ADEX DSE-OSCE

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DENTINâ„¢ | ADEX DSE-OSCE

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DENTIN™ | ADEX DSE-OSCE

COPYRIGHT ©2020-2021. DENTIN, LLC. ALL RIGHTS RESERVED. No part of this book may be produced, stored in a retrieval system, or transmitted in any form, or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission from the publisher. Produced by DENTIN, LLC dentin.co Printed in the United States

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DENTIN™ | ADEX DSE-OSCE

The ADEX DSE-OSCE is a comprehensive computer-based examination that consists of 165 multiple-choice items (15 are pilot questions for future versions). For each discipline tested, 80% of the questions are stand-alone, and 20% of the questions are interdisciplinary and case-based. The DSE-OSCE is a 4 hour exam administered on a one day As with all sections of the ADEX Dental Examination Series, the 18-month rule and 3-time failure rule apply to the DSE OSCE. DSE OSCE CONTENT PATIENT EVALUATION (PE) • Pathology (14%) • Physical Evaluation (6%): Anatomy, Identify Systemic Conditions, Radiology, Lab Diagnostics, and Pharmacological Therapeutics COMPREHENSIVE TREATMENT PLANNING (CTP) • Systemic Diseases, Medical Emergencies, Special Care/Oral Medicine (10%) •

Restorative Dentistry (12%)

Specialties (18%): Endodontics, Orthodontics, Oral Surgery, and Pediatric Dentistry 15-minute break

PERIODONTICS, PROSTHODONTICS, AND MEDICAL CONSIDERATIONS (PPMC) • Medical Consideration in Treatment Planning (Medical Emergencies and Infection Control) (8%) • Periodontics (16%) • Prosthodontics (16%)

165 QUESTIONS 20% (33)

40% (66)

40% (66)

ADEX DSE-OSCE SCORING: The final DSE-OSCE score is based on the percentage of items answered correctly and scaled to equate scores annually. Out of 100 possible points, a scaled SCORE OF 75 OR HIGHER IS REQUIRED TO PASS. Results are released in accordance with CDCA administrative procedures. The ADEX candidate MUST pass the DSE to pass the overall ADEX examination and achieve “ADEX Status.” Candidates may register for the DSE-OSCE through their online candidate profiles and may take the DSE-OSCE before or after the manikin or patient-based examination sections. DO NOT WORRY, STUDY HARD and TEST WITH CONFIDENCE, YOU WILL PASS THE ADEX DSE-OSCE WITH THE DENTIN ADEX DSE-OSCE STUDY GUIDE. Simulations of patients are illustrated through computer-enhanced photographs, radiographs, optical images of study, working models, laboratory data, and other clinical digitized reproductions. The DSE-OSCE is a computerized objective simulated clinical examination (OSCE). If you know the core foundation material in the DENTIN ADEX DSE-OSCE study guide, you will be well-prepared to answer any of the DSE-OSCE questions.

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DENTINâ„¢ | ADEX DSE-OSCE

DENTIN ADEX DSE-OSCE TABLE OF CONTENTS PATIENT EVALUATION (PE) General and Oral Pathology ........................................................................................... 4-115 General and Oral Pathology Potential ADEX DSE Exam Questions.......................... 116-124 Anatomy and Systemic Conditions ............................................................................. 125-153 Dental Radiology ........................................................................................................ 154-156 Pharmacological Therapeutics (Pharmacology) ......................................................... 157-172

COMPREHENSIVE TREATMENT PLANNING (CTP) Systemic Diseases, Special Needs, and Medical Emergencies ................................. 173-175 Restorative Dentistry .................................................................................................. 176-182 Specialties (Endodontics) ........................................................................................... 183-188 Specialties (Orthodontics and Pediatric Dentistry) ..................................................... 189-193 Specialties (Oral Surgery)........................................................................................... 194-198

PERIODONTICS, PROSTHODONTICS, AND MEDICAL CONSIDERATIONS (PPMC) Medical Considerations in Dental Treatment Planning ............................................... 199-206 Infection Control and OSHA ....................................................................................... 207-218 Periodontics ................................................................................................................ 219-294 Prosthodontics ............................................................................................................ 295-374

