NBDE II-2021-PREVIEW

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TABLE OF CONTENTS CHAPTER 1 ORAL PATHOLOGY METABOLIC & GENETIC DISEASES ....................................................................................................8 INFLAMMATORY JAW LESIONS .......................................................................................................15 CONNECTIVE TISSUE LESIONS ........................................................................................................17 BENIGN EPITHELIAL TUMORS ..........................................................................................................21 VERRUCAL PAPILLARY LESIONS .....................................................................................................24 NEOPLASMS ......................................................................................................................................25 ODONTOGENIC ABNORMALITIES ....................................................................................................34 WHITE LESIONS .................................................................................................................................41 BLOOD DISEASES .............................................................................................................................49 NEUROLOGIC & MUSCLE DISORDERS ............................................................................................56 NON-ODONTOGENIC CYSTS ............................................................................................................58 ODONTOGENIC CYSTS .....................................................................................................................60 NON-ODONTOGENIC TUMORS ........................................................................................................64 ODONTOGENIC TUMORS .................................................................................................................71 PIGMENTED LESIONS .......................................................................................................................77 RED-BLUE LESIONS ..........................................................................................................................80 PSEUDOCYSTS (NO EPITHELIAL LINING) ........................................................................................83 BENIGN SALIVARY GLAND TUMORS ...............................................................................................85 MALIGNANT SALIVARY GLAND TUMORS ........................................................................................88 ULCERATIVE CONDITIONS ...............................................................................................................92 VESICULO-BULLOUS DISEASES ......................................................................................................96 RADIOGRAPHIC PATHOLOGY ........................................................................................................104

CHAPTER 2 RADIOLOGY OSTEONECROSIS ............................................................................................................................113 DIGITAL RADIOGRAPHY ..................................................................................................................115 SECONDARY RADITION, COLLIMATION, FILTRATION ..................................................................116 PANORAMIC & CONE BEAM ...........................................................................................................119 CEPHALOMETRICS & BWX .............................................................................................................120 SUBMENTAL-VERTICAL ..................................................................................................................121 WATER’S VIEW .................................................................................................................................122 TOWNE’S VIEW ................................................................................................................................123 CHEMICALS, SOLUTION, & DEVELOPING ERRORS ......................................................................124 RADIOGRAPHIC TECHNIQUES & ERRORS ....................................................................................125

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CHAPTER 3 DENTAL EMERGENCY PROTOCOL & MEDICALLY COMPROMISED CONSIDERATIONS DENTAL EMERGENCY PROTOCOL ................................................................................................132 MEDICALLY COMPROMISED CONSIDERATIONS..........................................................................134

CHAPTER 4 DENTAL PHARMACOLOGY ANTIBIOTIC PRE-MEDICATION GUIDELINES .................................................................................138 CENTRAL NERVOUS SYSTEM ........................................................................................................141 ADRENERGICS (SYMPATHETICS)...................................................................................................143 ADRENERGIC AGONISTS ................................................................................................................145 ANTI-ADRENERGICS (SYMPATHOLYTIC AGENTS) .......................................................................149 CHOLINERGICS ...............................................................................................................................153 ANTI-CHOLINERGICS ......................................................................................................................156 NICOTINIC RECEPTOR ANTAGONISTS ..........................................................................................157 DRUG ADMINISTRATION ROUTES & METABOLISM ......................................................................159 DEA DRUG SCHEDULE ....................................................................................................................164 ANESTHETICS ..................................................................................................................................166 NITROUS OXIDE & GENERAL ANESTHESIA ...................................................................................171 ANTI-ANXIETY AGENTS ...................................................................................................................175 CARDIOVASCULAR AGENTS ..........................................................................................................179 ANTI-DEPRESSANTS .......................................................................................................................187 ANTI-PSYCHOTICS ..........................................................................................................................189 ANTI-HISTAMINES ...........................................................................................................................190 ANTI-CONVULSANTS ......................................................................................................................192 ANTIBIOTICS ....................................................................................................................................194 ANTI-FUNGALS & ANTI-PROTOZOALS...........................................................................................207 ANTI-VIRALS ....................................................................................................................................209 NSAIDS .............................................................................................................................................211 ACETAMINOPHEN & OPIODS..........................................................................................................217 ANTI-NEOPLASTIC (CANCER) DRUGS ...........................................................................................226 HYPOGLYCEMICS ...........................................................................................................................228

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CHAPTER 5 PROSTHODONTICS REMOVABLE PARTIAL DENTURES .................................................................................................230 MANDIBULAR MAJOR CONNECTORS ...........................................................................................231 MAXILLARY MAJOR CONNECTORS ...............................................................................................234 INDIRECT RETAINERS .....................................................................................................................237 DIRECT RETAINERS .........................................................................................................................240 RPD STRESS BREAKERS ................................................................................................................245 SURVEYING RPD ABUTMENTS.......................................................................................................247 COMPLETE DENTURES ...................................................................................................................250 MANDIBULAR COMPLETE DENTURES ..........................................................................................252 MAXILLARY COMPLETE DENTURES ..............................................................................................254 ORAL PATHOLOGY & ILL-FITTING COMPLETE DENTURES .........................................................256 IMMEDIATE DENTURES ...................................................................................................................258 OVERDENTURES & OCCLUSION ....................................................................................................260 DENTURE TEETH SELECTION .........................................................................................................271 PHONETICS ......................................................................................................................................274 FIXED PARTIAL DENTURES (CROWN & BRIDGE)...........................................................................275 PORCELAIN SHADE SELECTION ....................................................................................................279 PONTIC DESIGN ..............................................................................................................................280 CANTILEVER BRIDGES & PIER ABUTMENTS .................................................................................282 MARYLAND BRIDGE ........................................................................................................................284 BRIDGES & BRIDGE ABUTMENTS ..................................................................................................286 POST & CORES ................................................................................................................................289 PORCELAIN VENEERS .....................................................................................................................291 IMPRESSION MATERIALS & CEMENT ............................................................................................292 DENTAL IMPLANTS, IMPORTANT PEARLS, & OVERDENTURES ..................................................297

CHAPTER 6 OPERATIVE DENTISTRY DENTAL CEMENTS ..........................................................................................................................306 PREPARATION BASES & CAVITY LINERS ......................................................................................309 DENTAL CARIES ..............................................................................................................................313 GOLD ................................................................................................................................................300 COMPOSITE .....................................................................................................................................327 AMALGAM ........................................................................................................................................337 DENTAL BIOMATERIALS .................................................................................................................350 RESTORATIVE HAND INSTRUMENTS & BURS...............................................................................352

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CHAPTER 7 PERIODONTICS PERIODONTIUM & FIBERS ..............................................................................................................356 FLAPS, GRAFTS, & SURGERY .........................................................................................................362 GINGIVITIS & GINGIVAL CONDITIONS ............................................................................................371 PERIODONTITIS ...............................................................................................................................377 PLAQUE & CALCULUS.....................................................................................................................383 SCALING & ROOT PLANING (SRP) ..................................................................................................389 HYGIENE INSTRUMENTATION & POWER DRIVEN SCALERS .......................................................390 OCCLUSAL TRAUMA .......................................................................................................................398 ABSCESSES .....................................................................................................................................401 ORAL HYGIENE INSTRUCTION .......................................................................................................403

CHAPTER 8 ORAL SURGERY NERVE ANATOMY ............................................................................................................................409 ARTERIES & GLANDS ......................................................................................................................413 MUSCLES OF MASTICATION & TMJ ...............................................................................................417 FRACTURES .....................................................................................................................................422 GENERAL ANESTHESIA ...................................................................................................................427 LOCAL ANESTHESIA & COMPLICATIONS ......................................................................................433 NITROUS OXIDE ...............................................................................................................................440 EXODONTIA ......................................................................................................................................445 GRAFTS ............................................................................................................................................455 BIOPSY .............................................................................................................................................458 ORAL SURGERY CONDITIONS & TREATMENT CONSIDERATIONS..............................................460 CPR GUIDELINES.............................................................................................................................466 HORMONES, CALCIUM, BLOOD GLUCOSE ..................................................................................469

CHAPTER 9 ENDODONTICS TOOTH FRACTURES ........................................................................................................................475 FLAPS & SLOB RULE .......................................................................................................................477 PULPOTOMY, APEXIFICATION, APEXOGENESIS ..........................................................................479 DIRECT & INDIRECT PULP CAPPING..............................................................................................480 CANAL ACCESS & DEBRIDEMENT .................................................................................................482 GUTTA PERCHA OBTURATION .......................................................................................................483 IRRIGANTS & CHELATING AGENTS ................................................................................................484 ZOE, MTA, APICOECTOMY .............................................................................................................485 PERIRADICULAR SURGERY & CURETTAGE ..................................................................................486 ENDODONTIC INSTRUMENTATION ................................................................................................487 MANAGING AVULSION INJURIES ...................................................................................................489 EXTERNAL & INTERNAL RESORPTION ...........................................................................................491 PULP, DENTIN, CEMENTUM ...........................................................................................................493 MANDIBULAR & MAXILLARY ROOT ANATOMY .............................................................................497 RCT ADJUNCTS, INDICATIONS & CONTRAINDICATIONS .............................................................499 PERIAPICAL & PERIODONTAL ABSCESSES ..................................................................................501 PROBING LESIONS ..........................................................................................................................503

