DENTINâ„¢ | NBDHE 2020-2021
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DENTIN™ | NBDHE 2020-2021
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 and digitized in the United States of America
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DENTIN™ | NBDHE 2020-2021 IMPORTANT MESSAGE FOR HYGIENISTS PREPARING FOR THE NBDHE: DENTIN is so glad to help you prepare and pass the challenging NBDHE. You worked extremely hard to get into and complete hygiene school, and passing the NBDHE is your last major hurdle before entering into one of the top 10 professions as ranked by U.S. News and World Report. With that said, DENTIN finds that most students prepare 4-8 weeks in advance from the actual NBDHE test date. If you know the information in this study guide, you will confidently be able to answer any type of question (including testlets), and you WILL PASS THE NBDHE. Be positive, confident, and calm during the NBDHE, and you will pass! This DENTIN NBDHE study guide GUARANTEES comprehensive, clear, and concise information in that thoroughly provides the dental hygiene student with a SOLID FOUNDATION upon which to confidently answer any type of question format presented on the NBDHE. DENTIN backs this statement up with our 100% pass guarantee because we know the DENTIN NBDHE AND 1,001+ HIGH SPEED DRILLS are simply the best resources to pass the NBDHE. Your score is determined by two criteria (number of correct answers and a pre-determined conversion scale). A STANDARD SCORE of 75 is required to pass the NBDHE. Scores are mailed to you within 34 weeks after taking the exam, and will also be mailed to your program director and state licensing boards you indicate.
NBDHE SUMMARY The NBDHE consists of 350 multiple-choice examination items broken down as follows: COMPONENT A ANATOMY, HISTOLOGY & EMBRYOLOGY PHYSIOLOGY BIOCHEMISTRY & NUTRITION MICROBIOLOGY & IMMUNOLOGY ORAL & GENERAL PATHOLOGY PHARMACOLOGY ASSESSING PATIENTS RADIOLOGY PLANNING & MANAGING DENTAL HYGIENE CARE PERFORMING PERIODONTAL PROCEDURES USING PREVENTIVE AGENTS SUPPORTIVE TREATMENT SERVICES PROFESSIONAL RESPONSIBILITY COMMUNITY HEALTH & RESEARCH
NUMBER OF QUESTIONS 16 5 6 10 13 10 17 13 34 18 9 7 18 24
COMPONENT B (TESTLETS) *TESTS ABILITY TO APPLY COMPONENT A CONCEPTS *10-15 Dental Hygiene Patient Cases
150 QUESTIONS
NBDHE scores range from 49-99, with a MINIMUM PASSING SCORE of 75. Results are available within 3-4 weeks from the date the computerized exam is completed. Preparing with this study guide and DENTIN’s 1,000+ HIGH SPEED DRILLS GUARANTEES THAT YOU WILL PASS THE NBDHE.
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DENTINâ„¢ | NBDHE 2020-2021
TABLE OF CONTENTS ANATOMY AND PHYSIOLOGY Tongue and Salivary Glands .................................................................................................................9 Hard Palate, Soft Plate, Throat ...........................................................................................................14 Muscles of Mastication .......................................................................................................................16 Muscles of Facial Expression .............................................................................................................18 Hyoid Muscles ....................................................................................................................................20 Neck Muscles and Neck Triangles .....................................................................................................21 Cranial Nerves.....................................................................................................................................24 Osteology ............................................................................................................................................37 TMJ .....................................................................................................................................................43 Heart and Blood Supply to Head and Neck .......................................................................................45 Veins (Head and Neck) .......................................................................................................................49 Lymphatic System ..............................................................................................................................52 DENTIN 1,001+ High-Speed Drills Anatomy and Physiology Preview .........................................57
MICROBIOLOGY AND IMMUNOLOGY Cellular vs. Humoral Immunity ............................................................................................................58 Natural vs. Acquired Immunity ............................................................................................................59 Cellular Immunology ...........................................................................................................................61 Immunoglobulins (Antibodies) ............................................................................................................63 Hypersensitivity Reactions..................................................................................................................65 Bacteria ...............................................................................................................................................67 Fungi ...................................................................................................................................................76 RNA and DNA Viruses ........................................................................................................................78 DENTIN 1,001+ High-Speed Drills Microbiology and Immunology Preview ................................84
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DENTINâ„¢ | NBDHE 2020-2021
BIOCHEMISTRY AND NUTRITION Cells and Organelles ...........................................................................................................................85 Carbohydrates, Sugars, Glucose Metabolism ....................................................................................87 Nutritive and Non-Nutritive Sweeteners .............................................................................................91 Amino Acids, Proteins, Lipids (Fats) ...................................................................................................93 Vitamins and Vitamin Deficiencies ......................................................................................................98 Microminerals and Macrominerals....................................................................................................102 Weight Control and Eating Disorders ...............................................................................................106 DENTIN 1,001+ High-Speed Drills Biochemistry and Nutrition Preview ....................................108
EMBRYOLOGY AND HISTOLOGY Facial Development ..........................................................................................................................109 Tissues ..............................................................................................................................................112 Odontogenesis..................................................................................................................................115 Enamel and Dentin ............................................................................................................................119 Cementum and Pulp .........................................................................................................................123 DENTIN 1,001+ High Speed Drills Embryology and Histology Preview .....................................126
DENTAL ANATOMY AND OCCLUSION Tooth Eruption and Exfoliation .........................................................................................................127 Dental Occlusion ...............................................................................................................................129 Primary Tooth Anatomy ....................................................................................................................133 Permenant Tooth Anatomy ...............................................................................................................134 DENTIN 1,001+ High Speed Drills Dental Anatomy and Occlusion Preview .............................140
ANATOMY OF THE PERIODONTIUM AND PROVISION OF DENTAL HYGIENE CARE Free and Attached Gingiva ...............................................................................................................141 Periodontal Ligament (PDL) Fibers and Alveolar Bone .....................................................................143 Oral Mucosa......................................................................................................................................146 Classification of Periodontal Disease and Provision of Dental Hygiene Care ..................................148 Dental Plaque....................................................................................................................................155 Dental Calculus .................................................................................................................................158 Gingival Conditions and Treatment ..................................................................................................160
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DENTIN™ | NBDHE 2020-2021 Periodontal Disease and Treatment..................................................................................................165 CAL, Mobility, and Osseous Defects ................................................................................................167 Scaling and Root Planing and Gross Debridement ..........................................................................168 Periodontal Surgery, Grafting, Wound Healing.................................................................................169 Osseous Defects and Root Furcations .............................................................................................174 Dental Implants .................................................................................................................................177 DENTIN 1,001+ High Speed Drills Periodontology Preview ........................................................180 Hygiene Instrumentation ...................................................................................................................181 Instrument Sharpening .....................................................................................................................188 Polishing and Tooth Discoloration ....................................................................................................189 Preventative Agents (Fluoride, Dentrifices, Antimicrobials) ..............................................................191 Preventative Services and OHI .........................................................................................................200 Oral Health Indices ...........................................................................................................................205 Staging and Grading Periodontitis ....................................................................................................210 DENTIN 1,001+ High Speed Drills Provision of Dental Hygiene Services Preview ...................212
PHARMACOLOGY Drug Potency, Efficacy, and Adverse Reactions ..............................................................................213 Pharmacokinetics .............................................................................................................................215 Routes of Administration ..................................................................................................................216 Autonomic Nervous System (SANS and PANS) ...............................................................................218 PANS Drugs (Anti-cholinergics, Cholinergics, Muscarinics) .............................................................219 SANS Drugs (Adrenergics) ................................................................................................................220 Respiratory Drugs .............................................................................................................................222 Cardiovascular Drugs (Anti-Coagulants, Anti-Arrhythmics, Anti-Hypertensives) .............................226 Cardiovascular Drugs (Beta-Blockers, Cardiac Glycosides, Anti-Anginals, Statins) ........................232 Antihistamines and Gastrointestinal Drugs .......................................................................................237 Non-Opioid and Opioid Analgesics ..................................................................................................239 Anti-Anxiety Drugs, Anti-Depressants, and Anti-Convulsants .........................................................242 Hypoglycemics and Endocrine Imbalance Drugs .............................................................................246 Antibiotics and Prophylaxis Guidelines ............................................................................................251 Antivirals and Antifungals .................................................................................................................260 General and Local Anesthetics .........................................................................................................262 Nitrous Oxide (N2O) ...........................................................................................................................270 DEA Controlled Substances and Prescriptions ................................................................................272 DENTIN 1,001+ High Speed Drills Pharmacology Preview .........................................................274
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DENTINâ„¢ | NBDHE 2020-2021
ORAL AND GENERAL PATHOLOGY Pathology Terminology .....................................................................................................................275 Squamous Cells Carcinoma and Basal Cell Carcinoma ...................................................................277 Tongue Lesions.................................................................................................................................279 White Lesions ...................................................................................................................................283 Pigmented Lesions ...........................................................................................................................288 Connective Tissue Lesions ...............................................................................................................292 Inflammatory Soft Tissue Lesions .....................................................................................................294 Bone Lesions ....................................................................................................................................297 Ulcerative Lesions .............................................................................................................................298 Viral-Induced Ulcerative Lesions (Herpes) ........................................................................................303 Odontogenic Tumors ........................................................................................................................308 Odontogenic Cysts ...........................................................................................................................312 Non-Odontogenic Cysts ...................................................................................................................314 Salivary Gland Lesions......................................................................................................................315 Odontogenic Abnormalities ..............................................................................................................317 DENTIN 1,001+ High Speed Drill Pathology Preview ...................................................................327
SPECIAL NEEDS AND MEDICALLY COMPROMISED DENTAL TREATMENT MODIFICATIONS Asthma and COPD............................................................................................................................328 Cardiac Disorders .............................................................................................................................331 Blood Disorders ...............................................................................................................................335 Cancer Treatment and Dental Management.....................................................................................338 Developmental and Behavioral Disorders.........................................................................................341 Mental Health and Addiction Disorders (Tobacco, Alcohol, Substance Abuse)...............................343 Pregnancy .........................................................................................................................................349 Sensory Impairment and Geriatric Care ...........................................................................................350 Musculoskeletal and Skin Disorders .................................................................................................351 Neurological Disorders .....................................................................................................................356 DENTIN 1,001+ High Speed Drills Special Needs Preview..........................................................359
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DENTINâ„¢ | NBDHE 2020-2021
DENTAL BIOMATERIALS Terminology ......................................................................................................................................360 Amalgam, Composite, Whitening, and Sealants ..............................................................................362 Dental Adhesives, Cavity Liners and Bases, and Dental Cements...................................................365 Impression Materials .........................................................................................................................368 Gypsum, Waxes, and Casting Alloys ................................................................................................371 Radiographic Material Interpretation ...............................................................................................373 DENTIN 1,001+ High Speed Drills Dental Biomaterials Preview ................................................374
DENTAL RADIOLOGY Radiation Biology ..............................................................................................................................375 ALARA Techniques to Minimize Radiation Exposure .......................................................................377 X-Ray Tube Components .................................................................................................................380 kVp, Density, Contrast, and mA........................................................................................................381 Inverse Square Law, Half-Value Layer ..............................................................................................382 Image Quality (Sharpness, Magnification, Distortion) .......................................................................383 Dental Radiograph Film Processing and Errors ................................................................................384 Radiographic Techniques and Errors ...............................................................................................385 Panoramic Errors ..............................................................................................................................390 Anatomical Landmarks on Radiographs...........................................................................................392 DENTIN 1,001+ High Speed Drills Radiology Preview .................................................................398
PROFESSIONAL RESPONSIBILITY OSHA and Infection Control .............................................................................................................399 Ethical and Legal Principles, Professional Responsibility, and Informed Consent...........................406 Community Dental Health and Research..........................................................................................410 Epidemiology ....................................................................................................................................415 Research Methods, Variables, Statistics, Measures of Central Tendency .......................................417 DENTIN 1,001+ High Speed Drills Professional Responsibility Preview....................................428
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DENTIN™ | NBDHE 2020-2021
HEAD AND NECK ANATOMY AND PHYSIOLOGY SALIVARY GLANDS SALIVA-a watery substance in the mouth secreted by salivary glands. Consists of 95% water and 0.5% electrolytes, mucus, glycoproteins, enzymes, and antibacterial compounds like IgA and lysozyme. SODIUM BICARBONATE is a BUFFER in SALIVA. Salivary glands are EXOCRINE GLANDS because they have striated ducts lined by stratified cuboidal epithelial cells or simple low columnar epithelium. Salivary glands produce MUCOUS, SEROUS or BOTH types of secretions. Salivary flow is controlled by the PNS (parasympathetic nervous system from CN VII & IX). • • •
Parotid Glands and Glands of Von Ebner produce ONLY SEROUS secretions. Sublingual and buccal glands produce purely MUCOUS secretions. Submandibular glands produce mucous and serous secretions (mixed), but MOSTLY serous.
MINOR SALIVARY GLANDS: located on lips, cheek (purely mucous), tongue (Von Ebner’s glands-pure serous), and hard palate (in the posterolateral zone). MAJOR SALIVARY GLANDS (Parotid, Submandibular, & Sublingual) are compound tubuloalveolar glands that deliver salivary secretions into the mouth by way of large excretory ducts (Stenson’s, Wharton’s, and numerous small Rivian ducts). There are 3 major pairs of salivary glands: 1. PAROTID GLAND-the LARGEST salivary gland, and PURELY SEROUS (contains amylase to break down starches), located below and just anterior to the ear. Produces 25% of total saliva. Located anterior and below the ears. Each parotid is wrapped around the mandibular ramus and secretes saliva through STENSON’S DUCT. •
STENSON’S DUCT-drains the parotid gland and pierces the buccinator muscle and crosses the masseter muscle where it drains into the vestibule of the mouth opposite the maxillary 2nd molar.
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Innervation: entirely autonomic; parotid gland salivation is ultimately caused by the Glossopharyngeal nerve (IX).