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DENTIN™ | ADEX DSE-OSCE

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. • Caution with patients taking IV bisphosphonates (Zometa (zoledronic acid) & Aredia (pamidronate) for osteoporosis and cancer treatment respectively. •

Caution with patients taking oral bisphosphonates (Fosamax, Actonel, & Boniva). Occurs more common in patients taking IV bisphosphonates (.05-7%) and < 1% taking oral bisphosphonates. 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 AND DENSE. • Clinical Signs: abnormal bone & dental development, fragile bones, stunted growth anemia, spleen & liver enlargement, blindness, and progressive deafness.

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DENTIN™ | ADEX DSE-OSCE

4 TYPES OF MELANOMA: 1. Superficial Spreading Melanoma-the MOST COMMON form of malignant melanoma (65%), & most common cutaneous melanoma in Caucasians. The lesion is TAN, BROWN, BLACK, or ADMIXED on sun-exposed skin (especially BLACK). The cancer begins at one focus in the skin at the dermo-epidermal junction (DEJ). It initially grows in a horizontal plane, along and just above & below the dermo-epidermal junction (this is the “radial” growth phase of melanoma which predominates), and is clinically macular or only slightly elevated. The “vertical” growth phase is characterized by an increase in size, change in color, nodularity, and at times ulceration. 2. Nodular Melanoma-much less common (~13% of cutaneous melanomas). THERE IS NO “RADIAL” GROWTH PHASE (it exists only in the “vertical” growth phase). NM presents as a sharply defined nodule with degrees of pigmentation (may be pink (amelanotic melanoma) or black, and occurs more often on the back, head, and neck of men. 3. Lentigo Malignant Melanoma-even less common (~10% of cutaneous melanomas), and is most common in the ELDERY population. The lesion may grow for years in the “radial” growth phase before developing into the more aggressive “vertical” growth phase. This radial growth phase is known as lentigo maligna (melanotic freckle of Hutchinson), while the vertical growth phase is known as lentigo maligna melanoma. 4. Acrolentiginous Melanoma-occurs on the hands and feet with a reputation for being ignored by the patient, resulting in the development of metastic disease. NEVUS (MOLES)-nearly all moles are normal. Atypical (Dysplastic) nevi-unusual moles are generally larger than normal moles, and are flat or have a flat part, with irregular borders with variable shades of color (especially brown, but can be a Blue Nevus). The presence of dysplastic nevi may mark a greater risk of malignant melanoma developing on apparently normal skin. NEVUS

ACQUIRED NEVI (MOLES) – small, usually dark, skin growths that develop from pigmentproducing cells (melanocytes) in the skin. Fairly common on the skin and intra-orally (much more common than congenital nevi both intra-orally and extra-orally). When present, they are usually on the HARD PALATE, or may be on the gingiva and lips. Acquired nevi are microscopically classified into 5 subtypes:

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ODONTOGENIC ABNORMALITIES ABRASION – abnormal, PATHOLOGIC WEARING AWAY (LOSS) of tooth structure. 1. Toothbrush Abrasion-most often results in V-shaped wedges at the cervical margins in canines & premolars. Caused by using a hard bristle toothbrush and/or horizontal brushing strokes with a gritty dentifrice. 2. Occlusal Abrasion-results in flattened cusps on all posterior teeth & worn incisal edges due to chewing or biting on hard foods or objects, and chewing tobacco. ATTRITION –physiologic wearing-away of enamel & dentin due to NORMAL function or mainly excessive GRINDING/GRITTING/CLENCHING teeth together (BRUXING). The most noticeable effects are POLISHED FACETS (flat incisal edges that usually develop on the linguoincisal of maxillary canines & central incisors, and facioincisal of mandibular canines). Discolored tooth surfaces, and exposed dentin. ATTRITION (BRUXING/GRINDING)

EROSION – CHEMICAL loss of tooth structure from NON-MECHANICAL MEANS such as drinking acidic liquids (soda) or eating acidic foods. Common in BULIMCS due to regurgitated stomach acids. Affects smooth surfaces and occlusal surfaces of teeth. EROSION

INTRINSIC STAINING: can be caused by the following except DIABETES MELLITUS. • Dentinogenesis imperfecta-causes a translucent or opalescent hue, usually gray to bluish-brown. • Erythroblastosis fetalis- causes intrinsic stain that is bluish-black, greenish-blue, tan, or brown. • Porphyria-causes an intrinsic stain that is red or brownish. • Fluorosis-causes white opacities, or light brown to brownish-black.