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REVERSIBLE & IRREVERSIBLE PULPITIES, NECROSIS.................................................................503 RESTORING TEETH AFTER RCT .....................................................................................................505

CHAPTER 10 PEDIATRIC DENTISTRY ANTI-ANXIETY MEDICATIONS .........................................................................................................507 PULPAL TREATMENT ......................................................................................................................509 PEDIATRIC DISEASES & CONDITIONS ...........................................................................................512 TOOTH ABNORMALITIES ................................................................................................................522 TOOTH DEVELOPMENT & ERUPTION.............................................................................................524 PRIMARY DENTITION ......................................................................................................................528 FLUORIDE.........................................................................................................................................532 SEALANTS ........................................................................................................................................540 TOOTH TRAUMA ..............................................................................................................................542 BEHAVIOR MANAGEMENT ..............................................................................................................546

CHAPTER 11 ORTHODONTICS OVERBITE & OVERJET .....................................................................................................................549 MALOCCLUSION .............................................................................................................................550 ANGLE MALOCCLUSION CLASSIFICATION ...................................................................................551 CROSSBITES....................................................................................................................................554 CEPHALOMETRICS..........................................................................................................................556 MIXED DENTITION & ANALYSIS ......................................................................................................558 PRIMATE SPACES & SPACE MAINTENANCE .................................................................................559 ORTHODONTIC APPLIANCES .........................................................................................................564

CHAPTER 11 BEHAVIORAL SCIENCE, PUBLIC HEALTH, OSHA & INFECTION CONTROL BEHAVORIAL SCIENCE ...................................................................................................................573 PUBLIC HEALTH AND RESEARCH METHODS ...............................................................................579 ORAL HEALTH INDICES ...................................................................................................................585 OSHA AND INFECTION CONTROL ..................................................................................................587 DENTIN “1,001+ HIGH-SPEED DRILL NBDE II PREVIEW ............................................................599

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ORAL AND GENERAL PATHOLOGY INFLAMMATORY JAW LESIONS OSTEOMYELITIS –inflammation or infection of the bone marrow and adjacent bone, usually caused by bacteria (Staphylococci) due to trauma or surgery by a direct extension from a nearby infection, or via the bloodstream.

• Signs & Symptoms: pain, redness, swelling in the infected area, fever, and general malaise.

Radiographically, poorly circumscribed radiolucency with a central sclerotic nidus may be present.

CONDENSING OSTEITIS (CHRONIC FOCAL SCLEROSING OSTEOMYELITIS) – an unusual bone reaction to an infection (most often associated with a long-standing periapical infection) that occurs during instances of extremely high tissue resistance or in cases of low-grade infection.

There may be no signs or symptoms of the disease, other than mild pain associated with an infected pulp. Mandibular 1st molar is the tooth most commonly involved. Most often occurs in young patients.

• Radiographic Findings: periapical radiographs show pathognomonic, well-circumscribed radiopaque mass of sclerotic bone surrounding and extending below the apex of one or both roots. The entire root outline is always VISIBLE (important feature that radiographically distinguishes it from a benign cementoblastoma).

• A tooth with a condensing osteitis lesion can be treated with RCT or extracted, since the pulp is infected, and the infection has spread past the immediate periapical area. The sclerosing bone constituting the osteomyelitis is NOT attached to the tooth, so it remains after the tooth is treated or removed.

PERIAPICAL ABSCESS – usually arises from pulpal infection of a tooth due to carious involvement of the tooth. The cellular debris and/or infection that caused the tooth pulp to become necrotic, slowly filters out of the root tip, producing an inflammatory reaction around the root tip.

A periapical abscess can also occur after traumatic injury to a tooth, causing pulpal necrosis, and in cases of irritation of the periapical tissues (either by mechanical manipulation or application of chemicals) in endodontic procedures.

Clinical Features: • Acute Periapical Abscess: tooth is extremely painful to percussion (may feel slightly extruded from its socket), and is MOBILE. Radiograph presents only a slight thickening of the periodontal membrane (PDL). Not typically seen on periapical film because until it becomes chronic.

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Chronic Periapical Abscess: presents as a granuloma or cyst (radiolucent area at the root apex), but there are usually no clinical features or symptoms (asymptomatic).

• Treatment: establish DRAINAGE by opening the pulp chamber (RCT) or extracting the tooth.

If not treated, it can cause serious complications (i.e. osteomyelitis, cellulitis, & bacteremia).

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OSTEONECROSIS–bone death or necrosis; a rare complication of cancer patients (radiation and chemotherapy), patients with tumors or infectious embolic events, or with osteoporosis taking IV or oral bisphosphonates. May be caused by a defect in bone remodeling or wound healing (defect in osteoclast function).

BISPHOSPHONATE-OSTEONECROSIS (BON)-a dental phenomenon that may lead to surgical complications (bone necrosis) due to impaired wound healing after extractions, periodontal surgery, or RCT. OSTEONECROSIS

OSTEOPOROSIS – a reduction of total skeletal mass due to INCREASED BONE RESORPTION, causing predisposition to pathologic fractures caused by calcium or estrogen hormone deficiencies over a long time period. BONES BECOME LESS DENSE & BRITTLE. • Osteoporosis is most common in THIN, ELDERLY WHITE WOMEN. Treatment: estrogen therapy, calcium & vitamin D supplements, bisphosphonates.

OSTEOPETROSIS (“Albers-Schonberg Disease” or “Marble Bone Disease”) – an uncommon genetic disorder that manifests in infancy characterized by an OVERGROWTH & DENSENESS OF BONES due to a DEFECT IN OSTEOCLASTS which are needed for bone marrow formation. The long bones become dense and hard to the extent that BONE MARROW IS OBLITERATED (prevents bone marrow formation). BONES BECOME HARD BUT BRITTLE & DENSE. • Clinical Signs: abnormal bone & dental development, fragile bones, stunted growth anemia, spleen & liver enlargement, blindness, and progressive deafness.

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ENAMEL HYPOCALCIFICATION

AMELOGENESIS IMPERFECTA – an inherited hereditary ECTODERMAL DEFECT transmitted as a dominant trait that affects the deciduous & permanent dentition, causing enamel to be soft, thin, and yellow due to EXPOSED DENTIN through the thin enamel layer. Teeth are easily damaged and susceptible to decay. Crowns may or may not show discoloration. If discoloration is present, it varies depending on the type of disorder, ranging from yellow to dark brown.

• Open contacts between teeth and occlusal surfaces/incisal edges are often severely abraded.

• Radiographic findings are often distinctive & pathognomonic. When enamel is totally absent, the radiographic appearance makes the diagnosis obvious. When some enamel is present, thin radiopaque coverings on the proximal surfaces are visible. When anatomic crown forms are normal or near normal, the softness of the defective enamel may not be easily distinguished from dentin.

• Dentin, pulp, and cementum are NOT affected by AI (unlike dentinogenesis imperfecta).

Exception: AI will only show pulp obliteration if there is advanced abrasion with secondary dentin formation.

AMELOGENESIS IMPERFECTA

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WHITE LESIONS ORAL CANDIDIASIS (“THRUSH” OR “MONILIASIS”) – a FUNGAL infection of the oral cavity or vagina caused by a Candida species (usually Candida albicans) causing an inflammatory, pruritic infection with a thick, white discharge. Appears diffuse, curly or velvety white mucosal plaques on the cheeks, palate, and tongue that CAN BE WIPED OFF, leaving a red, raw, or bleeding surface. The most common symptoms are discomfort and burning of the mouth & throat, and altered taste.

• Candida is a yeast-like fungi and normal inhabitant of the oral cavity & vaginal tract, but is normally held in check by indigenous bacteria of these areas. Factors that stimulate Candida growth are extended use of antibiotics (antibiotics prescribed for a dental infection), steroids, diabetes, pregnancy, or vitamin deficiency (iron, folate, B12, zinc).

• Very common in patients on long-term antibiotic or chemotherapy, and immunosuppressed patients (AIDS).

• Treatment: topical with LOZENGES (Trouches) & mouth rinses (NYSTATIN is most widely used).

ACUTE PSEUDOMEMBRANOUS CANDIDIASIS – the most common oral candidiasis, usually found on the buccal mucosa, tongue, and soft palate. Oral cytology smears diagnose acute pseudomembranous candida by revealing budding organisms with branching pseudohyphae.

ANGULAR CHEILITIS (PERLECHE) – any chronic inflammatory lesion that occurs at the labial commissure (corners of mouth) due to unknown cause. Generally associated with LOSS OF VERTICAL DIMENSION in elderly patients. Mouth corners are painful, irritated, red, cracked, and scaly. Candida albicans fungus (Thrush) may grow in the corners of the mouth, keeping them sore.

• Predisposing Factors: Candida albicans infection, loss of inter-maxillary distance (decreased vertical dimension), trauma to the labial commissure due to prolonged dental treatment, & vitamin deficiencies (especially riboflavin or thiamine).

• Treatment: NYSTATIN will eliminate the FUNGAL infection only.

