph when pt chin is tipped upward

7) Important Diseases according to "Age":

• Fibrous Dysplasia---->Children

• Paget's Disease------>Adults over 50

• Aneurismal Bone Cyst---->Teenagers

• Cherubism----->Children

• Periapical Cemeno osseous Dsysplasia---->Middle aged black women

• Capillary Hemangioma---->1st week after Birth till 9 years old

• Cavernous Hemangioma---->Old Adults

8) Diagnostic Tumor:

T=Size;To=No envidence of tumor; T1= < 2 cm; T2=4 cm; T3=>4cm

N=Lymph node involvement, No=No palpable; N1=palpable homolateral Not Fixed; N2=palpable bilateral, Not fixed; N3= palpable, Fixed

M= distan Metastasis; Mo= No metastasis, M1= clinical or Rx evidence of metastasis.

46 9) Inmune Granulomas:

Immune granulomas can have a few different appearances, depending on their cause. Here’s a summary:

• Tuberculosis. Granulomas —in TB are sometimes called tubercles. They are caseating, meaning they are “cheesy” in gross appearance. Histologically, there is a bunch of amorphous, granular, necrotic debris in the center of the granuloma. You should see some acid-fast bacilli in there too.

• Leprosy —These granulomas are non-caseating, and an acid-fast stain should reveal bacilli.

• Syphilis— Granulomas in syphilis are called gummas; they have central necrosis (but not really caseating, because you can still see cell outlines) and a plasma cell infiltrate.

• Cat-scratch disease — These granulomas may be stellate in appearance. They contain neutrophils and some granular debris, but giant cells are rare.

• Sarcoidosis—Granulomas in sarcoidosis are non-caseating, with a lot of activated macrophages.

• Crohn’s disease— Sometimes you see non-caseating granulomas in the i n t e s t i n a l w a l l P O L Y P S i n p a t i e n t s w i t h C r o h n disease.GRANULOMATOUS GINGIVA HYPERTROPHY, bleeding rectal anus, oral granulomas, APTHOUS ULCER.

• Giant cell Granuloma— Giant cells=HYPERPARATHYROID. Giant cells bone=Dx Bence Jones. Most like Granular cell Myeloma (also linked to congenital epulis)

47 10) CYSTS:

• Periapical Cyst (Radicular cyst) (PC)—> most common on Non-Vital tooth. Necrotic pulp. When is Acute= “periapical abbess”, when is Chronic= dental GRANULOMA . Rest oF Malassez. Tx: RCT, apiecectomy or tooth extraction with apical curettage.

• Dentigerous Cyst (DC)—> crown of an impacted tooth (unerupted), least affected in 3rd molars, more affected in canines. From Reduced enamel epithelium (REE). Potential transform to AMELOBLASTOMA.

• Lateral Periodontal Cyst (LPC)—>unilocular or multilocular radiolucency in lateral periodontal membrane of adults, most common + in MANDIBULAR PREMOLAR Region LATERAL TO THE ROOT of tooth. From Dental Lamina (DL). Rx: well defined round or tear drops RL with opaque margin

• Bohn’s Nodules (Gingival Cyst of Newborn) —> neonate with multiple small gingival nodules on ALVEOLAR RIDGE. From rest of Dental Lamina (DL). No Tx necessary.

• Epstein Pearls (EP)—-> Baby with streaks on the PALATE

48 • Odontogenic Keratocyst (OKC) or Keratocystic Odontogenic tumor (KOTC)—>GORLYN syndrome. Aggressive, associated with “Nevoid Basal Cell Carcinoma”. POSTERIOR MANDIBLE. From Rest Dental Lamina (DL). PALMAR AND PLANTAR KERATOSIS, often BIFID RIB. Mnemonic: “OK Gordon Ba”. HIGH RECURRENCE. Calcified Falx cerebri.

• Calcifying Odontogenic Cyst (COC)—> is rare, “Ghost cells” keratinization (microscopically). Rx: RL with opaque foci. From Rest Dental Lamina (DL).

• Glandular Odontogenic Cyst (GOC)—>Rare, could be aggressive and recurrent . Sialo-odontogenic. From Rest Dental Lamina (DL).

• Dermoid Cyst—> contains structures such as hair, fluid, teeth, or skin glands that can be found on or in the skin. Located in FLOOR OF THE MOUTH and “ DOUGHY”

11) Odontogenic Tumors:

• Ameloblastoma —>+ most common EPITHELIAL ODONTOGENIC TUMOR. Benign but aggressive (local invasion),+ most common in MANDIBULAR-RAMUS area. Significant recurrence potential. Teeth are VITAL, slow growing and painless swelling. Mimic->”enamel organ”. Tto: wide excision to resection. Leads to DENTIGEROUS CYST (DC). Stellate reticulum BELL stage

Distinguish Ameloblastoma from OK—> reactive light microscopy

49 • Califying Epithelial Odontogenic Tumor (CEOT)—-> “PINDBORG TUMOR”. In MOLAR-RAMUS area. Similar to Ameloblastoma but Less (-) aggressive.

• Adenomatoid—> uncommon to rare odontogenic HAMARTOMA. Contain epitehlial duct like spaces and calcified enameled material. ANTERIOR JAW, Not recurrence.

• Odontogenic Mixoma (OM)—> uncommon to rare tumor of myxomatous connective tissue. Either jaw affected. RL= “Honey comb” pattern” or “soap- bubble lesion” appareance. CORTICAL EXPANSION AND ROOT DISPLACEMENT, always RL. Tx: surgical excision.

• Central Odontologoenic Tumor (COT) —-> rare tumor of Dense collagen with strands of epithelium. Rx: RL well defined in either jaw, multiplecular. Tx: surgical excision, FEW Recurrence

• Cementobalstoma—> Rx: well circumscribed “RO” mass of cementum and cementoblasts replacing the root of the tooth. Rare BENIGN neoplasms. VITAL tooth. + Most common in MANDIBLE AND POSTERIOR. Tx: tooth removed with lesion. No recurrence.

50 • Periapical cemento- osseous dyplasia or Cementoma (PCOD) —> apices of ANTERIOR MANDIBLE, teeth VITAL, No symptoms, Middle age Black Womans. Rx: “RL” circusscribed, gradually become opaque.

• Florida cemento oseeous dyplasia (FCOD) —> when involving both maxilla and mandible (entire jaw)

• Ameloblastic Fibroma and Ameloblastic Fibroodontoma—> CHILDRENS AND TEENS affected (12 years old) In MANDIBULAR MOLAR REGION. Rx: Unilocular or Multilocular with”Opacity”. Tx: enucleation or excision. Recurs.

• Odontoma—> + Most common tumor. In children and young adults. Rx: Opaque lesion” of Dental Hard tissues “MINIATURE TEETH”—> Compound Odontoma and Complex odontoma —> AMORPHOUS CONGLOMERATIONS OF MASS. Tx: curettage, No recurrence

• Adenomatoid Odontogenic Tumor (AOT)—> LESS RECURRENT, between canine-lateral. X-Ray: LESION goes to APEX

12) Abnormalities of Teeth:

• Anodontia—> a) complete—> all teeth are missing, b) partial—> congenitally missing teeth

51 • Oligodontia—> abcense of 6 or more teeth but not all

• Hypodontia—>only Few teeth

• Diphydontia—> having 2 successive set of teeth

• Fusion—> developmental union of 2 teeth. 2 buds 2 teeth.(2 roots)

• Concresence—>only the CEMENTUM of 2 teeth become united.

• Gemination—> division of a SINGLE TOOTH germ, incomplete formation of 2 teeth. 1 bud 2teeth (1 root).

• Dens in dente—> tooth within a tooth. + common lateral incisor.

• Ankylosis—> affected 1st and 2nd molar, percussion “Dull sound”.

• Abrasion—> abnormal loss of tooth structure due to NON- MASTICATORY physical friction. (TOOHBRUSH).

• Atrition —> wear of enamel due to normal function or excessive grinding (BRUXISM).

• Erosion—> acidic liquids (BULIMIA).

• Abfraction—> CERVICAL erosive lesions not attributed to any particular cause. Enamel “pop off”

• Amelogenesis Imperfecta—> Hereditary ECTODERMAL DEFFECT, affect enamel tissue intrinsecally, BOTH DENTITIONS AFFECTED, ENAMEL HYPOPLASIA, enamel is yellow, pitted; dentin, cementum and pulp is normal. OPEN BITE—> common finding in Type II and III. NO CONTACTS.

Type I (hypoplastic)—> defect in AMOUNT of enamel-BELL STAGE.

Type II (Hypomaturation)—> defect in final GROWTH AND MATURATION of enamel cristalites.

52 Type III (hypocalcified)—>defect in INITIAL crystalite, formation followed by defective growth.

• Dentinogenesis Imperfecta—> A.D. Intrinsic alteration of dentin, AFFECT BOTH DENTITIONS, PULP AFFECTED (oblitered type I and II ONLY, small or abcent), yellow opalent color, extreme occlusal wear, SHORT ROOTS, BELL-SHAPED crowns. Teeth are annual “translucent or opalent appearance” with color variantion from yellow-brown to gray. Tx: full crown coverage, NoT use as abutment.