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Facial nerve, retromandibular vein, & external carotid artery LIE INSIDE the parotid gland. EXTERNAL CAROTID ARTERY and its terminal branches (superficial temporal and maxillary arteries) inside the parotid, supply blood to the parotid gland.
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If a needle is advanced to far posteriorly during an inferior alveolar block injection, anesthesia of the mandibular teeth will NOT OCCUR because the needle has entered the PAROTID GLAND which can cause Bell’s Palsy (paralysis of the muscles of facial expression due to depositing anesthetic solution into the parotid gland).
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Lymphatic drainage of parotid gland is into the DEEP CERVICAL LYMPH NODES.
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Bilateral swelling of the PAROTID GLAND in a child with flu-like symptoms may indicate MUMPS (Epidemic Parotitis).
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SUBMANDIBULAR GLANDS (Submaxillary Glands)-large MIXED salivary glands beneath the FLOOR OF THE MOUTH that produce between 60-65% of total saliva. Lies next to a Stafne defect, the cortical bone depression on the lingual surface of the angle of the mandible. •
Submandibular gland is located SUPERIOR to the DIGASTRICS and INFERIOR to the MYLOHYOID muscle (divides the glands superficial and deep lobes).
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WHARTON’S DUCT (Submandibular Duct)-passes forward along side of the tongue, below the mucous membrane of the floor of the mouth. It is crossed by the LINGUAL NERVE and then lies between the sublingual gland and genioglossus muscle. It opens at the base of the frenulum of the tongue.
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Sublingual Caruncle-the site on either side of the lingual frenum where the submandibular (Wharton’s duct) and sublingual salivary glands empty into the oral cavity.
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Innervation: parasympathetic secretomotor from FACIAL NERVE (CN VII), which runs in the chroda tympani and lingual nerve (V3 branch). Same innervation as sublingual gland.
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Blood Supply: FACIAL & LINGUAL ARTERIES.
SUBLINGUAL GLANDS- SMALLEST SALIVERY GLAND that produces 10% of total saliva. Located in mouth floor under the tongue, close to the midline, and supported by the mylohyoid muscle. •
Sublingual glands have 8-20 small ducts (ducts of Rivinus) that empty onto the floor of the mouth at the sublingual fold (Bartholin’s Duct—not gland, which is the major sublingual gland duct that drains the sublingual gland and opens in the sublingual papilla in the mouth floor. Sublingual gland is a MIXED GLAND secreting mostly MUCOUS and some SEROUS ACINI.
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Innervation: parasympathetic secretomotor from FACIAL NERVE (CN-VII) that runs in the chorda tympani and lingual nerve (V3 branch). Same innervation as submandibular gland.
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Blood Supply: sublingual artery (a lingual artery branch, a branch of external carotid).
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Lymphatic Drainage: drain into submandibular and deep cervical lymph nodes.
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DENTIN™ | NBDHE 2020-2021
MUSCLES OF MASTICATION MUSCLES OF MASTICATION-four pairs of muscles responsible for biting, grinding, and mandibular movement during mastication. All muscles of mastication are innervated by TRIGEMINAL NERVE (V3mandibular division). Blood supply comes from the MAXILLARY ARTERY (external carotid artery branch). 1. TEMPORALIS-fan-shaped, originates from the temporal fossa floor (temple) and deep surface of the temporal fascia. It passes medially (downward and deep) to the zygomatic arch as a thick tendon before inserting on CORONOID PROCESS of mandible and anterior border of ramusposterior to 3rd molars). •
Anterior & superior fibers ELEVATE THE MANDIBLE. Temporalis posterior fibers RETRACT the MANDIBLE. Maintains resting position during when the mouth is closed. ELEVATES & RETRACTS the mandible.
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Inserts into the coronoid process of mandible and anterior border of the ramus.
2. MASSETER-paired muscle that originates from the ZYGOMATIC ARCH (cheekbone) that inserts and COVERS THE LATERAL SURFACE OF THE RAMUS (ANGLE OF MANDIBLE). ELEVATES MANDIBLE to occlude teeth. Forms a sling around the angle of the mandible. The stretch reflex maintains masseter muscle tone. MASSETER IS THE MOST POWERFUL MASTICATORY MUSCLE. The masseter is overworked, becomes prominent, and hypertrophies with chronic bruxism. 3. MEDIAL PTERYGOID-origin is the medial surface of the lateral pterygoid plate (sphenoid bone) and maxillary tuberosity. Inserts on medial surface of angle of mandible. ELEVATES (CLOSES) & slightly PROTRUDES MANDIBLE, & MOVES IT LATERALLY. Forms a sling around the angle of the mandible. • During an inferior alveolar block injection, the needle passes through the mucous membrane and buccinator muscle, and lies LATERAL to the medial pterygoid. If the anesthetic needle passes through the MEDIAL PTERYGOID MUSCLE OR BUCCINATOR during an inferior alveolar nerve block, trismus can result. •
Can cause TRISMUS if needle passes through the MEDIAL PTERYGOID during IA nerve block with anesthesia. TRISMUS (LOCKJAW)-limited mandibular opening due to SPASMS of a muscle of mastication.
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The MOST definite clinical sign indicating extension of an odontogenic infection into the masticator space is TRISMUS (difficulty opening the mouth due to a tonic spasm of mastication muscles).
4. LATERAL PTERYGOID (2 Heads)-mainly contained in the INFRATEMPORAL FOSSA (along with the maxillary artery and vein). Its origin is lateral pterygoid plate (inferior head) and infratemporal crest (superior head) greater wing of the sphenoid bone. BOTH HEADS INSERT into the neck of the mandibular condyle and TMJ articular disc to DEPRESS (OPEN) & PROTRUDE THE MANDIBLE & MOVE THE MANDIBLE LATERALLY (SIDE-TO-SIDE) when one side contracts. Works with the hyoid muscles to OPEN THE MOUTH. Temporalis, Medial Pterygoid, & Masseter all CLOSE (ELEVATE) THE MANDIBLE.
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DENTIN™ | NBDHE 2020-2021 All 4 muscles of mastication receive blood from MAXILLARY ARTERY’s PTERYGOID BRANCH (larger terminal branch of the external carotid artery). MUSCLES OF MASTICATION
MUSCLE OF MASTICATION MOVEMENT SUMMARY MOVEMENT MASTICATION MUSCLE ELEVATES MANDIBLE Masseter, Temporalis, Medial Pterygoid DEPRESSES MANDIBLE Lateral Pterygoid with Hyoid Muscles PROTRUDES & LATERAL MANDIBLE Lateral Pterygoid RETRUSION Temporalis
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DENTIN™ | NBDHE 2020-2021
CRANIAL NERVES
EFFERENT NERVE-a MOTOR nerve that carries impulses AWAY from the CNS (brain). AFFERENT NERVE- a SENSORY nerve that carries impulses TOWARD the CNS (brain). OLFACTORY NERVE (CN I)-a PURELY SENSORY nerve for SMELL that exits skull through the ethmoid bone’s perforated CRIBIFORM PLATE to enter the olfactory bulb where it synapses. Carries afferent impulses for smell. OPTIC NERVE (CN II)-a PURELY SENSORY nerve that arises from ganglion cells of the RETINA that converge at the optic disk. Enters the cranial cavity (exits skull) with the ophthalmic artery through the OPTIC FORAMEN (CANAL) of the sphenoid bone. • OPTIC NERVE (CN II) innervates the RETINA with PURE SENSORY fibers; conducts impulses of vision to the thalamus from where the visual pathway terminates in the visual cortex in the brain’s occipital lobe. OCULOMOTOR NERVE (CN III)- exits the skull through superior orbital fissure. Provides MOTOR FIBERS to most extra-ocular (extrinsic) muscles: medial, superior, and inferior recti; inferior oblique, & LEVATOR PALPEBRAE SUPERIORIS. • Responsible for EYE MOVEMENT and PUPIL CONSTRICTION. CN III postganglionic fibers supply sphincter pupillae and ciliary muscle of EYE LENS. •
Can be directly linked to PTOSIS (drooping of the upper eyelid).
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DENTIN™ | NBDHE 2020-2021
FACIAL NERVE (CN VII)
FACIAL NERVE (CN VII)-exits skull and emerges through the STYLOMASTOID FORAMEN. It contains SENSORY neurons that originate in the pons, traverses the facial canal of the temporal bone, and exit the skull through the stylomastoid foramen. FACIAL NERVE (CN VII) FUNCTIONS: 1. Motor innervation-motor to the MUSCLES OF FACIAL EXPRESSION, posterior belly of digastric muscle, styohyoid muscle, and stapedius muscle in the middle ear. LMN lesions of the facial nerve cause ipsilateral (same side) flaccid paralysis of the facial musculature (muscles of facial expression). 2. Motor parasympathetic-innervation to lacrimal gland for secretion of tears, and salivation from sublingual and submandibular glands. Note: parasympathetic innervation controlling salivation also originates in the glossopharyngeal nerve (CN IX). 3. Sensory-proprioception innervation to the same muscles listed for motor innervation. TASTE (sweet sensation) from taste buds on the anterior 2/3 of tongue, floor of mouth, and palate. •
Geniculate Ganglia-contains cell bodies of taste sensory neurons that innervate taste buds on anterior 2/3 of tongue. Facial nerve also contains parasympathetic fibers to the sublingual and submandibular salivary glands (via submandibular ganglion) and lacrimal glands (via pterygopalatine ganglion).
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TEMPOROMANDIBULAR JOINT (TMJ) TEMPEROMANDIBULAR JOINT (TMJ)-dual articulation between the condyle of the mandible and squamous portion (glenoid fossa) of the temporal bone (skull). • TMJ is a GINGLYMOARTHRODIAL JOINT (rotational and translational); it is a hinging AND sliding joint. It involves the condylar process of the mandible and glenoid (articular) fossa of the temporal bone. •
During SLIDING (GLIDING), the disk and condyle move forward (protrude by lateral pterygoid) and backward (retrude by temporalis).
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During HINGE (ROTATIONAL) MOVEMENT, the mandible is elevated (masseter, temporalis, medial pterygoid) and depressed (lateral pterygoid). Rotational movement occurs mainly between the disc and mandibular condyles in the lower synovial cavity.
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During mandibular lateral excursions (deviation) to one side, the TMJ glides on one side and rotates on the opposite side.
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Each TMJ is covered by a fibrous capsule, and the non-articular TMJ surfaces are covered with periosteum.
TMJ COMPONENTS: 1. Mandibular Condyles-elliptically-shaped mandibular bone, with its long axis oriented mediolaterally. Condyle ROTATES in the fossa, and slides forward along the articular fossa to the articular eminence (TRANSLATES); the TMJ disc normally moves with the condyle that is wrapped by the JOINT CAPSULE. 2. Articular Disc (Meniscus)-a FIBROCARTILAGE, saddle-shaped (bioconcave) tissue associated with the TMJ made of dense, irregular C.T. that SEPARATES THE CONDYLE & TEMPORAL BONE (it divides the TMJ into superior and inferior joint spaces and prevents bone-to-bone contact), and provides a smooth articulating surface. Thickest at the posterior, thinner in the center. It moves with the condyle under normal function. THE DISC IS SURROUNDED and PROTECTED by the FIBROUS C.T. JOINT CAPSULE. The disc is considered DISPLACED when it lies ANTERIOR to its usual position. •
CLICKING and POPPING when opening is caused by DISK DISPLACEMENT WITH REDUCTION.
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Painful and limited opening (< 30mm) WITHOUT SOUND is caused by DISK DISPLACEMENT WITHOUT REDUCTION. Normal, full opening is 40-50mm as measured from the maxillary and mandibular incisal edges.
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The best diagnostic imaging tests to examine DISK POSITION and FUNCTION is MAGNETIC RESONANCE IMAGING (MRI) or CT scan.
3. Articular Capsule-thick, fibrous tissue that surrounds the TMJ and is attached above to the articular eminence (tubercle) and to the margins of the mandibular fossa and below to the neck of the mandible. Synovial Membrane-lines the articular joint capsule in the superior and inferior spaces of the joint and PRODUCES SYNOVIAL FLUID for lubrication. It does not cover the articular surfaces or articular disc.
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4. Temporal Bone’s Articular Surface-composed of the concave articular fossa (glenoid fossa) and convex articular eminence (tubercle) that limits forward movement of the condyle. • SUBLUXATION (slipping of the condyle from its socket) occurs when the condyle head moves too far ANTERIORLY on articular eminence. Caused by injury to the articular capsule surrounding the TMJ. •
GOMPHOSIS-a type of fibrous joint in which the conical process is inserted into a socket-like portion, such as the styloid process in the temporal bone or the teeth in the dental alveoli.
3 TMJ LIGAMENTS: attach and determine the farthest boundaries of mandibular movement: 1. Temporomandibular ligament (lateral ligament)-runs from the articular eminence (tubercle) to the neck of the mandibular condyle. It provides lateral reinforcement for the capsule & PREVENTS POSTERIOR & INFERIOR DISPLACEMENT OF THE CONDYLE (prevents the mandible from excessive retraction or from moving backward). Resists posterior movement of the mandibular condyle, and is found on the lateral surfaces of the TMJ. 2. Stylomandibular ligament-separates the infratemporal region anteriorly from the parotid region behind. Runs from the styloid process of sphenoid bone to the angle of the mandible. Separates the parotid and submandibular salivary glands, and is taut when the mandible protrudes. 3. Sphenomandibular ligament-attaches to the spine of sphenoid bone and lingula of the mandible. Becomes taut when the mandible protrudes. A remnant of Meckel’s cartilage and a landmark when administering an IA nerve block. TEMPEROMANDIBULAR JOINT (TMJ)
TMJ SENSORY innervation is from V3 (mandibular branch of trigeminal) and bloods supply is from the EXTERNAL CAROTID ARTERY (superficial temporal branch). TMJ development occurs at 12 weeks in utero when the joint spaces and articular disc develop.
