Integrated National Board Dental Examination (Inbde) : Dentin Inbde Study Guide (2020-2021) WWW - Dentin.co

DENTIN INBDE STUDY GUIDE (2020-2021) www.dentin.
co
INTEGRATED NATIONAL BOARD DENTAL

EXAMINATION (INBDE)
The INBDE is a 500 multiple-choice examination scored as PASS or FAIL. The INBDE is 12
hours and 30 minutes and is taken over a period of 1-1/2 days.
• Day 1: examinee has 8 hours and 15 minutes to answer 360 questions.
• Day 2: examinee has 4 hours and 15 minutes to answer 140 questions.
The INBDE emphasizes the decision making process relevant to the safe practice of dentistry
by integrating the basic sciences with dental and clinical science.
The INBDE presents multiple choice questions accompanied by a Patient Box that contains
patient case information. The information in the Patient Box is information that would be available
to the dentist and dental hygienist during the patient visit. Examinees will need to extrapolate the
relevant information from the Patient Box and apply that information with their didactic and clinical
knowledge to correctly answer the exam questions.
INBDE CONTENT INBDE

PERCENTAGE
Molecular, Biochemical, Cellular and systems-level development, structure 12.2%
and function
General and Disease-Specific Pathology to assess patient risk 11.8
Pharmacology 10.6%
Biology of Microorganisms in Physiology and Pathology 10.6%
Behavior Sciences, Ethics, and Jurisprudence 10.6%
Genetics, Congenital and Developmental Diseases and Conditions and 10.6%
clinical features to assess patient risk
Research Methodology and Analysis and Informatic Tools 9.8%
Cellular and Molecular Bases of Immune and Non-Immune Host Defense 9.0%
Mechanisms
Physics and Chemistry to Explain the characteristics and technological 8.0%
application of biomaterials
Physics and Chemistry to Explain Biology and Pathobiology 6.8%
100%
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DENTIN INBDE STUDY GUIDE (2020-2021) www.dentin.co
INTRODUCTION: THE DENTIN INBDE STUDY METHOD:

Below is a sample PATIENT BOX that will be presented to you on the INBDE. Each patient box
contains specific patient information. You will be asked several questions covering multiple
disciplines related to the information provided in the patient box to test your dental knowledge and
ability to apply your knowledge to practical situations you may encounter as a dental professional.
The underlying format of the DENTIN study guide covers all of the required information you
will need to correctly understand and answer the INBDE patient box questions. Because it
is difficult to predict the exact information contained in the patient boxes, DENTIN has provided
you with the core foundational knowledge and material in this study guide that will enable
you to successfully answer any INBDE question and pass the exam.
The core INBDE material in this high-yield study guide contains over 2,100 prior and potential
INBDE SUCCESS STATEMENTS that have been carefully selected based on the material’s
clinical importance, relevance, and practical application.
To efficiently and effectively maximize your study time, DENTIN has reviewed thousands of pages
of detailed dental information and carefuly developed over 2,100 INBDE success statements
contained in this study guide. The statements are meticulously organized by subject and each
statement includes the correct answer in the statement, so you are learning the important
information with the correct response.
The DENTIN INBDE study guide is an amazing high-yield and effective study aid to successfully
pass the INBDE. As long as you invest the time and effort to study the INBDE success statements
in this study guide, YOU WILL PASS THE INBDE. BEST OF LUCK! DENTIN.
INBDE PATIENT BOX

PATIENT
Male, 68 years old
CHIEF COMPLAINT
“I have a bump on my gum near my bottom right
tooth”
BACKGROUND AND/OR PATIENT HISTORY

Prosthetic Heart Valve
Smokes E-cigarettes
Medications: Warfarin (Coumadin)
Penicillin allergy
CURRENT CLINICAL FINDINGS

#28 periapical radiolucency; no response to #2
endo ice or electric pulp test.
White coating on tongue that wipes off.
BP: 130/80
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TABLE OF CONTENTS
ANATOMICAL SCIENCES
Tongue ............................................................................................................................................ 1-26

Salivary Glands ............................................................................................................................. 27-56
Soft and Hard Plates, Throat, Sinuses.......................................................................................... 57-73
Muscles of Mastication ................................................................................................................. 74-88
Muscles of Facial Expression ....................................................................................................... 89-93
Hyoid Muscles ............................................................................................................................ 94-103
Neck Muscles and Neck Triangles ........................................................................................... 104-113
Cranial Nerves........................................................................................................................... 114-162
Lymphatic System .................................................................................................................... 163-188
Osteology and TMJ................................................................................................................... 189-212
Embryology and Histology ........................................................................................................ 213-285
DENTAL ANATOMY AND OCCLUSION
Dental Anatomy and Occlusion ................................................................................................ 286-441

Maxillary Canine........................................................................................................................ 442-467
Mandibular Canine .................................................................................................................... 468-487
Maxillary Lateral Incisor ............................................................................................................ 488-503
Mandibular Lateral Incisor ........................................................................................................ 504-510
Maxillary Central Incisor............................................................................................................ 511-513
Mandibular Central Incisor ........................................................................................................ 514-519
Maxillary First Premolar ............................................................................................................ 520-532
Mandibular First Premolar ........................................................................................................ 533-539
Maxillary Second Premolar ....................................................................................................... 540-544
Mandibular Second Premolar ................................................................................................... 545-549
Maxillary First Molar .................................................................................................................. 550-578
Mandibular First Molar .............................................................................................................. 579-596
Mandibular Second Molar ........................................................................................................ 597-609
Maxillary Second Molar ............................................................................................................ 610-623
Third Molars .............................................................................................................................. 624-634
Primary (Deciduous) Teeth ........................................................................................................ 635-650
MICROBIOLOGY AND PATHOLOGY
Biology of Microorganisms and Disease .................................................................................. 651-895

Odontogenic and Bone Lesions ............................................................................................... 896-944
Endocrine Pathology ................................................................................................................. 945-953
Musculoskeletal and Skin Pathology ........................................................................................ 954-967
Bacterial and Viral Oral Pathology ............................................................................................ 968-978
Blood Pathology ....................................................................................................................... 979-997
Oral White Lesions .................................................................................................................. 998-1008
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Pigmented Lesions ............................................................................................................... 1009-1017

Comprehensive Oral Pathology Review ....................................................................... Pages: 155-266
IMMUNOLOGY
Immunology .......................................................................................................................... 1018-1064
BIOCHEMISTRY, PHYSIOLOGY, AND NUTRITION
Biochemistry, Physiology, and Nutrition ............................................................................... 1065-1303
PHARMACOLOGY
Pharmacokinetics ................................................................................................................. 1304-1341

Respiratory Drugs ................................................................................................................. 1342-1352
Anticoagulants and Salicylates (Aspirin) ............................................................................... 1353-1374
Antihistamines and Proton Pump Inhibitors ......................................................................... 1375-1382
Opioid Analgesics ................................................................................................................. 1383-1393
Antibiotics and Antifungals ................................................................................................... 1394-1414
Antivirals and Viruses ............................................................................................................ 1415-1430
Local Anesthetics.................................................................................................................. 1431-1471
Anti-anxiety Agents and General Anesthesia ....................................................................... 1472-1491
Anti-hypertensive (Beta Blockers)......................................................................................... 1492-1503
Diuretics ................................................................................................................................ 1504-1507
ACE Inhibitors and Statins .................................................................................................... 1508-1513
Anti-Anginal Drugs ................................................................................................................ 1514-1516
Anti-Convulsant Drugs .......................................................................................................... 1517-1519
Hypoglycemics and Endocrine Imbalance Drugs ................................................................. 1520-1539
PROVISION OF DENTAL CARE
Periodontics .......................................................................................................................... 1540-1598

Endodontics .......................................................................................................................... 1599-1670
Oral Surgery .......................................................................................................................... 1671-1726
Orthodontics and Pediatric Dentistry.................................................................................... 1727-1793
Biomaterials, Operative Dentistry, and Prosthodontics ........................................................ 1794-1889
PROFESSIONAL ETHICS, PATIENT MANAGEMENT, OSHA