ANGUAL CHELITIS (PERLECHE)

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ACTINIC CHEILITIS (SOLAR CHEILITIS/FARMER’S LIP) – a PRE-MALIGNANT condition caused by chronic and excessive exposure to the UV sunlight radiation. A counterpart of actinic keratosis of the skin, and can also develop into squamous cell carcinoma. There is thick, WHITISH discoloration of the lip at the border of the lip and skin, and loss of the usually sharp demarcation between the red of the lip and normal skin (vermillion border). May lead to SCC, so it must be treated.

ACTINIC CHEILITIS

LEUKOEDEMA – a condition that mimics leukoplakia as it appears to be a WHITE PATCH, but is a just a VARIANT OF NORMAL MUCOSA. Varies from a filmy opalescence of the mucosa in the early stages, to a more definite grayish-white cast with a coarsely wrinkled surface in later stages. Usually occurs BILATERALLY and along the occlusal line in the bicuspid and molar region. Diagnostically, one can stretch the tissue and the white disappears (Important: Leukoplakia DOES NOT DISAPPEAR WHEN STRETCHED). NO TREATMENT REQUIRED. LEUKOEDEMA

WHITE SPONGE NEVUS (FAMILIAL WHITE FOLDED DYSPLASIA)–an often genetic and benign BUCCAL MUCOSAL ABNORMALITY (often mistaken for leukoplakia. Characterized by WHITE (pearly or opalescent), CORRUGATED THICK SOFT FOLDING OF THE BUCCAL MUCOSA (bilaterally). Can also occur on the labial mucosa, alveolar ridge, and floor of mouth.

Almost NEVER found on the gingival margin & dorsal of tongue. NO TREATMENT NECESSARY.

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GEOGRAPHIC TONGUE

FISSURED TONGUE (“SCROTAL TONGUE”) –a DEEP, usually asymptomatic (maybe painful if infected with Candida Albicans) MEDIAN FISSURE with laterally radiating grooves that vary in number, but are usually symmetrically arranged across the DORSUM (TOP) OF THE TONGUE. Rare in children, but incidence increases with age. Found in Melkersson-Rosenthal Syndrome (along with Cheilitis Granulomatosum & Facial Nerve Paralysis).

FISSURED TONGUE

STOMATITIS NICOTINA (“PIPE-SMOKER’S PALATE” OR NICOTINIC STOMATITIS): the initial clinical response is generalized palatal erythroplakia then becomes a white hyperkeratotic area with small red dots. Related to pipe smoking (tobacco), occurs ONLY ON THE PALATE, and mainly affects males. The palate is initially red & inflamed, then develops a diffuse, grayish-white, thickened, multi-nodular popular appearance with a small red “spot” in the center of each tiny nodule. This “spot” corresponds to orifices of palatal salivary gland ducts.

Treatment: None, except to stop smoking. Not usually premalignant.

• Found ONLY on the palate (palate is leathery white and full of keratin (hyperkeratosis with RED DOTS (inflamed minor salivary glands). The only lesion produced by tobacco that is not cancerous. Usually a white, generalized area with red dots on the hard palate that are PAINLESS & non-indurated. White areas with multiple red dots (inflamed salivary glands in the palate).

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RADIOLOGY Radiographs show shading from black to white (most radiolucent to most radiopaque). From least to most radiopaque: (PDL space, dentin, enamel, ZOE, and amalgam).

Radiopaque Structures & Dense Materials: metals, enamel, dentin, and bone that INHIBIT the passage of x-rays and appear WHITE on the processed film. Less radiation penetrates the structure and reaches the film.

Radiolucent Structures and Materials: less dense materials like soft tissue and air space that appear gray to black on processed film) ALLOWING RADIATION to pass through by absorbing very little radiation. More radiation penetrates the structure and reaches the film. § Radiolucent Lesions-appear every time bone is DESTROYED. Unilocular & Multilocular are terms only used to describe radiolucent lesions.

1. well-defined unilocular (one cavity): border is well-defined. Most benign lesions are unilocular, well-defined.

2. well-defined multilocular: border is well-defined with several cavities.

3. well-defined honeycomb or soap bubble (multilocular): 4. diffuse-cannot follow the border of the radiolucency: 90% of the time it is cancer. If loss of cortical plates, the first diagnosis is cancer.

OSTEORADIONECROSIS-the necrosis of bone produced by ionizing radiation that is more common in the MANDIBLE than maxilla due to the richer vascular supply to the maxilla, and because the mandible is more often irradiated. The most common factors precipitating osteoradionecrosis are pre-irradiation & post-irradiation extractions, and periodontal disease. Damage to blood vessels (not nerves or muscles) predisposes a patient to developing osteoradionecrosis. A complications that can occur with patients taking IV Bisphosphonates or oral bisphosphonates for more than three years orally (i.e. Fosamax).

Osteoradionecrosis is more common IN THE MANDIBLE probably because of the richer vascular supply to the maxilla and the fact that the mandible is more frequently irradiated. Caution with patients on IV bisphosphonates or if taking oral bisphosphonates (i.e. Fosamax).

• May occur after dental extractions.

• The most common factors precipitating osteoradionecrosis are pre and post irradiation extractions and periodontal disease.

OSTEONECROSIS

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CONE BEAM CBCT

CEPHALOMETRICS (“Lateral Head Radiograph)-a technique employing oriented radiographs for the purpose of making head measurements used to study craniofacial growth, diagnosis, planning orthodontic treatment, and evaluation of treated cases. Cephalometrics are useful to assess tooth-to-tooth, bone-to-bone, and tooth-to-bone relationships. Serial cephalometric films can show the amount and direction of growth. §

Lateral head radiograph (cephalometric x-ray) must be compared with “normal” lateral radiographs from an accepted norm. Linear and angular measurements are obtained using known anatomical landmarks in the lateral head radiography of the patient.

These measurements are then compared with those considered WNL, thus enabling the orthodontist to assess aberrations in the dentition and jaw structures that cause malocclusion.

§

Cephalometric radiographic analysis includes hard tissue structures (bone & teeth), and measurements of soft tissue structures (nose, lips, soft tissue chin).

§

Superimposition of longitudinal cephalometric studies is generally on a reference plane and registration point to best demonstrate the growth of structures farthest from the plane and point. The most stable area from which to evaluate craniofacial growth is the anterior cranial base due to its early cessation (stopping) of growth.

BITEWING RADIOGRAPHS-an intraoral radiograph MOST useful to detect INTERPROXIMAL CARIES and demonstrate alveolar bone resorption (periodontitis).

Bitewings show the crowns of both maxillary & mandibular teeth, but NOT the root apices. The main reason to take bitewings is to detect interproximal caries. § Bitewings are most useful to monitor the progression of periodontal disease as they show the crestal bone levels and interproximal areas of both arches. For the film to be of diagnostic use, the quality of the dimensional accuracy, open contacts, and optimum contrast and image clarity must be excellent. When taking bitewings, the film is placed in either a horizontal or vertical position.

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RADIOGRAPHIC TECHNIQUES & ERRORS VERTICAL ANGULATION-directing x-rays so they pass vertically through the part being examined. This is accomplished by positioning the tubehead and direction of the central ray in an up-and-down (vertical) plane. Foreshortening & Elongation are produced by INCORRECT VERTICAL ANGULATION. §

Foreshortening-a shortened image is caused by excessive vertical angulation. The teeth APPEAR TO SHORT due to either too much vertical angulation, or poor chair position.

§

Elongation-an elongated image is caused by insufficient (too little) vertical angulation. Elongation is the MOST COMMON error when taking dental radiographs where the teeth APPEAR TOO LONG due to either too little vertical angulation, or the film not being parallel to the long axis of the teeth or the occlusal plane not being parallel to the floor.

Vertical Angulation

HORIZONTAL ANGULATION-maintaining the central ray at 0° as the tube is moved around the head. This is accomplished by positioning the tubehead and direction of the central ray in a sideto-side (horizontal) plane. The general rule for horizontal angulation is the central ray should be perpendicular to the mean antero-posterior plane of the teeth being x-rayed. §

Overlapping-interproximal areas are overlapped due to incorrect horizontal tube angulation (central x-ray was not directed perpendicular to the curvature of the arch and through the contacts). Overlapping reduces the diagnostic quality of film to detect interproximal caries since teeth images are superimposed on each other).

The central ray is at 0° when the x-ray tube is adjusted so the central ray is parallel to the floor. If the tubehead is directed at the floor, it is positive angulation. If the x-ray tubehead is directed toward the ceiling, it is negative angulation.

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DENTAL EMERGENCY PROTOCOL ANAPHYLACTIC REACTION (allergic reaction develops in seconds or minutes) after local anesthetic, nitrous, or dental material exposure. LIFE-THREATENING causing BRONCHOSPAM & DROP IN B.P. (EPI pen bronchodilates and raises patient’s BP): 1. Call 911 and position the conscious patient in a comfortable position.

2. Get the preloaded EPI syringe in the emergency kit and inject EPI pen into patient’s DELTOID, TONGUE, or LATERAL THIGH. 3. Re-administer EPI pen in 5 minutes ONLY IF SYMPTOMS PERSIST.

CHEST PAIN (ANGINA PECTORIS)—patient has tight, heavy, or constricted chest pain and may clench their fist against their chest.

1. Call 911 and position patient so he/she is comfortable and ask if they have their nitroglycerin tablets or spray on them. If not, give 2 sprays of NITROGLYCERIN (vasodilator) onto the patient’s tongue.