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DENTIN™ | ADEX DSE-OSCE

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

Leukoedema’s white appearance is caused by water inside spinous cells, causing light to reflect back as whitish. Differential Diagnosis: leukoplakia, white sponge nevus, and benign intraepithelial dyskeratosis.

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.

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DENTIN™ | ADEX DSE-OSCE

ORAL PATHOLOGY AND RADIOLOGY “DENTIN SUCCESS STATEMENTS” ODONTOGENIC AND BONE LESIONS 1.

Oral manifestations associated with TRISOMY 21 (DOWN SYNDROME) include bullshaped molars (TAURODONTISM), some missing teeth (HYPODONTIA), increased gingivitis and periodontal disease, and DECREASED CARIES.

2.

Patient with DOWN SYNDROME (TRISOMY 21) would present with the CLASS III malocclusion (protruded mandible).

3.

The MOST common site for oral cancer is the LATERAL BORDER OF THE TONGUE.

4.

The 5-year survival rate for head and neck cancer is approximately FIFTY-PERCENT (50%).

5.

Three major risk factors for head and neck cancer are ALCOHOL, TOBACCO, and HUMAN PAPILLOMAVIRUS (HPV).

6.

Stages of PERIAPICAL CEMENTAL DYSPLASIA when viewed radiographically in a middle-aged African American female are: RADIOLUCENT (Stage 1), MIXED (Stage 2), & RADIOPAQUE (Stage 3).

7.

Inflammation and fissuring at the corners of the mouth (labial commissures) caused by CANDIDA ALBICANS, RIBOFLAVIN (B2) DEFICIENCY, or ILL-FITTING DENTURE (DECREASED VERTICAL DIMENSION) is called ANGULAR CHEILITIS (PERLECHE).

8.

Appropriate medications for ANGULAR CHEILITIS are MYCOLOG II topical cream (Nystatin + Triamcinolone) or DERMAZENE topical cream (iodoquinol + hydrocortisone).

9.

A 28-year old pregnant patient presents with a pedunculated, raspberry-like, BENIGN softtissue growth on her INTERDENTAL PAPILLAE. The lesion is ulcerated, smooth, red, and bleeds easily. The lesion is due to local tissue irritation or injury but can also occur during due to progesterone changes. This lesion accurately describes a PYOGENIC GRANULOMA (PREGNANCY TUMOR).

10.

A MALIGNANT tumor of BONE-FORMING tissue is an OSTEOSARCOMA.

11.

A BENIGN radiopaque BONY OVERGROWTH or protuberance of pre-existing bone found at the MIDLINE of the HARD PALATE and/or mandibular lingual surfaces is an EXOSTOSIS (TORI = OSTEOMA).

12.

The panorex of a 30-year-old female reveals a painless, unilocular radiolucency with welldefined margins around the CROWN of an impacted permanent mandibular 3rd molar. This is a DENTIGEROUS CYST (FOLLICULAR CYST).

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DENTIN™ | ADEX DSE-OSCE

ANATOMY AND SYSTEMIC CONDITIONS TONGUE 1.

HYPOGLOSSAL NERVE (CN XII) provides MOTOR to ALL TONGUE INTRINSIC & EXTRINSIC MUSCLES EXCEPT “PALATOGLOSSUS” which is innervated by the VAGUS NERVE (PHARYNGEAL PLEXUS).

2.

EXTRINSIC TONGUE MUSCLES are named based on their ORIGIN.

3.

During contraction, the tongue muscle that PROTRUDES the tongue is GENIOGLOSSUS.

4.

During contraction, the tongue muscle that DEPRESSES the tongue’s sides is HYOGLOSSUS.

5.

During contraction, the extrinsic tongue muscle that ELEVATES and RETRACTS the tongue is STYLOGLOSSUS.