Ethical and Legal Principles; Informed Consent .................................................................. 1890-1908
Special Needs and Medical Emergencies ............................................................................ 1909-1945
Research Method, Variables, and Statistics ......................................................................... 1946-1996
Oral Health Indices and Prevention ...................................................................................... 1997-2077
OSHA and Infection Control ................................................................................................. 2078-2110
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ANATOMICAL SCIENCES
TONGUE
1. HYPOGLOSSAL NERVE (CN XII) provides MOTOR to ALL TONGUE INTRINSIC &
EXTRINSIC MUSCLES EXCEPT “PALATOGLOSSUS” which is innervated by the VAGUS
NERVE (PHARYNGEAL PLEXUS).
2. EXTRINSIC TONGUE MUSCLES are named based on their ORIGIN.
3. During contraction, the tongue muscle that PROTRUDES the tongue is GENIOGLOSSUS.
4. During contraction, the tongue muscle that DEPRESSES the tongue’s sides is HYOGLOSSUS.
5. During contraction, the extrinsic tongue muscle that ELEVATES and RETRACTS the tongue is
STYLOGLOSSUS.
6. During contraction, the tongue muscle that ELEVATES the tongue’s base and DEPRESSES
the soft palate is PALATOGLOSSUS.
7. The soft palate is elevated during swallowing and initiation of esophageal peristalsis by the
VAGUS NERVE.
8. LINGUAL NERVE provides general SENSORY to the TONGUE’S ANTERIOR 2/3.
9. GLOSSOPHARYNGEAL NERVE provides sensory and taste to TONGUE’S POSTERIOR 1/3.
10. The tongue is innervated by cranial nerves VII, IX, X, and XII.
11. LINGUAL ARTERY provides the MAIN blood supply to the TONGUE.
12. Tongue tip and lower lip, floor of the mouth, mandibular incisors, and the chin bilaterally DRAIN
INTO the SUBMENTAL LYMPH NODES.
13. REMAINING anterior tongue 2/3 drains into the SUBMANDIBULAR and DEEP CERVICAL
LYMPH NODES.
14. A severe abscess of a maxillary tooth will drain via the SUBMANDIBULAR LYMPH NODES.
15. FILLIFORM PAPILLAE are the most NUMEROUS, NO TASTE BUDS, & cause HAIRY
TONGUE.
16. STAINING & ELONGATION of the FILLIFORM PAPILLAE due to accumulation of oral bacteria
or fungi is indicative of HAIRY TONGUE.
17. The best treatment for BLACK HAIRY TONGUE is to improve oral hygiene by routine TONGUE
BRUSHING or SCRAPING and TOBACCO CESSATION.
18. ATROPHY (areas of erythema) of FILLIFORM PAPILLAE may be due to GEOGRAPHIC

TONGUE (ERYTHEMA MIGRANS).
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19. The loss of numerous FILIFORM PAPILLAE during iron-deficiency anemia may result in a RED,
BEEFY TONGUE.
20. 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.
21. The tongue’s LOWEST taste threshold region occurs in the POSTERIOR TO BITTERNESS.
22. An oral manifestation often caused by HEMANGIOMAS and common to both ACROMEGALY
and TRISOMY 21 (DOWN SYNDROME) is MACROGLOSSIA.
23. MACROGOSSIA signs and symptoms include DYSPNEA, DYSPHAGIA, DYSPHONIA, and
ANGULAR CHEILITIS.
24. A congenital anomaly of EXCESSIVE TONGUE ADHESION to the mouth floor caused by a
SHORT, THICK LINGUAL FRENUM is ANKYLOGLOSSIA (TONGUE TIE).
25. The objective of ANKYLOGLOSSIA treatment is to improve tongue movement, speech, and
oral hygiene via a FRENECTOMY.
26. The simplest LYMPHOID ORGAN located at the base of the tongue are the LINGUAL
TONSILS.
SALIVARY GLANDS
27. A calcification or obstruction to WHARTON’S DUCT can result in SIALOLITHIASIS (Salivary

Stones) or a RANULA.
28. Compared to plasma, saliva contains HIGHER ion levels of POTASSIUM and BICARBONATE
and LOWER levels of SODIUM and CHLORIDE due to active transport of salivary glands that
is involved with saliva production.
29. A bluish-pink fluid-filled nodule on the LOWER LIP’s inner surface is most likely a MUCOCELE.
30. A bluish-pink fluid-filled nodule on the FLOOR OF THE MOUTH is most likely a RANULA.
31. The treatment for a MUCOCELE and RANULA if they do not improve or resolve on their own
is SURGICAL EXCISION or MARSUPIALIZATION.
32. The purely serous MINOR SALIVARY GLANDS on the tongue are GLANDS OF VON
EBNER.
33. The LARGEST and PURELY SEROUS salivary gland is the PAROTID GLAND.
34. The PAROTID GLAND produces PURELY SEROUS saliva containing secretory IgA,
lysozymes, thiocynate, and salivary amylase.
35. STENSONS’S DUCT drains the PAROTID GLAND.
36. The SUBLINGUAL and SUBMANDIBULAR GLANDS are MIXED GLANDS (mostly mucous
and some serous).
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37. The SUBLINGUAL and BUCCAL GLANDS produce PURELY MUCOUS secretions.
38. The minor salivary glands and sublingual glands produce primarily MUCUS secretions to
protect and lubricate the oral tissues.
39. MINOR SALIVARY GLANDS are located on the LIPS, CHEEK, TONGUE, and HARD
PALATE.
40. MAJOR SALIVARY GLANDS are the PAROTID, SUBMANDIBULAR, & SUBLINGUAL
glands.
41. Bilateral swelling of the PAROTID gland in a child with flu-like symptoms may be indicative of
MUMPS (EPIDEMIC PAROTITIS).
42. The PAROTID GLAND and SUBLINGUAL GLAND lymphatic drainage are through the DEEP
CERVICAL LYMPH NODES.
43. The EXTERNAL CAROTID ARTERY supplies blood to the PAROTID GLAND.
44. The salivary glands responsible for 60-65% of total salivary flow are the SUBMANDIBULAR
GLANDS.
45. The SUBMANDIBULAR GLAND is located SUPERIOR to the DIGASTRICS and INFERIOR
to the MYLOHYOID muscle.
46. The SUBLINGUAL and SUBMANDIBULAR glands are both oriented just SUPERIOR to the
MYLOHYOID MUSCLE.
47. WHARTON’S DUCT drains the SUBMANDIBULAR GLANDS.
48. Most SALIVARY GLAND TUMORS originate from DUCTS.
49. SUBLINGUAL & SUBMANDIBULAR GLANDS are innervated by the FACIAL NERVE (CN
VII).
50. SUBMANDIBULAR SALIVARY GLANDS are best examined using BIMANUAL PALPATION
by rolling the lymph nodes over the mandible’s inferior border.
51. The SMALLEST salivary gland is the SUBLINGUAL GLAND.
52. The SUBMENTAL GLANDS are best examined using BILATERAL DIGITAL PALPATION.
53. A 51-year old female is currently undergoing radiation therapy for thyroid cancer and was also
previously diagnosed with rheumatoid arthritis. She complains of joint pain, dry mouth and has
rampant caries. She often has to use lip balm due to cracking lips and her parotid glands are
bilaterally enlarged. Her symptoms are consistent with SJOGREN’S SYNDROME.
54. The MOST COMMON BENIGN SALIVARY GLAND TUMOR that affects the major and minor
salivary glands as a slow-growing, painless swelling is a PLEOMORPHIC ADENOMA.
55. The GREAT AURICULAR NERVE provides sensory innervation to the SKIN directly overlying
the PAROTID GLAND.
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56. A rare congenital anomaly involving the ABSENCE OF ONE OR MORE of the MAJOR
SALIVARY GLANDS is SALIVARY GLAND APLASIA.
SOFT AND HARD PALATES, THROAT AND SINUSES

57. The mobile soft-tissue fold posterior to the hard palate that separates the ORAL CAVITY
from the NASOPHARYNX is the SOFT PALATE.
58. The ROOF OF THE MOUTH is 1/3 SOFT PALATE and 2/3 HARD PALATE.
59. All skeletal muscles that comprise the SOFT PALATE are innervated by the
PHARYNGEAL NERVE PLEXUS except TENSOR VELI PALATINI.
60. TENSOR VELI PALATINI is the only SOFT PALATE MUSCLE innervated by the
MANDIBULAR DIVISION (V3) of the trigeminal nerve.
61. Most blood supply to the HARD PALATE is directly vascularized by the GREATER
PALATINE ARTERY.
62. The GREATER PALATINE NERVE BLOCK provides anesthesia to the palatal mucosa
anterior to the maxillary first premolar and to the posterior hard palate up to the midline, but
DOES NOT INNERVATE TEETH.
63. Most blood supply to the SOFT PALATE comes from the GREATER & LESSER
PALATINE ARTERIES.
64. Rapidly adapting encapsulated MECHANORECEPTORS of LIGHT PRESSURE,

discriminative touch, and low frequency vibration located in C.T. papillae under the
epithelial layer to permit the palate to discriminate sensory information are MEISSNER
CORPUSCLES.
65. Rapidly adapting encapsulated mechanoreceptors of DEEP PRESSURE, stretch, and high
frequency vibration are PACINIAN CORPUSCLES.
66. The SIMPLEST LYMPHOID structures found in the POSTERIOR WALL of the
NASOPHARYNX are the PHARYNGEAL TONSILS.
67. The LARYNX is evaluated by being moved gently side-to-side by BIMANUAL