2. Dental treatment can continue if patient and doctor are comfortable.

Important: do not give spray/tablets if the patient has chest pain and feels faint or dizzy (means BP is dropping), or if the patient took VIAGRA within 24hrs. ________________________________________________________________________ HEART ATTACK: after chest pain, patient says their pain is getting worse, patient has taken 3 doses of nitroglycerin at five minute intervals and pain continues, or the chest pain went away but comes back, or the patient has had no history of heart disease or chest pain. CRUSHING, INTENSE, RADIATING PAIN from the chest to the stomach or to the left side of the neck, jaw, left arm, and/or pinkie finger (tingles). SKIN TURNS ASHEN GRAY & PATIENT MAY SWEAT PROFUSELY. 1. Call 911 and position the patient so they are comfortable.

2. Administer 50% nitrous oxide & 50% oxygen (has same effect as IV Morphine) for pain and delivers more oxygen to the muscles/brain.

3. Give two sprays of nitroglycerin on patient’s tongue and have the patient CHEW 1 tablet of adult-dose ASPRIN (325mg) EXCEPT if patient is allergic to aspirin, has a bleeding disorder, or gastric/peptic ulcer. ASPIRIN prevents clot from getting bigger.

CARDIAC ARREST (UNCONSCIOUS PATIENT): 1. Call 911 while dentist lays the patient flat in dental chair with their feet ELEVATED. 2. (CAB): Dentist starts chest compressions, check airway and open with the HEAD LIFT/CHIN TILT and then check for breathing and carotid pulse (in the groove under and to the side of the Adam’s Apple). Follow CAB (compressions, airway, and breathing)-new AHA guideline.

3. Dentist gives CPR (30 chest compressions for every 2 breaths). 30:2 ratio. 120 compressions/minute.

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DENTAL CONSIDERATIONS FOR MEDICALLY COMPROMISED PATIENTS CHRONIC OBSTRUCTIVE PULMONARY DISEASE (Asthma, Bronchitis, Emphysema): • Sit patient upright in dental chair.

• No rubber dam in severe cases.

• No N2O if severe emphysema.

• Avoid barbiturates, narcotics, anti-histamines.

• Avoid erythromycin, clarithromycin if patient takes theophylline.

ASTHMA: • Have patient bring their bronchodilator inhaler to each appointment.

• Avoid Aspirin, NSAIDs, narcotics/barbiturates.

• Avoid Erythromycin if patient takes theophylline.

• Avoid sulfite-containing local anesthetics.

• Can use N2O or Diazepam for anxious patient.

• Use pulse oximeter if necessary.

TUBERCULOSIS: • Active TB: consult with physician before treatment and only treat emergencies.

• Prior TB (Non-Active): Use caution, get good medical history, periodic chest-x-rays to rule-out reactivation. If patient is TB-free confirmed by physician, treat as a normal patient. May be taking ISONIAZID (INH) for 6 months to 1 year prophylactically.

VIRAL HEPATITIS (B,C,D,E): • Active Hepatitis: Consult with physician and treat on emergency basis only.

• Non-Active Hepatitis: consult with physician, treat as normal.

DIABETES MELLITUS: • In uncontrolled diabetics, they are prone to infection and poor-wound healing.

• Insulin patients: eat normal meal before appointment (schedule morning or midmorning).

• Have sugar (OJ) available in case of diabetic shock.

• With well-controlled diabetics, no alteration of treatment plan is required unless. Treat as usual.

HYPERTHYROIDISM (Thyrotoxicosis): overactive thyroid produces too much T3 and/or T4 most commonly caused by Grave’s disease.

• Avoid EPI and other vasoconstrictors in untreated patients.

HEMODIALYSIS: renal replacement therapy to remove creatine, urea, and free water from the blood during kidney failure.

• Delay treatment until off dialysis machine for at least 4 hours (because of heparin). Best to schedule dental appointment the day after hemodialysis.

• Pre-treatment screen for bleeding disorders.

• Avoid drugs metabolized by the kidneys.

• Consider antibiotic prophylaxis to minimize effects of bacteremia.

• Avoid BP cuff on arm containing the shunt.

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DENTAL PHARMACOLOGY DRUG ADMINISTRATION ROUTES DRUG ADMINISTRATION ROUTES: drug’s onset of action is PRIMARILY determined by the RATE of ABSORPTION. The major effect of a drug is a factor (is determined by) how much of the drug is FREE IN PLASMA. ENTERAL ROUTE OF ADMINISTRATION (ORAL, RECTAL, SUBLINGUAL): 1. Oral Route (P.O.)-takes ~30min for the onset of a drug’s effect after swallowed. The oral route allows the use of many different dosage forms like tablets, capsules, and liquids. ¶ Oral route is an example of an ENTERAL ROUTE of administration. It is the most common route where the drug is swallowed. It is the most convenient for safe drug administration. It is safe, painless, and economical. The oral route is the safest and easiest route for drug administration, but it is also the most unpredictable and least effective route available. ¶ Oral route is most known for its significant hepatic “FIRST PASS” metabolism.

The oral administration of a drug is the one most accepted by patients. It is convenient because drugs can be given via tablets or capsules that contain an exact dose, making it easy for the patient to take the drug without assistance. ¶ After oral administration, drugs are generally absorbed best from the DUODENUM which has a large surface area due the presence of villi and microvilli. ¶ Drugs taken by mouth have to be absorbed (usually from the small intestine) before they can be transported to their site of action. Absorption may be slow, unpredictable and irregular due to the presence of variable amounts of food in different stages of digestion and to the varying degrees of acidity and alkalinity of the digestive juices.

Moreover, blood from the intestinal tract passes first to the liver (some drugs are metabolized in the liver, while others may be stored there to be released only slowly).

These considerations make it clear that oral administration is usually NOT USED IN MEDICAL EMERGENCIES or other occasions when a rapid effect is needed. ¶ Oral Route Disadvantage: drugs must be absorbed (usually from the small intestine) before they can be transported to their site of action. Blood from the intestinal tract passes first to the liver (some drugs are metabolized in the liver “first-pass effect”, while others may be stored there to be released slowly). This consideration makes it clear that oral administration is not suitable in emergencies or other occasions when a rapid effect is needed. Emotional stress decreases the rate of absorption of a drug when given orally.

2. RECTAL ROUTE: administered as creams, enemas, or suppositories if the patient is VOMITING or UNCONSCIOUS. Not often used for systemic effects because drugs are poorly and irregularly absorbed rectally and there is POOR PATIENT ACCEPTANCE. 3. BUCCAL OR SUBLINGUAL ROUTE-a tablet is placed under the tongue or in the cheek (ex: Nitroglycerin for angina pectoris).

19

NITROUS OXIDE Nitrous Oxide (N2O)-a slight sweet smelling, colorless, inert gas at room temperature and pressure that cannot produce general anesthesia EXCEPT if administered at concentrations > 80% (thus, it cannot be used as a single agent to produce general anesthesia). At these concentrations, the lack of oxygen causes hypoxia. Inhalant anesthetics like halothane & isoflurane can produce general anesthesia at concentrations of 3-5%, thus are very useful in anesthesia. Nitrous oxide is stored under pressure in steel cylinders painted blue. Oxygen is stored in green tanks. §

Advantages of Nitrous Oxide Analgesia: rapid onset of action, elevates pain threshold, produces euphoria, pleasant induction, titratable, rapid and complete recovery, virtually no adverse effects in absence of hypoxia, therapeutic for many medically compromised patients, and is suitable for all ages.

§

Nitrous oxide is used to produce SEDATION & MILD ANALGESIA. Nitrous oxide’s main therapeutic effect is relaxation/sedation (mild analgesia is a secondary effect).

N2O is usually used in 30-50% concentrations along with pure oxygen. It is a colorless, nonirritating gas at root temperature and pressure, and is non-flammable and non-explosive.

Nitrous oxide delivery machines are pre-equipped with a failsafe mechanism that will not allow less than 20% oxygen to be delivered to the patient (nitrous oxide MUST be coupled with AT LEAST 20% oxygen). Nitrous oxide does not have local anesthetic (analgesic) properties. Thus, local anesthesia must be used in conjunction with nitrous oxide any procedure where pain is anticipated.

§

Onset of sedation occurs within 5 min and the recovery is just as rapid. The FIRST SYMPTOM of nitrous oxide onset is TINGLING OF THE HANDS. It is excreted unchanged by the lungs. Most common complaint from patients taking N2O is mild nausea.

Always give the patient 100% oxygen after the procedure to prevent diffusion hypoxia.

§

N2O is quickly absorbed from the lungs and is physically dissolved in the blood. There is no biotransformation, and the gas is rapidly excreted by the lungs when the concentration gradient is reversed. It is recommended that the patient be maintained on oxygen for 5-10 minutes AFTER the sedation period. Nitrous oxide has a rapid onset (5min) and rapid recovery (5min).

§

Contraindications: patients with upper respiratory infections, emphysema, bronchitis, 1st trimester of pregnancy (long-term exposure to low nitrous oxide doses can increase the incidence of spontaneous abortions), and in patients where communication is difficult (i.e. autistic patients). Nitrous is never used on patients with a contagious disease as it is difficult to sterilize the entire tubing. Environmental contamination by nitrous oxide is kept to a minimum by employing a scavenger system.