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DENTIN™ | NBDHE 2020-2021
DENTIN “1,001+ HIGH SPEED DRILLS” PREVIEW ANATOMY AND PHYSIOLOGY 1.
HYPOGLOSSAL NERVE (CN XII) provides MOTOR to ALL TONGUE INTRINSIC & EXTRINSIC MUSCLES EXCEPT “PALATOGLOSSUS” which is innervated by the VAGUS NERVE (PHARYNGEAL PLEXUS).
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During contraction, the tongue muscle that PROTRUDES the tongue is GENIOGLOSSUS.
3.
LINGUAL NERVE provides general SENSORY to the TONGUE’S ANTERIOR 2/3.
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LINGUAL ARTERY provides the MAIN blood supply to the TONGUE.
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Tongue tip and lower lip, floor of the mouth, mandibular incisors, and the chin bilaterally DRAIN INTO the SUBMENTAL LYMPH NODES.
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FILLIFORM PAPILLAE are the most NUMEROUS, NO TASTE BUDS, & cause HAIRY TONGUE.
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STAINING & ELONGATION of the FILLIFORM PAPILLAE due to accumulation of oral bacteria or fungi is indicative of HAIRY TONGUE.
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CIRCUMVALLATE PAPILLAE are the LARGEST, but LEAST NUMEROUS arranged in an inverted “v” shaped row with TASTE buds next to VON EBNER’S GLAND (purely serous) on the posterior tongue.
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The tongue’s LOWEST taste threshold region occurs in the POSTERIOR TO BITTERNESS.
10.
An oral manifestation often caused by HEMANGIOMAS and common to both ACROMEGALY and TRISOMY 21 (DOWN SYNDROME) is MACROGLOSSIA.
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MACROGOSSIA signs and symptoms include DYSPNEA, DYSPHAGIA, DYSPHONIA, and ANGULAR CHEILITIS.
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The simplest LYMPHOID ORGAN located at the base of the tongue are the LINGUAL TONSILS.
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Bilateral swelling of the PAROTID gland in a child with flu-like symptoms may be indicative of MUMPS (EPIDEMIC PAROTITIS).
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SUBMANDIBULAR SALIVARY GLANDS are best examined using BIMANUAL PALPATION by rolling the lymph nodes over the mandible’s inferior border.
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The muscles of mastication are the MASSETER, TEMPORALIS, MEDIAL PTERYGOID AND LATERAL PTERYGOID.
NOW AVAILABLE! DENTIN (1,001+) “HIGH SPEED DRILLS” NBDHE To purchase the full NBDHE 1,001+ High Speed Drills, visit dentin.co
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DENTIN™ | NBDHE 2020-2021
MICROBIOLOGY AND IMMUNOLOGY MAIN FUNCTION of the IMMUNE SYSTEM is to prevent or limit infections by microorganisms (bacteria, viruses, fungi, and parasites). All cells in the immune system were derived from PRIMITIVE CELLS IN BONE MARROW. The immune system becomes fully functional at six-months after birth. ACQUIRED IMMUNITY (ADAPTIVE IMMUNITY): the immune system’s LONG-TERM MEMORY response that occurs after exposure to a specific pathogen, and improves with repeated exposures to prepare the immune system against future similar pathogens. A specific immune response that targets the pathogen that stimulated the response. Ex: Vaccinations. Acquired immunity occurs naturally (innate) and artificially, and can be ACTIVE or PASSIVE. •
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ACTIVE IMMUNITY-the host actively produces an immune response consisting of antibodies and activated helper and cytotoxic T lymphocytes. The main advantage of active immunity is RESISTANCE IS LONG TERM (years). The major disadvantage is its SLOW ONSET. o
Natural (Innate) Immunity (Non-Specific): a person’s natural born resistance to all pathogens (fungi, bacteria, viruses, parasites). A person is exposed to an antigen and the body produces antibodies. Natural immunity is NOT acquired from prior antigen exposure, does NOT improve after exposure, and has NO MEMORY. Ex: skin and mucous membrane barriers, salivary enzymes, natural killer cells, neutrophils, and complement proteins. Processes like inflammation and phagocytosis by macrophages.
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Artificially Active immunity-vaccination with killed, inactivated, or attenuated bacteria or toxoid.
PASSIVE IMMUNITY-antibodies are preformed in another host. It is not as permanent and does not last as long as active immunity. Main advantage is IMMEDIATE AVAILABILITY OF ANTIBODIES; the major disadvantage is the SHORT DURATION (months). o
Naturally Passive immunity-antibodies (IgG) passed from mother to fetus during pregnancy and IgA passed from mother to newborn during breast-feeding.
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Artificially Passive immunity-injection of immune serum or gamma-globulin.
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ACQUIRED IMMUNITY occurs AFTER EXPOSURE to an agent, improves upon repeated exposure, and is specific. Mediated by antibodies and T-lymphocytes (T helper and cytotoxic T cells). The cells responsible for acquired immunity have long-term memory for a specific antigen. Acquired immunity is specific, improves after repeated exposure, and has “long-term” memory for an antigen.
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Acquired immunity includes both humoral and cell-mediated immunity. Antibodies are produced by B-cells to specifically target the pathogen that caused their production by plasma cells. Pathogens are “remembered” by memory B cells and memory T cells.
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BIOCHEMISTRY AND NUTRITION BIOCHEMISTRY-study of chemical processes within and relative to living organisms and structures, functions, and interactions of proteins, nucleic acids, carbohydrates, and lipids that provide cell structure and carry out the many functions associated with life.
CELL AND ORGANELLES CELL-the basic structural, functional, and biological unit of the human body that consists of: 1. CYTOPLASM-viscous clear watery gel of the cell body that surrounds the nucleus, converts raw materials into energy. A clear, thin film of protoplasm (cell membrane) always surrounds the cytoplasm. Most synthesizing activities occur in the cytoplasm. Contains organelles and is the site of all metabolic activity. 2. CELL (Plasma) MEMBRANE-a semi-permeable membrane that is the cell’s external boundary and separates it from other cells and from the external environment. • Consists of a double layer of phospholipids and proteins. A selectively permeable membrane that forms the protoplasmic boundary of all cells. Cholesterol is the MOST ABUNDANT non-phospholipid component of the cell membrane. •
Controls the exchange or passage of materials between the cell and its environment by various processes (i.e. osmosis, phagocytosis, pinocytosis, and secretion).
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FUNCTION OF CELL MEMBRANE is primarily to regulate the flow of material in and out of the cell. The cytoplasmic membrane is a selectively permeable barrier (movement of molecules across the membrane is selectively restricted). •
Polar (hydrophilic “water loving”)-molecules or groups soluble in water (ions, glucose, urea). Molecules and ions LARGE & POLAR move across the membrane via TRANSPORT SYSTEMS.
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Nonpolar (hydrophobic)-molecules or groups poorly soluble in water (oxygen, carbon dioxide, alcohol). SMALL, NONPOLAR molecules easily penetrate the biologic membrane quiet readily.
3. GOLGI Apparatus (Golgi Body)-the CELL’S POST-OFFICE that synthesizes COMPLEX CARBOHYDRATES that combine with proteins produced by RER to form secretory products (e.g. lipoproteins). Golgi body packages proteins into membrane-bound vesicles inside the cell before the vesicles are secreted via exocytosis. Also involved in lipid transport and lysosome formation. 4. LYSOSOMES-digestive bodies formed in the golgi apparatus that break down foreign or damaged materials in cells. Contain hydrolytic enzymes for phagocytosis and digestion.
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NUTRITION NUTRITION-the interaction of nutrients and other substances consumed by the body as food for survival, maintenance, growth, reproduction, repair, wellness, and disease. NUTRIENTS-organic and inorganic food components consumed for survival and growth. • Organic nutrients: carbohydrates, fats, amino acids (building blocks of proteins), and vitamins. •
Inorganic nutrients: minerals, water, and oxygen.
CARBOHYDRATES, SUGARS, AND SWEETENERS CARBOHYDRATES-organic compounds composed of carbon, hydrogen, and oxygen. Converted into glucose by the digestive system for cellular energy. Carbohydrates are THE MOST IMPORTANT & ABUNDANT ENERGY SOURCE FOR BODY METABOLISM and contain 4 calories per gram. Monosaccharides, disaccharides, and polysaccharides are carbohydrates. • The RDA for digestible carbohydrates is 130 grams/day. Minimum adult intake is 50 grams/day to prevent using amino acids and proteins as an energy source. •
At least 45%-65% of total caloric intake should come from carbohydrates for a healthy diet. Based on a 2,000 calorie diet, 225 grams (900 calories) should come from carbohydrates daily.
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Carbohydrates “spare proteins” because they provide the body with energy. Protein “sparing” conserves muscles tissue and allows the body to use proteins for rebuilding muscle, and producing enzymes and antibodies.
1. MONOSACCHARIDES-the most BASIC and SIMPLE units of carbohydrates and sugar. Glucose is stored as glycogen, circulates in blood, and is metabolized to provide cellular energy (4 kilocalories/gram) for the CNS and red-blood cells (RBCs). •
GLUCOSE (Dextrose)-the “BLOOD SUGAR” and most important simple sugar in human metabolism. The body’s primary source of cellular energy. Glucose Sources: pasta, whole grains, legumes, potatoes, vegetables, grapes, and honey. 100% of the carbohydrates consumed are converted into glucose. Glucose is the immediate and PREFERRED energy source for CELLULAR METABOLISM. The MOST CARIOGENIC and sticks to occlusal surfaces.
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FRUCTOSE (Levulose)-the FRUIT SUGAR that bonds with glucose to form the disaccharide sucrose. The SWEETEST of all natural carbohydrates (sugars). Sources: fruits, vegetables, honey, maple and corn syrup.
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GALACTOSE-binds to glucose to form the disaccharide lactose (in mammary glands during lactation for breast milk), binds lipids to make glycolipids (blood groups A, B, AB), and binds proteins to form glycoproteins (cell membranes). Most absorbed galactose enters the LIVER and converted to glucose then incorporated into glycogen or used as energy. Less sweet than glucose or fructose. Sources: dairy products (milk, yogurt).
2. DISACCHARIDES-a carbohydrate (sugar) formed by two monosaccharides that undergo a condensation reaction (loss of water).
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2. BULIMIA NERVOSA-cycles of binge eating followed by compensatory purging by vomiting, laxatives, or diuretic abuse to prevent weight gain due to a preoccupation and distorted image of weight and body shape. •
Oral Manifestations: PERIMOLYSIS (enamel erosion on the palatal surfaces of maxillary teeth due to constant acid exposure and subsequent thermal sensitivity), parotid gland enlargement, xerostomia, increased caries risk, and angular cheilitis. Dental restorations appear elevated from the adjacent teeth.
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Behavioral Traits: 90% are college-aged females with low self-esteem, impulsive, and clinically depressed. Self-critical (guilt and shame) and often turn to food for comfort. Normal to slightly overweight, and are aware the behavior is abnormal. LOWER SEROTONIN LEVELS IN THE BRAIN.
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Bulimia Symptoms: abnormal bowel function, bloating, dehydration, dry skin, fatigue, irregular heartbeat, amenorrhea, extremity tingling, muscle cramps. Vomits at least twice per week and eats between 1,500-12,000 calories in a binge. After vomiting, bulimic should rinse with water and wait 1-2 hours to brush teeth due to remaining HCL stomach acid in the mouth that can harm enamel.
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Treatment: teach approach between physician and eating disorder therapist to normalize eating behavior and stop compensatory purging.
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The best topical fluoride for bulimics to promote enamel remineralization is SODIUM FLUORIDE (5% NaF). Baking soda (sodium bicarbonate) rinses neutralize HCL from vomiting. BULEMIC ACID EROSION
BINGE EATING DISORDER (BED)-the most common eating disorder in the U.S. characterized by recurrent binge eating without compensatory behaviors (vomiting or laxatives) to counter the binges. • Most people with BED are overweight or obese with recurrent episodes of eating large amounts of food within a specific time period (ex: 2 hours). Binges at least once per week for at least three months. •
Eats even when not hungry and until uncomfortably full. Often eats alone or in secret, and feels depressed, and SHAME or GUILT about the binge eating.
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ODONTOGENESIS
ODONTOGENESIS: the process of tooth development from embryonic cells, including tooth growth and eruption. Primary (deciduous) teeth formation begins at 6-8 weeks prenatally, while permanent teeth begin formation in the 20th week of embryonic development. GERM LAYER-three pronounced primary cell layers formed during embryogenesis that give rise to all body tissues and organs through organogenesis. 3 developmental primary germ layers: 1. ENDODERM-innermost layer that forms the epithelial linings of the digestive tract and lines all glands and internal organs. Forms stomach, colon, liver, pancreas, bladder, trachea, lungs, pharynx, and thyroid. 2. MESODERM-located between endoderm and ectoderm and begins the process of cellular differentiation. Forms cardiac, skeletal, and smooth muscle, bone, cartilage, C.T., adipose, circulatory system, lymphatic system, RBCs, pulp, cementum, and periodontal attachment. 3. ECTODERM-forms the outermost body layer that differentiates to form the oral cavity lining and ENAMEL (from ectoderm that lines the stomodeum). Forms the salivary glands, nervous system (PNS and CNS), nostrils, sweat glands, hair and nails. •
PULP, CEMENTUM, & DENTIN develop from underlying C.T. ECTOMESENCHYME (derived from embryonic ectoderm adjacent to underlying mesenchymal tissue).
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Teeth Develop from MESODERM and ECTODERM.
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ECTODERM: dental lamina®enamel organ®IEE®ameloblasts®enamel
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DENTAL TISSUE ANATOMY ENAMEL ENAMEL-the HARDEST substance in the body and HIGHLY MINERALIZED STRUCTURE containing 95-96% inorganic matter formed from AMELOBLASTS from the inner enamel epithelium (IEE). •
Hydroxyapatite-made of calcium and phosphate, and is the largest mineral constituent (9095%) of enamel’s inorganic matter. Fluoride and zinc are minor inorganic constituents.