PALPATION.
68. The PARANASAL SINUSES drain through the NASAL MEATUSES.
69. The nasal cavity is separated from the oral cavity by the PALATINE BONE.
70. PARANASAL SINUSES are the MAXILLARY, FRONTAL, ETHMOIDAL, & SPHENOIDAL
sinuses.
71. The shape of the MAXILLARY SINUS most closely resembles a PYRAMID.
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72. The MAXILLARY SINUS FLOOR is formed from the ALVEOLAR PROCESS OF THE
MAXILLA.
73. MAXILLARY SINUSITIS may often accompany a TOOTHACHE.
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MUSCLES OF MASTICATION
74. The MASSETER originates from the ZYGOMATIC ARCH (cheekbone) and inserts on and
covers the LATERAL SURFACE OF THE RAMUS (ANGLE) OF THE MANDIBLE.
75. All muscles of mastication are innervated by TRIGEMINAL NERVE (MANDIBULAR

DIVISION-V3).
76. BLOOD SUPPLY to the muscles of mastication comes from the PTERYGOID BRANCH of
the MAXILLARY ARTERY.
77. BLOOD SUPPLY to the PERIODONTAL LIGAMENT (PDL) arises from the MAXILLARY
ARTERY.
78. The artery that arises behind the neck of the mandible and runs medially to the neck of the
mandibular condyle before passing into the pterygopalatine fossa is the MAXILLARY
ARTERY.
79. The muscles of mastication are the MASSETER, TEMPORALIS, MEDIAL PTERYGOID
AND LATERAL PTERYGOID.
80. The GREATEST MASTICATORY FORCE is produced by the MASSETER MUSCLE.
81. Repeated muscle contraction from CLENCHING TEETH causes HYPERTROPHY of the
MASSETER MUSCLE.
82. The muscle of mastication responsible for ELEVATING and RETRACTING the mandible
is the TEMPORALIS.
83. The muscle of mastication that INSERTS into the CORONOID PROCESS is
TEMPORALIS.
84. Mandibular movements produced by the LATERAL PTERYGOIDS are OPENING

(DEPRESSION), PROTRUSION, and LATERAL EXCURSION (side-to-side).
85. The LATERAL PTERYGOID is mainly contained in the INFRATEMPORAL FOSSA with
the maxillary artery and vein.
86. TEMPORALIS, MEDIAL PTERYGOID & MASSETER all CLOSE (ELEVATE) THE
MANDIBLE.
87. A few days after an inferior alveolar nerve block, a patient complains of soreness, spasm,
and limited opening. The patient most likely developed TRISMUS as a result of the needle
penetrating through the MEDIAL PTERYGOID.
88. A patient with a maximum opening of 25mm (limited opening) could be caused by
CONDYLAR ANKYLOSIS, HYPERTROPHY OF THE CORNOID PROCESS, or
PERICORONITIS, NOT by fatigue of the masseter muscle.
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MUSCLES OF FACIAL EXPRESSION
89. TASTE and MOTOR innervation to the MUSCLES OF FACIAL EXPRESSION comes from
the FACIAL NERVE (CN VII).
90. BLOOD SUPPLY to the MUSCLES OF FACIAL EXPRESSION comes from the FACIAL
ARTERY (external carotid artery branch).
91. The muscle of facial expression located between the maxilla and mandible that
COMPRESSES the CHEEKS and LIPS against the teeth to prevent food accumulation in
that area is the BUCCINATOR.
92. The thin quadrilateral muscle that originates from the MAXILLARY and MANDIBULAR
ALVEOLAR PROCESSS and PTERYGOMANDIBULAR RAPHE to aids in whistling or
smiling is the BUCCINATOR.
93. The most effective way to examine the MENTALIS MUSCLE is by DIGITAL PALPATION.
HYOID MUSCLES
94. HYOID MUSCLES together with the LATERAL PTERYGOID MUSCLE DEPRESSES THE
MANDIBLE.
95. HYOID MUSCLES are INNERVATED by the FACIAL NERVE (CN-VII) and TRIGEMINAL
NERVE (CN-V).
96. The DIGASTRIC, MYLOHYOID, GENIOHYOID, & STYLOHYOID are all SUPRAHYOID
MUSCLES.
97. The group of muscles that attach superior to the HYOID BONE and are responsible for
SWALLOWING are the SUPRAHYOID MUSCLES.
98. The ANTERIOR DIGASTRIC BELLY is innervated by the TRIGEMINAL NERVE (V3).
99. The POSTERIOR DIGASTRIC BELLY is innervated by the FACIAL NERVE (CN-VII).
100. The MOUTH FLOOR is formed mainly by the MYLOHYOID MUSCLE.
101. Taking periapical radiographs of mandibular molars can be difficult if the MYLOHYOID
MUSCLE IS NOT RELAXED.
102. MOTOR INNERVATION to the INFRAHYOID MUSCLES (TOSS) comes from ANSA
CERVICALIS (the cervical plexus loop).
103. THYROHYOID, OMOHYOID, STERNOHYOID, & STERNOTHYROID (TOSS), are all

INFRAHYOID MUSCLES.
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NECK MUSCLES AND NECK TRIANGLES

104. The muscle that separates the neck’s anterior & posterior triangles and TILTS and
ROTATES THE HEAD is the STERNOCLEIDOMASTOID.
105. The muscular landmark palpated during an extra-oral examination that runs adjacent to the
CERVICAL LYMPH NODES is the STERNOCLEIDOMASTOID.
106. The muscle that ELEVATES and ADDUCTS the SCAPULA and produces the
“SHOULDER SHRUG” is the TRAPEZIUS.
107. BREATH SOUNDS OF RESPIRATION are best heard by placing a stethoscope on the
TRIANGLE OF AUSCULTATION.
108. The neck’s ANTERIOR TRIANGLE consists of the CAROTID, SUBMANDIBULAR,

SUBMENTAL, and OMOTRACHEAL triangles.
109. The neck’s POSTERIOR TRIANGLE is formed by the OCCIPITAL and OMOCLAVICULAR
triangles.
110. The LARYNX, TRACHEA, THYROID GLAND, and CAROTID SHEATH are all contents of
the lesser anterior OMOTRACHEAL TRIANGLE.
111. The COMMON CAROTID ARTERY, INTERNAL JUGULAR VEIN, and VAGUS NERVE
are all contained within the CAROTID SHEATH
112. The POSTERIOR TRIANGLE contains the CERVICAL & BRACHIAL PLEXUS,
SUBCLAVIAN ARTERY, and ACCESSORY NERVE (CN-XI).
113. The only UNPAIRED TRIANGLE of the neck is the SUBMENTAL TRIANGLE.
CRANIAL NERVES AND BLOOD VESSELS
114. A MOTOR nerve that carries impulses AWAY from the CNS is an EFFERENT NERVE.
115. A SENSORY nerve that carries impulses TOWARD the CNS is an AFFERENT NERVE.
116. The OLFACTORY NERVE (CN-I) exists the skull through the ETHMOID BONE’S
CRIBIFORM PLATE and is responsible for SMELL.
117. TWO cranial nerves that are PURELY SENSORY are the OPTIC NERVE and
OLFACTORY NERVE.
118. The OPTIC NERVE (CN-II) provides PURE SENSORY innervation to the RETINA.
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119. The cranial nerve responsible for EYE MOVEMENT and PUPIL CONSTRICTION that can
be directly linked to PTOSIS (drooping of the upper eyelid) is the OCULOMOTOR NERVE
(CN III).
120. The cranial nerve responsible for EYE MOVEMENT and PUPIL CONSTRICTION is the
OCULOMOTOR NERVE (CN-III).
121. PTOSIS (drooping of the upper eyelid) is most likely due to damage to the OCULOMOTOR
NERVE (CN-III).
122. The cranial nerve that supplies MOTOR function to the eye’s SUPERIOR OBLIQUE
MUSCLE is the TROCHLEAR NERVE (CN-IV).
123. The cranial nerve directly linked to DOUBLE VISION (DIPLOPIA) is the TROCHLEAR
NERVE (CN-IV).
124. The cranial nerve that supplies MOTOR function to the eye’s LATERAL RECTUS
MUSCLE is the ABDUCENS NERVE (CN-VI).
125. The ABDUCENS NERVE’S NUCLEUS is located in the PONS.
126. Cranial nerves III (OCULOMOTOR), IV (TROCHLEAR), and VI (ABDUCENS) innervate

the EYES.
127. The LARGEST CRANIAL NERVE and MAJOR SENSORY NERVE to the FACE is the
TRIGEMINAL NERVE (CN V).
128. The TRIGEMINAL nerve’s 3 DIVISIONS are MANIBULAR (V3), MAXILLARY (V2) &
OPHTHALMIC (V3).
129. The MAXILLARY DIVISION (V2) of the trigeminal exits the skull through FORAMEN
ROTUNDUM.
130. The MIDFACE, PALATE, PARANASAL SINUSES, and MAXILLARY TEETH receive
SENSORY innervation from the MAXILLARY DIVISION (V2) of the TRIGEMINAL.
131. The MANDIBULAR DIVISION (V3) exits the skull through FORAMEN OVALE.
132. The MANDIBULAR DIVISION (V3) of the trigeminal nerve is SENSORY and MOTOR.
133. Branches of the MANDIBULAR DIVISION (V3) of the trigeminal nerve are the BUCCAL,
LINGUAL, and MENTAL nerves.
134. A branch of V3 that carries sensation from the mandibular teeth and exits the
MANDIBULAR FORAMEN is the INFERIOR ALVEOLAR NERVE.
135. Motor innervation to the MUSCLES OF MASTICATION and MYLOHYOID MUSCLES are
supplied by the MANDIBULAR DIVISION (V3) of the TRIGEMINAL NERVE.
136. FACIAL NERVE (CN VII) exits the skull and emerges through the STYLOMASTOID
FORAMEN.
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137. BELLS PALSY is caused by damage to the FACIAL NERVE (CN VII).
138. The FACIAL NERVE provides TASTE sensation to the TONGUE’S ANTERIOR 2/3.
139. A FACIAL NERVE (CN-VII) branch that provides TASTE to the TONGUE’s ANTERIOR
2/3 AND SECRETOMOTOR innervation to the SUBMANDIBULAR and SUBLINGUAL
glands is CHORDA TYMPANI.
140. GLOSSOPHARYNGEAL NERVE provides TASTE sensation to the TONGUE’S