Type I—> associated with OSTEOGENESIS IMPERFECTA, “blue sclera”, primary teeth are more affected. PULPLESS

Type II—> +common. Not bone involvement. PULPLESS. + COMMON TYPE.

Type III—> “Brandwine type”-> Only Dentin as II, multiple pulp exposures, PA- RL and variable rx appearance. SHELL TEETH. LARGE PULP CHANBER

• Dentin Dysplasia—> A.D intrinsic alteration of dentin. AFFECT BOTH DENTITIONS. HAVE GRANULOMAS AND CYSTS. “HAVE RL”

Type I (radicular dysplasia)—> +common, NORMAL COLOR of teeth and , pulp obliterated,SHORT ROOT (surrounded by granulomas or cyst, residual fragments of pulp (chevrons), frequent abcess. PULPLESS.

Type II (coronal dysplasia)—> Color of primary tooth-opalescent and permanents have normal color. Coronal pulp-is enlarged, NO Periapical RL. LARGE PULP CHAMBERS.

53 • Regional Odontodysplasia or Odontogenesis Imperfecta—-> NO hereditary. Unknown cause, SHORT ROOTS, OPEN APICES, enlarged pulp chambers, PERMANENT + AFFECTED, MAXILLARY ANTERIOR . Rx: “Ghost teeth”. Tx: EXT.

• Enamel Hypoplasia—> enamel is hard but thin in AMOUNT. Lack of contact between the teeth, rapid breakdown of occlusal surfaces, Yelowish-brown stain. AFFECT BOTH DENTITIONS

• Turner’s Hypoplasia—> ONLY PERMANENTS are affected, caused by “physical damage” or “PA infections” to the primary tooth. Single tooth affected.

• Enamel hypocalcification—> heredityary, enamel is SOFT and under calcified, NORMAL QUANTITY. Defect in the mineralizedion of teeth. “CHALKY TEETH”

13) Intrinsic Stains:

• Erythroblastosis Fetalis—> bluish-black, greens-blue, tan or brown

• Porphiria—> red or brownish

• Fluorosis—>white opacities or light brown to brownish-black

• Pulpal injury—> Pink and become orange-brown to bluish- black

• Internal resortion—> “Pinkish”. Tx: RCT

54 • Tetracycline—> from light yellow-orange to dark gray-brown.

• Hypomineralized—> white to brown

14) Fibro- Osseous Lesion (Non- Odontogenic):

• Cementifying Fibroma or Ossifying Fibroma (CF)—> to ossifying fibroma. BONY TUMOR, NON-ODONTOGENIC fibrosseous lesion. Located in BODY OF MANDIBLE. Rx:Well circumscribed radioopaque Foci. TX: Curettage or excision. Rare recurrence.

• Fibrous Dysplasia—> Mc-Cune Albright Syndrome=“ Cafe au Lait Spots“ . uncommon rare, uncapsulated . Involves the ENTIRE HALF JAW, + common in MAXILLA, CHILDREN (pre-puberty). Rx: DIFFUSE OPPACITY, tooth is VITAL “Ground Glass appearance”. Tx; surgical recon touring for cosmetic appareance.

• Osteoblastoma—> Young adults, 50% of pain. Rx: “RO” mass of bone and osteoblasts. Tx: surgical excision. Few recurrence.

15) Giant Cell Lesions:

• Peripheral Giant Cell Granuloma (PGCG)—> reactive lesion, RED to PURPLE GINGIVAL MASS. Exclusive in gingiva. TX: Excision

55 • Central Giant Cell (CGC)—> Tumor, ANTERIOR MANDIBLE, + most in CHILDREN. Rx: “RL” located.

• Aneurismal Bone Cyst (ABC)—> PSEUDOCYST (NO EPITHELIAL LINNING). Rx: multilocular, excision

• Hyperparathyroidism—-> VON RECKLINHAUSEN’S DISEASE OF BONE.(not to be confused with von Recklinghausen's disease, neurofibromatosis type I). Decresed VIT. D. Multiple bone lesions, Incresed PTH. Rx:Lost of lamina dura and tooth roots. Systemic signs: kidney stones, metastatic calcification, osteoporosis, neurological problems and arrhythmia.

• Cherubism—> autosomal dominant (A.D.), CONDITION OF THE JAW, BILATERAL JAW EXPANSION, in CHILDRENS, Symetrical swelling in 1 or both jaws. Rx: “Soap- Bubble” appearance. Tx: No tto

• Langerhans Cell Disease (LCD)—> abnormal proliferation of Langerhans cells. a) Eosinophilic Granuloma= Chronic localized form, bone only; b) Hand Schüller Christian= Chronic disseminated form (bone, exophthalmus and diabetes mellitus); c) Letter Size disease= acute disseminated form (skin, bone, internal organ lesion). IS FATAL. Rx: “Punched-Out appearance”arround tooth “Floating in the air”. Tx: Excison, radiation, chemotherapy.

• Paget’s disease—> disturbance of bones, ADULTS >50 YEARS. Enlargements of bones, DENTURES BECOME TOO TIGHT, bony pain. Tx Biphosphonates for suppression of bone resorption. Rx: “Cotton Wool Appearance” IN SKULL. Can transfer to OSTEOSARCOMA. Develop slowly. INCREASED ALKALINE PHOSPHATASE

16) Bone Inflammatory Diseases:

• Osteomyelitis—> apex of the tooth for long standing pulpitis a) Acute Osteomyelitis—> causes extension of periodical abcess (Staphylococcus

56 and Streptococcus) and periodontal disease, bacteremia. BONE OF THE JAWS. RX: “Moth-Eating appearance”. Staphylococcus and Streotococcus. PAIN; b) Chronic Osteomyelitis—> GARRE’S, Involves periosteum. Tx: tooth removal, antibiotics; c) Diffuse sclerosing Osteomyelitis—. due to chronic periodontal disease in middle-age BLACK FEMALES bone sclerosis “RO”. d) Biphosphonates-related osteonecrosis of the Jaws.

• Garre’s Osteomyelitis—> chronic osteomielitis with proliferateve osteitis. “periosteal inflammatory reaction”. Rx: “Onion-Skin appearance”. Tx: EXT and antibiotics.

**Remember—> Garre’s osteomyelitis and Ewing’s sacoma are both Rx “onion-skin appearance“

17) Bone Malignancies:

• Osteosarcoma—>+ common primary malignant tumor, Rx DIFFUSE, radiating pattern, PDL Invasion, Simmetrical Widening of PDL, loss of trabeculae mass, could metastasis to brain and lungs. Osteosarcoma prognosis better in mandible as compare to maxilla. +Most common in MANDIBLE, PAIN, Swelling, paresthesia. Young people. Rx: “sun burst” or “Sun-Ray” appareance.

• Chondrosarcoma—>are radioresistant. rare sarcoma of the JAWS.

• Ewing’s Sarcoma—> rare “round- cells” . CHILDREN, Rx: “RL”. RAMUS OF THE MANDIBLE. + MALES. 5-30 years old, destruction of alveolar bone, loosening of teeth, mucosal ulcers, increased metastasis. Rx: “Moth-eaten” erosion costed with expansion.

• Burkitt’s Lymophoma—> factor causal-EBV

• Metastasic carcinoma—> Rx: “RL” to Opaque. From breast, lung, prostate, kidney

57 • Multiple Myeloma—> rx: “punched-out appearance”. Bone pain, Bence jone protein.

18) Weak bone:

• Osteomalacia—> softening of bones caused by deficiency of Vit D. (adults)

In Children=Rickets disease, is osteomalacia in children, DELAYED ERUPTION, malocclusion and increase caries rate

19) Hereditary Conditions:

• White Sponge Nevus—>autosomal dominant (A.D), Asymptomatic, WHITE SPONGY appearing in BUCCAL MUCOSA BILATERALLY. TX: No tto, biopsy.

• Epidermolyasis Bullosa—>autosomal dominant (A.D), BLISTER, SCAMING, Hypoplastic teeth

• Hereditary Hemorragic Telangectasia—> autosomal dominant (A.D), RED MACULES, PAPULES, epistaxis.

• Cleidocranial Dysplasia—> loss of clavicles, SUPERNUMERARY TEETH, HYPERTELORISM, RETAINED PRIMARY TEETH, fontanelles failed to close.

• Hereditary Ectodermal Dysplasia—> X linked recessive. Lack of sweat glands, abnormal skin, SPARSE HAIR, nails, teeth. Partial or complete anondontia. CONICAL TEETH. Apparence OLD AGE

• Gardner’s Syndrome—>Autosomal Dominant (A.D). INTESTINAL POLYPOSIS, IMPACTED SUPERNUMERARY TEETH, MULTIPLES

58 ODONTOMAS, Skin lesions. Lead to Colorectal cancer ADENOCARCINOMA.

What has Polyps like—> peuts jeghers syndrome and crown’s disease

• Osteopetrosis—> Albers-Schoberg diseases, MARBLE BONE. Bone sclerosis (lacl of bone remodeling and resorption), BONE PAIN, blindness, deafness, anemia.