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Due to enamel’s high inorganic content, it appears optically clear on a histologic slide.
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Enamel also consists of an organic matrix (1-2%) and water (4%) that decreases as enamel matures. At the same time, the inorganic content increases. In its mature state, enamel is 96% inorganic mineral.
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Enamel is the HARDEST substance in the body, lacks nerve supply, and is a good thermal insulator. Dentin acts as a cushion for enamel to help withstand the forces of mastication.
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Enamel is made of enamel rods (prisms), rod sheaths (organic matrix), and a cementing interred substance (inter-prismatic substance).
ENAMEL RODS (Enamel Prisms)-the fundamental morphologic unit of enamel. Each enamel rod is formed in increments by a single-enamel forming cell (AMELOBLAST). Each enamel rod traverses uninterrupted through the entire thickness of enamel. There are 5-12 million enamel rods per crown. Enamel rods increase in diameter (from 4 up to 8 microns) as they flare outward from the DEJ. •
Enamel rods are aligned PERPENDICULAR TO THE DENTINOENAMEL JUNCTION (DEJ), except in cervical regions of permanent teeth (oriented somewhat apically).
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Hunter-Schreger Bands-alternating light and dark lines seen in enamel that begin at the DEJ and end before they reach the enamel surface. Represent areas of enamel rods cut in crosssection dispersed between areas of rods cut longitudinally.
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Striae/Lines of Retzius-incremental growth rings, lines, or bands in enamel due to mineralization. Its terminal ends form perikymata. Run obliquely from the DEJ to the enamel surface, and are 20-80um apart. They are BROWN in preparations of mature enamel.
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Perikymata-external wavy lines (small transverse ridges and pits) on the tooth’s outer surface formed from normal ENAMEL APPOSITION. Most prominent on canines, and can wear away from bruxism.
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Enamel Tufts-small, fan-shaped, hypocalcified structures of enamel rods that project from the DEJ into the enamel proper (function is unknown).
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Enamel Spindles-elongated odontoblastic processes (hair-like) ends that traverse the DEJ from the underlying odontoblast into enamel. May serve as pain receptors. Dentinal tubules hold the odontoblastic processes. Fluid movement inside the tubules cause pain (Hydrodynamic Theory). Enamel spindles are short dentinal tubules that extend from the DEJ into enamel and are more prevalent at cusp tips.
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DENTAL ANATOMY AND OCCLUSION TOOTH ERUPTION AND EXFOLIATION THERE ARE 3 DENTITION PERIODS: 1. Primary dentition (6 months - 6 years). 2. Mixed dentition (6-12 years). 3. Permanent dentition (12+ years). PRIMARY TEETH: primary tooth eruption is typically complete by 30 months and begins forming as early as SIX WEEKS in utero as the dental lamina. Primary teeth begin to calcify at 4 months in utero. •
PRIMARY SPACES-developmental spaces normally present from the time the teeth erupt caused by growth of the maxilla and mandible. Required for proper alignment of the permanent incisors.
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THERE ARE NO PREMOLARS IN THE PRIMARY DENTITION.
MIXED DENTITION-a dentition phase during which some of the teeth in the oral cavity are permanent, and some are deciduous (primary). The earliest indication of a mixed dentition consists of the primary dentition and permanent mandibular 1st molars. • The last teeth to erupt are the maxillary canine or mandibular 2nd premolar, thus these teeth are most likely to become impacted due to lack of eruption space. PERMANENT TEETH begin to develop at 4 MONTHS in utero. Maxillary and mandibular 1st molars begin to calcify at birth (1st molars are the first to begin calcification). Mandibular 3rd molars are the last teeth to begin calcifying (at about 8-10 years of age). •
After permanent teeth have reached full occlusion, small tooth movements occur to compensate for wear at the contact areas (by mesial drift) and occlusal surfaces (by deposition of cementum at the root apex).
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3rd molars are most likely to become impacted in the permanent dentition.
EXFOLIATION-process of shedding primary teeth and subsequent replacement by permenant teeth. Exfoliation typically lasts from ages 6-12 years. • Primary central incisors exfoliate between 6-8 years old. • Primary lateral incisors exfoliate between 7-9 years old. • Primary first and second molars exfoliate between 10-12 years old. • Primary canines exfoliate between 9-12 years old. PRIMARY DENTITION (20 TEETH) ERUPTION SCHEDULE DECICUOUS TOOTH MANDIBULAR MAXILLARY Central Incisor 6-10 months 8-12 months Lateral Incisor 10-16-months 9-13 months 1st Molar 14-18 months 13-19 months Canines 17-23 months 16-22 months 2nd Molar 23-31 months 25-33 months *Girl’s teeth typically erupt before boy’s teeth, and mandibular teeth erupt before maxillary teeth.
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Primary Tooth Eruption Sequence: mand central—mand lateral incisor---mand 1st molar First permanent tooth (typically the 1st molar), erupts by age 6 years and starts the MIXED DENTITION stage, which typically lasts to age 12-13 years when the last primary tooth (maxillary canine or mandibular 2nd molar exfoliates. DECIDUOUS (primary) teeth begin to FORM at SIX WEEKS in utero, and start to calcify at 4 months in utero. • 6-year old child typically has ALL (20) PRIMARY TEETH & 4 PERMANENT FIRST MOLARS (“6year molars”) clinically visible in the mouth. • Mandibular central incisors erupt between ages 6-7 years. • Maxillary central incisors erupt between ages 7-8 years. PERMANENT DENTITION ERUPTION SCHEDULE PERMANENT TOOTH 1st Molar Central Incisor Lateral Incisor Canine 1st Premolar 2nd Premolar 2nd Molar 3rd Molar
MANDIBULAR 6-7 years 6-7 years 7-8 years 9-10 years 10-12 years 11-12 years 11-13 years 17-21 years
MAXILLARY 6-7 years 7-8 years 8-9 years 11-12 years 10-11 years 10-12 years 12-13 years 17-21 years
Important: MANDIBULAR FIRST MOLAR (#19, #30) is the first PERMANENT tooth to erupt.
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DENTAL OCCLUSION ANGLE’S CLASSIFICATION OF HUMAN OCCLUSION (MALOCCLUSION): uses the MB CUSP of the permanent maxillary 1st molar and BUCCAL GROOVE of the mandibular 1st molar as the REFERENCE POINTS to classify the permanent dentition occlusion. CLASS I-the MB cusp of the maxillary permanent 1st molar occludes IN THE BUCCAL GROOVE of the mandibular permanent 1st molar. Normal and the most common occlusion (70% of population). •
Maxillary central incisors OVERLAP mandibular centrals.
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CANINE RELATIONSHIP: maxillary canine lies in the labial embrasure between the mandibular canine and mandibular first premolar (maxillary canine occludes with the distal half of the mandibular canine and mesial half of the mandibular first premolar). The mesial slope of the maxillary canine coincides with the distal slope of the mandibular canine.
CURVE OF SPEE-the two-dimensional concave ANTERIOR-POSTERIOR CURVATURE of the MANDIBULAR OCCLUSAL PLANE starting at the canine cusp tip, continuing through all posterior buccal cusp tips and anterior ramus, and ending at the mandibular condyle. • Curves upward from anterior to posterior. • On the Curve of Spee, molar crowns tilt MESIALLY and roots tilt DISTALLY.
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ANATOMY OF THE PERIODONTIUM
PERIODONTOLOGY-dental specialty that studies teeth supporting structures (periodontium), conditions and diseases that affect it, and methods to diagnose, treat, and prevent periodontium diseases. PERIODONTIUM-the HARD and SOFT tissues that surround and support teeth. Consists of the gingiva, PDL, cementum, alveolar bone & supporting bone. Main functions are to support, protect, and nourish the teeth.
GINGIVA FREE GINGIVA (Unattached or Marginal Gingiva)-the tissue collar not attached to tooth or alveolar bone that consists of: 1. Gingival Margin-the most coronal part of the free gingiva. 2. Free Gingival Groove-a shallow line or depression that separates FREE gingiva from ATTACHED gingiva. Present in 33% of adults. 3. Gingival Sulcus-shallow groove between the marginal gingiva & tooth surface, bound by sulcular epithelium laterally, and by junctional epithelium apically. 4. Interdental (Interproximal) Gingiva-occupies the interdental spaces above (coronal) to the alveolar bone crest.
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PERIODONTAL LIGAMENT (PDL)
PERIODONTAL LIGAMENT (PDL)-a complex, highly cellular and vascular, soft, fibrous connective tissue composed mainly of TYPE 1 COLLAGEN FIBERS and contains numerous cells (fibroblasts), blood vessels, nerves, & extracellular substances. The primary cells of the PDL are FIBROBLASTS.
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ANKYLOSIS-the FUSION of ALVEOLAR BONE and ROOT due to INFECTION OR TRAUMA TO THE PERIODONTAL LIGAMENT. The ankylosed tooth has lost its PDL space and radiolucent ligament space on periapical radiograph. ALVEOLAR BONE
ANKYLOSIS
ALVEOLAR PROCESS-the bony part of the maxilla and mandible that HOUSES THE TEETH. Consists of two main parts: 1. Alveolar Bone Proper-the only essential part of the bone socket (alveolar process) that is always present. It is a thin inner layer of compact lamellar bone that immediately surrounds the root where PDL fibers attach. It is a perforated cribiform plate through which vessels and nerves pass between the PDL and bone marrow. It consists of two layers of bone (compact lamellar bone & layer of bundle bone (the layer that PDL fibers insert into). Alveolar bone proper helps form the attachment apparatus. 2. Supporting Alveolar Bone-is not always present, but surrounds the alveolar bone proper to provide SUPPORT to the socket (alveolar process) and consists of: ยง Cortical Plate (compact lamellar bone)-forms the outer and inner alveolar process plates, and is thicker in the mandible than in the maxilla. ยง
Spongy Bone (cancellated bone)-fills in the area between the cortical plates of bone. Spongy bone is NOT present in the anterior region of the mouth (here the cortical plate is fused to the cribiform plate) nor over radicular buccal bone of maxillary posterior teeth.
ORAL MUCOSA ALL ORAL MUCOSA is STRATIFIED SQUAMOUS EPITHELIUM regardless if it is keratinized or nonkeratinized. The oral mucosa also has a C.T. lamina propria that is separated by a basement membrane (which becomes the DEJ in the developing tooth). 3 MAJOR FUNCTIONAL TYPES OF ORAL MUCOSA: 1. Masticatory Mucosa-composed of free & attached gingiva, and hard palate mucosa. The epithelium of these tissues is KERATINIZED stratified squamous epithelium, and the lamina propria is a dense, thick, firm C.T. containing collagenous fibers. Note: the surface epithelium of the gingiva is highly impermeable making it resistant to bacterial invasion. 2. Lining (Reflective) Mucosa-a NON-KERATINIZED tissue that contains a submucosa. It covers the inside of lips, cheek, vestibule, lateral surfaces of the alveolar process, floor of mouth, soft palate,
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CLASSIFICATION OF PERIODONTAL DISEASE & PROVISION OF DENTAL HYGIENE CARE STAGING AND GRADING PERIODONTITIS The 2017 World Workshop on the Classiciation 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
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)
Extent and Distribution: For each stage (I through IV), describe the extent of periodontitis as either localized (< 30% of teeth involved), generalized, or molar/incisor pattern.
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PERIODONTAL DISEASE 4 STAGES OF THE PERIODONTAL LESION (INITIAL, EARLY, ESTABLISHED, & ADVANCED) 1. INITIAL LESION (2-4 Days): no changes clinically after plaque accumulation, but increases in capillary permeability and gingival crevicular fluid flow occur, and there is an increase in PMNs (neutrophilic leukocytes). PMNs are the FIRST LINE OF DEFENSE and first cells to migrate into the gingival sulcus and JE when inflammation caused by plaque formation in the initial lesion of gingivitis occurs. Evident histologically as gingival inflammation. 2. EARLY LESION (Gingivitis 4-7 Days): and extension of the initial lesion. The area of destruction becomes larger with persistence of inflammation. Clinical signs of GINGIVITIS are evident and leukocyte invade (mainly lymphocytes 75%) C.T. The sulcular lining becomes ulcerated and inflamed causing BOP. COLLAGEN DESTRUCTION OCCURS and PMNs invade the sulcus. Macrophages, plasma cells (secrete IgG), and mast cells (release histamine) are present. JE (sulcular lining) develops RETE PEGS (epithelial extensions or fusion sites of epithelial ridges where stippling occurs) histologically. 3. ESTABLISHED LESION (2-3 weeks): occurs 2-3 weeks after plaque accumulation. Gingival erythema occurs due to capillary proliferation and PLASMA CELLS DOMINATE (produce IgG and IgA). EPITHELIAL PROLIFERATION and APICAL MIGRATION OF JE STARTS. C.T. below the JE is destroyed. NO BONE LOSS, but continued collagen loss. May be with or without pocket formation. Gingival color changes occur starting at the papillary and marginal tissues and progressing to the attached gingiva. Gingiva is reddish with a bluish hue due to venous return impairment and moderately inflamed gingiva.
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DENTINâ&#x201E;¢ | NBDHE 2020-2021 4. ADVANCED LESION (3 weeks-life): the IRREVERSIBLE transition from gingivitis to periodontitis (lesion extends from the gingiva into supporting alveolar bone and PDL). PERIODONTAL POCKET FORMATION, gingival ulceration and suppuration, ALVEOLAR BONE and PDL DESTRUCTION. JE continues to migrate apically and detaches from the root surface (causing mobility and drifting). Dense infiltrate of plasma cells and macrophages. Bone marrow is converted into fibrous C.T.