POSTERIOR 1/3.
141. The only cranial nerve NOT RESTRICTED TO THE HEAD & NECK and THE DOMINANT
NERVE TO THE HEART is the VAGUS NERVE (CN X).
142. Parasympathetic innervation to the heart, lungs, esophagus, small intestines, and stomach
are all supplied by the VAGUS NERVE (CN X).
143. The VAGUS NERVE (CN X) provides all parasympathetic innervation to the body’s vital
organs from the neck to the transverse colon; originates in the MEDULLA OBLONGATA.
144. The cranial nerve involved in SHOULDER SHRUGGING and HEAD TURNING is the
ACCESSORY NERVE (CN XI).
145. The ACCESSORY NERVE (CN XI) supplies MOTOR function & innervation to the
TRAPEZIUS & STERNOCLEIDOMASTIOD muscles.
146. The cranial nerve with the MOST EXTENSIVE DISTRIBUTION that carries MOST
parasympathetic output from the BRAIN is the VAGUS NERVE (CN X).
147. The cranial nerves with MIXED FUNCTION (MOTOR & SENSORY) are V, VII, IX, and X.
148. The cranial nerves with ONLY SENSORY FUNCTION are I, II, and VIII.
149. The cranial nerves with STRICTLY MOTOR FUNCTION are III, IV, VI, XI, XII.
150. The HYPOGLOSSAL NERVE (CN-XII) is responsible for TONGUE MOVEMENT.
151. VESTIBULOCOCHLEAR (CN-VIII) is the cranial nerve responsible for BALANCE and
HEARING.
152. The major artery palpated against the larynx during a MEDICAL EMERGENCY (CPR) of
an adult or child due its pulse reliability is the COMMON CAROTID ARTERY.
153. The major artery that is most reliable when checking an infant’s BLOOD PRESSURE or
PULSE is the BRACHIAL ARTERY.
154. The major artery most reliable to check ADULT HEART RATE is the RADIAL ARTERY.
155. A blood vessel that transports DEOXYGENATED BLOOD from the tissues BACK TO THE
HEART is a VEIN.
14
156. BLOOD PRESSURE is HIGHEST in ARTERIES and LOWEST in VEINS.
157. The greatest drop in blood pressure occurs at the transition from ARTERIES to
ARTERIOLES.
158. Excessive vasoconstriction of the digital arteries and arterioles that causes cyanosis of the
digits in the hands and feet and resulting cold sensation is consistent with findings with
RAYNAUD’S PHENOMENON.
159. The buccal gingiva innervation and blood supply overlying the maxillary molars are provided
by the POSTERIOR-SUPERIOR ALVEOLAR nerve and vessels. The facial gingiva
covering the maxillary incisors and canines are supplied by the ANTERIOR-SUPERIOR
ALVEOLAR nerves and blood vessels. BOTH TRUE.
160. The INTERNAL CAROTID ARTERY is the primary blood supply to the brain, while the
EXTERNAL CAROTID ARTERY supplies blood to the face, scalp, skull, and meninges.
BOTH TRUE.
161. A patient whose pupils do not dilate (remain small) in a dimly lit room can be attributed to
an injury to the SUPERIOR CERVICAL SYMPATHETIC GANGLION that innervates the
dilator pupillae muscle.
162. The MARGINAL MANDIBULAR branch of the FACIAL NERVE innervates the risorius
muscle and muscles of the lower lip.
15
LYMPHATIC SYSTEM
163. Superficial lymphatic vessels that drain the BREAST, CHEST, & ARM are AXILLARY
LYMPH NODES.
164. A MAIN function of LYMPH NODES is to FILTER BLOOD & LYMPH by removing and
destroying circulating antigens.
165. LYMPHATIC SYSTEM functions include FIGHTING INFECTION, FILTERING BLOOD and
LYMPH, and producing LYMPHOCYTES (WBCs).
166. Lymph node enlargement due to infection, inflammation, or cancer is

LYMPHADENOPATHY.
167. LARGE LYMPH NODE CLUSTERS are present in the AXILLARY, CERVICAL, and
INGUINAL REGIONS, but NOT in the lower extremities.
168. The SIMPLEST LYMPHATIC TISSUE presenting clinically as a MUCOSA SWELLING

posterior to the soft palate (OROPHARYNX) are TONSILS.
169. LYMPHOID TISSUE comprise lymph nodes, is COMPOSED OF RETICULAR C.T.,

produce antibodies, and store lymphocytes.
170. The most extensive component of lymphoid tissue that functions to protect open
passages from ANTIGENS by lining mucosa throughout the body such as in the
APPENDIX and TONSILS is called MALT (MUCOSA-ASSOCIATED LYMPHATIC
TISSUE).
171. LYMPH is composed of WBC (lymphocytes), water, ions, and plasma proteins.
172. The LARGEST LYMPHOID ORGAN that FILTERS blood by breaking down damaged
RBC, stores platelets and iron, and removes microbes is the SPLEEN.
173. LYMPH flows in ONE DIRECTION (UPWARD TOWARDS THE NECK), while BLOOD
flows in a continuous loop.
174. When there is LYMPHATIC OBSTRUCTION, EDEMA (SWELLING) occurs DISTAL to the
obstruction.
175. Mechanical pressure in the brain from trauma that compresses cerebral vasculature and
causes subsequent ischemia from diminished oxygen and blood flow delivery to CNS
tissues describes the physiological mechanism of CEREBRAL EDEMA.
176. LYMPH FLOW occurs and is maintained by skeletal muscle contraction, valves in lymph
vessel walls to prevent “backflow”, and by breathing.
177. LYMPHATIC CAPILLARIES are MORE PERMEABLE than BLOOD CAPILLARIES.
178. LYMPH IS CARRIED AWAY from a lymph node by EFFERENT LYMPHATIC VESSELS.
16
179. The LYMPHATIC SYSTEM drains into the VENOUS SYSTEM.
180. Most lymph is RETURNED TO THE BLOOD at the junction of LEFT INTERNAL JUGULAR
+ SUBCLAVIAN VEINS.
181. LYMPH TRANSPORT depends on the movement of adjacent tissues like SKELETAL
MUSCLES.
182. LYMPHOCYTES become IMMUNOCOMPETENT due to THYMIC HORMONES.
183. The SPLEEN, THYMUS, TONSILS, and ADENOIDS all produce LYMPHOCYTES.
184. The maturation site for IMMATURE T-CELL DEVELOPMENT into LYMPHOCYTES in
children is the THYMUS.
185. The THYMUS initially INCREASES in size during childhood, then DECREASES in size
and atrophies during ADULTHOOD.
186. The THYMUS does NOT contain lymphatics and is the only lymphoid organ that DOES
NOT DIRECTLY FIGHT ANTIGENS.
187. The THYMUS is located in the SUPERIOR MEDIASTINUM.
188. Lymphocytes that DO NOT reach the thymus become B-CELLS.
OSTEOLOGY AND TEMPEROMANDIBULAR JOINT

189. The TMJ is a GINGLYMOARTHRODIAL JOINT with ROTATIONAL
and TRANSLATIONAL movement.
190. During TRANSLATION (SLIDING), the disk

and condyle move FORWARD and BACKWARD in the upper joint
space.
191. During ROTATION (HINGE), the mandible is ELEVATED and DEPRESSED.
192. Depression movement of the mandible into the open position occurs along the horizontal
hinge axis in the lower joint space that is purely ROTATIONAL.
193. The TEMPEROMANDIBULAR JOINT (TMJ) has DUAL

ARTICULATION between the MANDIBULAR CONDYLE and GLENOID FOSSA of the
temporal bone (skull).
194. SENSORY SUPPLY:V3(Post: Auriculotemporal branch of V3 and Ant: Deep temporal

and Massetric branch of V3)andBLOOD SUPPLY is from the EXTERNAL CAROTID
ARTERY (superficial temporal branch).
195. MAXIMUM BLOOD SUPPLY is found in RETRODISCAL PAD of the TMJ’s