20) Neoplasm:

• SCC (Squamous Cell Carcinoma)—> also called Epidermoid carcinoma. Most malignant cancer oral.Least oral cancer=Whites. Worst rate SCC= Black men. The etiology is external factor and stress. Xerostomia— increase risk of SCC. Most—LATERAL BORDER OF TONGUE, Incisional biopsy . 1rst most common LOWER LIP—> “sun exposure”, 1st most common intraoral LATERAL BORDER OF TONGUE; 2nd most common intraoral FLOOR OF THE MOUTH kerathoacanthoma —>looks likeSCC

• Basal cell Carcinoma—> Malignant Epithelial cell Tumor. Central CRATER that crust and bleeds + common NOSE. LIP

• Multiple Myeloma—> abnormal plasma cell, BENCE JONES PROTEINURIA. Rx: “punched- out appearance” . JAWS, MOLAR, RAMUS AREA, SKULL.

• Melanomas—> Vertical growth phase. In this phase metastasis is possible.

59 21) Other Diseases:

• Neurofibromatosis—-> VON RECKLINHAUSEN DISESE, soft nodules, “Cafe-au-lait spots”, macular pigmentation of the skin, SUPERNUMERARY TEETH; LISH NODULE ON IRIS, NEUROFIBROMAS. Neurofibroma—> if solitary on tongue, buccal mucosa, vestibule, if multiple Syndrome Neurofibromatosis.

**Remember—> “cafe-au-lait spots” common in Neurofibromatosis (Von Recklinhausen disease) and Mc June Albright Syndrome (polyostotic fibers dysplasia)

• Lupus Erythematosus—> collagen/CT multisystem disease. Unknown cause. Women 10x more frequently. Avg age =31years old. Malar rash, kidney problems 50% of time & lead to organ failure. Pericarditis also frequent complication; warty vegetations on valves =Libman-Sacks endocarditis. Oral lesions if evident- palate, B mucosa, gingiva

• Cavernous Sinus Thrombosis —> infection of the upper lip, involved canine space or man. ant. teeth, danger triangle of face (No valves in the veins). Signs= 1)HEADACHE, 2) blurred vision. Afraid because valveless veins and infection can go back to brain. Bacterias involved= Staphylococcus aureus and Streptococcus. Its life threatening and requires immediate Tx.

• Ludwing Angina—>Submandibular, sublingual and submental. NO retropharyngeal. Bilateral celulitis, swelling, pain, raising of the tongue, swelling of the neck, malaise, fever, dysphasiagia, and severe cases stridor or difficulty breathing. edema of the glottis is the main complication of Ludwing angina.

Infection of mnd 2nd pm goes into or root of 3rd molar disappears — >submandibular space

60 If you have an infection in in the lateral pharyngeal space—>the Medial pterygoid will involved

• Lymphoma Hodgkin—> “Reed- Sternberg cells”for Dx. Painless

• Hairy tongue— hypertrophy of Filiform papilla

• Pyogenic granuloma—Raspberry like appearance.

• Erythema Multiform—“Target lesions”/“Bull’s eyes”. “Erythematous, bleeding swelling”, between premolars and canine, RAPID growth (Rapid change in size), PINK growth, most seen in PREGNANT Woman.

• Scarlet Fever— “strawberry tongue” inflamed

• Focal cemento osseous dyplasia —>post mandible, caucasians

• Florida cemento oseeous dyplasia —> when involving both maxilla and mandible

• Cystic Fibrosis —->early morning appointment are NOT recommended, avoid GA, upright position, short appointments, enamel hypoplasia, lower lip everted, dental development and eruption delayed.

• Epulis fissuratum caused by—>over extended denture, traumatic occlusion

• Epithelial hyperkerathosis—> bilateral white lines on the occlusal plane (linea alba)

• Fordyce Granules—-> ectopic SEBACEOUS GLANDS

• PenphigoiD (Deep)—-> SUBepithelial separation,—> Autoinmune disorder more severe, blisters, vesicle. DESCAMATIVE GINGIVITIS. NO acantholysis. Less severe.

61 • PenphiguS (Surface)—> SUPRAbasal epithelial, intraepithelial (vesicles) —-> less severe, YES acantolysis. Nicolsky +. Most severe .Tzanc cells.

• Descamative gingivitis —> associated with—> Pemphigoid and Liquen Planus because they are SUBepithelial.

• Epidermolisis Bullosa—> child small blisters that develop from mild provocation over areas of stress—ie elbows and knees****

• Traumatic Neuroma—> most common in a patient that has a denture and a firm, swelling under the buccal flange midway between incisors and molars

• Fibroma—-> NO coliflowerlike, similar to epulis fissurathum, caused by HYPERPLASIA

• Leukoplakia—> INCISION BIOPSY. incise multiple areas it it is possible.

• Erytroplakia—> smokers, red points in soft palate. SEVERE DYSPLASIA. Carcinoma in situ and dysplasia.

• Kerathoacanthoma—> Resembles to SCC, 16 weeks and then disappears

• Leukoedema—>DISSAPEARS upon stretching, ALWAYS BILATERAL, Blanches, no Tx, Grayishp-White Lesion.

• Addison’s disease—> Decreased Cortisol BRONZING OF ENTIRE SKIN, PIGMENTATION OF GINGIVA, TONGUE HARD PALATE, BUCCAL MUCOSA

• Cushing syndrome—> Increased Cortisol, 20-30 years old. NO PIGMENTATION in oral cavity

• Carcinoma—-> is malignant EPITTHELIAL NEOPLASM

• Sarcoma—> is malignant MESENCHIMAL NEOPLASM (C.T)

62 • Actinomycosis—> bacterial infection of Actinomyces israelii, “LUMPY JAW”, SULFUR GRANULES. due to previous infection, surgery. DRAINING FISTULA.

• Tuberculosis—> large ulcers, painless chronic, TONGUE BASE AND GINGIVA. Primary lesionsCervical Lymph nodes, larynx and middle ear. Secondary lesion are in tongue, palate and lips.

• Sarcoidosis—> LUNG growth, granulomas, inframmatory cells, lymph nodes. Is similar to TB. Tx: corticosteroids

22)Leukemia:

Leukemia is bone marrow disease involving uncontrolled increase in White blood cells.

• ALL (Acute Lymphocytic Leukemia)—> +common leukemia in CHILDREN. + responseveness to treatment.

• AML (Acute Myelogenous Leukemia)—> + malignant. ADULTS

• CLL (Chronic Lymphocitic Leukemia)—>LEAST Malignant. Most common in OLDER patients, the pathologic finding is lymph node enlargement.

• CML (Chronic Myelogenous Leukemia)—> FATAL. PHILADELPHIA CHROMOSOME.

Patients signs and symptoms: young person, fatigued and has Jacked-up mouth, gums always bleeds.

Pt had erythematous and gingival enlargement over past 5 weeks. And increased report of bruising on body – cause is acute leukemia: Specifically, AML

63 23) Blood Disorders:

• Plummer- Vinson Syndrome—> IRON DEFIciency anemia. “Spoon shaped finger nails”. Complication SCC tongue and throat, predispose to cause carcinoma. + common in middle age woman.

• Aplastic Anemia (AA)—> “Red blood cells are DEFECTIVE”, usually fatal. Drugs like Cloranfenicol can cause A.A,. Associated with “Drug Toxicity”.

• S i c k l e C e l l A n e m i a ( S C A ) — - > R B C d i s c o r “ C r e c e n t shapoed”.Production of abnormal hermoglobin. + common in FEMALE <30 years old.

• Purpura Spots—> “pintpoint spots”, extravasation blood capillaries.

Thrombocitopenic Purpura(TP)—>”Werlhof dissen”multiple bruises, petequias in palate, gingival hemorraghea.

Thrombotic Thrombocitopenic Purpura (TTP)—> severe and FATAL. large purport spots > 3mm, echymoses. Tooth extraction is contraindicated due to excessive bleeding.

• Agranulocytosis—> severe dec. in granulocytes (neutrophils). Also caused by “antithyroid drugs”: methimazole, carbimazole, and propilthiouracil. RAPID PERIODONTAL DESTRUCTION, oral ulcers and gingival bleeding.

• Pernicious Anemia (PA)—> lack of secretion of intrinsic factor necessary for the absorption of Vit B12. patients consult dentist to relieve “GLOSITIS”

• Erythroblastosis Fetalis—> fetus Rh+ is incompatible with, mothers the fetus RBC, leading to anemia. + common ABO incompatiblety and less common Rh incompatiblelity is the most severe.

64 24) Connective Tissue Lesions:

• Traumatic neuroma—> MENTAL FORAMEN

• Neurilemoma—. benign neoplasm’

• Schawamoma—> + common in TONGUE

• Fibromatosis—> benign. +common in MANDIBLE, locally aggressive and inflictrative

• Lynphangiomas—-> benign “HAMARTOMAS” TONGUE (growth as same rate of surrounding tissues.NO malignant change.

• Pyogenic Granulomas—> GINGIVA + common

• Epulis granulomatosum—> caused by retained foreign material “iatrigenic” malpraxis.

• MEN Syndrome (Multiple Endocrine Neoplasia Syndromes)—> A.D

MEN I—>tumors or hyperplasia pituitary, parathyroids, adrenal cortex, pancreatic islets.