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DENTIN™ | NBDHE 2020-2021 CLINICAL ATTACHMENT LOSS (CAL): measures the distance from the CEJ to the pocket/sulcus base (pocket depth) + gingival recession. Gingival hyperplasia/enlargement is always subtracted from the final pocket depth measured. CAL increases as periodontal disease progresses, and is the MOST CRITICAL factor that determines the extent of periodontium damage. •
An indication that gingivitis has progressed to periodontitis is the presence of CLINICAL ATTACHMENT LOSS (not gingival recession, widened PDL, or bleeding on probing).
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Improper scaling in shallow pockets CAN cause CAL. A periodontal pocket results from bone loss due to APICAL migration of the junctional epithelium (JE). CLINICAL ATTACHMENT LOSS (CAL)
The two MOST CRITICAL FACTORS to determine the prognosis of a periodontally involved tooth are MOBILITY & ATTACHMENT LOSS (the most critical). Periodontal pocket formation causes apical migration of the JE, destruction of C.T. attachment (PDL), and alveolar bone resorption. GOALS OF PERIODONTAL THERAPY: to preserve the natural dentition, periodontium, and peri-implant tissues and to maintain and improve periodontal health, comfort, esthetics and function. After a comprehensive periodontal exam is performed a combination of SRP, antibiotics, proper home care, and periodontal maintenance all help control and eliminate periodontal inflammation signs (redness, swelling, suppuration, and BOP) to achieve a functional clinical attachment level. BARRIERS TO PERIODONTAL THERAPY: patient refuses the recommended treatment and periodontally hopeless teeth/implants. Patients who decline periodontal therapy should sign and date a refusal form that explains the benefits of periodontal treatment and risks of not receiving treatment. The signed refusal form should become part of the dental record. MAIN OBJECTIVE OF ROOT PLANING is to provide optimally smooth root surfaces to reduce the potential for bacterial accumulation and achieve soft-tissue reattachment. ROOT PLANING is the instrumentation applied to the root surface to remove deposits and smooth the root surface.
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DENTIN™ | NBDHE 2020-2021 SCALING & ROOT PLANING (SRP: D4341 & D4342)-techniques of instrumentation applied to the root surface to remove plaque, calcified deposits, bacteria, endotoxins, and soft or rough diseased cementum. When thoroughly performed, SRP produce a smooth, clean, hard polished root surface. Cementum, dentin, and calculus are removed during root planing. Diseased cementum contains embedded calculus, bacteria, and endotoxins. •
SRP is the primary treatment to control and ELIMINATE periodontal inflammation. In simple cases, SRP reduces shallow pockets and the number of bacteria in these shallow pockets, and may be the only treatment necessary. Deeper pockets may require open-flap debridement to allow visible access to clean root surfaces. In advanced periodontal disease where surgery may not be possible, SRP is the only feasible treatment.
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Since plaque and deposit removal is the definitive treatment for periodontal inflammation, SRP is more often used than any other type of therapy. Clinical changes that occur one week after SRP include reduced pocket depths and reduced gingival inflammation.
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BEST CLINICAL AID to determine if subgingival calculus is removed is using an EXPLORER and BITE-WING X-RAYS to clinically detect and show the presence of inter-proximal calculus.
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When extensive SRP must be performed, the best approach is to schedule a SERIES of appointments to scale and root plane a segment or quadrant of teeth at a time thoroughly and completely (ex: can SRP the right side at one appointment and the left side at another appointment). DO NOT do gross debridement (subgingival and supragingival) of the entire mouth, and then schedule a series of appointments for fine scaling and polishing.
GROSS (FULL MOUTH) DEBRIDEMENT (D4355): the gross removal of plaque and calculus that INTERFERE with the dentist’s ability to perform a comprehensive oral evaluation. Gross debridement does not eliminate the need for additional periodontal therapy procedures. D4355 is performed before any SRP, prophylaxis, or evaluation procedure. •
Hygienist should explain to the patient “a debridement will remove thick or dense plaque and tartar on the teeth so the dentist can perform a thorough examination and I can obtain accurate probing measurements around your teeth.” It is important that if subsequent probing depths (> 5mm), bone loss, and inflammation reveal periodontal disease, that the hygienist educate the patient of the importance and necessity of future SRP appointments to ensure the patient’s periodontal disease does not progress.
RE-EVALUATION AT 4-6 WEEKS: the most important factor to evaluate at the 4-6 weeks re-evaluation after initial periodontal therapy is the DEGREE OF INFLAMMATION PRESENT. The absence of gingival inflammation and bleeding is the BEST indicator of treatment success at the 4-6 week re-evaluation. PERIODONTAL MAINTENANCE (D4910): performed after the SRP re-evaluation period (4-6 weeks) at 3, 4, or 6-month intervals. PM is the periodic assessment and preventative treatment for early detection and treatment of recurrent periodontal disease. The maximum periodontal-care interval recommended for periodontal maintenance therapy is 3 MONTHS. • The most critical factor to evaluate during a periodontal re-evaluation at 4-6 weeks to determine if a patient is maintaining adequate plaque control and the effectiveness of periodontal therapy (SRP) is the ABSENCE OF BLEEDING DURING CIRCUMFERENTIAL PROBING (TISSUE RESPONSE). •
The most important factor to determine the frequency of patient recare appointments for periodontal maintenance is THE EFFECTIVENESS OF PATIENT’S ORAL HYGIENE.
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The more REMAINING osseous walls around a tooth with an INFRABONY POCKET, the BETTER THE PROGNOSIS. Thus, the INFRABONY POCKET with the WORST prognosis is a ONE-WALL HEMISEPTUM or RAMP DEFECT.
FENESTRATION-an OPENING or “WINDOW” in the solid cortical plate of COMPACT BONE on the buccal/facial or lingual bony surface that exposes the tooth root so the root surface directly contacts the gingival or alveolar mucosa, but the marginal bone is in tact. Distinguished from a dehiscence since a fenestration is BORDERED BY ALVEOLAR BONE along its coronal aspect. DEHISCENCE-alveolar bone loss (usually on the buccal/facial surface) leaving a characteristic OVAL, ROOT-EXPOSED DEFECT from the CEJ apically. Denuded areas extend through the marginal bone. The defect may be 1-2mm long or extend the full root length. 3 characteristic features of dehiscence are gingival recession, root exposure, and alveolar bone loss.
FENESTRATION “WINDOW”
DEHISCENCE
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HYGIENE INSTRUMENTATION MODIFIED PEN GRASP-the MOST common and RECOMMENDED GRASP for periodontal instruments to allow the greatest intricacy or delicacy of touch. With the modified pen grasp, the index finger and thumb hold the handle and the middle finger rests on the shank. The ring finger supports the hand and instrument. TACTILE SENSITIVITY-the ability to distinguish between degrees of tooth surface smoothness or roughness. SHANK DESIGN: • Thick, Rigid Shank: is stronger, less flexible, and provides less tactile sensitivity. Stronger, more rigid shanks are used to remove HEAVY calculus deposits. •
Flexible, Less Rigid Shank: provides greater tactile sensitivity and removes FINE calculus during root planing.
•
Straight Shank: used in anterior areas, while longer (contra-angled) shanks are used in harder to reach posterior areas.
STROKE-the action of an instrument performing the task for which is was designed. Instruments are often named based on the task they perform. •
PROBING STROKE (Walking Stroke)-upward and downward movement within a periodontal pocket.
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EXPLORATORY STROKE (Assessment Stroke)-used to assess the smoothness or roughness of the tooth surface (tactile sensitivity) and the effectiveness of instrumentation. Instrument handle is grasped lightly to increase tactile sensitivity. o
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Periodontal Explorer-used to detect calculus with a LIGHT instrument grasp (not firm) to increase tactile sensitivity. The lateral side of the instrument tip is placed in contact with the tooth surface when exploring for calculus.
SCALING STROKE-a short, powerful “pull” stroke to remove calculus (more pressure). Initiated in the forearm and transmitted from the wrist to the hand with slight flexing of the fingers. Wrist rotation is synchronized with forearm movement. o
Sequence and control of strokes is important. If heavy lateral pressure is continued with long, even strokes, it produces a smooth, but “ditched” root surface. To avoid this, deliberate transition from short, powerful scaling strokes, to longer, lighter root planing strokes are made as soon as the calculus and initial roughness are removed.
o
Preferably, the motion to initiate a SCALING STROKE is generated from the FOREARM. Although fingers may be used to initiate the scaling stroke in some situations, a powerful scaling stroke cannot be initiated in the wrist or fingers. Hence, is not carried out independently without using the forearm. The MODIFIED PEN GRASP is the most useful grasp for periodontal instruments.
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TOOTH DISCOLORATION AND ORIGIN EXOGENOUS EXTRINSIC STAINS: ARE REMOVED BY SCALING and POLISHING. After a period of time, green and tobacco stains may become incorporated inside the tooth, at which point they become endogenous intrinsic stains. Stained root cementum is removed by scaling and polishing. •
BROWN: a thin, translucent, acquired pigmented pellicle. Color is due to TANNIN. Occurs in patients who do not brush sufficiently or who use a dentrifice with inadequate cleansing (associated with poor oral hygiene and drinking coffee, tea, red wine, and certain fruit juices).
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BLACK: a thin, black line on the facial and lingual surfaces of teeth near the gingival/cervical margin, and as a diffuse patch on proximal surfaces. Caused by chromogenic gram (-) bacteria (especially Actinomyces species), iron, and insoluble ferric sulfide. Chromogenic bacteria are also implicated in causing ORANGE STAINS.
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DARK BROWNISH-BLACK: tobacco products dark brown or black resulting from coal tar combustion products and from penetration of pits & fissures, enamel, and dentin by tobacco juices.
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ORANGE: present mainly on ANTERIOR TEETH caused by CHROMOGENIC BACTERIA from poor oral hygiene.
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GREEN: caused by poor oral hygiene and chromogenic bacteria, fungi, or gingival bleeding.
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GREENISH-YELLOW: common in children. Green discoloration is attributed to fluorescent bacteria.
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BLUISH-GREEN (METALLIC): common in industrial workers who inhale metallic dust from occupational exposure, or due to orally administered drugs containing metals or metal salts. Metal stains vary from green due to copper and nickel, to black stains due to iron, silver, and manganese.
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YELLOWISH-BROWN & BROWN: caused by prolonged use of CHLORHEXIDINE GLUCONATE or STANNOUS FLUORIDE (SnF2) due to the reaction of the TIN ION (Sn).
IMPORTANT: ORGANGE, GREEN, & BROWN STAINS ON ATERIOR TEETH ARE TYPCIALLY DUE TO POOR ORAL HYGIENE. ENDOGENOUS INTRINSIC STAINS-originate from a source outside the tooth and becomes incorporated inside tooth structure. CANNOT BE REMOVED BY SCALING and POLISHING. Causes: •
Dentinogenesis imperfecta-causes a translucent or opalescent gray to bluish-brown hue. Adverse effect of osteogenesis imperfecta (brittle bones).
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Erythroblastosis fetalis- causes intrinsic stain that is bluish-black, greenish-blue, tan, or brown.
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PORPHYRIA-high levels of the protein in RBCs can cause intrinsic reddish-brown stain.
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DENTAL FLUOROSIS-an “irreversible” diffuse symmetric hypomineralization disorder of ameloblasts due to excessive fluoride intake during ENAMEL’s calcification/mineralization period. NOT CAUSED BY REPEATED TOPICAL FLUORIDE APPLICATION.
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PREVENTATIVE SERVICES AND OHI PRIMARY ORAL HEALTH SERVICES: provide preventive therapies and are implemented to prevent, reverse, or arrest a disease process. Examples: mechanical plaque removal, dietary restriction/limitation of sucrose, and professional fluoride treatments. • Application of HYDROPHOBIC resin-based (longer retention) or glass-ionomer cements SEALANTS to prevent pit and fissure caries. Most sealants are urethane dimethacrylate or bisphenol A-glycidyl methacrylate monomers. • Fluoride mouth-rinse application for a caries-free nine-year old. • Fabrication and delivery of an athletic mouth guard or occlusal splint to prevent BRUXISM, CLENCHING, and HEAD INJURIES. • Oral Cancer and TMD Screening. SECONDARY ORAL HEALTH SERVICES: controlling or treating an oral health disease or condition after it occurs. Examples: periodontal therapy, restorative (composites), or extractions (for non-restorable teeth). TERTIARY SERVICES: replacing lost tissues to rehabilitate oral structures. Examples: denture fabrication and delivery, dental implants, and dental bridges.
DENTRIFICES DENTRIFICES-its ingredients provide THERAPEUTIC and COSMETIC benefits to reduce plaque, calculus, stain, caries, gingivitis, hypersensitivity, and halitosis. Dentifrices contain 400-1500 ppm depending on fluoride compound they contain. Dentrifice Ingredients: • Carbamide Peroxide/Hydrogen Peroxide-used as a whitening agent in toothpastes. •
Detergents-provide a FOAMING ACTION to loosen debris and acts as a surfactant. Ex: Sodium lauryl sulfate.
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Dicalcium Phosphate-the dentrifice component most likely to inactivate the fluoride ion.
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Stannous Fluoride-added to prevent caries or reduce dentinal hypersensitivity.
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Humectants-prevent drying and separation.
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Potassium nitrate, Sodium Citrate, and Strontium Chloride for ANTI-HYPERSENSITIVITY.
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Preservatives-extends the dentrifice shelf-life.
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Pyrophosphates- helps control TARTER and CALCULUS.
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Triclosan-the most commonly used broad-spectrum antibacterial agent in oral care products. Ex: Colgate Total. Some effectiveness in reducing plaque/gingivitis.
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Abrasives: silica, calcium carbonate, dicalcium phosphate (may inactivate F-), dicalcium phosphate dehydrate, and SODIUM BICARBONATE (BAKING SODA).