BILAMINAR ZONE.
17
196. The RETRODISCAL PAD contains COLLAGEN, VENOUS PLEXUS, ELASTIC & NERVE
FIBERS, and FAT.
197. The TMJ posterior attachment tissues located between the posterior portion of the TMJ
DISC and CAPSULE that allows the condyle to move forward, is the BILAMINAR ZONE.
198. SUPERIOR & INFERIOR LAMINAS and RETRODISCAL PAD form the TMJ’s BILAMINAR
ZONE.
199. The dense, irregular, and saddle-shaped (bioconcave) FIBROCARTILAGE that

SEPARATES THE CONDYLE & TEMPORAL BONE to prevent bone-to-bone contact and
provide a smooth articulating surface is the ARTICULAR DISC (MENISCUS).
200. The ARTICULAR DISC is surrounded and protected by the FIBROUS C.T. JOINT
CAPSULE.
201. The ARTICULAR DISC is the fibrous C.T. between the condyle head and glenoid fossa to
allow ROTATION and TRANSLATION of the mandible.
202. The bioconcave-shaped ARTICULAR DISC of the TMJ is AVASCULAR and NON-
INNERVATED.
203. SPACES located above and below the TMJ’s fibrous disk are SYNOVIAL CAVITIES.
204. The main function of SYNOVIAL FLUID is TMJ LUBRICATION and NUTRITION.
205. TEMPEROMANDIBULAR, STYLOMANDIBULAR, and SPHENOMANDIBULAR are the

TMJ LIGAMENTS.
206. TEMPEROMANDIBULAR LIGAMENT provides lateral reinforcement for the capsule &
PREVENTS POSTERIOR & INFERIOR DISPLACEMENT OF THE CONDYLE.
207. STYLOMANDIBULAR LIGAMENT separates the PAROTID & SUBMANDIBULAR

salivary glands
208. CLICKING and POPPING when opening is due to DISK DISPLACEMENT WITH
REDUCTION.
209. SOUNDLESS, PAINFUL, and LIMITED OPENING (< 30mm) is due to DISK
DISPLACEMENT WITHOUT REDUCTION.
210. SUBLUXATION (slipping of the condyle from its socket) occurs when the condyle head
moves too far ANTERIORLY on ARTICULAR EMINENCE.
211. The best diagnostic imaging test to examine DISK POSITION and DISK FUNCTION is
MAGNETIC RESONANCE IMAGING (MRI).
212. Approximately 85% of TMJ and orofacial pain cases are MUSCLE-RELATED. Thus, non-
surgical, minimally invasive TMJ and orofacial pain trigger-point muscle injections with
botulinum toxin (Botox) are highly effective to treat facial esthetics, TMJ/orofacial pain,
and bruxism. BOTH TRUE.
18
EMBRYOLOGY AND HISTOLOGY

213. MECKEL’S CARTILAGE forms from the MANDIBULAR PROCESS and forms the
cartilaginous bar of the MANDIBULAR ARCH (FIRST BRANCHIAL ARCH).
214. Formation of the MANDIBLE and MAXILLA occurs by INTERMEMBRANOUS

OSSIFICATION.
215. The thin multi-layered epithelium that covers enamel and forms the JUNCTIONAL
EPITHELIUM after tooth eruption is the REDUCED ENAMEL EPITHELIUM (REE).
216. The REDUCED ENAMEL EPITHELIUM (REE) is derived from AMELOBLASTS,

STRATUM INTERMEDIUM, STELLATE RETICULUM, and OUTER ENAMEL
EPITHELIUM.
217. The FIRST layer of DENTIN formed that lies closest to the DEJ, contains KORFF’S
FIBERS, and makes up the majority of the tooth is MANTLE DENTIN.
218. Prematurely erupted primary teeth devoid of enamel defects that are present at birth and
are typically retained are NATAL TEETH.
219. On MULTI-ROOTED TEETH, DENTIN FORMATION is FASTEST at the PULP CHAMBER

FLOOR and ROOF.
220. Dentin formed by the gradual, but continuous deposition of odontoblasts AFTER ROOT
FORMATION is complete and is continuous with primary dentin is SECONDARY DENTIN.
221. DENTIN that forms as a defense mechanism from a pre-existing odontoblast due to
external insult like CARIES or iatrogenic drilling is TERTIARY DENTIN.
222. Formation of the DENTINAL TUBULE WALLS consist of PERITUBULAR DENTIN.
223. Glassy, translucent dentin that increases with age, and prolongs pulp vitality due to its
occlusion with calcific material in the root’s apical third and midway between the DEJ and
pulp surface is SCLEROTIC DENTIN.
224. The most common form of DENTINOGENESIS IMPERFECTA (DI) that is not associated
with Osteogenesis Imperfecta and is known as hereditary opalescent dentin is DI TYPE II.
225. The composition of DENTIN is 35% ORGANIC and 65% INORGANIC. Most of the organic
substance of dentin is TYPE I COLLAGEN.
226. DENTIN’s organic material consists of COLLAGEN FIBRILS and GROUND

SUBSTANCE, and its inorganic material is HYDROXYAPATITE CRYSTALS.
227. The HARDEST (MOST HIGHLY MINERALIZED) dentin is INTRATUBULAR

(PERITUBULAR) DENTIN.
19
228. The dentin formed AFTER the apical foramen is closed in response to stimuli produced
by carious that causes gradual narrowing of the pulp chamber and canals over time is
SECONDARY DENTIN.
229. The MAIN component of ENAMEL responsible for enamel’s hardness is INORGANIC
MATTER.
230. The direction of ENAMEL RODS in the CERVICAL THIRD of permenant teeth is in the
GINGIVAL DIRECTION.
231. The HARDEST AND MOST MINERALIZED TISSUE in the body due to its 95% inorganic
composition is ENAMEL.
232. The rate of dentin deposition is FASTER in the coronal portion of the tooth, and SLOWER
in the radicular portion.
233. Each DENTINAL TUBULE contains the odontoblast cell process called TOMES’ FIBERS.
234. DENTIN, PULP, and CEMENTUM are derived from MESODERM.
235. PULP and DENTIN and are formed from the inner and outer cells of the DENTAL PAPILLA
respectively.
236. PULP FUNCTIONS are NUTRITIVE, SENSORY, PROTECTIVE, and FORMATIVE.

However, the pulps PRIMARY function is to FORM DENTIN FROM ODONTOBLASTS.
237. Pulpal tissue projections in the pulp chamber roof that correspond to the prominence of
crown cusps or lobes are PULP HORNS.
238. A single canal lies between the pulp chamber and root apex in a TYPE 1 canal
configuration, while two separate canals exist the pulp chamber floor and unite to form
one canal with a single apex in a TYPE II canal configuration. BOTH TRUE.
239. Two separate canals leave the pulp chamber floor, remain separated, and form two
apices with a TYPE III canal configuration. One canal exists the pulp chamber floor,
bifurcates into two distinct canals to form two apices in a TYPE IV canal configuration.
240. The SOFTEST (LEAST MINERALIZED) dental tissue is CEMENTUM.
241. The enamel organ location responsible for ROOT FORMATION that gives rise to
HERTWIG’S EPITHELIAL ROOT SHEATH is the CERVICAL LOOP.
242. A round, solidary, and smooth calcified remnant of HERTWIG’S EPITHELIAL ROOT
SHEATH that is visible radiographically in the molar furcation or at the CEJ resulting in
periodontal pocket formation and inflammation, but cannot be dislodged with SRP, is an
ENAMEL PEARL.
243. ODONTOGENESIS STAGES in sequence are INITIATION, BUD, CAP, BELL, &
MATURATION.
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244. The proliferative stage of odontogenesis that occurs between weeks 9-10 of tooth
development during which time the ENAMEL ORGAN DEVELOPS from the dental lamina
is the CAP STAGE.
245. The composition of CEMENTUM is 50% INORGANIC (hydroxyapatite), 40% ORGANIC