MEN II—> “Sipple’s Syndrome” PTH hyperplasia or adenoma, Pheochromocytomad of Adrenal medulla, medullary carcinoma of the thyroid gland

Men I and II DO NOT have ORAL manifestations of mucosal neuromas

MEN III—-> “mucocutaneous neuromas”, multiple exophitic masses in buccal mucosa, tongue or lips. “MUCOSAL NEUROMAS” MEDULLARY CARCINOMA OF THE THYROID

• Neurofibromatosis—> Von Recklinghousen Disease, mustiples neuronibromas, “Cafe-au-lait spots”—> 6 or more than 1.5 cm, Iris Frekling “Lish spots”, axillary freckling “Crow’s sign”

65 • Leiomioma—> smooth muscle

• Rhabdomioma—> skeletal muscle

• Scleroderma—> systemic disease, progressive “Tissue fibrosis”. Excessive production of type I and II collagen. CREST SYNDROME. WIDENNING OF PDL, LOSS OF RAMUS MANDIBLE. Blue fingers, hair loss and hardness skin

25) Herpes and Virus disese:

• Gingivostomatitis Herpetica —>caused by Herpes Simplex type I. Initial presentation during the first ("primary") herpes simplex infection. of greater severity than herpes labialis (cold sores) which is often the subsequent presentations. is the most common viral infection of the mouth, affects both the Free and attached mucosa. Tx:Acyclovir, valacyclovir, pencyclovir, famciclovir

85% of population have—> herpes

Peak prevalence of herpes between—> 2-3 years of age

The most common cause of Bells Palsy is—> Herpes simplex

• Primary Herpes Stomartitis—> young persons, fever, vesicles (contagious when are present). Most are SUBCLINICAL

• Recurrent intraoral herpes—> mucosa overlaying bone, Hard palate (most common site). Reactivation from the Primary herpes

• 2ndary Herpes—> Lip, gingival, palate

• Herpes—>over Keratinized tissue

• Herpes Withlow—> FINGER

• Post-Herpetic Neuralgia—> caused by Herpes zoster

66 DRUG OF CHOICE: DO NOT GIVE corticosteroids in herpes

Acyclovir—->herpes I, II, VZV,EBV. Best treatment for herpes, inhibit mRNA poluymerase,15 mg/kg, 5 times/day x 7 days Ganciclovir (IV): CMV or (valancyclovir – oral)

Primary HSV: PALLATIVE.

Tx is supportive—topical before eating, analgesics, maintain fluid/ electrolyte balance, anti-viral agents.

• KAPOSI Sarcoma—> Malignant neoplasm, most common associated with AIDS, purple-brown spongy nodules, caused by Human Herpes 8, most likely on HARD PALATE.

• Aphthous ulcer—> NON-Kerathinized tissue

• Epstein Barr Virus (EBV)—> associated with BURKITT’S LYMPHOMA. Nasopharyngeal carcinoma, hairy leukoplakia (non-malignant in AIDS patients), INFECTIOUS MONONUCLEOSIS. IgM antibodies

• Paramyxovirus—> cause MEASLES (RUBEOLA)= KOPLIK’S SPOTS (surround by red ring, No wipe off); and MUMPS (PAPERAS)= cause deafness in childrens and Orchitis in males infertility

26) Hepatitis:

• Hepatitis A—> Fecal-oral transmission

• Hepatitis B—> Parenteral or sexual transmission. 6-8 weeks inoculation

• Hepatitis C—> Cirrhosis and “hepatocelular carcinoma”

• Hepatitis D—> Only in pat. with episodes or hepatitis B

• Hepatitis E—> enterically (like A)

67 27) Papiloma:

Papilloma: verrucous, pedunculated or sessile, COLIFLOWER looking, most common benign neoplasm,EPITHELIAL TISSUE ORIGIN, posterior border of the tongue, lips, gingiva or soft palate,

• Heck disease (also known as focal or multifocal epithelial hyperplasia) —> is an asymptomatic, benign neoplastic condition characterized by multiple white to “pinkish papules” that occur diffusely in the oral cavity. Caused Human papilloma virus types 13 and 32.

• Condyloma Acuminatum—> genital wort, HPV (human papilomavirus) types 6 and 11.

• Verrucous carcinoma—-> buccal vestibule, most common on smokeless tabacco,HPV 16 and 18 (verrucous leukoplakia), large broad base exophytic papillary leukoplakia lesion.

28) Salivary gland tumors:

*Most common salivary gland tumor: Pleomorphic adenoma

*MOST COMMON SITE = MINOR GLANDS OF PALATE

*MOST COMMON TUMOR OF PAROTID GLAND*

• Pleomorphic Adenoma—>Most common BENIGN Major & Minor salivary glands. Mixed tumor, Best prognosis. PAROTID GLAND=+ common in woman

• Adenoid Cystic Carcinoma—> Most common MALIGNANT. Minor. salivary gland. Neurotrophic factor. Adenomatoid Worst prognosis. PERINEURAL INVASION(neurotrophic factor). Most common on PALATE. “Swiss cheese” microscopic patterns

68 • Mucoepidermoid Carcinoma—> Most common MALIGNANT Major salivary gland.

• Warthin’s tumor—> PAROTID neoplasm. + in males over 50 years old. 2nd benign + common Parotids ‘

+most common site of minor intraoral MINOR S.G neoplasm—> PALATE

+common site of interior MAJOR S.G neoplasm—-> PAROTID

• Necrotizing Sialiometaplasia—-> lesion of MINOR S.G, in adults males Hard palate related to isquemia. Mimic malignant neoplasm (SCC and mucoepidermoid carcinoma)

• Mucocele—>mucus extravasation “bluish hue”, due to TRAUMA to minor S.G excretory duct. + frequent LOWER LIP, painless

• Mucoretention cyst—> less common, No meanical trauma.

• RANULA—> due to mucus plug, FLOOR OF THE MOUTH, Blue mass under TONGUE

• Sialodochitis—> “sausage links”

• Sialolithiasis—> calcified salivary stone, submandibular duct (Wharton’s duct). Tx: surgically remove submandibular gland (cannulate the duct and remove).

• Frey’s Syndrome—-> STRONG SALIVATION, auriculotemporal syndrome, SWEETS BEFORE EATING PAROTID GLAND, due to surgery in parotid.

• Whartin’s tumor—> PAROTID GLAND

• Stafne deffect—> salivary glan DEPRESSION DEFFECT, salivary inclusion

69 29) Other Syndromes:

• Sjögren Syndrome—> AUTOINMUNE DISESE, Xerostomy, dry eye, Parotid. Linked with LYMPHOMA. Affect kerathoconjuntivitis and genital. DRY MOUTH. Destruction of salivary glands an tear duct. RHEUMATOID ARTHRITIS often accompanies Sjögren Syndrome. Lab test: SSA/SSB ANA patterns

• Benchets Syndrome—> produce aphthous ulcers, genital ulcers and uveitis. Rare disorder cause severe neurological complications.

• Triad Steven jhonson Syndrome—> Severe expression of Erythema Multiform. Triad a) stomatitis, b) eye lesion, c) skin lesion

• Teacher Collins Syndrome—> also called mandibulofacial dsyostosis. Loss of zygomatic bone, mandibular hypoplasia, malformed ears and eyelids.

70 • Mc- Cune Albright Syndrome—->Alkaline Phosphatase increased. Severe form of Polyostotic FIBROUS DYSPLASIA, “Cafe-au-lait spots” in skin. PREMATURE PUBERTY IN FEMALE (hallmark). Transform to OSTEOSARCOMA. Rx: “RO” well circumscribed.”Ground-glass appearance”. Dx differencial=Ossifying fibroma. VITAL TOOTH.

• Cherubism—> familial fibrous dysplasia

• Peutz- Jeghers Syndrome—>FRECKLES on LOWER LIP 5 year old and oral mucosa. “POLYPS INTESTINES”. Dx differential= Gardner's syndrome.

• Papillon Lefvre Syndrome—->periodontitis, Hyperkerathosis hand/feet, premature tooth loss (4 years old)

• Pierre Robinson Syndrome—> micrognatia, glssoptosism cleft palate and abcense of gag reflex

• Sturge Weber Syndrome—> Vascular malformation eye, HEMANGIOMA, and “Port Wine Stain.

71 30) Disease with Triads:

• Syphilis—highly infectious stage of sylphilis are the first two stages. Copper colored vesicles on palm and soles of the feet. Syphilis CHANCRE resembles= aphthous ulcers

Hutchinson Triad (syphilis)—> a) Interstitial keratintis, b) Hutchinson incisors, c) Eight VIII nerve deafness

• Hand Schüler- Christian Triad: associated with multifocal Langerhans cell histiocytosis. Triad: a) diabetes insipidus, b) exophthalmos, and c) bone lesions (langerhams disease SKULL ). Oral signs: bad breath, sore mouth, loose teeth, lesion are sharply. X-Ray: “punched out radiolucency” and teeth appear “Floating in the Air”.

72 31) Candidiasis:

• Systemic antifungal in HIV patient —>Fluconazole (Diflucan)

• Candidasis in cancer patients due to —->Chemotherapy

• Inhaled methacholine (steroid) produce—> oral candidiasis

• Candidiasis—-> patches that scraped off. Tx= Nystatin.