The fluoride concentration is most dentifrices ranges between 900-1500ppm.
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ORAL HEALTH INDICES (MEASURING DISEASE AND CONDITIONS) DENTAL INDEX: an efficient numerical and objective method to measure the incidence, prevalence, and severity of a REVERSIBLE OR IRREVERSIBLE oral disease or condition in a population. Helps the dental clinician collect data and summarize the clinical observations found. The information is then compared and classified, and can be used to develop preventative programs. Ideal Index Qualities: • Valid by measuring what it is supposed to measure. • Reliably measures with consistency. • Quantifiable and analyzable • Useful (simple, clear, and objective). • Sensitive to changes in disease. • Clinically significant and acceptable by subjects. REVERSIBLE INDEX-measures reversible or treatable oral conditions like GINGIVITIS or PLAQUE that can increase or decrease on future examinations. Ex: Loe and Silness gingival index. IRREVERSIBLE INDEX-measures irreversible oral conditions like DENTAL CARIES, FLUOROSIS, or PERIODONTAL DISEASE. The index scores do not decrease on future examination. Ex: DMFT/DMFS. SIMPLE INDEX-measures the presence or absence of a disease. Ex: Silness and Loe Plaque Index. CUMULATIVE INDEX-measures all past and present evidence of a disease. Ex: DMFT index.
GINGIVITIS INDICES GINGIVAL INDEX (GI)-a REVERSIBLE index to assess the SEVERITY OF GINGIVITIS (gingival inflammation) based on color, consistency, and BOP. • Gingivitis is most commonly scored using the LOE-SILNESS gingival index which grades the gingiva based on the four surfaces of each tooth based on inflammation and bleeding. •
GI, Papillary, Marginal, & Attached Gingiva Index (PMA Index) are confined to measurements within the gingiva. PMA index is used to record the prevalence and severity of gingivitis in school children. The presence or absence of gingivitis is noted in the gingival papillae, gingival margin, and attached gingiva.
SULCULAR BLEEDING INDEX (SBI)-a REVERSIBLE dental index that detects EARLY signs of GINGIVITIS using a periodontal probe with a 0.5mm tip. The scoring range around 8 anterior teeth (4 maxillary and 4 mandibular) is from 0-5. 0 = Healthy. Useful for short-term clinical trials.
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DENTIN 1,001+ HIGH SPEED DRILLS PROVISION OF DENTAL HYGIENE SERVICES PREVIEW 1. The MOST DIFFICULT anatomical areas on teeth that can limit the effectiveness of removing calculus during SRP are the MESIAL surfaces of maxillary premolars, PROXIMAL surfaces of mandibular incisors, and TRIFURCATIONS of maxillary first molars. 2. Gingivitis is controlled when THERE IS NO BLEEDING WHEN FLOSSING OR PROBING. 3. When root planing, VERTICAL STROKES are used first, followed by oblique, then horizontal strokes. LIGHT PRESSURE is used with root planing strokes to maximize TACTILE sensitivity. 4. The probe must be WALKED along the entire gingival sulcus perimeter because the DEPTH of the epithelial attachment VARIES. 5. Ultrasonic scaling devices use either magnetostrictive or piezoelectric technology to convert electrical energy into physical energy at the instrument tip. The tip vibrates from 25,000-40,000 6. The BEST CRITERION to evaluate the success of SRP is NO BLEEDING ON PROBING (since BOP indicates active inflammatory periodontal disease). 7. The MOST EFFECTIVE practical and cost-effective method to prevent dental caries for children ages 6-12 years old in communities with established water systems is FLUORIDATION. FLUORIDE SOURCES include drinking water, supplements, toothpaste, and mouth rinse. 8. OPTIMAL WATER FLUORIDATION LEVEL established by the EPA is 1.0ppm. Historically, the recommended natural fluoride concentration in drinking water ranged from 0.7 to 1.2 ppm depending on CLIMATE TEMPERATURE. 9. Adults ingest 1-3 mg of fluoride DAILY. 10. DIETARY FLUORIDE SUPPLMENTS are NOT RECOMMENDED DURING PREGNANCY (ONLY CHILDREN) living in areas with inadequate community water fluoridation. 11. The only condition contraindicated with WATER FLUORIDATION is a patient with KIDNEY FAILURE on RENAL DIALYSIS since it requires the use of mineral-free water. 12. An IRREVERSIBLE oral condition caused by excessive and prolonged ingestion of fluoride that causes ENAMEL MOTTLING and PITTING is called DENTAL FLUOROSIS. 13. The pH of SODIUM FLUORIDE (NaF) is best described as NEUTRAL (7.0). 14. The greatest uptake of FLUORIDE ION occurs in OUTER ENAMEL LAYER (not dentin or cementum). 15. Fluoride’s cariostatic effect occurs during the CALCIFICATION STAGE of tooth development. 16. The tooth surface that derives the greatest benefit from WATER FLUORIDATION and FLUORIDE MOUTHRINSE are PROXIMAL SURFACES. 17. The toothpaste/dentrifice component most likely to inactivate the fluoride ion is DICALCIUM PHOSPHATE.
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PHARMACOLOGY The dental hygienist’s knowledge of pharmacology is critical to obtain and review patient medical history since a patient’s medical history can impact dental treatment considerations and contraindications, how one responds to dental emergencies, scheduling patient appointment times and duration, and administering drugs in the dental office as appropriate. LOG DOSE-EFFECT CURVE-a drug’s therapeutic range (plotted where the dose sharply increases) versus a drug’s maximum response (where the curve plateaus). Log-Dose-Effect Curve graphs a DRUG DOSE vs. DRUG RESPONSE.
DRUG POTENCY-a function of the AMOUNT of drug required to produce an effect. THE SMALLER THE DOSE, THE GREATER THE POTENCY. Potency measures a drug’s activity expressed in the amount required to produce an effect of given intensity. A highly potent drug causes a greater response at low concentrations, while a lower potency drug causes a smaller response at low concentrations. • Drug Potency is the relative concentration of AT LEAST TWO DRUGS that produce the same effect. The effect usually chosen is 50% of the maximal effect and the dose causing this effect is the EC50. Potency is mainly determined by the affinity of the drug receptor. The smaller the EC50, the greater drug potency. Potency is a comparative term (one drug is more potent than another drug). • Ex: Drug A in a dose of 10mg produces the same magnitude of response as Drug B in a dose of 50mg. The following is true: Drug A is 5x as potent as Drug B, but Drug A is not potent in and of itself. Also, if Drug A has a greater efficacy than Drug B, then Drug A is capable of producing a greater maximum effect than Drug B. DRUG EFFICACY (“Intrinsic Ability”, “Maximal” or “Ceiling Effect”)-the ability of a drug to produce a desired therapeutic effect REGARDLESS OF DOSE. The maximum effect a drug can cause, regardless of the dose. Administering more drug DOES NOT increase efficacy, but often simply increases the chance of an adverse drug reaction. DRUG EFFICACY AND POTENCY ARE NOT RELATED. • When comparing drugs with respect to intensity of response, the drug that produces the greatest maximum effect has the highest efficacy. • Ceiling dose (effect) is closely related to drug EFFICACY.
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ANTIBIOTICS (ANTIMICROBIALS) ANTAGONISM-the interaction between two or more drugs (antibiotics) that have opposite effects. Antagonism may block or reduce the effectiveness of one or both of the drugs to produce LESS EFFECT than either drug alone. SYNERGISM-occurs when two drugs are combined to produce a GREATER EFFECT than either drug would produce alone. Ex: Acetaminophen + codeine (Tylenol 3). BACTERICIDAL- a substance or antibiotic’s ability to IRREVERSIBLY destroy and kill bacteria. BACTERIOSTATIC-a biological or chemical agent that prevents bacteria growth by inhibiting reproducing or multiplication, but does not necessarily kill the bacteria. MINIMUM INHIBITORY CONCENTRATION (MIC)-the LOWEST concentration of an antimicrobial drug required to inhibit the visible growth of a microorganism after incubation. RESISTANCE-an organism’s natural or acquired ability to resist the effects of an anti-infective agent. The single most important factor leading to antibiotic resistance worldwide is ANTIBIOTIC USE. SPECTRUM-the broad or narrow range of an antibiotic’s activity against bacteria. Ex: Penicillins are broad-spectrum antibiotics, effective against gram (-) and gram (+), while Sulfonamides are narrowspectrum antibiotics, effective against only aerobic bacteria. PENICILLIN-BACTERICIDAL antibiotics that INHIBIT BACTERIA CELL-WALL SYNTHESIS BY CELL LYSIS. Penicillins are INEFFECTIVE against viruses, fungi, and Rickettsia (gram (-) bacteria). Penicillins and Cephalosporins have the beta-lactam ring that is critical for their antibacterial activity. Common penicillin derivatives effective against rapidly growing bacteria during the logarithmic phase and are SAFE during pregnancy include: 1. Penicillin VK-has the HIGHEST DRUG ALLERGY INCIDENCE, but the antibiotic of choice in DENTISTRY for oral infections to treat non-penicillinase producing gram (+) staphylococcal infections in non-allergic patients. Penicillin VK is more acid stable against gastric acids (reliable oral absorption, so better than Penicillin G). Safe during pregnancy, and does not penetrate bony tissue or teeth of children (unlike tetracyclines). Adverse effects: hypersensitivity reaction that causes a skin rash, and rarely anaphylaxis. 2. Amoxicillin-effective against gram (+) and (-) bacteria with good absorption, but ineffective against beta-lactamase (penicillinase-producing) bacteria, so it is combined with Clavulanic Acid to form Augmentin. TID is the preferred dosing. Amoxicillin Treats: acute otitis media, sinusitis, skin and urinary tract infections, and is prophylactically prescribed when indicated to prevent BACTERIAL ENDOCARDITIS. 3. Augmentin-resistant against amoxicillin-resistant (penicillinase-producing) bacteria that produce beta-lactamase enzyme that typically break down the penicillin beta-lactam ring. Augmentin combines Amoxicillin + Clavulanic Acid to prevent beta-lactamase enzyme from destroying the beta-lactam ring. If penicillinase is cultured from an infection, AUGMENTIN (amoxicillin + clavulanic acid) should be given NOT just Amoxicillin.
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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 DIFFUSION HYPOXIA. Nitrous oxide is an INCOMPLETE ANESTHETIC and is the most common inhaled anesthetic used for sedation and anxiety reduction. Nitrous oxide is stored under pressure in steel BLUE cylinders. Oxygen is stored in GREEN cylinder tanks. §
Advantages of Nitrous Oxide Analgesia: rapid onset of action and recovery, works by elevating the pain threshold (not by decreasing PNS), produces euphoria, pleasant induction, titratable, virtually no adverse effects in absence of hypoxia, therapeutic for many medically compromised patients, and is suitable for all ages.
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Nitrous oxide works on the CNS to produce SEDATION & MILD ANALGESIA BY RAISING THE PAIN THRESHOLD. 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, non-irritating 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.
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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 for 3-5 minutes after the procedure to prevent DIFFUSION HYPOXIA.
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N2O is quickly absorbed from the lungs and is physically dissolved in the blood. There is NO BIOTRANSFORMATION, and nitrous is rapidly excreted by the lungs when the concentration gradient is reversed (it is not metabolized by the body). 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). Vomiting and nausea are adverse effects of a nitrous oxide overdose. Sweating is caused by vasodilation of vessels in the extremities.
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N2O Contraindications: patients with upper respiratory infections (URI), COPD (emphysema, bronchitis), cystic fibrosis, 1st TRIMESTOR OF PREGNANCY (long-term exposure to low nitrous oxide doses can increase spontaneous abortion incidence), and in patients where communication is difficult (i.e. autistic patients or language barrier) or emotional/behavioral instability. 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. CHF is a relative contraindication for N2O administration.
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Important: Nitrous oxide is a SEDATIVE and NOT a general anesthetic since hypoxic levels are required to produce anesthesia. N2O is used alone to produce sedation or in combination with inhalation agents to supplement the anesthetic response.
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N2O can effectively REDUCE OROFACIAL MUSCLE TONE IN CEREBRAL PALSY PATIENTS during dental treatment and is BENEFICIAL TO ASTHMATICS.
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A hypersensitive GAG REFLEX on an anxious patient is best suppressed using N2O-O2 sedation.
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ORAL AND GENERAL PATHOLOGY SQUAMOUS CELL CARCINOMA (EPIDERMOID CARCINOMA)-the MOST COMMON MALIGNANCY IN THE ORAL CAVITY (90%). Occurs more often in the oral cavity than any other type of cancer (90% of all malignant oral cavity neoplasms). 50% mortality rate within 5 years. •
Clinical Description: SCC is a malignant squamous EPITHELIAL TUMOR that starts clinically as a white plaque (leukoplakia that doesn’t rub off) then changes into an exophytic ulcerative mass. During clinical exams, be highly cautious of red or white lesions. Can appear RED, irregular, indurated, non-painful lesion, or as a WHITE lesion caused by sun exposure (lower lip). Lasts > 1 month.
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SCC of the tongue quickly and initially metastasizes to the CERVICAL LYMPH NODES in the neck due to the tongue’s mobility and richly endowed lymphatics and vasculature. SCC then spreads to more distant organ sites like the liver and lungs. It rarely spreads to bone.
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Intra-oral Sites: SCC can occur anywhere in the mouth, but the most common intra-oral sites are the posterior VENTRO-LATERAL TONGUE BORDERS and MOUTH FLOOR. Can also occur on the soft and hard palates, buccal mucosa, gingival tissues, and other areas on the tongue (rarely on the tongue dorsum).
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LIPS: THE MOST COMMON LOCATION FOR SCC (more than intra-orally). 95% of all SCC are found on the LOWER LIP (vermillion of the lower lip) of which 90-98% of lower lip cancers occur in MALES 60+ due to chronic sun exposure & pipe smoking. This location (lips) is etiologically related to race, complexion, pipe smoking, and sunlight. It is a PAINLESS ulcer and keratotic plaque. The most common extra-oral site for SCC is the vermillion border of the LOWER LIP, but it can also occur on the face.