6.

During contraction, the tongue muscle that ELEVATES the tongue’s base and DEPRESSES the soft palate is PALATOGLOSSUS.

7.

The soft palate is elevated during swallowing and initiation of esophageal peristalsis by the VAGUS NERVE.

8.

LINGUAL NERVE provides general SENSORY to the TONGUE’S ANTERIOR 2/3.

9.

GLOSSOPHARYNGEAL NERVE provides sensory and taste to TONGUE’S POSTERIOR 1/3.

10.

The tongue is innervated by cranial nerves VII, IX, X, and XII.

11.

LINGUAL ARTERY provides the MAIN blood supply to the TONGUE.

12.

Tongue tip and lower lip, floor of the mouth, mandibular incisors, and the chin bilaterally DRAIN INTO the SUBMENTAL LYMPH NODES.

13.

REMAINING anterior tongue 2/3 drains into the SUBMANDIBULAR and DEEP CERVICAL LYMPH NODES.

14.

A severe abscess of a maxillary tooth will drain via the SUBMANDIBULAR LYMPH NODES.

15.

FILLIFORM PAPILLAE are the most NUMEROUS, NO TASTE BUDS, and cause HAIRY TONGUE.

16.

STAINING & ELONGATION of the FILLIFORM PAPILLAE due to accumulation of oral bacteria or fungi is indicative of HAIRY TONGUE.

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DENTINâ„¢ | ADEX DSE-OSCE

PHARMACOLOGICAL THERAPEUTICS PHARMACOKINETICS ANTIBIOTICS AND ANTIFUNGALS 1.

The penicillin derivative when combined with clavulanic acid that is MOST EFFECTIVE against bacteria that produce the beta-lactamase enzyme is AMOXICILLIN.

2.

The antibiotic of choice in DENTISTRY for non-penicillinase producing oral infections in a pregnant woman who denies allergies is PENICILLIN VK.

3.

The period of initial SLOW BACTERIAL GROWTH, no cell division, and stable metabolic activity is the LAG PHASE.

4.

If penicillinase is cultured from an infection, AUGMENTIN (amoxicillin + clavulanic acid) should be given NOT just Amoxicillin.

5.

PENICILLINS are effective against bacteria by INHIBITING CELL WALL SYNTHESIS BY LYSIS.

6.

The prophylactic antibiotic of choice and dosage in a non-penicillin allergic patient one-hour before dental treatment to prevent bacterial endocarditis is AMOXICILLIN (2 grams).

7.

AMOXICILLIN and AMPICILLIN are contraindicated in patients with INFECTIOUS MONONUCLEOSIS due to the increased risk of MACULOPAPULAR EXANTHEMS.

8.

A MAJOR disadvantage of penicillin compared to other antibiotics is its high incidence of ALLERGIC REACTIONS.

9.

The FIRST antibiotic PRE-MEDICATION ALTERNATIVE for a penicillin-allergic patient with congenital heart disease and artificial heart valves is CLINDAMYCIN (600mg before the dental procedure).

10.

A 62-year old male with no allergies presents for root planing. He had bilateral hip replacement surgery nearly two years ago without complication, has mitral valve prolapse with regurgitation, and has a cardiac pacemaker. The appropriate antibiotic prophylaxis is PRE-MEDICATION IS NOT REQUIRED.

11.

Antibiotic prophylaxis to prevent infective endocarditis is REQUIRED for patients with PROSTHETIC HEART VALVES, HISTORY OF ENDOCARDITIS, or TETROLOGY OF FALLOT.

12.

A rare, but dangerous adverse effect of taking CLINDAMYCIN is PSEUDOMEMBRANOUS COLITIS (overgrowth of Clostridium difficile that produces a toxin causing colitis).

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DENTIN™ | ADEX DSE-OSCE

COMPREHENSIVE TREATMENT PLANNING (CTP) SPECIAL NEEDS AND MEDICAL EMERGENCIES 1.

In PARKINSON’S DISEASE neurons in the BASAL GANGLIA to DEGENERATE, causing DECREASED DOPAMINE production.

2.