§

Important: Nitrous oxide is a SEDATIVE, NOT a general anesthetic because hypoxic levels are required to produce anesthesia. It is used alone to produce sedation or in combination with inhalation agents to supplement the anesthetic response.

20

ANTI-CONVULSANTS (ANTI-EPILEPTICS) EPILEPSY-a neurological disorder characterized by sudden, recurring attacks of motor, sensory, or psychic malfunction with or without loss of consciousness or convulsive seizures. The goal of anti-convulsant therapy is to reduce or eliminate these seizures. § Carbamazepine (Tegretol)-used a prophylaxis for partial seizures with complex symptomatology (psychomotor and temporal lobe seizures). Also treats tonic-clonic seizures (grand mal), and pain associated with TRIGEMINAL NEURALGIA by blocking Na+ channels. Adverse effects: diplopia, ataxia, enzyme induction, and blood dyscrasias, but rarely causes aplastic anemia. §

Diazepam (Valium)-treats STATUS EPILEPTICUS and emergency treatment of seizures.

May cause drowsiness, dizziness, and ataxia.

§

Ethosuximide (Zarontin)-the preferred drug for effectively treating absence seizures because it causes minimal sedation by BLOCKING CALCIUM CHANNELS. Adverse Effects: GI distress, lethargy, headache.

§

Gabapentin (Neurontin)-used as an adjunct to treat partial seizures.

§

Phenytoin (Dilantin)-treats tonic-clonic (grand mal) seizures. The rate of gingival hyperplasia is diminished by proper oral hygiene. Produces Na+ channel blockade.

Phenytoin is the most extensively used of all anti-epileptics, used IV for status epilepticus.

Phenytoin-induced gingival hyperplasia is a common adverse effect that may partially or completely obscure teeth crowns.

§

Valproic Acid (Depokote or Depakene)-also a preferred drug for effectively treating complex partial seizures, and adjunctively in patients with multiple seizure types, including absence seizures because it causes minimal sedation. It functions by causing neuronal membrane hyperpolarization. Adverse Effects: GI distress, lethargy, headache, blood dyscrasias, hepatotoxicity & liver failure.

§

Most of the commonly used anti-convulsants are CNS depressants. Thus, respiratory depression may occur with overdosage of anti-convulsants.

PARKINSON’S DISEASE-a slowly progressing, degenerative disorder of the nervous system with several distinguishing features: tremor (shaking) when at rest, sluggish initiation of movements, and muscle rigidity. In Parkinson’s disease, nerve cells in the BASAL GANGLIA DEGENERATE, causing decreased dopamine production. It may be treated, but not cured with various drugs: 1. Carbidopa-a drug used to treat PARKINSON’S DISEASE, but only works when combined with LEVODOPA (treats Parkinson’s Disease to replenish the brain’s supply of dopamine, which is the deficient neurotransmitter in Parkinson’s. § Administering Carbidopa + Levodopa = Sinemet, which reduces the required dose of levodopa by ~75%. When levodopa is given alone, most of the dose is metabolized before it reaches the brain. Thus, large doses are required and can cause unwanted side-effects. §

Carbidopa inhibits the peripheral decarboxylation of levodopa to simultaneously reduce peripheral side-effects and to allow more levodopa to reach the brain.

21

ANTIBIOTICS Sulfonamides (“Sulfa drugs”)-BACTERIOSTATIC agents structurally similar to Paraaminobenzoic Acid (PABA) which is the basis for their antibacterial actions. Bacteria require PABA to synthesize folic acid which is needed to synthesize bacteria cellular components for bacterial cell growth. Due to the structural similarities between sulfonamides and PABA, the sulfonamides COMPETE with PABA to inhibit PABAs actions, which prevents bacterial folic acid synthesis to inhibit cellular growth. Sulfonamides are “sulfa drugs” because their molecules contain sulfur atoms and their unique structure gives them their unique antibacterial mechanism of inhibiting folic acid synthesis and cell growth. § Sulfonamides DO NOT TREAT dental infections because of a low degree of effectiveness against oral pathogens. However, they are used primarily in medicine to treat URINARY TRACT INFECTIONS (UTIs). §

Bactrim-the brand name of combining Trimethoprim + Sulfamethoxazole. Bactrim is the drug of choice for many UTIs. Note: Trimethoprim component is an antimicrobial, while Sulfamethoxazole is a sulfonamide.

3 Allergic Reactions to Penicillin: a RASH is the most common sign/manifestation of an allergy to PENICILLIN. The most common adverse effect of penicillin therapy is an allergic reaction. These reactions occur in up to 10% of patients receiving penicillin.

1. Acute/Immediate Onset Reactions (Anaphylactic Shock)-occurs within 30min and are IgE mediated. Characterized by urticaria, angioedema, bronchoconstriction, GI disturbances, and shock. Death can result quickly if treatment is not given immediately (parenteral administration of EPI). This is rare, but can occur especially with oral dosing. § Cephalosporins: are definitely contraindicated for penicillin-allergic patients who exhibit immediate-type reactions.

§

Ex: a patient was given penicillin 15min ago and develops laryngeal edema, urticaria (welts that itch), severe hypotension, GI disturbances, bronchoconstriction (airway constriction), and shock. This patient is having an anaphylactic reaction (anaphylactic shock).

§

An anaphylactic reaction can be fatal if countermeasures like injecting EPI are not taken promptly. EPI prevents the release of substances from mast cells and antagonizes the actions of histamine and leukotrienes of smooth muscle.

2. Accelerated Allergic Reaction-occurs 30-48hrs after administration of penicillin.

Manifestations are urticaria, pruritus, wheezing, mild laryngeal edema, and local inflammatory reactions. Not life-threatening.

3. Delayed Allergic Reaction (Skin Rash)-occurs after 2-3 days. Approximately 80-90% of all allergic reactions occurring with penicillin are “delayed”, manifested by mild skin rashes (the most prevalent allergic manifestation).

Hypersensitivity Reactions-occur in up to 10% of patients receiving penicillin. Manifestations range from a mild rash to anaphylaxis. The rash may be urticarial, vesicular, bullous, or maculopapular. Rarely thrombopenic purpura develops.

22

PROSTHODONTICS REMOVABLE PARTIAL DENTURES KENNEDY CLASSIFICATIONS-based on the MOST POSTERIOR EDENTULOUS AREA to be restored. Although Class III & IV RPDs are entirely supported by abutment teeth, Class I and II RPDs are supported by abutment teeth, residual ridges, subjacent tissues, and fibrous C.T. overlying the alveolar process. Alveolar ridge resorption under the distal extension RPD is reduced by maximizing coverage of these supporting areas. Periodontal damage to abutment teeth is avoided with firm tissue support (maintaining a stable base-tissue relationship).

1. Class I: bilateral edentulous areas posterior to the natural teeth. BILATERAL DISTAL EXTENSION. 2. Class II: unilateral edentulous area posterior to remaining natural teeth. UNILATERAL DISTAL EXTENSION. Kennedy Class I and II must have a MESIAL REST on the abutment next to the posterior edentulous space.

3. Class III: unilateral edentulous area with natural teeth both anterior and posterior to it. A tooth-borne RPD because it depends entirely on abutment teeth for support .

4. Class IV: a single, but bilateral (it must cross the midline), edentulous area anterior to the remaining natural teeth. Anterior teeth are missing and across the midline. DOES NOT HAVE MODIFICATION SPACES. A tooth-borne RPD type because it depends entirely on abutment teeth for support. OCCLUSAL RESTS ARE PLACED ON THE DISTAL OF FIRST PREMOLARS! OCCLUSION RIMS-the resultant product after adding base-plate wax to a record base to approximate the tooth position and arch form expected in the completed denture. Functions: § Determine and establish the patient’s VDO (vertical dimension of occlusion) and level of occlusal plane. § Make maxillo-mandibular preliminary jaw relation records. § Establish and locate the future position of denture teeth (arch for the lips, cheeks, tongue). § Maxillary rim is 22mm and mandibular rim 18mm.

When recording CR for an RPD, the occlusion rim is attached to the completed partial denture metal framework instead of to a record base as used with a complete denture.

Inferior surface of the maxillary occlusion rim should be PARALLEL to CAMPER’S LINE (the line/plane running from the inferior border of the nose ala to the superior border of the ear tragus).

Significance of Camper’s Line: the occlusal plane, established by the wax occlusion rims surfaces is parallel to Camper’s line & inter-pupillary line.

23

Impression making of Complete Dentures Recommend using a technique that: 4 Affords placement and control of the impression material in recording border tissues (border molding).

4 Results in minimal tissue displacement under the denture (registers tissues in their passive position).

4 Depends on the oral conditions present.

4 Best impression technique for a patient with loose hyperplastic tissue is to register the tissue in its PASSIVE position. There must be intimate contact of the impression material with the tissue.

MANDIBULAR COMPLETE DENTURES

MANDIBULAR COMPLETE DENTURES: a primary support (stress-bearing) area is the BUCCAL SHELF because of its bone structure (resists resorption because it is dense cortical bone and does not change) and its trabeculation right angle (parallel) relationship to the occlusal plane. • A SECONDARY peripheral seal area for a mandibular complete denture is the anterior lingual border.