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SCC is most easily managed when found on the LOWER LIP. SCC is the most common malignant oral tumor, representing >90% of all oral malignancies. SCC is 9-10 times more common in males than females, and while it is seen in all ages, its highest incidence is after age 40yrs. SCC IS MORE COMMON ON THE LIPS than intra-orally.
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95% of lip carcinomas occur on the LOWER LIP, and are usually discovered early and only a small percentage show lymph node metastasis. The prognosis is very good.
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MOUTH FLOOR: 2nd MOST COMMON INTRA-ORAL SITE FOR CANCER, mainly in the ANTERIOR SEGMENT on either side of the midline near salivary gland orifices. Caused by tobacco and alcohol. Pre-malignant lesions of squamous epithelium most often occur here. VERY POOR PROGNOSIS. Typically effects men 40-60yrs. Presents as a painless ulcer with leukoplakia and erythroplakia. THE LOCATION WITH THE WORST PROGNOSIS.
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SCC Risk Factors: tobacco (smoke and smokeless) and alcohol (so best to recommend nonalcoholic oral mouth rinses), painful and ill-fitting dentures, syphilis, chronic inflammation, and Plummer-Vinson Syndrome. 2x more common in males > 40-65 years old.
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Treatment: surgical excision, radiation (may cause xerostomia, caries, skin erythema, and osteoradionecrosis), chemotherapy, or treatment combination. SCC prognosis depends on its size, location, and existence or absence of metastasis.
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DENTIN™ | NBDHE 2020-2021 •
SCC also occurs on the tongue’s ventral surface (under the tongue), however the tongue dorsum and tip are the LEAST likely sites (most uncommon locations). Tongue cancer causes more deaths than any other malignant lesion in other regions of the head and neck because the tongue is a highly mobile organ richly endowed with lymphatics & blood vessels that facilitate metastasis. Tongue cancer most commonly metastasizes to the CERVICAL LYMPH NODES, and RARELY gives rise to skeletal metastasis.
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SCC of the tongue metastasizes fast, and the prognosis is not as good as lower lip SCC.
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More common on the LOWER LIP than intra-orally (some consider the lower lip extra-oral, however sun exposure is the primary risk factor). The most common intra-oral site is the lateral border & ventral surface of the TONGUE (from this site, SCC often metastasizes to cervical lymph nodes). Dorsal tongue surface is almost never affected.
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Treatment of choice for ORAL CANCER (SCC) IS SURGERY.
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Mostly effects men > 60yrs. on the posterior lateral border and middle 1/3 of the tongue. Presents as a painless ulcer with leukoplakia and erythroplakia. SCC OF MOUTH FLOOR AND LOWER LIP
BASAL CELL CARCINOMA–a MALIGNANT epithelial cell tumor that begins as a papule that enlarges peripherally, forming a central crater that erodes, crusts, and bleeds. Only found on the skin, and NEVER orally due to EXCESSIVE SUN EXPOSURE (UV radiation) or to x-rays. Metastasis is rare, but the local invasion by direct extension destroys underlying and adjacent tissues. Often develops on exposed skin surfaces, face (nose), and scalp in middle-aged or elderly people. Treatment: eradicate the lesion by electrodessication or cryotherapy. BASAL CELL CARCINOMA IS THE MOST COMMON SKIN CANCER, that usually appears as an ulcerated, crateriform lesion. It may look exactly like SCC, but RARELY produces metastasis with a much better prognosis than SCC. • •
BASAL CELL CARCINOMASA ARE NEVER FOUND IN THE MOUTH (INTRA-ORALLY). MAY BE ASSOCIATED WITH ODONTOGENIC KERATOCYST (OKC).
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TONGUE LESIONS LIPOMA–a BENIGN soft tissue tumor derived from ADIPOSE (FAT) tissue (C.T. origin). It is smooth or lobulated, sessile or pedunculated (foot-shaped), soft, movable, painless, yellowish-white nodular mass. Vessels are visible on the surface. Locations: mouth floor, buccal mucosa, and TONGUE. YELLOWISH MASS covered by normal mucosa. Easier to diagnose because it is yellowish, soft, smooth, and movable, and FLOATS IN FORMALIN WHEN BIOPSIED. •
Microscopic Features: lobules of mature fat separated by delicate C.T. septae.
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Treatment: conservative excision. Recurrence is rare. Remove surgically only if it becomes painful, tender, infected, or enlarges to where it becomes bothersome. LIPOMA
MACROGLOSSIA-a rare, severe tongue enlargement causing difficulty speaking, eating, swallowing, and sleeping (obstructive sleep apnea). Caused by many congenital and acquired conditions. Usually occurs in children. • Most commonly caused by VASCULAR FORMATIONS (lymphangioma or hemangioma) and muscular hypertrophy. •
People who are edentulous (no teeth) create more room for the tongue to expand laterally to cause problems with dentures and may also cause pseudomacroglossia.
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MACROGLOSSIA is an oral manifestation of DOWN SYNDROME (TRISOMY 21), HYPOTHYROIDISM, ACROMEGALY (HYPERPITUITARISM) a hormonal disorder where the ANTERIOR pituitary gland produces excess growth hormone) due to a benign pituitary tumor (adenoma) AFTER fusion of long bone epiphyses. Other acromegaly oral features: thick lips, teeth tipped buccally or lingually, long roots, and protruded mandible. Also found with lymphangioma.
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No treatment for mild cases. Speech therapy or reduction glossectomy surgery if indicated.
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DENTIN™ | NBDHE 2020-2021
BENIGN MIGRATORY GLOSSITIS (GEOGRAPHIC TONGUE = ERYTHEMA MIGRANS): a HARMLESS, USUALLY PAINLESS with a possible slight burning sensation. A common condition that involves the tongue’s DORSAL and LATERAL BORDERS. Cause is unknown (idopathic), but may be stress-induced. • Occurs due to desquamation and atrophy of FILIFORM papillae (no taste buds ad atrophic). One or more irregular-shaped erythematous patches on the tongue exist. •
Clinical Presentation: Tongue center is redder then the rest of the tongue, and edges of the red patch (erythema) are surrounded by a whitish or yellow perimeter/border. The patches appear and remain for a short time, heal, then reappear at another site (the condition comes and goes). NO TREATMENT and they disappear spontaneously. Geographic Tongue often occurs with Fissured Tongue. GEOGRAPHIC TONGUE
FISSURED TONGUE (“SCROTAL OR FURROWED TONGUE”)–a DEEP, usually asymptomatic, but may be painful if infected with Candida Albicans or food debris. MEDIAN FISSURE with laterally radiating, symmetrical GROOVES that vary in number across the TONGUE DORSUM (TOP). Cause is unknown, but may be a normal variant. • Rare in children, but incidence increases with age. Found in Melkersson-Rosenthal Syndrome (along with Cheilitis Granulomatosum and Facial Nerve (CN-VII) Paralysis). •
TREATMENT: BRUSH THE TONGUE WITH A SOFT-BRISTLE TOOTHBRUSH. FISSURED TONGUE
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DENTIN™ | NBDHE 2020-2021 HAIRY TONGUE–a benign asymptomatic condition of HYPERTROPHY, STAINING, and ELONGATION of the FILIFORM PAPILLAE on the tongue dorsum (may be linked to tobacco, alcohol, antibiotics, Candida Albicans, radiation therapy, poor oral hygiene, steroids, or certain foods). •
Tongue’s complete DORSAL SURFACE is “HAIRY” due to stained and elongated FILIFORM PAPILLAE (which have no taste buds), appear yellowish-white, green, brown or black. This is not Hairy Leukoplakia, but is simply DISCOLORATION of the DORSUM tongue surface, elongation and hyperkeratosis of the FILIFORM PAPILLAE.
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ETIOLOGY: overgrowth of fungal microorganisms due to smoking or poor oral hygiene. Treatment: BRUSH THE TONGUE WITH A SOFT-BRISTLE TOOTHBRUSH. HAIRY TONGUE
MEDIAN RHOMBOID GLOSSITIS (Central Papillary Atrophy)-areas of redness and loss of lingual papillae on the tongue dorsum midline just anterior to the circumvallate papillae that often affects MIDDLE-AGED ADULTS. A permanent end-result of a CHROINC CANDIDA ALBICANS INFECTION (fungal). Most susceptible in diabetics, IMMUNOSUPPRESED patients, and patients on long-term antibiotic therapy. •
Clinical Features: smooth, denuded, BEEFY-RED LESION (erythematous) devoid of filiform papillae on the MIDLINE of TONGUE DORSUM, just anterior to the circumvallate papillae. Generally asymptomatic, and NO TREATMENT is usually necessary. MEDIAN RHOMBOID GLOSSITIS
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DENTIN™ | NBDHE 2020-2021
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)-a chronic, progressive AUTOIMMUNE inflammatory disease where the immune system attacks healthy tissue causing JOINT PAIN and SWELLING. Skin lesions are the most common clinical manifestation, often the BUTTERFLY RASH (MALAR RASH) over the nose bridge with facial inflammation and scarring. The primary lab test to diagnose SLE is the ANTINUCLEAR ANTIBODY TITER combined with clinical findings. (British musician SEAL has the rash due to DLE = discoid lupus erythematosus). 90% affected are women (15-44 years). Cause is unknown, but may be genetic or environmental. • Treatment: aspirin and/or non-steroidal anti-inflammatories (NSAIDs) to ease symptoms.
PEMPHIGUS VULGARIS–a chronic RARE SKIN DISEASE due to an autoimmune disorder that causes intra-epithelial blistering of the skin and mucous membranes. Characterized by the formation of vesicles and bullae produced by dyhesion (acantholysis) of epidermal cells due to an autoimmune mechanism where antibodies attack the intracellular junction of epithelium (autoantibodies to desmosomes that link two cells together). Usually occurs after age 30 years (ages 30-50yrs), and occurs more frequently in JEWISH people and more common in WOMEN. • The primary skin lesion is a FLACCID BLISTER WITH CLEAR FLUID ON HEALTHY SKIN. •
Oral lesions are often the FIRST MANIFESTATION. Intact bullae are rare in the oral cavity, rather, large areas of ulceration and erosions covered by white or blood-tinged exudates. Sometimes, areas of epithelium will slide off simply by rubbing of an apparently unaffected area (NIKOLSKY’S SIGN is an indication of Pemphigus vulgaris that may also be found in BMMP). This sign occurs when normal epithelium is separated at the basal layer and is RUBBED OFF when pressed with a sliding motion. Blister is within the epithelium (intra-epithelial). Pemphigus is OFTEN FATAL WITHOUT TREATMENT, which includes high-dose systemic steroids or chemotherapy (Methotrexate).
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Pemphigus Vulgaris is more severe than Pemphigoid (BP). Patient has vesicles on the skin. GINGIVA is red, inflamed and is the most common location in mouth
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The Pels-Macht test is helpful to diagnose PEMPHIGUS VULGARIS.
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DENTIN™ | NBDHE 2020-2021
SALIVARY GLAND LESIONS MUCOCELE-a movable and painless, BLUISH-PINK, FLUID-FILLED NODULE (< 1 cm in diameter consisting of solid tissue) most common on the INNER LOWER LIP (but may also occur on the gingiva palate, or tongue). Caused by trauma or obstruction to the salivary gland excretory duct and spillage of mucin into the surrounding soft tissues. Common in children and young adults. Treatment: can resolve on their own, but may require surgical excision and may recur if the causative salivary gland is not removed. MUCOCELE RANULA
RANULA-a clear-to-bluish swelling (resembles a frog’s belly) of C.T. consisting of mucin from a ruptured salivary gland due to local trauma on the MOUTH FLOOR. A MOUTH FLOOR MUCOCELE caused by WHARTON’S DUCT obstruction (submandibular salivary gland duct and ducts of Rivini of the sublingual gland). SIALOLITHIASIS (Salivary Stones)-a calcified mass (sialolith) that forms inside a SUBMANDIBULAR SALIVARY GLAND or duct (WHARTON’S DUCT) causing obstruction that results in PAIN and SWELLING that worsens before or during meals. Can also cause xerostomia and difficulty swallowing. A sialolith stone is crystallized calcium phosphate and calcium carbonate. SIALOLITHIASIS
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DENTIN™ | NBDHE 2020-2021 1. ATTRITION–the PHYSIOLOGICAL wearing away of enamel and dentin due to NORMAL function or excessive GRINDING or CLENCHING teeth together (TOOTH-TO-TOOTH CONTACT). BRUXISM-pathologic attrition due to teeth grinding. The most noticeable effects are POLISHED FACETS (flat incisal edges that usually develop on the linguoincisal of maxillary canines and central incisors, and facioincisal of mandibular canines). Discolored tooth surfaces, and exposed dentin. Age-related process NOT DUE TO CARIES. •
CLENCHING- parafunctional habit that involves constant or intermittent mandibular closure under vertical pressure (holding the teeth together and tightening the mastication muscles). Typically results in less wear than BRUXISM (GRINDING).
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BRUXISM-moving the mandible while the teeth are together. Grinding usually during sleep causing muscle and joint pain and discomfort. Bruxism decreases with age. ATTRITION (BRUXING/GRINDING)
2. ABRASION-the pathologic loss of tooth structure (wearing away) by mechanical forces from a foreign object (overzealous/aggressive brushing, nail biting, or pipe smoking habit). Abrasion is NOT caused by mastication or tooth-to-tooth contact. Abrasion causes v-shaped cervical notches. ABRASION
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DENTIN™ | NBDHE 2020-2021
SPECIAL NEEDS AND MEDICALLY COMPROMISED DENTAL TREATMENT MODIFICATIONS 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 hygienists 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.
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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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AVOID BARBITURATES and local anesthetics with SODIUM METABISULFIDE.