• Sistemic tx for candida—>Amphotericin B

• Rhomboid tongue—> type of candidiasis (redness in the middle of the tongue)

32) Thyroid diseses:

• Hyperthyroidism—-> a) Grave’s disease also known as toxic diffuse goiter (exophthalmus) is the acute and severe form of

73 hyperthyroidism.b) Thyrotoxic Shock=dyaphoresis (excessive sweating), tachycardia, fever, increased HTN, exophthalmus, loss of weight. c) Thyroid Storm= severe version

Thyrotoxocosis= DIAPHORESIS, FEVER, and THACHICARDIA

• Hypothyroidism—> in a) Child= CRETINISM (underdevelop mandible, overdevelop maxilla, enlarge tongue, DELAYED ERUPTION); b) in Adults=MYXEDEMA. Sings and symptoms: gain wight, BRADYCARDIA, cold temperature, fatigue, constipation, Thin hair. Tx= Levothyroxin c) Hashimoto—>most common cause of hypothyroidism, autoimmune disease.

• Hypoparathyroidism—> important consequencence of HYPOCALCEMIA = clinical manifestation of TETANY. Give Vit. D

• Hyperparathyroidism—> Too much PTH . Vit. D deficiency, HYPERCALCEMIA. INCREASED ALKALINE PHOSPHATASE. a) Osteoporosis, b) Kidney Stones, c)Central Giant cell granuloma. Tx: depend the type

Decreased alkaline phosphatasia is—> hypophosphatasia

33) Cleft Palate/ Lip:

• Cleft Palate—> occurs 8-10 th week embryonic life. 1:2000

• Cleft Lip—> the medial nasal process fails to fuse with the lateral portion of the maxillary process. 1: 1000—> 6-7 weeks

74 RADIOLOGY

1) Diagnostic Xray:

• Waters view--->Maxillary sinus and Mid-facial tractures

• Bite wing------>Interproximally caries

• Periapical- ---->Periapical tissue & Periodontal disease

• Submentovertex--->Zygomatic fracture

• Panoramic—-> mandibular fracture

• Reverse Towne’s—> condyle fracture

• Lateral Cephalometric--->Face growth

• Posterior-Anterior of skull--- >Skull vault

• Reveres Towns---->Condylar necks

• MRI------>TMJ

• CBCT----- >Implant & Endo

2) Safety:

• If NO barrier—> 6 feet, 9-135 degrees

• MAX DOSE of personal radiation—>YEAR= 50 Msv, Per Month= 4 Msv, Per Week= 1 Msv.

• Colimation—> reduce area of exposure-reduce amount of scattered radiation because reduce the size of the x Ray Beam.

• Switch ROUND to RECTANGULAR—> greater decrease in overall radiation

75 3) Panoramic errors:

• Inverted curve of spee—->chin too high (chin up)—> REVERSE SMILE (Frown)

• Exagerated curve of spee—>chin too low (chin down)—> STEEPER SMILE

• If patient is positioned TOO FAR backward —> the WIDER the images of the anterior teeth.

• If Pano, short upper roots—> patient didn’t put tongue on the top of their mouth

Correction

• To reduce Penumbra—> decrease Object/ film distance

• Larger Penumbra—> decrease contrast, more unsharpness

4) Periapical errors:

• Incorrect HORIZONTAL angulation —produce OVERLAP

• EXCESSIVE VERTICAL angulation—> produce FORESHORTENING tooth

• INSUFFICIENT VERTICAL angulation—>produce ELONGATION of tooth

• Perpendicular to Object but Not to Film—> Elongation

• Perpendicular to Film but Not to Object—> Foreshortening

• X-Ray too white—> low mA (underexposed), exposure too short, incorrect focal-fit distance

• X-Ray too dark—-> too long in developer solution (overexposed), high mA, exposure too long, kVp too high

76 5) General principles in radiology:

• Film based xray mean manual------higher resolution and need higher radiation exposure

• Disadvantages of digital imaging------rigidity and thickness of sensor, dec resolution, higher intial cost and unknown sensor lifespan.

• Higher KVP------long scale contrast------lower contrast Lower KVP------shorter scale contrast------higher contrast PID------size increases------lower magnification PID------size decreases------higher magnification

• Radiopaque------rays does not pass------bone enamel, dentine, metals

• Radiolucent------rays passes------soft tissues,

• Developing solution gets weaker------film gets lighter

• Yellowish brown film------insufficient fixing or rinsing

• Foggy film------outdated, improper storage or light leak

• Amalgam is most radiopaque

• Effects of radiations are not visible immediately

• Effects of radiation exposure are additive.

• Cell nucleus is more sensitive than cytoplasm, Radiation causes cell death by------apoptosis, chromosomal abnormalities, preventing successful mitosis

• Osteoradionecrosis------hypo cellularity, hypoxia, hypo vascularity.

77 • No effects on embryo or fetus from low doses radiation uses in dental radiography.

• Radiotherapy------tumor in advance stage, deeply invasive, radiosensitive.

• Radiation------xerostomia persisted beyond a year less likely to shows return of the function.

• Higher KVP------greater energy levels, shorter wave length, more penetration and less absorption

• To increase the film density------increase mA, KVP, decrease the source object.

• Paralleling technique------long cone------increase exposure time

• Poor contrast------due to high KVP

• Periodontal bone levels will not be represented accurately by bisecting technique

6) Radiosensitive/radioresistant tissues:

• RadioSensitive tissues—> a) Bone marrow, b) Reproductive cells, c) Inmature cells, d) Lymphoid cells, e)Intestine

**Most radiosensitive—> Hematopoietic Bone Marrow

**X-Ray damage cells by—>hydrolysis of water H2O2 molecule

• RadioResistants tissues—>a) Salivary glands, b) Kidney, c) Liver, d) Muscle

**LEAST sensitive or MOST RADIORESISTANT —> Muscle

• Osteoradionecrosis—> Biphosphonates with radiation. Must be above 65 gys. MORE IN MANDIBLE

78 SURGERY AND PAIN CONTROL

1) Le Fort:

• Le Fort I osteotomy (Horizontal, Maxillary sinus) —>advancement; or treatment of upper jaw malocclusion and cleft palate. Used to treat maxillary “retrognathia”. LOWER MIDFACE, “Floating palate”.MOST COMMON SURGERY FOR MAXILLA.

Example= patient Class III—> Le fort 1 with BSSO

• Le Fort II osteotomy (Pyramidal, Periorbital) —>treatment of upper jaw “fractures”. Involvement of the INFERIOR ORBITAL RIM(infraorbirtal nerve). Pathognomonic sign= periorbital echimosis, hematoma.

• Le Fort III osteotomy (Transverse)—> treatment of “midface" problems and deficiencies. ENTIRE MIDFACE, NASOETMOIDAL COMPLEX, Craniofacial dissociation.

Occlusal discrepancy—> mandibular fracture sign.

Angle fracture of mandible—> increase chance of IAN paresthesia and numbness (lower lip)

2) Blood Values:

• Platelets Count:

-Normal value—> 150K- 450K

-Platelets required for surgery—> 75K

-Intraoperative bleeding—> 40-70K

-Spontaneous bleeding—> less than<20K

79 • Hematocrit:

-Normal value for men—> 38.8 to 50 %

-Normal value for women—> 34.9 to 44.5%

-Required for surgery —> 30%

• PT (prothrombin time):

-Normal Value: 11-13.5 seconds

-PT increases in warfarin, liver diseases, vit-k deffiency, antibiotics, and fat malabsorption.

• PTT (partial thromboplastin time):

-Normal Value: 25-35 seconds

-PTT increases in Heparin, von willbrand disease, hemophilia

• INR (International Normalized ratio) :

-Ideally INR —> 0.8- 1.2 normal INR—> 1 (12 sec)

-Ideally INR for Pt having anticoagulant —->between 2 and 3.5

Note: it should not be higher than 4 and lower than 3 before extractions which mat indicate or fuse bleeding for simple extractions

-Pt should be —->lower than <4 for moderate bleeding

-Included and impacted third molar surgeries or multiple extractions- it should be less than <3

-If —->over > 5 no surgical treatment

80

Example:

* Heparin—> PTT

* Haemophilia—-> PTT

* Coumarin—> INR

* ALCOHOLIC—> INR

* Aspirin—-> bleeding time

• A1C:

• In most labs, the normal range is 4-5.9 %.

• In poorly controlled diabetes, its 8.0% or above

• In well controlled patients it's less than 7.0%.

3) 2013 ADA Guidelines: According to these guidelines, antibiotic prophylaxis should be considered for people with:

• Artificial heart valves.

• A history of an infection of the lining of the heart or heart valves known as infective endocarditis.

81 • A heart transplant in which a problem develops with one of the valves inside the heart.

• Heart conditions that are present from birth, such as: Unrepaired cyanotic congenital heart disease, including people with palliative shunts and conduit.

• Defects repaired with a prosthetic material or device—whether placed by surgery or catheter intervention—during the first six months after repair.

• Cases in which a heart defect has been repaired, but a residual defect remains at the site or adjacent to the site of the prosthetic patch or prosthetic device used for the repair.

4) Antibiotic prophylaxis guidelines:

• Have been developed for people who have orthopedic implants such as artificial joints. In 2012, the ADA and American Association of Orthopedic Surgeons updated the recommendations and no longer recommend antibiotics for everyone with artificial joints. As a result, your healthcare provider may rely more on your personal medical history to determine when antibiotics are appropriate for people with orthopedic implants.