24

MAXILLARY COMPLETE DENTURES

PRIMARY support denture bearing areas (stress-bearing area) are the RESIDUAL RIDGES and PALATE. SECONDARY support area are the PALATAL RUGAE. Secondary RETENTIVE area is the glandular region on each side of the midline.

POSTERIOR PALATAL SEAL-extends through the HAMULAR NOTCHES in the maxilla, and passes 2mm in front of the FOVEA PALATINAE. It is in an area of immovable tissue and compensates for denture processing errors. Posterior palatine salivary glands help maintain peripheral seal.

4 Mark it in the mouth with a Thompson stick and carve/scribe this area into the cast.

4 Compensates for acrylic shrinkage and is in IMMOVABLE TISSUE. 4 Butterfly shape and in shallower in the center and hamular notch areas.

4 Carried ~5mm ANTERIOR TO THE VIBRATING LINE.

25

DENTIN™ | NBDE II

IMMEDIATE DENTURES All new dentures should be evaluated 24hrs after delivery to correct any undetected errors.

Tissue trauma attributed to denture function manifests as hyperemia, inflammation, ulceration, and pain. The basic sequence of the clinical procedure for a 24hr recall appointment is: 1. Remove the dentures from the mouth and thoroughly examine the mouth.

2. Ask the patient about the areas of tissue trauma observed. Permit the patient to describe additional complaints.

3. After collecting all diagnostic information, the dentist can determine the source of the problem and cure.

During the first few days after inserting complete dentures, the patient should expect some difficulty in masticating most foods and excessive saliva due to reflex parasympathetic stimulation of the salivary glands. Over time, this will subside and return to normal.

Ideal treatment is to fabricate the maxillary & mandibular immediate dentures simultaneously to avoid setting maxillary teeth to the likely malpositions of the remaining mandibular teeth. § If the master casts are altered in an immediate denture procedure (e.g. elimination of gross undercuts), it is advisable to construct a second transparent denture base using a surgical stent or template. The stent is placed over the ridge after the teeth are extracted.

Pressure points and undercuts are readily visible and surgical ridge correction can be performed. §

Duplicating a master cast to construct a surgical stent/template that is to be used at the time of immediate denture insertion is best made after wax elimination and after the cast is trimmed. Do not make a 2nd denture set for at least 6 months.

2 Step Schedule for Tooth Extraction Prior o delivery of IMMEDIATE COMPLETE dentures: 1. Step 1: extract all posterior teeth EXCEPT a maxillary first premolar and its opposing tooth to provide a posterior “stop” to maintain the VDO. 2. Step 2: after the posterior residual ridges exhibit acceptable healing, the 2nd treatment phase (denture fabrication) can begin. Anterior teeth are extracted at the time of denture insertion.

To help the patient get through the first day of wearing immediate dentures, instruct them to NOT REMOVE THE DENTURES, eat soft foods, and return in 24hrs for the first adjustment/evaluation. KEEP THEM IN THE MOUTH FOR 24hrs after delivery.

26

DENTIN™ | NBDE II

DENTAL IMPLANTS IMPLANT-a prosthetic device made of alloplastic materials implanted into the oral tissue beneath the mucosal and/or periosteal layer and/or within the bone, to provide retention and support for a fixed or removable prosthesis.

DENTAL IMPLANTS are classified based on their anchorage component as it relates to bone: 1. Eposteal- receives its primary support by resting on the bone.

2. Endosteal (used mainly today), placed into alveolar and/or basal bone of the mandible or maxilla, and transects only one cortical plate. Ex: Blade, ramus frame, or root form implant.

3. Subperiosteal-placed directly beneath periosteum overlying the bony cortex.

4. Transosteal (Staple Bone Implant)- penetrates BOTH cortical plates and the full thickness of alveolar bone. Combines the subperiosteal and endosteal components.

5. Intra-mucosal Implants-inserted into the oral mucosa which is used as the attachment site for the metal inserts.

Dental Implant Systems: subperiosteal, transosteal, and ENDOSSEOUS (most common).

Placing endosseous implants is a predictable procedure.

IMPLANT MATERIALS: 1. Metallic: most popular material today (TITANIUM). Other metallic implants are stainless steel, cobalt chromium molybdenum alloy, and vitallium.

2. Ceramic & Ceramic Coated: can coat metallic implant with a plasma spray or coated to produce a bioactive surface. Non-reactive ceramic materials are also present.

3. Polymeric: only used as adjuncts stress distribution along with implant, not used as implants themselves.

4. Carbon: made of carbon + stainless steel with a modulus of elasticity equal to bone and dentin. Brittleness can lead to fracture.

Criteria for Implant Success: • No persistent signs/symptoms of pain, infection, neuropathies, paresthesia.

• Implant immobility and no continuous peri-implant radiolucency.

• Negligible progressive bone loss (< 0.2mm annually) after physiologic remodeling during the first year of function.

• Patient/dentist satisfaction with the implant restoration.

Biointegration-direct biochemical bond of bone to the titanium implant surface at the electron microscope level. Independent of any mechanical interlocking.

Osseointegration-direct attachment or connection of osseous tissue to an inert, alloplastic material without intervening with connective tissue. Direct contact between bone and implant surface.

27

DENTINâ&#x201E;˘ | NBDE II IMPLANT OSSEOINTEGRATION

Implants have a peri-implant soft tissue seal where junctional epithelium attaches to the implant surface by HEMIDESMOSOMES. Main reasons implants fail to integrate: premature loading, apical migration of junctional epithelium, overheating during placement, loose fitting implants, and patients with medical risk factors or contraindications.

Implants have > 90% success rate for both maxillary & mandibular implants. Implants with rough surfaces offer advantages than smooth surface implants, and implants placed in the mandible have higher success rates than in the maxilla.

3-D computerized tomography (CT) scans provide the most accurate information about regional anatomy (maxillary sinuses, foramina, mandibular canal, adjacent teeth/roots).

28

DENTIN™ | NBDE II FERRULE EFFECT-the preparation margin (finish line) MUST extend at beyond (apical) to the core and into SOUND TOOTH STRUCTURE. Ferrule is the 1.5- 2mm or so of sound root structure apical to the core that the margins of the crown should engage to PROTECT AGAINST ROOT FRACTURE. A ferrule makes post-retained full-coverage restorations significantly more retentive and dramatically strengthens the tooth to resist fracture. It surrounds the circumference of the tooth, holding it together like the metal bands around the head of a wooden mallet.

• Preparation for a post-core should preserve solid tooth structure. The margin should be APICAL to the dowel-core margin to enable the crown to girdle the tooth and brace it externally.

• If the tooth is flush with the gingiva, fabricating a post-core and crown without encircling the tooth structure by the crown walls can cause ROOT FRACTURE.

Advantages of POST + CORE, rather than a post crown to restore RCT treated teeth: 4 Marginal adaptation and fit of the restoration is independent on the fit of the post.

4 Restoration can be replaced in the future if needed, without disturbing the post and core.

4 If the endodontically treated tooth is to serve as a bridge abutment, it is not necessary to make the root canal preparation parallel with the line of draw of other preparations (it can be treated as an independent abutment).

• Post and core is made separate from the final restoration. The crown is fabricated and cemented over the core just as a restoration is placed over a preparation done on tooth structure.

• Post and core can be used for teeth with little or no clinical crown, but with roots with adequate length, bulk, and straightness. For posterior teeth with less extensive destruction of coronal tooth structure, or teeth with less favorable root configurations, a pin-retained amalgam or composite core can be used.

29

DENTIN™ | NBDE II

IMPLANT OVERDENTURES An overdenture supported by two implants (implant-retained overdenture) is the PRIMARY prosthetic approach for an edentulous mandible. Attachments provide overdenture retention and stability via 4 attachments, and selecting the optimal mandibular overdenture attachment depends on required retention, jaw morphology/anatomy, oral function, and patient recall compliance.

1. O-ring 2. Bar-clip attachments 3. Ball attachment: highly reliable, independent attachment that allows rotational freedom to allow stress release. Ball attachments place less stress on implants and produces less bending movement than bar-clip attachments. More favorable in distributing stress around an implant than a locater attachment. Ball attachments with minimum collar heights are preferred over locators when there is restricted vertical space to address stress concerns. Transfers the least stress to peri-implant bone when a unilateral load is applied. More resilient than a locator, thus causes more uniform and less maximum stress.

4. Locator attachment: a self-aligning independent attachment with dual retention, comes in different vertical heights, and provides good resiliency, retention, and durability. Transfers more stress than a bar-clip. Very rigid to restrict overdenture movement and can generate more stress than ball attachments on the peri-implant bone.

Adequate restorative space such as interocclusal distance, phonetics, and esthetics are critical in successful implant overdenture treatment.

Minimum vertical restorative space required for implant-supported overdentures attachments: • Locator attachments = 8.5mm.

• Ball attachments = 10-12mm.

• O-ring attachment = 10-12mm.

• Bar clip attachments = 13-14mm.

IDEAL LOCATION FOR A MANDIBULAR TWO IMPLANT OVERDENTURE IS THE LATERAL INCISOR AREA WITH SHORT ATTACHMENTS.

At least 12mm vertical restorative space is needed for mandibular implant-supported overdenture.