(collagen and protein), and 10% WATER.
246. The proportions of inorganic HYDROXYAPATITE in ENAMEL (92%), DENTIN (75%), and
CEMENTUM (45%).
247. CEMENTUM is THICKEST at the ROOT’S APICAL THIRD and THINNEST at the
CORONAL THIRD.
248. The root’s coronal 2/3 is comprised of ACELLULAR CEMENTUM and its apical 1/3 and
furcation are comprised of CELLULAR CEMENTUM.
249. The cells responsible for producing DENTIN are ODONTOBLASTS.
250. The epithelial cells responsible for producing ENAMEL are AMELOBLASTS that develop
from the INNER ENAMEL EPITHELIUM.
251. The MOST COMMON tooth development and mineralization abnormality caused by a
disturbance in AMELOBLASTS during enamel matrix formation due to trauma, localized
infection, or excessive systemic fluoride ingestion is ENAMEL HYPOPLASIA.
252. A person’s natural tooth color is determined primarily by the THICKNESS OF ENAMEL and
UNDERLYING DENTIN COLOR. Depending on the enamel thickness, teeth may appear
lighter or darker.
253. The structural boundary that develops from the basement membrane and separates the
INNER ENAMEL EPITHELIUM from the DENTAL PAPILLA is the DENTINOENAMEL
JUNCTION (DEJ).
254. The DEJ occurs at the JUNCTION of the DENTAL PAPILLA and INNER ENAMEL
EPITHELIUM.
255. DENTAL PAPILLA CELLS contact the INNER ENAMEL EPITHELIUM.
256. The primary purpose of the DENTINOENAMEL JUNCTION (DEJ) is to prevent the
propagation of cracks from enamel into dentin.
257. Wavy lines on the tooth’s outer surface that result from normal ENAMEL APPOSITION are
called PERIKYMATA.
258. The incremental growth rings or bands that run obliquely from the DEJ to the enamel surface
due to mineralization are called STRIAE OF RETZIUS.
259. The average distance between STRIAE OF RETZIUS is 20-80µm.
21
260. Facial and oral development begins at WEEK 3 with the formation of the STOMODEUM
(the depression lined by ectoderm that lies between the brain and pericardium in an embryo
that forms the primitive MOUTH).
261. ENAMEL formation originates from ECTODERM.
262. An organ or tissue at its EARLIEST RECOGNIZABLE STAGE during prenatal development
is the PRIMORDIUM.
263. TONGUE DEVELOPMENT occurs during the 4th-8th week as a triangular swelling.
264. Branchial arches 1-4, bilateral lingual buds, tuberculum impar, and copula form the
TONGUE.
265. The FIRST PART OF THE FACE to form in the embryo is the MANDIBLE.
266. FACIAL DEVELOPMENT is complete by the 12th WEEK.
267. A relatively rare, autosomal dominant craniofacial developmental disorder caused by

abnormal development of the FIRST and SECOND branchial arches resulting in a retruded
mandible, narrow face, and hypoplasia of the mandibular condyle and zygoma is
TREACHER COLLINS SYNDROME (Mandibulofacial Dysostosis).
268. The TRIGEMINAL NERVE is the most critical cranial nerve to facial or oral structures and
is derived from the 1st BRANCHIAL ARCH.
269. An autosomal dominant craniofacial disorder caused by a fibroblast growth factor 2 mutation
(FGF2) resulting in maxillary hypoplasia, shallow orbits, and crowded maxillary teeth in
posterior crossbite is CROUZON SYNDROME (Craniofacial Dysostosis).
270. MOST ABUNDANT CELLS in CONNECTIVE TISSUE are FIBROBLASTS &

MACROPHAGES.
271. The MOST ABUNDANT CARTILAGE IN BODY that covers the articular surfaces of all
synovial joints is HYALINE CARTILAGE.
272. APPOSITIONAL and INTERSTITIAL processes are responsible for CARTILAGE

FORMATION.
273. ALL ORAL MUCOSA is STRATIFIED SQUAMOUS EPITHELIUM regardless if it is

keratinized or non-keratinized.
274. The HARD PALATE and ATTACHED GINGIVA are KERATINIZED EPITHELIUM.
275. The junctional and crevicular epitheliums, interdental papilla, marginal gingiva, soft palate,
buccal mucosa, and alveolar mucosa are all NON-KERATINIZED.
276. The JUNCTIONAL EPITHELIUM contains HEMIDESMOMES & BASAL LAMINA and is
derived from the REDUCED ENAMEL EPITHELIUM during tooth development.
22
277. TERMINAL PORTIONS of the PDL principal collage fibers EMBEDDED in CEMENTUM
and ALVEOLAR BONE are SHARPEY’S FIBERS.
278. CEMENTUM contains SHARPEY’S FIBERS that run perpendicular to its surface and
COLLAGEN FIBERS that run parallel to the its surface.
279. The MAIN FUNCTION of CEMENTUM is to ATTACH & ANCHOR THE PDL PRINCIPAL
FIBERS TO THE ROOT from the surrounding alveolar bone.
280. The non-keratinized STRATIFIED SQUAMOUS EPITHELIUM that FORMS THE

GINGIVAL SULCUS BASE is the JUNCTIONAL EPITHELIUM.
281. JUNCTIONAL EPITHELIUM is SHORTER at the POCKET BASE than at the SULCUS
BASE.
282. The MOST ABUNDANT cells in the PERIODONTAL LIGAMENT (PDL) responsible for
collagen synthesis are FIBROBLASTS.
283. The PDL is composed primarily of TYPE 1 COLLAGEN FIBERS.
284. The SHAPE of the PERIODONTAL LIGAMENT most closely resembles an HOUR-GLASS.
285. The MOST NUMEROUS PDL fibers located on the root’s middle third that provide the
PRIMARY tooth support during mastication and reduce forceful impaction into the alveolus
are the OBLIQUE FIBERS.
23
DENTAL ANATOMY AND OCCLUSION
286. GINGIVAL FIBERS attach tooth CEMENTUM to GINGIVA, while PDL FIBERS attach tooth
CEMENTUM to BONE.
287. The PDL is 0.2mm wide, but DECREASES in THICKNESS to 0.1mm in older adults due
to the deposition of CEMENTUM and BONE.
288. A permenant tooth’s CERVICAL LINE has the GREATEST CURVATURE DEPTH on the
MESIAL.
289. The GINGIVAL FIBERS (not PDL fibers) that extend inter-proximally (tooth-to-tooth) over
the alveolar crest of bone and are embedded in the CEMENTUM of adjacent teeth are
TRANSSEPETAL FIBERS.
290. The CREST of interdental bone should typically FOLLOW A PARALLEL LINE BETWEEN
ADJACENT CEMENTOENAMEL JUNCTIONS (CEJs).
291. The MOST NUMEROUS PDL fibers located in the root’s MIDDLE THIRD that run from
cementum OBLIQUELY to insert into bone CORONALLY are OBLIQUE FIBERS.
292. The MAIN function of OBLIQUE FIBERS is to provide tooth support during function and
reduce and resist INSTRUSIVE and ROTATIONAL FORCES into the alveolus.
293. The two-dimensional 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 is the CURVE OF
SPEE.
294. The MEDIOLATERAL U-SHAPED CURVE of the occlusal plane of maxillary and
mandibular posterior teeth is the CURVE OF WILSON.
295. The HORIZONTAL overlap or protrusion of the maxillary anteriors, common in Class II,
division I malocclusion is OVERJET.
296. Average OVERJET is 2-4 mm. Think of a jet airplane flying across the sky.
297. A patient whose mandibular incisors lie ANTERIOR to the maxillary incisors best
describes REVERSE OVERJET.
298. The VERTICAL overlap of maxillary anteriors over mandibular anteriors common in Class
II, division II malocclusion is OVERBITE. Ex: Chewing up and down in a vertical motion.
299. A RETRUDED MANDIBLE with FLARING OF ALL MAXILLARY ANTERIORS is

characteristic of CLASS II, DIVISION I MALOCCLUSION.
300. A skeletal malocclusion due to its RETROGNATHIC FACIAL PROFILE positioning the
maxillary first molar’s MB cusp tip to lie MESIAL to the MB groove of the mandibular first
molar is a CLASS II MALOCCLUSION.
24
301. A skeletal malocclusion due to its PROGNATHIC FACIAL PROFILE where the mandibular
teeth are positioned mesial to the maxillary teeth and anterior may be in crossbite or edge-
to-edge is a CLASS III MALOCCLUSION.
302. A RETRUDED MANDIBLE with FLARING AND RETRUSION OF SOME MAXILLARY

ANTERIORS best describes a CLASS II, DIVISION II MALOCCLUSION.
303. The maxillary first molar MB CUSP is directly above and aligns with the MB GROOVE
of the mandibular first molar in a CLASS I OCCLUSION.
304. Lateral misalignment of the arches resulting in the BUCCAL positioning of the mandibular
molars relative to the maxillary molars is POSTERIOR CROSSBITE.
305. A WEDGE-SHAPED DEFECT along the gingival margin caused by FLEXURE at the
CEMENTOENAMEL JUNTION (CEJ) during biting, chewing, or grinding is ABFRACTION.
306. The visible or palpable movement or VIBRATION of teeth (especially incisors) during
normal occlusal contact/forces is FREMITUS.
307. Tooth movement caused by occlusal forces is FREMITUS.
308. The common CRACKLING sound in the TMJ caused by improper movement of the
articular disc and mandibular condyle is CREPITUS.
309. A widened PDL on radiographs, mobility, wear facets, fremitus, pain on percussion and/or
during occlusal contact, are all clinical signs of OCCLUSAL TRAUMA.
310. BALANCING SIDE INTERFERENCES (contact on the non-working side) are most
damaging to teeth and can induce joint pain, along with muscle and ligament damage on
the working side.
311. POSTERIOR OCCLUSAL INTERFERENCES are removed and by adjusting distal facing
maxillary posteriors and/or mesial facing mandibular teeth (DUML).
312. LATERAL AND VERTICAL INTERFERENCES of CR to MI are reduced by adjusting the

buccal inclines of maxillary posteriors and lingual inclines of mandibular posteriors (BULL).
313. The multiple teeth contacts of mainly the premolars, but that may also include the canines
and/or laterals to support and allow POSTERIOR DISCLUSION, especially when the
canines are small or missing is GROUP FUNCTION.
314. Tooth contact before the mandible closes into centric relation (CR) is
DEFLECTIVE/PREMATURE CONTACT.
315. The tooth with the LONGEST CROWN in the oral cavity is the MANDIBULAR CANINE.
316. The roots of the MAXILLARY FIRST PREMOLAR and MANDIBULAR FIRST MOLAR
mesial root are both HOUR-GLASS SHAPED.
317. The tooth with the GREATEST MESIODISTAL LENGTH is the MANDIBULAR 1st MOLAR.
25
318. The maximum OPENING (DEPRESSING) distance of the mandible in the average adult is
50mm.
319. Centric occlusion is a TOOTH-GUIDED POSITION, while centric relation is a LIGAMENT-