• For example, antibiotic prophylaxis might be useful for patients who also have compromised immune systems (due to, for instance, diabetes, rheumatoid arthritis, cancer, chemotherapy, and chronic steroid use), which increases the risk of orthopedic implant infection.

82

83 5) LA (local anesthetics):

Epinephrine dose:

• Normal patient—>0.2mg/200 mg or 11 cartridges

• CVS patients —->0.04/40 mg or 2 cartridges

• O2 is indicated for the treatment of all types of syncope except hyperventilation syndrome.

• Most important function of vasoconstrictor in LA is increase the depth and duration of action.

• Affinity for epinephrine 50% Alpha and 50% Beta.. while levonordefrin 75%Alpha and 25% Beta..(ep z more potent than L)

• LA------blockage—different size----smaller unmylinated fibers 1st than larger mylinated fibers or same size than mylinated fibers 1st and unmylinated later

• Procaine Not available in North America

84

85 6) Rescue CPR:

• Rescue breathing------1breath every 5seconds or 10-12 breath/min

• Chest compression-----depress the sternum---1.5-2 inches and 30 compression every 2 breath. 30/2—100/min

• Most of the oral bleeding can be controlled by pressure pack.

• Rescue breathing in children—> after every 3 seconds and in adults after 5-6 seconds

• Compression rate children—> 100/min

• Compression/ventilation ratio children—-> 30/2

• Compression depth: 1.5-2inches in adults while in children 1/3rd to 1/2of depth of chest

7) Nitrous Oxide/ Oxigen:

• Oxygen no less than 20% in nitrous oxide.

• oxygen is green ciliander; NO2 blue cylinder

• Adults= 70/30

• Children= Max 50% of NO2. 50/50

• After NO2 —> Patient must have 100% oxygen—. IF NO diffusion hypoxia

• Used in children to alleviate—> ANXIETY

• Minimum oxygen flow rate——3L/min

86 • In chilldren’s sedative mostly------chloral hydrate, -bitter taste and GIT irritation. Example=Hydroxizine is used with chloral hydrate because it decreese nausea.

• YES NO2 for (no contraindicated)—> for asthmatic and sickle cell anemia patients

• Contraindicated—-> COPD, respiratory infection, phenumotorax, 1st trimester pregnancy, contagious disease, middle ear infection, sinus infection, bowel obstruction, head injury.

• Adverse effect—-> nausea

In

asthma....avoid anti histamine, minimize epinephrine dose , avoid asprin and avoid erythromycin and clarithromycin if pt also taking theophylline

87 8) Implants:

• Biological width in implant —>3-4mm and in tooth 1-2mm

• Minimum Bone height—> 10mm is required for dental implant

• IAN and IMPLANT distance—-> 2mm

• Implant to vital structures—->2 mm

• Implant ant. to mental foramen—> 5mm

• Implant and implant—-> 3 mm

• Soft tissue height surrounding implant—->2-4mm

• Implant and tooth—> 1.5 mm

• Implant in all directions—> 1.5 al around

• Minimum implant length------10mm and maximum 16mm

• Amount of bone loss —>0.2mm/year

• Minimum amount of space required for 4mm dental implant is 7mm(4+1.5+1.5)

• The highest failure rate of implant —>in posterior maxilla D4.

• Most popular implant is —>root form.

• Implant of choice in very atrophic mandible is...... transosseous

• When there is adequate length/depth but insufficient width------blade form implant we use.

• Implant limit on heat—> 47c* for less than 1 min

• Primary stability—-> is primary objective of surgical implant placement

• Fibers grow—>PARALLEL WITH CUFF LIKE

88 • High Torque +Low Speed—> Implants

9) Implants Contraindication:

• Uncontrolled diabetes

• Immunocompromised patients

• Volume and height of bone(anatomic considerations)

• Bisphosphonate therary

• Bruxism tobacco(relative)

• Cleft palate

• Young kids

Note: AGE and CARDIOVASCULAR disease does NOT affect implants

89 10) Forceps:

Maxillary Forceps:

• #150—> ALL maxillary

• #65—> BAYONET (incisors and root)

• #88—-> CROWNHORN (molar R&L)

Mandibular Forceps:

• #151—> ALL mandibular

• #151A—>premolars only

• #23—> CROWNHORN (molars R & L)

• #74—->ASH (mandibular premolars)

• #17—> mandibular molars NOT FUSED

• #222—> Molars FUSED

90 ORTHODONTICS

1) Bone Development:

• Intramembranous ossification —-> Cranial vault, clavicle, maxilla and body mandible except ant. part

• Endochondral ossification—> takes place in cartilage, produce woven bone that is then remodeled. Anterior part of the mandible (symphysis), Coronoid process and condylar process.

• Major site of vertical growth in mandible is condyle

• Growth spurt-----girls 12 and boys 14

• Class 3 maloclusion------difficulty in f and v sound

• Class 2 malocclusion------retrognathism and over bite

• Sunday bite...... patients with skeletal class 2-----bring the mandible forward to improve the appearance

• Pathologic occlusion can cause------TMJ problem, wear facets, pulpal changes, periodontal changes

• Premature exfoliation of primary teeth———hyperparathyroidism

• ANB*------less than 4 class 1 and more than 4 class 2

• Early mesial shift uses primate spaces and late mesial shift uses LEEWAY spaces.

• Terminal plane relationship of primary mand 2nd molar —>determines the future ant-postposition of 1st permanent molar.

• Mesial step ------class 1, flush terminal if late mesial shift occurs it develops on class 1 other wise in class 2, and in distal step it develops in class 2.

91 • Indirect bonding bracket technique—->more complex, more technique sensitive and control of flash mean excess cement remove easily and is usually is lingual ortho

• Nance appliance------premature loss of primary maxillary teeth Lingual arch------inc arch length, anchorage purpose, space maintainer

• Lip bumber-----distalization of molar, uprighting of mesialy and lingual tipped molars, inc arch length and interposition of soft tissue in b/w upper and lower teeth

• Head gear modif—>y the growth of maxilla, anchorage purpose, protract or retract the maxillary teeth and traction purpose Head gear.. maximum----14 hours minimum 8 hours and average 10-12 hours Orthopedic force ------250-450 and for mov of teeth -----100-200N

• Easiest movement—>mesially and tipping

• PROBLEM with simple removable appliance is —->lack of patient cooperation, improper activation and poor design

• Maxillary incisor rotation—>in mixed dentition not treated------treated in early permanent dentition with removable appliance

• Condition where bands used instead of brackets —>short clinical crown, labial and lingual attachment required, better anchorage and SS crown where incompatible bonding.

• Elastics are always attach —>to brackets and arch wire —>and never to naked tooth

• Elastics class 1------inter maxillary; class 2------intra maxillary for class 2 malocc; class 3: intra maxillary used for class 3 malocc; and edge to edge bite class 4 cross bite

• Center of resistance—->single rooted tooth------1/3rd to 1⁄2 from the alveolar crest to root apex and in multi rooted tooth apical to furcation.

92 • Effects of head gear —>restrict the anterior growth of maxilla, distalize the molar and extrusion of molar particularly with cervical p H G. timings female 8.5-10.5 and male 9.5-11.5

• Post cross bite and mild ant cross bite—> should be treated as soon as possible and severe Ant cross bite —->in 2nd stage

• Most commonly used appliance for palatal expansion—> is HYRAX type. Activation 0.25turn/day and produce expan of 0.5mm/day Mild post cross bite in children——HAWLEY type removable appliance with jack screw.

• Q helix, W arch------uni /bi lateral cross bite + rotating molars

• Corrected ant cross bite is best retained by...... normal incisor relation

• Skeletal cross bite------smooth closure and functional cross bite caused by thumb sucking

• Long face —>predispose the patient to class 2

• Short face—> to class 3.

• Most stable point in growing skull from ceph point is Sella turcica

• Compression side------osteoclastic activity———resorption

• Tension side------osteoblastic activity------deposition

93 PERIODONTICS

1) Bacteria:

• In newly born child—> oral cavity germ free then after 12 hours microflora appears and after 6 months S,mutans and sanguis present

• After 5 years oral bacteria of child resembles that of adult

• Earliest bacteria found in plaque—-> S. sanguis

• Adult periodontitis—>P.gingivalis

• ANUG—>spirochetes

• Agressive Periodontitis —>A.A

• Pregnancy —>P intermedia, g enlargement in 2nd or 3rd month

• Puberty —>capnocytophagia, P.intermedia,

2) Microbial Complexes:

• EARLY COLONIZERS of plaque------actinomycis, streptococcus

• Green complex—————-ACE——————Actinobacillus, Capnocytophagia, E corrodens

• Orange————————PCF------Fusobacterium, Camphylobacter, Prevotella

• Red------TTP------T forsythia, T denticola, P ginigivilis

94 • Most perio disease —>max 1st and 2nd molar

• Desquamative ginigivitis—> red atrophic, glazed gingiva, middle age women, spares the marginal gingiva, involve attached gingiva, needed biopsy, role of plaque is vague. Phemphigus, Phemphigoid, Liquen Planus, ch Ulcerative Stomatitis, linear IgA disease, dermatitis Herpetiform, LE, EM