30

DENTIN™ | NBDE II

RESTORATIVE DENTISTRY DENTAL CEMENTS (LUTING AGENTS) GLASS IONOMER CEMENT (GIC)-are hybrids of silicate and polycarboxylate cements designed to combine the fluoride releasing properties of silicate particles with the chemically adhesive and more biocompatible characteristics of the polyacrylic acid matrix compared to the extremely acidic matrix of silicate cement. GICs are mixed powder-liquid component systems. The powder (calcium-aluminofluorosilicate glass) reacts with a liquid (polyacrylic acid) to form a cement of glass particles surrounded by a matrix of fluoride elements. §

GIC Advantages: 4 Releases fluoride (anti-cariogenic). Upon setting, GICs can inhibit recurrent caries development at its margins because it releases fluoride from its surface. GIC can also absorb fluoride when local ionic concentrations are high, then slowly release fluoride when the environment concentration decreases, thus acting as a FLUORIDE SPONGE. 4 Chemical adhesion to the prepared tooth and certain materials. Micromechanical bond to composite resins.

4 High biocompatibility, thus with enough dentin remaining (.5-1mm) no pulpal protective agent (calcium hydroxide) is required.

4 Good thermal insulators (equal to natural dentin).Thermal expansion is similar to that of tooth structure.

4 After the initial setting period, GICs have low solubility in the mouth. It is the least soluble cement (compared to zinc phosphate and zinc polycarboxylate cements).

§

GIC Disadvantage: has a higher cement film thickness than zinc phosphate cement.

§

Only GIC is used as a cement (luting agent) AND permanent restorative material. GIC are often used for root surface carious lesions (Class V restorations) due to the potential advantage of fluoride release to help control spread of caries. GIC is used as a luting agent and for Class V restorations with composite “sandwich technique”.

§

GICs are composed of aluminosilicate powder and polycarboxylate liquid.

CLASSES OF GLASS IONOMER CEMENTS (GIC): 1. Conventional GIC-used as a luting agent. Ex: Ketac-Cem. 2. Light-cured GIC-used as a liner or base (the liquid version has HEMA added to it).

Advantages: extended working time, short on-demand setting times, as a set mass it is stronger, more adhesive, and more resistant to desiccation than self-cured glass ionomers.

Ex: Vitrebond & XR Ionomer.

3. Resin-Modified (Hybrid) Light Cured GIC-used for any application where glass ionomers are good choices (the liquid has HEMA added to it). Ex: Fuji-II LC. Advantages of hybrid light cured ionomers: esthetics, bond strength, and coefficient of thermal expansion.

31

DENTIN™ | NBDE II

DENTAL BIOMATERIALS ADHESION-the attraction of unlike molecules. Adhesive potential is predicted by measuring the spreading or wetting of the adhesive over a substrate surface. This is done by determining the contact angle of the drop of adhesive as it spreads out. The smaller the contact angle, the greater wetting & potential for adhesion. 2 types of adhesion: § physical forces (van der Waals forces). § chemical forces (chemisorption).

COHESION-the attraction of similar molecules.

STRAIN-the actual change in shape or deformation that accompanies any stress. 3 Types of Stresses: 1. Compression-the squeezing of material by external forces. If the wire were a thin metal rod on a firm (hard) surface with a weight on the top, it would spread the weight (stress) across the entire rod. Here the rod’s atoms are being pushed together.

2. Tension-the pulling of a member or part of a member, resulting in an increase in length. If a long metal wire were hung from the ceiling with a weight on one end, the weight would place a force on the wire. Inside the wire, the force spreads evenly through the whole wire. If enough force or weight were put on the end of the wire, it could cause the wire to stretch. The wire’s atoms are being pulled apart by the weight or force on the wire.

3. Shear-the sliding of one layer of a material relative to another layer of material. Ex: two blocks of wood nailed together. If one block was pushed to the right, and the other block pushed to the left, the nails experience a shear stress at the point where the two blocks of wood meet. If pushed hard enough, the nails could bend or break.

TOUGHNESS-the total energy absorbed to the point of fracture (the property of being difficult to break). It is affected by yield strength, percent elongation, and modulus of elasticity. ¶ The mechanical property of toughness is affected by yield strength, tensile strength, percent elongation, and modulus of elasticity.

BRITTLENESS-the opposite of toughness. A brittle material is vulnerable to fracture at or near its proportional limit. A brittle material has a high compressive strength, but low tensile strength (i.e. amalgam). This is why amalgam preparations doe NOT have beveled margins (they need butt joints).

MODULUS OF ELASTICITY-a measure of a material’s stiffness or rigidity (the ratio of stress to strain below the elastic limit). ¶ The higher the modulus of elasticity, the stiffer (more rigid) the material. ¶ Rank these materials in order of INCREASING modulus of elasticity (MPa): GLASS IONOMER (5520 MPa) < COMPOSITE (16,600 MPa) < DENTIN (19,300 MPa) < ENAMEL (90,000 MPa) < GOLD ALLOY (96,000 MPa).

RESILIENCE-the energy that a material can absorb before the onset of any plastic deformation.

GALVANIC SHOCK-a clinical phenomenon where an electrical charge is created when two dissimilar metals come into contact.

32

DENTIN™ | NBDE II

PERIODONTICS STAGING AND GRADING PERIODONTITIS The 2017 World Workshop on the Classification of Periodontal and Peri-Implant Disease and Conditions was co-presented by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) PERIODONTITIS STAGING-a method to classify the severity and extent of a patient’s disease based on the measurable amount of destroyed and/or damaged tissue as a result of periodontitis and to assess the specific factors that may attribute to the complexity of long-term case management.

Initial stage is determined using clinical attachment loss (CAL). If CAL is not available, radiographic bone loss (RBL) should be used. Tooth loss due to periodontitis may modify stage definition. One or more complexity factors may shift the stage to a higher level. See perio.org/2017wwdc for additional information.

PERIODONTITIS Interdental CAL (site of greatest loss)

STAGE I 1-2mm

STAGE II 3-4mm

STAGE III >5mm

STAGE IV >5mm

SEVERITY

RADIOGRAPHIC BONE LOSS (RBL)

Coronal 1/3 (<15%)

Coronal 1/3 (15%-33%)

Extending to root’s middle 1/3 and beyond apically

SEVERITY

TOOTH LOSS (due to periodontitis)

No Tooth Loss

No Tooth Loss

< 4 Teeth

Extending to root’s middle 1/3 and beyond apically < 5 Teeth

SEVERITY

COMPLEXITY

LOCAL

Max probe depth < 4mm Mostly Horizontal Bone loss

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Max probe depth < 5mm Mostly Horizontal Bone loss

Stage II complexity with probings > 6mm, vertical bone loss >3mm, Class II or III furcation involvement, and moderate ridge defects

Stage III complexity with need for complex therapy due to masticatory dysfunction, sencondary occlusal trauma (mobility > 2 degrees), severe ridge defects, bite collapse, drifting, flaring, < 20 teeth remain (10 opposing pairs)

DENTIN™ | NBDE II

FLAPS, GRAFTS, AND PERIODONTAL SURGERY Autogenous Free Gingival Graft-an autogenous graft of gingiva placed on a viable C.T. bed where initially buccal or labial mucosa were present. Usually, the donor site from where the graft is taken is an edentulous region or palatal area. The graft epithelium undergoes degeneration after it is placed, then sloughs. The epithelium is reconstructed in ~1 week by the adjacent epithelium and proliferation of surviving donor basal cells. In 2 weeks, tissue reforms, but maturation is not complete until 10-16 weeks. The healing time required is proportional to the graft’s thickness. The greatest amount of shrinkage occurs within the first 6 weeks. §

Free gingival graft-involves removing a section of attached gingiva from another area of the mouth (usually the hard palate or an edentulous region) and suturing it to the recipient site. FGG success depends on the graft being immobilized at the recipient site. A FGG is used to increase the zone of attached gingiva and possibility of gaining root coverage. The difficulty in getting complete root coverage lies in the fact that an avascular graft is placed over a root surface also devoid of blood supply.

§

FGG retains NONE of its own blood supply and is totally dependent on the bed of recipient blood vessels. The FGG receives its nutrients from the viable C.T. bed.

§

MAIN reason a FGG fails is disruption of the vascular supply before engraftment.

Infection is the second most common reason of FGG failure.

FREE GINGIVAL GRAFT INDICATIONS: § Prevent further recession and successfully widen (increase the width) of attached gingiva. §

Cover non-pathologic dehiscence and fenestrations.

§

Performed with a frenectomy to prevent reformation of high frenal attachments.

§

Cover a root surface with a narrow denudation. FGG may or may not yield a successful result when used to obtain root coverage (the result is not highly predictable in root coverage cases).

§

Used therapeutically to widen attached gingiva after recession occurs, and to prophylactically prevent recession where the band of attached gingiva is narrow, and of a thin, delicate consistency.

§

Correct localized narrow recessions or clefts, but NOT DEEP WIDE RECESSIONS. In such cases, the laterally repositioned flap (a pedicle graft) has a greater predictability. FGG is rarely used on facial or lingual surfaces of mandibular 3rd molars (especially facial).

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FGG Healing: involves revascularization of the graft. The graft’s top layers are revascularized last. Thus, the epithelium dies off (degenerates), producing the necrotic slough. During healing, the epithelium of FGG degenerates (necrotic slough), and reepithelization occurs by proliferation of epithelial cells from adjacent tissue and surviving basal cells of the graft tissue.