GUIDED POSITION and is independent of tooth contact.
320. The most SUPERIOR POINT in POSSELT’S ENVELOPE OF MOTION is MICP

(MAXIMUM INTERCUSPATION).
321. BORDER MOVEMENTS of POSSELT’S ENVELOPE represent THE MOST EXTREME

POSITIONS THAT THE MANDIBLE CAN ASSUME.
322. The complete intercuspation of opposing teeth independent of condylar position is

MAXIMUM INTERCUSPATION (MICP).
323. The angle difference between the non-working condylar path and sagittal plane as viewed
in the horizontal plane that varies between 6-8 degrees is the BENNETT ANGLE.
324. The lateral shift of the mandible toward the WORKING CONDYLE that occurs during the
EARLIEST stage of lateral excursion is BENNETT MOVEMENT.
325. The side that the mandible is moving towards is the WORKING side, while the side
opposite the working side is the NON-WORKING (BALANCING) side.
326. During LEFT lateral mandibular excursion, the right side is the NON-WORKING side and
the right condyle is ORBITING.
327. The habitual or natural condyle position in the fossa when the teeth contact when the
mandible is in centric relation is CENTRIC OCCLUSION.
328. CENTRIC RELATION is the non-habitual tooth contact that occurs when the condyle head
is seated in its most ANTERIOR and SUPERIOR position within the glenoid fossa.
329. With respect to Posselt’s Envelope of mandibular motion, there is NO BORDER

MOVEMENT in the REST POSITION.
330. The SUPERIOR SURFACE of Posselt’s Envelop is determined by TOOTH CONTACTS.
331. The superior compartment of the articular disc permits only GLIDING MOVEMENTS,
while the inferior compartment permits both ROTATION and GLIDING movements.
332. When mandibular opening exceeds 20-25mm, mandibular TRANSLATION occurs.
333. As the mandible grows, it remodels SUPERIORLY and POSTERIORLY to lengthen the
mandibular arch to accommodate enlarging tooth buds and future erupting teeth.
334. Cusp ridges are separated from marginal ridges by fine enamel DEVELOPMENTAL
GROOVES.
26
335. The JOINING of two triangular ridges on POSTERIOR TEETH form TRANSVERSE
RIDGES.
336. INCISAL PROMINENCES found on newly erupted permenant anterior teeth that often wear
away with age, but may last a lifetime in patients with an anterior open bite, are called
MAMELONS.
337. An abnormal invagination of the enamel organ into the dental papilla that appears as a
“tooth within a tooth” on radiographs and most commonly seen in maxillary lateral incisors
is a DENS-IN-DENTE (DENS INVAGINATUS).
338. The MOST COMMON SUPERNUMERARY TOOTH located at the maxillary midline
between the central incisors is a MESIODENS.
339. A type of fusion common in maxillary 2nd and 3rd molars where two adjacent teeth are
connected only by CEMENTUM is CONCRESCENCE.
340. A common type of focal enamel hypoplasia due to trauma or infection in a deciduous tooth
that subsequently affects the bud development of the permenant tooth is TURNER’S
TOOTH.
341. BULL-SHAPED MOLARS with an elongated clinical crown, large pulp chamber, short roots
and an apically positioned furcation best describes TAURODONTISM.
342. Prominent inclusion cysts along the mid-palatine raphe that are simply remnants of trapped
epithelium along the raphe during fetal development are EPSTEIN’S PEARLS.
343. Keratin-filled inclusion cysts along the buccal and lingual aspects of the dental ridges in
newborns that are merely remnants of mucous gland tissue are BOHN’S NODULES.
344. CONGENITAL SYPHILLIS induced enamel hypoplasia characterized by DWARFED

FIRST MOLARS with cusps covered in globular enamel growths and pitted occlusal
surfaces are called MULBERRY MOLARS.
345. Small, widely spaced, SCREW-DRIVER SHAPED MAXILLARY INCISORS with deep
incisal notches due to an exposure to a congenital infection by TREPONEMA PALLIDUM
during tooth formation are HUTCHINSON INCISORS.
346. Factors that may contribute to tooth malposition include ANKYLOSIS, MESIODENS,
THUMB-SUCKING HABIT, and DELAYED EXFOLIATION of deciduous teeth.
347. The size difference between the primary posterior teeth and permenant canine and first and
second premolar is the LEEWAY SPACE.
348. The most common primary maxillary and mandibular second molar relationship is the
FLUSH TERMINAL PLANE.
349. The MESIAL STEP primary molar occlusion can develop into a CLASS I or CLASS III molar
relationship, while the DISTAL STEP primary molar occlusion develops into a CLASS II
molar occlusion. BOTH TRUE.
27
350. The most common clinical manifestation of a MICRODONTIA is the MAXILLARY PEG
LATERAL.
351. The PHYSIOLOGICAL/MECHANICAL WEARING AWAY of enamel and dentin due to

normal age-related tooth-to-tooth contact or excessive GRINDING (BRUXISM) or
CLENCHING teeth is ATTRITION.
352. The wearing away of tooth structure by mechanical means other than opposing teeth such
as a toothbrush and primary cause of gingival recession is ABRASION.
353. Loss of tooth structure from a chemical process such as HCL from bulimia or excessive
dietary acid in the absence of bacteria is EROSION.
354. Holding the teeth together and tightening the muscles of mastication is CLENCHING, while
moving the mandible while the teeth are together is GRINDING (BRUXISM).
355. While the PRIMARY cause of BRUXISM is STRESS and ANXIETY, other contributing
factors include SLEEP DISORDERS (sleep apnea), MALOCCLUSION, NEUROLOGICAL
CONDITIONS, SMOKING, and ALCOHOL consumption.
356. Sustained mandibular movement with increased muscle activity and contraction beyond
normal functions of speech, mastication, and chewing is PARAFUNCTIONAL ACTIVITY.
357. Parafunctional activities include CLENCHING, GRINDING, and ONYCHOPHAGIA (nail

biting).
358. GINGIVA + PDL + CEMENTUM + ALVEOLAR BONE and often the JUNCTIONAL
EPITHELIUM are collectively called the PERIODONTIUM.
359. The dense C.T. that lies beneath the masticatory mucosa and attaches directly to
periosteum is the LAMINA PROPRIA.
360. The layer of the lamina propria that forms FINGER-LIKE EXTENSIONS in the
depressions delineated by the rete ridges is the PAPILLARY LAYER.
361. Specialized rivet-like structures on the inner basal surface of keratinocytes that attach one
cell to the basement membrane and extracellular matrix to promote tissue integrity and
strength are HEMIDESMOSOMES.
362. DENTIN and PULP arise from the DENTAL PAPILLA.
363. The enamel organ, dental papilla, and dental follicle form the TOOTH GERM.
364. Mineralized bacterial plaque that may be supragingival or subgingival and form on all tooth
surfaces and dental prosthesis is CALCULUS.
365. The calcification of plaque begins within 24 hours.
366. Characteristics of SUBGINGIVAL CALCULUS include dark brown to greenish black

appearance, located below the crest of marginal gingiva, difficult to remove from the root
surface, and best identified via a tactile exam (explorer).
28
367. Highly calcified deposits that appear as radiopaque projections into the interdental space
on bitewing or periapical radiographs is INTERPROXIMAL CALCULUS.
368. The primary crystalline form that comprises CALCULUS is HYDROXYAPATITE.
369. The most abundant INORGANIC compound found in SUPRAGINGIVAL CALCULUS is