CARBIDOPA-LEVODOPA (Sinemet) is the current MOST EFFECTIVE combination to treat PARKINSON’S DISEASE by replenishing dopamine.

3.

The opioid and CNS stimulant that can produce PARKINSON-LIKE EFFECTS due to altered dopamine levels is METHAMPHETAMINE (crystal meth).

4.

A 13 year-old child during a routine prophylaxis had a sudden lapse of consciousness that began with a blank stare and ended quickly within 10-15 seconds with complete and immediate recovery. This child most likely had an ABSENCE (PETITE MAL) SEIZURE.

5.

A patient undergoing RENAL DIALYSIS for ESRD should schedule their dental hygiene appointment THE DAY AFTER DIALYSIS.

6.

When treating a pregnant patient, position patient on her LEFT SIDE with a FOLDED TOWEL or PILLOW UNDER HER RIGHT HIP to elevate the hip and prevent vascular compression.

drug

RESTORATIVE DENTISTRY 1.

Pit and fissure SEALANTS are generally comprised of FILLED BIS-GMA RESIN, an ideal material for occlusal surfaces due to their high wear resistance.

2.

The tooth preparation reduction for metal-ceramic restorations is 1.5-2.0mm to allow for 0.5mm metal thickness and 1.0-1.5mm thickness of porcelain.

3.

The most effective etching solution to prepare the enamel surface for dental sealants is 35%-50% PHOSPHORIC ACID.

4.

HYDROCOLLOIDS like ALGINATE are aqueous and HYDROPHILLIC (water-loving), while ELASTOMERS like POLYVINYL SILOXANES are non-aqueous and HYDROPHOBIC.

5.

Indications for using ZOE paste are final impressions for removable dentures (edentulous ridges) and as a surgical dressing after grafting to provide comfort.

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DENTIN™ | ADEX DSE-OSCE

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™ | ADEX DSE-OSCE

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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DENTIN™ | ADEX DSE-OSCE

PERIODONTICS, PROSTHODONTICS AND MEDICAL CONSIDERATIONS (PPMC) MEDICAL CONSIDERATIONS IN DENTAL TREATMENT PLANNING SPECIAL NEEDS: defined by the Commission on Dental Accreditation as patients whose medical, physical, or social situations make it necessary to modify regular dental routines in order to provide dental treatment that is specifically tailored to the individual. As dental professionals, we must modify the usual course of dental treatment modalities we provide to effectively render oral health care to special need patients. The dental professional’s role is to TREAT THE ENTIRE PERSON. Familiarize yourself with the special need patient’s condition and medical history, and modify treatment as needed to ensure that the dental appointment is as comfortable and as effective as possible. It is critical to effectively communicate with the patient and their guardian or caregiver, as well as other healthcare providers during the course of treating the special needs patient. Develop a treatment plan that considers any barriers to patient care such as resources, cultural values or beliefs, and personal abilities and limitations.

ASTHMA AND COPD PATIENTS ASTHMA-a chronic respiratory disease associated with airway obstruction, recurrent attacks of paroxysmal dyspnea (shortness of breath), and wheezing due to spasmodic contraction of the bronchi. • Asthma effects 17 million adults and 6 million children in the U.S. (1.1 in 100,000 asthma deaths annually. •

Clinical Manifestations: bronchi constriction, coughing, wheezing, chest tightness, and shortness of breath.

Oral Manifestations: increased caries risk, xerostomia, enamel defects, increased gingivitis and periodontal disease (possibly due to mouth-breathing), higher rates of malocclusion (overjet, overbite, posterior crossbite, high palatal vault).

ASTHMA MEDICATIONS: • Bronchodilators (ALBUTEROL INHALERS) can have adverse oral effects like oral candidiasis, xerostomia, decreased salivary flow rate, and increased caries. •

ASPIRIN and NSAIDs should be AVOIDED (due to allergies/hypersensitivity) as they can trigger a severe asthma attack (bronchoconstriction).