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DENTIN™ | NBDE II

4 STAGES OF THE PERIODONTAL LESION (INITIAL, EARLY, ESTABLISHED, AND ADVANCED) 1. Initial Lesion (2-4 Days): no clinical changes, vasodilation of small capillaries, increase in leukocytes (PMNs), and increased gingival fluid flow. PMNs (neutrophilic leukocytes) are the first line of defense and first cells to migrate into the gingival sulcus when inflammation caused by plaque formation in the initial lesion of gingivitis occurs.

2. Early Lesion (Gingivitis 4-7 Days): clinical signs of GINGIVITS appear. Leukocyte infiltration into C.T. Sulcular lining develops RETE PEGS. Collagen destruction occurs and the sulcular lining is ulcerated. The area of destruction becomes larger with persistence of inflammation. Leukocytes invade C.T. and are dominated by lymphocytes (3/4 of all cells), macrophages, plasma cells (secrete IgG), and mast cells (release histamine). PMNs in sulcus.

3. Established Lesion (2-3 weeks): gingival erythema occurs due to capillary proliferation.

Changes in gingival color occur starting at the papillary and marginal tissues, then progressing to attached gingiva. Gingival enlargement (may increase probing depths); plasma cells become prominent, and widened intercellular spaces in the pocket lining.

4. Advanced Lesion: the IRREVERSIBLE transition from gingivitis to periodontitis. JE becomes detached from the root surface as it migrates apically. Osteoclasts and bone loss.

Clinical Criteria To Evaluate During a Periodontal Exam (besides color, tone, contour, & gingiva size): 1. Level of Free Gingival Margin relative to the CEJ: the normal level of epithelial attachment should be on enamel or at the CEJ (this places the free gingival margin 2-3mm coronal to the sulcular base).

2. Periodontal Pocket Depth: all measurements > 3mm are recorded for sulcular depth, including any reading that locates the free gingival crest < 2mm at or below the CEJ. • Shallow pockets attached at the level of the apical third of the root connote more severe destruction than deep pockets attached at the root’s coronal third. When the gingival margin coincides with the cementoenamel junction (CEJ), the loss of attachment = the pocket depth.

• Provides the most accurate assessment of periodontal pocket depth.

3. Loss of Attachment: determined by measuring the distance between the CEJ to the base of the attachment.

• Attachment level-the position of the junctional epithelium at the base of a sulcus (pocket). In health, the JE is on enamel or at the CEJ. In disease, the JE migrates apically along the root surface. It is measured from an established reference point (CEJ or restoration margin) to the attachment with a periodontal probe. The periodontal pocket is measured from a changeable point (margin of free gingiva) to the attachment level.

4. Mobility: grades 1, 2, and 3. Use two instruments to test mobility. A depressible tooth has grade 3 mobility.

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DENTIN™ | NBDE II

ABSCESSES s

PERIODONAL PROBING will reveal deep pockets associated with the periodontal abscess. Vitality tests, thermal and electric tests will exclude the pulp as the unlikely cause of symptoms as the tooth with a periodontal abscess is usually vital. Methods to distinguish a periodontal abscess from a pulpal (periapical) abscess is done via periodontal probing, EPT, thermal testing. However, a periapical radiograph is not a good diagnostic method to distinguish between a periodontal and pulpal abscess.

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MOST COMMON symptom a patient will report with a periodontal abscess is ACUTE PAIN that is constant, severe, and dull throbbing. Thermal changes do not elicit or modify the discomfort. The onset of this discomfort is rapid and becomes progressively more intense. The patient may also notice an increase in tooth mobility, and say it is difficult to close their teeth together without striking the involved tooth first, causing increased pain.

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The periodontal abscess can be an acute exacerbation of chronic periodontal disease and may occur when the infection passes into the tissue through the pocket epithelium.

Such abscesses are often the result of blockage of the narrow openings of tortuous or deep infrabony pockets.

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Radiographic findings associated with the periodontal abscess are NOT specific.

There may be no change radiographically in the early acute lesion. However, often there is a localized discrete radiolucency lateral to the root or in a furcation which can cause rapid alveolar bone destruction.

s

Treatment of the acute periodontal abscess is determined initially by whether there is localization of the abscess (if there is, drainage is the treatment). If the abscess is not localized, the patient is placed on antibiotics (Penicillin V) and instructed to rinse with warm saline. Clindamycin can be used in penicillin allergic patients.

Periodontal-Endodontic Abscess: • Signs and symptoms are not always consistent, but include radiographic involvement of the periodontium and periapex, significant probing depths, percussion and pulpal sensitivity. Each case may or may not present with all of these signs and symptoms. In the presence of both a chronic endodontic and periodontal lesion, both lesions must be treated to achieve complete healing.

•

Treatment: RCT (pulp is treated first and after the periodontal condition is re-evaluated 23 months after the completion of endodontic therapy). Antibiotic therapy, SRP, and periodontal surgery if needed, is performed 2-3 months after the completion of RCT.

PERIODONTAL CYST-is usually asymptomatic and without grossly detectable changes, but may present as a localized tender swelling. Radiographically, an interproximal periodontal cyst appears on the side of the root as a radiolucent area bordered by a radiopaque line. Its radiographic appearance cannot be differentiated from a periodontal abscess.

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DENTIN™ | NBDE II

PROVISION OF SPECIALTY CARE ENDODONTICS 1.

A highly-effective root canal irrigant due to its antimicrobial action, substantivity, low toxicity, and because it does not interfere with the bond strength of resin cement to root dentin and a fiber post is 2% CHLORHEXIDINE GLUCONATE (CHX).

2.

The least effective endodontic treatment for primary teeth with extensive caries is the DIRECT PULP CAP. Pulp-capping should be limited to small exposures produced by mechanical means or pin-point caries. BOTH TRUE.

3.

The most widely used endodontic irrigant that is bactericidal, dissolves organic pulp and collagen, but does not remove the smear layer is NaOCl (SODIUM HYPOCHLORITE).

4.

CBCT 3D imaging should be used only when the patient’s history and clinical exam demonstrate the patient benefits outweigh the potential risks. CBCT should not be used routinely for endodontic diagnosis or for screening purposes in the absence of clinical signs and symptoms. BOTH TRUE.

5.

The pulp disinfectant used as an irrigant and chelating agent that kills bacteria by extracting bacterial surface proteins by combining with metal ions in the bacterial envelops is EDTA (ETHYLENEDIAMINE TETRA-ACETIC ACID).

PROVISION OF SPECIALTY CARE ORTHODONTICS AND PEDIATRIC DENTISTRY 1.

The most common chronic condition of rampant caries in the primary dentition due to intake of dietary sugars, nighttime feeding, and inadequate oral hygiene is EARLY CHILDHOOD CARIES (ECC).

2.

The most effective orthodontic appliance to retract or retrude protruding or flared maxillary incisors into proper arch alignment is the HAWLEY REMOVALBE APPLIANCE WITH CLASPS AND LABIAL BOW.

3.

The two major causes of orthodontic relapse are CONTINUED UNFAVORABLE GROWTH and SOFT TISSUE REBOUND.

4.

The most common congenitally missing permenant teeth (besides 3rd molars) are MAXILLARY LATERAL INCISORS and MANDIBULAR SECOND PREMOLARS.

5.

It is NOT recommended to attempt to replant an avulsed primary tooth back into its socket.

It is recommended to immediately replant an avulsed permenant tooth with open apices, clean roots, and that has only been out of the mouth for < 60 minutes back into its socket.

BOTH TRUE.

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DENTIN™ | NBDE II

PROVISION OF SPECIALTY CARE ORAL SURGERY 1.

A patient with severe restriction of opening, deviation to the affected side, and decreased lateral excursions to the contralateral side most likely has TMJ INTRACAPSULAR ANKYLOSIS. A patient whose mandible deviates to the left on opening may be due to intracapsular ankylosis of the LEFT TMJ.

2.

The average volume of the maxillary sinus is 15 mL.

3.

The maxillary sinus cavity lining that is elevated when insufficient bone height is present prior to dental implant placement is the SCHNEIDERIAN MEMBRANE.

4.

The most common surgical complication during or after sinus augmentation (lift) is SCHNEIDERIAN MEMBRANE PERFORATION.

5.

The maxillary sinus communicates with the nasal cavity through the OSTIUM.

6.

ASTHMA is NOT a contraindication for the administration of nitrous oxide. Nitrous oxide should NOT be administered to patients with drug-related dependencies, cobalamin deficiency, or during the first trimester of pregnancy. BOTH TRUE.

7.

The MOST COMMON pathological condition of the maxillary sinus is INFLAMMATORY DISEASE.

8.

The most common HYDROXYAPATITE.

9.

An example of a type of XENOGRAFT that can be alone or combination with other grafting materials is DEPROTEINIZED BOVINE BONE.

10.

The ability of a graft to act as a SCAFFOLD for new bone formation is OSTEOCONDUCTION.

11.

The ability of a graft to induce OSTEOBLASTIC DIFFRENTIATION of a host’s undifferentiated cells is OSTEOINDUCTION.

ALLOPLASTIC

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DENTINâ&#x201E;¢ | NBDE II

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