• Localized aggressive periodontitis------puberty, familial pattern, incisor and molar, AA, absence of plaque. Depressed chemotaxis

• IL1 and TNF 1-----bone resorption and IL8 chemotactic factor

95 • LIPO POLYSACHRIDES CAUSES------bone resorption and inhibit osteogenesis and chemotaxis

• As the severity of inflamation increses plasma cells increases

• Bleeding on probing is associated with—> red complex

3) Maxillary Sinus Communication:

• 2mm of communication —->don’t do anything and follow up

• 2-6 mm —> place gel foam (surgical), suture (figure of eight suture), decongestant and antibiotic , inform patient

• more than 6 mm —> buccal flap

4) Biological Width:

• Gingival Sulcus—> 0.69 mm • Junctional Epithelium —> 0.97 mm • Connective Tissue attachment —> 1.07 mm

96 5) Furcation:

• Furcation type 1and 2—>GTR (Guided Tissue Regeneration) • Furcation type 3 —> reposition flap surgery

6) Hemisection/Amputation:

• Hemisection —-> for mandibular molars. Hemisection in furcation class II and III. • Root amputation —-> for maxillary 1st and 2nd molar

7) Incisons:

• Bleeding points—> used to guide incision

• Distal wedge—>Is limited to formation of the Ramus. NO on 3rd molars when not enough keratin or attached gingiva

8) Gingivectomy:

Heals by —-> 2nd secondary Intention. LJE (Long junctional Epithelium)

Incison —> EXTERNAL BEVEL INCISION-starts from outside of the gingival margin to the crest of bone.

ABOVE THE MUCOGINGIVAL JUNCTION • Indications—> a) SUPRAbony pocket, b)Gingival hyperplasia

• Contraindication—> a) Little attached gingiva, b) High smile line, c) INFRAbony pockets, d) Recontouring osseous, e) botton of the pocket is apical the mucongival junction,

97 • Epithelium Growth over CI (connective tissue)—> 0.5-1 mm/day (related to gingivectomy)

9) Flaps:

Heals by —-> primary Intention

• Modified Widman Flap —-> 3 incisions= a) Internal bevel, b) Sulcular and c) , just instrumentation but does not reduce pocket depth, does NOT extend beyond the mucogingival junction, YES 2-3 mm beyond alveolar crest, pocket shrinkage because of healing.

• Undisplaced Flap------instrumentation + pocket wall removal. Pocket depth reduction. Excisional procedure of the gingiva= gingivectomy, internal bevel gingivectomy, but also reverse bevel. Final placement of flap determined by incision. Example: do Undisplaced flap when a tooth had epithelium above CEJ

Undisplaced and gingivectomy—-> are to flap procedure to remove the pocket wall

• Apically displaced ——> Internal bevel incision. Full thickness, indication------moderate to deep pocket, furcation involvement, crown lengthening root plaining, access for surgery. Pocket elimination by apical position and/or increase the width of attached gingiva. Best position is 2mm apical to the alveolar crest. DO NOT USE FOR EXTRUSION CANINE. Example: FOR CROWN LENGTHENING (apical repositioned flap, osteotomy and obtectomy); Long jxn epith was coronal to CEJ and margin was around cej,

98 • Lateral Positioned Flap (Pedicle Graft)—-> for wide/deep GINGIVAL RECESSION. Inadequate zone of attached gingiva, isolated area of gingival recession and CI (connective tissue) are donor site, lack of sufficient attached gingiva, fenestration and dehiscence.

**Type of healing in SRP and free gingival graft—> LJE and CT

• Lateral Positioned Flap (Pedicle Graft)—-> for wide/deep GINGIVAL RECESSION. Inadequate zone of attached gingiva, isolated area of gingival recession and CI (connective tissue) are donor site, lack of sufficient attached gingiva, fenestration and dehiscence.

• Most freq performed type of perio surgery is Undisplaced (un repositioned) flap.

• Periodontal flap preferred for mandibular anteriors—> Lateral repositioning is done for gingival recession.

• Goal of Perio Flap—> regeneration of PDL cementum and bone.

10) Graft:

Heals by —-> tertiary Intention

• Free Gingival Graft—>for localized narrow recession. Graft receives it’s eptithelium from – adjacent tissue (blood supply from CT). Epithelial formation in 1 week and complete maturation in 10-16weeks. Ideal thickness of free gingival graft is 1-1.5m. Greater palatine bundle can be affected (donor side).

Epithelial for graft come from—> DONOR EPITHELIUM

**Type of healing in SRP and free gingival graft—> LJE and CT

• Connective Tissue Graft—->need two surgical sites (disadvantage)

99 ‘

11) Bone Grafts:

Osteoinductive property—> cause growth of bone. Autograft is the most.

• Autogenous bone graft—> from the own patient. Is inductive+conductive and have the greatest osteogenic potential.

• Allograft —>3 types. Cadaver Bone

1.Fresh frozen------rarely used b/c of transmission of disease

2.freeze dried------osteoconductive potential only 3.demineralized freeze dried------lack strength+ostoconductive+inductive potential(b/c of BMP exposed)

• Xenograft—-> animal bone. osteoconductive potential only

100 12) GTR:

• Guided tissue regeneration (GTR)—> is a procedure that blocks the re- population of the root surface by long junctional epithelium and gingival connective tissue to allow cells from the periodontal ligament and bone to re-populate the periodontal defect.

• Best prognosis—-> narrow 3 wall deffect

• Most successful GTR—>better for Class II FURCATIONS (cul-de-sac)

• LEAST successful—> for class III furcations

• The purpose of GTR is to prevent: Long J.E, migration of PDL cells Migration of CT cells.

• Use barrier—> CORONAL movement of cells

Class 1,2 Gingival recession —->good prognosis,

3 Gingival recession—> partial coverage

4 Gingival recession —>poor prognosis

• GTR------non resorbable mem removed after 3-6 weks,

• Recession= migration of free gingival margin apical to CEJ (CEJ- marginal gingiva)

• Periodontal attachment loss=GR+P pocket( if recession we ADD (+)it and if hyperplasia we SUBSTRACT (-)it)

• Most common cause of gingival recession—> is abrasion or tooth injury

13) Fenestration/Dehicense:

• Fenestration —> HOLE in bone that expose the root

• Dehicense—> the loss of buccal or lingual bone overlying a tooth roo

101 PHARMACOLOGY

1) M C A T and TBB Contraindicated in Pregnancy:

• Metronidazole - Tetracyclines

• Chloramphinacol -Barbiturates

• Aminoglycoside -Benzodiazepines

• Tetracyclin

102 2) Drug Overdose:

• Diazepam treats —> Lidocaine overdose

• Flumanzenil—> Benzodiazepines overdose. Example: Diazepam overdose

• Neostigmine, Physostigmine treats —> Atropine overdose (cholinestrase inhibitors overdose)

• Nalaxone treats—> Opioid overdose

• Milk & Calcium for —>fluoride Highest overdose .

• Heparin—> protamine sulfate

• Physostigmine —> TCA (Tricyclic antidepressants) overdose

• Vit K —> Warfarin overdose

• Glucagon—>Beta blocker overdose

• Physostigmine—> Atropine overdose

• Beta blocker —> Theophylline overdose

• Pralidoxime —> Organophosphate poisoning

Pralidoxime antidote for Organophosphate and pesticide poisoning

• N acetylcysteine—> Acetaminophen overdose

• Aspirin overdose—> Potassium salt and sodium bicarbonate

• Calcium sodium ( EDTA) —> lead poisoning

• Dimercaprol, Penicillamin, EDTA —>mercury poising

103 Example: Dimercaprol can treat Heavy metal toxicity medication.It can treat arsenic, gold, and mercury poisoning. It can also treat lead poisoning when given with other medications.

• Phenytoin ,Lidocaine, Magnesium —> Digitalis

• Alpha Blocker—>Epinephrine toxicity

• Disulfiram—>Alcohol overdose

3) Drug Interactions:

• Anticholinergic drugs are contraindicated —> glaucoma

• Erythromycin with penicillin—->antagonism

• Tetracycline with penicillin —> cancel each other. (bacteriostatic/ bactericidal)

• Sulfonamides and Trimethoprim —> sinergism->interfere folic acid

• Seldane with Erythromycin—>causes cardiac arrhythmia

• Broad spectrum antibiotics with Coumadin (anticoagulants)— >incresed coagulation action and reduction in vitamin K resources.

• Penicilin G with Probenecid —>decrease renal excretion of penicilin G

• Tetracicline with antiacids—>reduce effectiveness of tetracyclines

• Ampicilin with oral contraceptives—-> reduce effectiveness of oral contraceptives, rapid excretion of steroids from body

• Erythromycin with Digoxin—> inhibitit effectiveness of the drug

• NSAIDs with Lithium/ Methotrexate —-> decrease elimination of Li/ Metro and more side effects.

104 • NSAIDs with Diuretics —> decrees action of diuretics

• NSAIDs with Warfarin —> increase bleeding

• NSAIDs with Alcohol —> bleeding ulcers

• NSAIDs with Antihypertensives —> increase hypertension (antagonist)

• NSAIDs with Cyclosporine —> negates the effect of cyclosporine on kidney function

• Opioids with Barbiturates —>depress respiratory by rendering respiratory center less sensitive to CO2

• Opioids with Benzodiazeopines—-> respiratory depression

• Opioids (Meperidine) with CNS depressants —->antihistamines, seizure medications, muscle relaxants, sedatives and TCA

• Opioids and Alcohol —> increase the sedative effect of both, and increases the risk of death from overdose.