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TYLEONOL (ACETAMINOPHEN) and NITROUS OXIDE-OXYGEN SEDATION are typically safe with mild-to-moderate ASTHMA (nitrous oxide can help relieve stress). Stress and bisulfites may trigger an asthma attack. DO NOT USE NITROUS during episodes of wheezing or patients with severe asthma. STRESS MANAGEMENT IS KEY WITH ASTHMATICS.
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AVOID ERYTHROMYCIN and PHENOBARBITALS for asthma patients taking THEOPHYLLINE (bronchodilator).
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DENTIN™ | NBDHE 2020-2021
RADIOGRAPHIC TECHNIQUES AND ERRORS VERTICAL ANGULATION-directing x-rays so they pass vertically through the object being examined. This is accomplished by positioning the tubehead and directing the central x-ray in an up-and-down (vertical) plane. Increasing or decreasing vertical angulation affects IMAGE LENGTH and can cause distortion. Foreshortening and Elongation are produced by INCORRECT VERTICAL ANGULATION. VERTICAL ANGULATION (5º-8º)
FORESHORTENING-a shortened image is caused by EXCESSIVE VERTICAL ANGULATION. Teeth APPEAR TOO SHORT due to either too much vertical angulation, or poor chair position. FORESHORTENING
ELONGATION
ELONGATION-caused by INSUFFICIENT (TOO LITTLE) VERTICAL ANGULATION. Elongation is the MOST COMMON angulation causing TEETH TO APPEAR TOO LONG due to either too little vertical angulation, or from the film not being parallel to the tooth’s long axis, or the occlusal plane being parallel to the floor. Elongation also occurs if non-digital film is bent on the roof of the mouth.
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DENTIN™ | NBDHE 2020-2021
HORIZONTAL ANGULATION-maintaining the central x-ray beam at 0° as the tube is moved around the patient’s head. Accomplished by positioning the tubehead and direction of the central ray in a side-toside (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 imaged. •
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 interproximal tooth contacts). Overlapping reduces the diagnostic quality of film to detect interproximal caries since teeth images are superimposed on each other).
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To prevent overlapped contacts on bitewing and periapical images, the x-ray beam is directed THROUGH THE INTERPROXIMAL CONTACTS with proper horizontal angulation.
INCORRECT HORIZONTAL ANGULATION
CORRECT HORIZONTAL ANGULATION
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. BISECTING ANGLE TECHNIQUE-the film image EQUALS the tooth length when the central ray is directed at 90° to the imaginary bisector. The dental clinician must bisect the angle formed by the image receptor and the tooth’s long axis (aim the central ray at right angles to an imaginary line that bisects the angle formed by the tooth’s long axis and receptor’s plane). The bisecting angle technique works as follows to produce a tooth image that is accurate ONLY if done correctly. •
With the BISECTING ANGLE TECHNIQUE, the beam’s central ray is directed at RIGHT ANGLES to an IMAGINARY LINE that bisects that angle formed by the tooth’s long axis and image receptor.
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BISECTING ANGLE TECHNIQUE is NOT the preferred method of dental imaging due to IMAGE DISTORTION, but may be used only if the paralleling technique is impractical such as with SMALL MOUTH, LOW PALATAL VAULTS, LARGE PALATAL TORI, SHORT LINGUAL FRENUM (TONGUE TIE), or POOR PATIENT COOPERATION.
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X-ray film is placed along the tooth’s lingual/palatal surface. At the point where the film contacts the tooth, an angle is formed by the plane of the film, and tooth’s long axis.
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DENTIN™ | NBDHE 2020-2021 •
The dental operator taking the x-ray must visualize a plane that bisects this angle (this plane is the imaginary bisector, which creates two equal angles and provides a common side for the two imaginary equal triangles. The central ray is positioned perpendicular to the imaginary bisector.
PROFESSIONAL RESPONSIBILITY 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. HAZARD COMMUNICATION STANDARD: requires DENTISTS to ENSURE CHEMICAL SAFETY IN THE WORKPLACE by providing training, protective attire, labeling chemical containers, and maintaining MSDS.
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DENTIN™ | NBDHE 2020-2021
ETHICS AND LEGAL PRINCIPLES, DENTAL PROFESSIONAL RESPONSIBILITY, AND INFORMED CONSENT ADHA CODE OF ETHICS-to attain high levels of consciousness, decision-making, and practice by members of the dental hygiene profession. The ethical rules and principles of professional conduct for the practice of dentistry are set forth in the ADA’s publication “Principles of Ethics and Code of Professional Conduct”. Ethical principles found in the ADHA Code of Ethics code include justice, autonomy, and beneficence. HYGIENE CORE VALUES: 1. AUTONOMY-refers to the PATIENT (not the hygiene professional) as a rational individual to make an INFORMED, un-coerced DECISION. Patients have the right to freedom of choice, privacy, and right to informed consent with full disclosure of treatment to make informed decisions about their personal dental care. The act of self-determination. To inform patients about their treatment, to be truthful, and protect patient confidentiality. Autonomy is the self-determination and ability of a person to be self-governing and self-directing. 2. JUSTICE-provides all patients with equal and fair access to high-quality, cost-effective dental care without bias (being impartial and fair). Dental professionals have an obligation to provide care to patients in need. Denying treatment because an individual is infected with HIV, HBV, or another bloodborne disease based solely on that fact is UNETHICAL and a violation of the ADHA’s core value of JUSTICE. 3. BENEFICENCE-the dental practitioner’s MAIN GOAL is to promote the individual’s and public’s welfare and well-being (requires the removal of an existing harm). The act of doing good. Ex: oral health education, sealant programs, free community dental screenings. Always practice to DO GOOD and do no harm. •
The Dental Hygiene Practice Act and Dental Practice Act are STATUTES enacted to PROTECT THE PUBLIC.
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Statutes-formal written laws that specify legal requirements enacted by the legislative branch of government. Statutes command or prohibit something, or declare a policy.
4. NON-MALEFICENCE-refers to the PRACTITIONER (HYGIENST) “DOING NO HARM” and providing services to protect all patients from harm in a manner that protects and minimizes harm to them and others involved in their treatment. Ex: ensuring pre-medication is taken as indicated, providing eye protection, or ensuring all required instruments are properly sterilized. 5. VERACITY-states a health professional should be HONEST and TRUTHFUL and provide full disclosure to the patient, abstain from misrepresentation or deceit, and report known lapses of standards of care. Veracity is the basis of trust between the patient and dental provider. Ex: hygienist’s responsibility to inform the patient of a broken restoration during a clinical examination. 6. CONFIDENTIALITY-a core duty of dental practice that requires the practitioner to keep the patient’s personal health information private unless the patient provides WRITTEN consent to release the information. ALWAYS FOLLOW HIPPA.
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DENTIN™ | NBDHE 2020-2021
COMMUNITY DENTAL HEALTH AND RESEARCH Aside from private practice, there is an increased emphasis on improving public access to oral healthcare services. Thus, tremendous opportunities exist for dental hygienists to promote public oral health through public education, direct community-based oral health prevention programs, and state Medicaid programs. The following table compares the procedural terminology between community based and private dental practice: PROCEDURAL COMPARISON COMMUNITY DENTAL PRACTICE PRIVATE PRACTICE Survey and Needs Assessment (Initial Health History and Exam Assessment) Data Analysis (Diagnosis) Diagnosis Program Planning and Operation Treatment Planning and Treatment Funding Payment Appraisal or Evaluation Evaluation GOVERNMENT LEVELS OF COMMUNITY DENTAL HEALTH (4 LEVELS): 1. INTERNATIONAL LEVEL: coordinates programs for underdeveloped nations, gathers epidemiologic data to international comparison, and develops ways to summarize treatment needs of international populations using minimal equipment such as the CPITN or Community Periodontal Index of Treatment Needs. Ex: World Health Organization. 2. FEDERAL LEVEL: addresses U.S. oral health problems, under the auspices of the Department of Health and Human Services (DHHS), which published “Healthy People 2010” (a comprehensive, national health promotion and disease prevention agenda). Provide grants (finances) to states to administer oral health services. Federal Level Examples: • Department of Health & Human Services (DHHS) • Center for Disease Control (CDC) • National Institute of Health (NIH) • Health Resources & Services Administration (HRSA). • Agency for Healthcare Research & Quality (AHRQ) • U.S. Food & Drug Administration (FDA) • Federal Dental Health Services (FDS) •
Block Grant-a lump sum of money given to a group to use at their discretion for the requested need.
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Line Item Grant-a limp sum of money given to a group for a specific purpose.
3. STATE LEVEL: provides consultation services to local health departments and directly administers some statewide oral health programs. Ex: Smiles for Children or Dentaquest Foundation (Medicaid). Apply for Federal grants to fund state-specific oral health programs. The most important function of the state health department is to provide CONSULTATIVE ASSISTANCE.
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DENTIN™ | NBDHE 2020-2021
RESEARCH METHODS, VARIABLES, AND STATISTICS PILOT STUDY-purpose is to conduct a TRIAL RUN of the planned study on a small sample. RANDOMIZED CONTROL TRIALS (RCT)-a scientific experiment where subjects are allocated randomly to receive on of several clinical interventions. REDUCES BIAS AND PROVIDES STRONGEST FORM OF EVIDENCE. RCT IS THE GOLD STANDARD OF SCIENTIFIC TESTING FOR NEW MEDICAL INTERVENTIONS. DESCRIPTIVE STUDIES-a study not truly experimental and provides information about the naturally occurring health status, behavior, attitudes, or characteristics of a certain group. Describes the extent of a disease or condition within a population and its relationship with other variables. Helps reveal patterns and connections that may otherwise go unnoticed. The primary goal is to assess a sample at a SPECIFIC POINT IN TIME without bias to determine who has disease and where and when the disease is occurring. Does NOT test a hypothesis, but attempts to increase the understanding of diseases by SURVEYING with a cross-sectional design. 3 Reasons to Conduct a Descriptive Study: 1. Identify areas for further research. 2. Help in planning resource allocation (needs assessment). 3. Provide information about a disease or condition. EXPERIMENTAL STUDY-a study where a treatment, procedure, or program is intentionally introduced and a result or outcome is observed. Examines the causes, preventions, and treatments for diseases or outcomes. The investigator actively manipulates and determines which group receives the agent or exposure to be studied. Experimental studies test a research HYPOTHESES to establish CAUSE AND EFFECT between two factors (ex: flossing and gingivitis). Conducted in CONTROLLED ENVIRONMENTS like a laboratory. • Hypothesis-an educated guess or proposition that attempts to explain a set of facts or natural phenomenon. Tested using the scientific method. Goal is to help explain the focus and direction of the experiment or research. It states the research purpose and identifies the variables used. •
Null Hypothesis (H0)-a hypothesis that a researcher tries to disprove, reject, or nullify. A high p-value prevents the researcher from rejecting the null hypothesis. The null hypothesis is often an initial claim that researchers specify using previous research or knowledge. Ex: brushing the tongue does NOT reduce candida and halitosis.
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Alternative Hypothesis (H1)-contradicts the null hypothesis (the alternative explanation when the null hypothesis is rejected). What you may believe to be true or hope to prove true. Ex: brushing the tongue does reduces candida and halitosis.
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Treatment Group: the participants who receive the experimental treatment, and whose effect is being studied.
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Control Group: participants who do not receive the experimental treatment being studied, but receive a PLACEBO (fake treatment), a standard non-experimental treatment, or no treatment at all to account for psychological phenomenon (“placebo effect”).
BLIND STUDY: all study participants are UNAWARE as to whether they are the experimental group, or control group. Attempts to control ONLY PARTICIPANT BIAS and ensure the placebo effect will not only effect the experimental group. DOUBLE-BLIND STUDY- a study where BOTH subjects and researcher are unaware of which subjects belong to the experimental group or the control group to PREVENT RESEARCHER AND SUBJECT BIAS.
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DENTIN™ | NBDHE 2020-2021
DENTIN 1,001+ HIGH SPEED DRILLS PROFESSIONAL RESPONSIBILITY PREVIEW 1. The measure of central tendency that would locate the midpoint of sample data using a DATA MATRIX is the MEDIAN. 2. The DIFFERENCE between high and low scores on a data matrix that is affected by OUTLIERS is the RANGE. 3. Steam Under Pressure Autoclaves and Chemical Vapor Autoclaves: used for sterilization should be BIOLOGICALLY MONITORED/tested AT LEAST WEEKLY. 4. An expected level of certain diseases found regularly in a certain populations in particular areas or during particular time periods like the INFLUENZA during winter, or Malaria in tropical regions, is an ENDEMIC. 5. The PERCENTAGE of people in a population suffering from a particular disease or condition at a given point in time is PREVALANCE. 6. The research sample that yields the GREATEST BIAS POTENTIAL is a JUDGEMENT SAMPLE. 7. The extent that a test measures what it is intended to measure is VALIDITY. 8. The CLOSER the CORRELATION CO-EFFICIENT to +1 or -1, the STRONGER CORRELATION and more probable the CAUSE & EFFECT. 9. An evidence-based approach to prevent and manage CARIES by assessing risk levels that form intervention guidelines before irreversible tooth damage occurs is CAMBRA. 10. PERSONAL PROTECTIVE EQUIPMENT includes GLOVES, GOWNS, EYE PROTECTION, FACE SHIELD, and MASKS. 11. ALCOHOLS, CHLORHEXIDINE, IODOPHORS, PHENOLS, and QUATERNARY AMMONIUM are all examples of DISINFECTANTS. 12. Opportunistic pathogens that inhabit biofilm inside dental unit water lines are PSEUDOMONAS AERUGINOSA & LEGIONELLA PNEUMOPHILIA. 13. BIOLOGICAL INDICATORS (BI) test the proper functioning of sterilization cycles AT LEAST WEEKLY.
YOU ARE PREPARED FOR THE NBDHE WITH DENTIN™
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