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DENTIN™ | ADEX DSE-OSCE

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)-describes several pulmonary disorders due to chronic airflow limitation that is not fully reversible. COPD affects ~25 million Americans and is most commonly caused by smoking tobacco and second-hand smoke. COPD can also be caused by environmental pollutants (chemicals, dust, fumes), or genetics. •

COPD Signs: increased breathlessness (shortness), frequent coughing (with or without sputum), wheezing, or chest tightness.

COPD includes CHRONIC BRONCHITIS and EMPHYSEMA (destruction of alveolar walls).

COPD DENTAL MANAGEMENT: 1. Determine the severity of COPD and degree that it is controlled. If controlled, the hygienist’s goal is to maintain the patient’s COPD status during dental treatment. 2. Encourage the patient to stop smoking (smoking cessation) at EVERY appointment for patients who smoke. 3. SHORT APPOINTMENTS that treat the patient in the UPRIGHT or SEMI-SUPINE position in the dental chair (not raising the chair slowly). Ensure patient has their short-acting rescue inhaler (Albuterol or Xopenex) and it is easily accessible during the appointment. Beta-2 agonist. 4. MINIMIZE STRESS with stress-reduction techniques since COPD typically has co-morbid conditions like hypertension and cardiovascular disease. 5. AVOID medications that can induce respiratory depression like barbiturates, opioid analgesics, antihistamines, erythromycin, and nitrous oxide-oxygen. Do not use with patient taking THEOPHYLLINE (bronchodilator). 6. AVOID N2O, rubber dams, power-driven polishers, and ultrasonic scaling instruments. ASTHMA is NOT part of COPD. While nitrous oxide is beneficial for asthmatics, it is NOT for COPD. 7. XEROSTOMIA, ALTERED TASTE, and INCREASED CARIES RISK are associated with anticholinergic drugs ATROVENT and SPIRIVA (mainstay drugs for COPD because as they allow bronchodilation and mucous reduction. However, they reduce moisture.

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DENTIN™ | ADEX DSE-OSCE

OSHA AND INFECTION CONTROL STANDARD (“UNIVERSAL”) INFECTION CONTROL PRECAUTIONS-a method of infection control in which all human blood and certain body fluids (saliva in dentistry) are treated as if known to be infectious for HIV, HBV, HCV, and other blood borne pathogens. The same infection control procedures are used for all patients. A set of infection control and safety procedures to protect against bloodborne disease transmission by treating blood and blood-contaminated body fluids as if they are infectious. • A thorough medical history is obtained for all patients at the initial visit and updated and reviewed at subsequent visits. However, since not all patients with infectious diseases are identified simply from a medical history, physical exam, or readily available lab tests, the CDC introduced the concept and practice of “STANDARD PRECAUTIONS” by treating all body fluids as infectious EXCEPT SWEAT. • Universal precautions are effective in preventing disease transmission from dental worker to patient, patient to dental worker, and patient-to-patient. • The MOST EFFECTIVE methods to prevent infection and disease transmission are HAND WASHING (30-60 seconds) and PRACTICING UNIVERSAL PRECAUTIONS. • The SAFEST TECHNIQUE to recap an anesthetic needle is the ONE-HANDED SCOOP TECHNIQUE. • To dispose extracted teeth with amalgam, DO NOT THROW IN RED BAGS, DO NOT PUT IN THE TRASH, AND DO NOT BLEACH. Dispose using a SERVICE that disposes mercury/amalgam. OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION (OSHA)-federal government agency who purpose is to assure safe and healthy work conditions for employees, enforce standards, and provide training, outreach, education, and assistance. OSHA BLOODBORNE PATHOGENS STANDARD-a comprehensive rule that sets forth the specific requirements OSHA believes will prevent the transmission of blood borne diseases to EMPLOYEES (not patients or employers). • OSHA regulates CONTAMINATED SHARPS (any contaminated object that can penetrate the skin, including, but not limited to needles, scalpels, broken glass, broken capillary tubes, and exposed ends of dental wires). There may be other objects used in the dental office that are sharps, and if they become contaminated with blood or other potentially infectious materials (including saliva), then they must be regulated. • Upon an “exposure incident”, immediately wash the injured area with antimicrobial soap and water, and inform the employer about the incident. OHSA requires an exposure incident report be completed and filed in the employee’s medical record.