• Opioids with Naloxone —> cancel each other

• Ciprofloxacin ——> inhibits Methadone

• Rifampicin (anti-tuberculosis)—-> increases Methadone

• Epinephrine with Histamine —> antagonism effect the exactly opposite to Histamine

• Acetaminophen with Codeine —> synergism

• Epinephrine with Nytroglycerine —> physiologic antagonism

• Epinephrine with Propranolol (non selective B blocker)—> antagonism effect. Increase BP and decrease HR. Hypertensive Crisis (lead to stroke), and anaphorixis that don’t respond to epinephrine.

105 NOTE: All Beta blockers, specially the non selective Beta Blockers —> inhibit the response of Epinephrine in anaphylaxis, also have increase risk, incidence and severity in anaphylaxis (epinephrine will not have an effect, won’t work).

• Meperidine DO NOT GIVE with MAO inhibitors

• Erythromycin should NOT BE GIVEN with Theophiline (bronchodilator)

• Lidocaine with Beta Blocker —-> reduce blood flow to liver, decrease clearance of the drug (increase blood pressure but decrease HR.

• Lidocaine with Cimetidine—> inhibit microsomal ensymes, decrease lidocaine clearance

• Alcohol with Barbiturates —> Valium, narcotics. Phenotiazine—> synergism

• Cimetidine (antiacid, antihistamine) —> increase activity of Warfarin and Carbamazepine (Tegretol for Trigeminal Neuralgia).

• Macrolides like Erythromicin —> inhibit metabolism of Seldane

• Cocaine—> inhibit uptake of catecholamines

• Epinephrine with Propranolol —> Antagonist effect, so increase BP but decrease HR (Bradychardia)

• Anesthesia in Vein—> increase HR but decrease BP

• Lidocaine and Propranolol —> reduce blood flow, decrease clearance of the drug, increase BP, decrease HR.

• Tetracyclines , Penicilins with Oral contraceptives —> reduce effect of oral contraceptive

• Clarithromycin with Calcium Ch Blockers—>hypotension, death

106 • Sedatives with Antihypertensives —>sedatives inhibits P450 and increase action of antihypertensives but mostly of the sedatives=depression of CNS

• CHF patient on digitalis —->avoid epinephrine or limited dose to 0.036mg, avoid calry or erythromycin, avoid gag reflex and epinephrine cords, place in upright position/semi supine and avoid NSAIDs

• Chamomile should NOT be given—> in patient taking anticoagulant

HERB interactions:

• St. John’s Wort—-> NO with BZ and HIV (INDAVIR) drugs

• Saw Palmetto

• Gingo biloba

• Yinseg

Oral Biphosphonates:

• Oral Biphosphonates with antihypertensives—> renal damage with use of diuretics. Sure to take in hydrated patients.

• Biphosphonates with NSAIDs, ahminoglycosides, antivirals and diuretics—> renal damage

• Biphosphonates with NSAIDs—>irritate gastric mucosa due to the GI effect of the Biphosphonate.

4) Antifungal drugs: a) Polyene antifungals:

107 • Nytatin —>topical for mucocutaneous infection

• Amptericin B —>systemic b) Azole antifungals:

• Ketoconazole —>BOTH topical for mucocutaneous or oral for systemic

• Miconazole —>topical for mucocutaneous

• Clotrimazole —> topical for mucocutaneous

• Fluconazole —>systemic

• Itraconazole —>systemic

• Voraconazole —> systemic

• Posaconazole —> systemic

5) Anticholinergics:

Reduce Salivary secretion (cause Xerostomia), Increase HR, Mydriasis, constipation….

• ATROPINE—> antidote for Organophospahate

108 • SCOPOLAMINE—-> used for eye drops to cause midriasis

*Physostigmine—-> Revert effect, example: atropine poisoning

*Pralidoxime—->organophosphate cholinesterase inhibitor

6) Cholinergics:

Increase saliva (Treat xerostomia), low HR, Miosis….

• PILOCARPINA

• NEOSTIGMINE

• METHACHOLINE

7) Xerostomy caused by:

• Antihypertensive • Anticholinergics • Antidepressants • Antihistamines • Bronchodilators • Sedatives

109 PATIENT MANAGEMENT

1) Types of studies:

• Case Series: study some clinical cases of jaw necrosis.

• Cross Sectional: Interview all patients at the school for jaw necrosis and use of biophosphate at one time.

• Case Control Study:Identify patients with and without jaw necrosis, follow them for use of biophospate.

• Cohort Study: Enroll all patients at the school and follow them for years to see who develops jaw necrosis.

• Deterministic: dosage dependent, in deterministic there a limit only after it reaches that limit effect will occur. It will increase with increase in dose.

• Stochastic: it is not dose dependent any amount will cause effect

2) Charge to patient $$:

• UNBUNDLING: "the separating of a dental procedure into component parts with each part having a charge so that the cumulative charge of the components is greater than the total charge to patients who are not beneficiaries of a dental benefit plan for the same procedure."

• BUNDLING "the systematic combining of distinct dental procedures by third- party payers that results in a reduced benefit for the patient/ beneficiary."

• UPCODING or overcoding: "reporting a more complex and/or higher cost procedure than was actually performed."

110 • DOWNCODING: "a practice of third-party payers in which the benefit code has been changed to a less complex and/or lower cost procedure than was reported except where delineated in contract agreements."

In Epidemiology a confounder is: not part of the real association between exposure and disease o predicts disease unequally distributed between exposure groups o A researcher can only control a study or analysis for confounders that are: known, measurable Example: Grey hair predicts heart disease if it is put into a multiple regression model because it is unequally distributed between people who do have heart disease (the elderly) and those who don't (the young). Grey hair confounds thinking about heart disease because it is not a cause of heart disease. Strategies to reduce confounding are: o randomization (aim is random distribution of confounders between study groups) o restriction (restrict entry to study of individuals with confounding factors - risks bias in itself) o matching (of individuals or groups, aim for equal distribution of confounders) o stratification (confounders are distributed evenly within each stratum) o adjustment (usually distorted by choice of standard) o multivariate analysis (only works if you can identify and measure the confounders)

3) Types of study:

• Case Control Study—-> is a RETROSPECTIVE, “Effect-to cause”, starts WITH disease, COMPARES people WITH or WITHOUT disease and also looks back to see how the risk for the disease is compared to actually getting that disease. Fewer study subject, ODDS RATIO, RARE diseases, SHORT duration. Example: 4 people with disease and dentist want to report

• Cohort Study—-> is a PROSPECTIVE study, “Cause-Effect”, measures incidence and exposure, starts with people EXPOSED to RISK factor or suspected cause , FATAL disease, LARGE number of subjects, To

111 DEVELOP CERTAIN DISEASE, RISK QUOTIENT (Relative risk ratio), Investigate CAUSE of disease, LARGE DURATION. Example: a) study among smokers and non-smokers, in a period of 6 years (200-2006) to develop a disease.

• T- test—-> 2 groups compared that are different statistically. Standard deviation=UNKNOWN. Analyze statistically difference between 2 MEANS. SMALL SAMPLE.

• Z- Test—> 2 groups compared that are different statistically. Standard deviation=KNONW. LARGE SAMPLE

• Cross- Sectional Study—-> EPIDEMIOLOGICAL. Study ENTIRE POPULATION. Prevalence and Rate. Study all variables, simultaneously ONE POINT AT A TIME

• Clinical Trials—-> “Cause-Effect”. randomization and blinding, to compare EFFECT OF TREATMENT with NO-Treatment. LARGE GROUPS of people. Evaluate EFFECTIVENESS of MEDICATIONS or medical devices by monitoring their effects. Conducted by Universities, medical projects, independent researches, private industry. Example: a) Study group A and B give some agents for plaque control, then compare wich agent is more effective; b) a study to determinate the effectiveness of a new antihistamine to 25 allergic patients, 13 patients give the new drug and the other 12 patients give placebo, assigned one drug.

• Correlation Study—-> measure linear relation between 2 factors. NO cause effect.

• ANOVA—> analysis of VARIANCE. Example: means of caries risk assessment for 3 groups.

• Regression analysis—> compare 2 CONSTANT variables

112 • Chi-Square Test—> 2 COMMON variables, 2 NON-PARAMETRIC DATA, independent variables, metric data.

• Longitudinal Study—> study certain set of people, Long period of time.

• Cross- Secctional Study—> EPIDEMIOLOGIC, data collect, SAME POINT OF TIME. Example: a) researcher wants to find incidence of oral cancer in nursing home; b) Teacher doing survey on kids, c) Myastenia Gravis patients are involved in a study, the doctor is conducting a study and is trying to find how many of these patients have periodontitis. d) Gave patient survey about their treatment.

• Double- blind Study—> NO 2 control group.

4) Hypotesis:

• If p-value<0.05 reject null

• If p-value>0.05 fail to reject null

113 5) Panel:

• PPO------open panel ------can go to any dentist

• HMO------closed panel------specific dentist

6) Types of Operant Conditioning:

!

114