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DENTIN™ | ADEX DSE-OSCE

OSHA AND INFECTION CONTROL “DENTIN SUCCESS STATEMENTS” 1.

The MOST EFFECTIVE methods to prevent infection and disease transmission are HAND WASHING and PRACTICING UNIVERSAL PRECAUTIONS.

2.

HANDS should be thoroughly washed IMMEDIATELY after removing gloves to prevent microbial growth on the hands due to the warm temperature and moisture within the glove.

3.

The MOST common antimicrobial agent present in hand sanitizers for disinfection is ALCOHOL.

4.

OSHA’S BLOODBORNE PATHOGEN STANDARD establishes requirements for EMPLOYERS to implement to prevent the transmission of blood-borne diseases to EMPLOYEES.

5.

The HAZARD COMMUNICATION STANDARD requires DENTISTS to ENSURE CHEMICAL SAFETY IN THE WORKPLACE by providing training, protective attire, labeling chemical containers, and maintaining MSDS.

6.

PERSONAL PROTECTIVE EQUIPMENT PROTECTION, FACE SHIELD, & MASKS.

18

includes

GLOVES,

GOWNS,

EYE


DENTIN™ | ADEX DSE-OSCE

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™ | ADEX DSE-OSCE

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).

s

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.

20


DENTIN™ | ADEX DSE-OSCE

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.

21


DENTIN™ | ADEX DSE-OSCE

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.

s

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.

s

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.

s

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.

22


DENTIN™ | ADEX DSE-OSCE

PERIODONTICS ADEX DSE-OSCE DENTIN SUCCESS STATEMENTS 1.

MANDIBLE and MAXILLA formation occurs by INTERMEMBRANOUS OSSIFICATION.

2.

The thin multi-layered epithelium that covers enamel and forms the JUNCTIONAL EPITHELIUM after tooth eruption is the REDUCED ENAMEL EPITHELIUM (REE).

3.

The REDUCED ENAMEL EPITHELIUM (REE) is derived from AMELOBLASTS, STRATUM INTERMEDIUM, STELLATE RETICULUM, and OUTER ENAMEL EPITHELIUM.

4.

The FIRST layer of DENTIN formed that lies closest to the DEJ, contains KORFF’S FIBERS, and makes up the majority of the tooth is MANTLE DENTIN.

5.

The HARDEST (MOST HIGHLY (PERITUBULAR) DENTIN.

6.

The dentin formed AFTER the apical foramen is closed in response to stimuli produced by carious that causes gradual narrowing of the pulp chamber and canals over time is SECONDARY DENTIN.

7.

The INFRABONY POCKET with the LEAST FAVORABLE prognosis is a ONE-WALL HEMISEPTUM or RAMP DEFECT.

8.

A SUPRABONY POCKET due to CORONAL expansion of marginal tissue without attachment loss is a PSEUDOPOCKET. A 4-mm probing of the junctional epithelium at the CEJ due to gingival margin hyperplasia WITHOUT the loss of any supporting periodontal tissues, and no apical migration of the JE is a PSEUDOPOCKET.

9.

MINERALIZED)

dentin

is

INTRATUBULAR

10.

The periodontal procedure that reshapes or recontours NON-SUPPORTING ALVEOLAR BONE without disturbing PDL fibers is an OSTEOPLASTY.

11.

A true periodontal pocket is distinguished from a “pseudopocket” by the APICAL MIGRATION OF THE JUNCTIONAL EPITHELIUM.

12.

A WINDOW or OPENING in the solid cortical plate of COMPACT BONE located on the buccal/facial surface that exposes a tooth root is a FENESTRATION.

23


DENTIN™ | ADEX DSE-OSCE

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.

24


DENTIN™ | ADEX DSE-OSCE

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.

25


DENTINâ„¢ | ADEX DSE-OSCE

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.

26


DENTIN™ | ADEX DSE-OSCE

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.

27


DENTIN™ | ADEX DSE-OSCE

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.

28


DENTIN™ | ADEX DSE-OSCE

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).

29


DENTINâ„¢ | ADEX DSE-OSCE

STUDY HARD TEST WITH CONFIDENCE

www.dentin.co

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