75% CALCIUM PHOSPHATE.
370. The HARDEST (MOST HIGHLY MINERALIZED) dentin is INTRATUBULAR

(PERITUBULAR) DENTIN.
371. The dentin formed AFTER the apical foramen is closed in response to any irritating
stimuli causing gradual narrowing of the pulp chamber and canals over time is
SECONDARY DENTIN (REPARATIVE).
372. Dentin produced on the surface or pre-existing dentin of the pulp chamber after
dentinogenesis is complete is REPARATIVE DENTIN.
373. The MAIN component of ENAMEL responsible for enamel’s hardness is INORGANIC
MATTER.
374. The HARDEST AND MOST MINERALIZED TISSUE in the body due to its 95% inorganic
composition is ENAMEL.
375. The rate of dentin deposition is FASTER in the coronal portion of the tooth, and SLOWER
in the radicular portion.
376. Each DENTINAL TUBULE contains the odontoblast cell process called TOMES’ FIBERS.
377. DENTIN, PULP, and CEMENTUM are derived from MESODERM.
378. PULP and DENTIN and are formed from the inner and outer cells of the DENTAL PAPILLA
respectively.
379. PULP FUNCTIONS are NUTRITIVE, SENSORY, PROTECTIVE, and FORMATIVE,

although its PRIMARY function is to FORM DENTIN FROM ODONTOBLASTS.
380. The removal of tooth structure by odontoclasts from the pulpal side of the tooth is
INTERNAL RESORPTION.
381. Natural changes in structure and function as the dentin-pulp complex ages include
increased presence of pulp stones, decreased volume of pulpal tissue, and increased dentin
deposition.
382. The SOFTEST (LEAST MINERALIZED) dental tissue is CEMENTUM.
383. The enamel organ location responsible for ROOT FORMATION that gives rise to
HERTWIG’S EPITHELIAL ROOT SHEATH is the CERVICAL LOOP.
29
384. A round, solidary, and smooth calcified remnant of HERTWIG’S EPITHELIAL ROOT
SHEATH that is visible radiographically in the molar furcation or at the CEJ resulting in
periodontal pocket formation and inflammation, but cannot be dislodged with SRP, is an
ENAMEL PEARL.
385. ODONTOGENESIS STAGES in sequence are INITIATION, BUD, CAP, BELL, and
MATURATION.
386. CALCIFICATION is initially detected during the LATE BELL STAGE of odontogenesis.
387. The bud organizes to form the three-layered ENAMEL ORGAN formed by IEE, OEE, and
stellate reticulum during the CAP STAGE of odontogenesis.
388. The proliferative stage of odontogenesis that occurs between weeks 9-10 of tooth
development during which time the ENAMEL ORGAN DEVELOPS from the dental lamina
is the CAP STAGE.
389. The appearance of the DENTAL LAMINA occurs during the 6th-7th week in utero.
390. The composition of CEMENTUM is 50% INORGANIC (hydroxyapatite), 40% ORGANIC

(collagen and protein), and 10% WATER.
391. CEMENTUM is THICKEST at the ROOT’S APICAL THIRD and THINNEST at the
CORONAL THIRD.
392. The root’s coronal 2/3 is comprised of ACELLULAR CEMENTUM and its apical 1/3 and
furcation are comprised of CELLULAR CEMENTUM.
393. FURCATION INVOLVEMENT is classified mainly by HORIZONTAL bone destruction that

follows the inflammatory process of periodontal disease and etiology of progressive clinical
attachment loss by bacterial plaque. TRUE STATEMENT.
394. Cementum that contains CEMENTOCYTES in their lacunae is CELLULAR CEMENTUM.
395. An OSTEOCYTE-LIKE cell with numerous processes that is trapped inside a lacuna in
tooth cementum is a CEMENTOCYTE.
396. A non-neoplastic condition characterized by excess cementum deposition on the root

surfaces of one or more teeth (especially premolars) is HYPERCEMENTOSIS.
397. Characteristics of HYPERCEMENTOSIS include increased frequency with age, thickening

or blunting of the root surface radiographically, and most commonly affects root APICES.
398. The cells responsible for producing DENTIN are ODONTOBLASTS.
399. The epithelial cells responsible for producing ENAMEL are AMELOBLASTS that develop
from the INNER ENAMEL EPITHELIUM.
400. The MOST COMMON tooth development and mineralization abnormality caused by a
disturbance in AMELOBLASTS during enamel matrix formation due to trauma, localized
infection, or excessive systemic fluoride ingestion is ENAMEL HYPOPLASIA.
30
401. The structural boundary that develops from the basement membrane and separates the
INNER ENAMEL EPITHELIUM from the DENTAL PAPILLA is the DENTINOENAMEL
JUNCTION (DEJ).
402. The primary purpose of the DENTINOENAMEL JUNCTION (DEJ) is to prevent the
propagation of cracks from enamel into dentin.
403. Wavy lines on the tooth’s outer surface that result from normal ENAMEL APPOSITION are
called PERIKYMATA.
404. The incremental growth rings or bands that run obliquely from the DEJ to the enamel surface
due to mineralization are called STRIAE OF RETZIUS.
405. The distance established by the junctional epithelium and C.T. attachment to the root
surface (the height of the deepest point of the SULCUS BASE and ALVEOLAR CREST
OF BONE is the BIOLOGIC WIDTH.
406. VIOLATING BIOLOGIC WIDTH leads to pain, gingival inflammation, and alveolar bone
loss. Thus, the all restoration margins must be at least 3 mm from the ALVEOLAR CREST
OF BONE.
407. Oral structure that demarcates the ATTACHED GINGIVA from ALVEOLAR MUCOSA,
separating keratinized and non-keratinized tissue is the MUCOGINGIVAL JUNCTION.
408. CLINICAL ATTACHMENT LOSS (CAL) is the distance from CEJ to the POCKET
(SULCUS) BASE + GINGIVAL RECESSION.
409. An indication that gingivitis has progressed to periodontitis is the presence of CLINICAL
ATTACHMENT LOSS.
410. Periodontitis is ALWAYS PRECEDED by gingivitis, but gingivitis does NOT always
progress to periodontitis.
411. PERIODONTITIS is marked by APICAL MIGRATION of the JUNCTIONAL EPITHELIUM

from the CEJ, loss of C.T. attachment and PDL, and bone destruction.
412. The FUSION OF ALVEOLAR BONE AND ROOT due to infection or trauma to the
PERIODONTAL LIGAMENT (PDL) is ANKYLOSIS.
413. A joint that binds the tooth root to the surrounding dental alveoli sockets in the maxilla
and mandible is GOMPHOSIS (Dentoalveolar Syndesmosis).
414. PDL fibers FOUND ONLY ON MULTI-ROOTED TEETH are INTERRADICULAR FIBERS.
415. When the mandible moves from CENTRIC OCCLUSION (CO) to EDGE-TO-EDGE, the
mandibular condyles move FORWARD (ANTERIOR) and DOWNWARD (INFERIOR).
416. The percentage of the population that has a mandibular shift from initial tooth contact in
centric relation (CR) moving to MI is 90%.
31
417. The NON-WORKING condyle moves DOWNWARD, FORWARD, and MEDIAL.
418. ANTERIOR GUIDANCE plays a MAJOR ROLE in DISCLUDING POSTERIOR TEETH

during LATERO-PROTRUSIVE mandibular movement.
419. The optimal tooth relationship for POSTERIOR DISCULSION during lateral excursions is
CANINE GUIDANCE.
420. During NON-MASTICATORY SWALLOWING the teeth contact in the INTERCUSPAL

POSITION (CENTRIC OCCLUSION).
421. INTERCUSPAL POSITION (CENTRIC OCCLUSION) is exclusively determined by TOOTH

CONTACT.
422. When chewing food the condyle’s NON-WORKING side moves in an INFERIOR,
ANTERIOR, MEDIAL direction.
423. NON-WORKING SIDE inward mandibular movement relative to the maxilla causing
cuspal slope interferences between the facial incline of maxillary palatal cusps and lingual
incline of mandibular buccal cusps is MEDIOTRUSIVE MOVEMENT.
424. ELEVATION of the mandible from the POSTURAL POSITION to CENTRIC OCCLUSION
occurs via the ANTERIOR FIBERS of TEMPORALIS.
425. The MUSCLE-GUIDED physiological rest position located 2-4mm below the intercuspal
position (CO) is the POSTURAL POSITION.
426. MANDIBULAR BORDER POSITIONS are located on the EXTERIOR (OUTSIDE) of

POSSELT’S ENVELOPE OF MOTION.
427. The arrangement of teeth viewed from the OCCLUSAL plane is typically PARABOLIC (U-
SHAPED).
428. From an occlusal plane view, the mandibular premolars and molars are typically aligned in
a STRAIGHT LINE.
429. In posterior teeth, the number of DEVELOPMENTAL LOBES typically coincides with the
number of CUSPS.
430. THIRD MOLARS may develop from 4 or 5 DEVELOPMENTAL LOBES.
431. Permenant FIRST MOLARS and MANDIBULAR SECOND PREMOLARS develop from 5
LOBES; all other teeth develop from 4 LOBES.
432. Permenant FIRST MOLARS begin to calcify at birth and they are the first permenant
tooth to erupt in the oral cavity.
433. All teeth have DISTAL marginal ridges.
434. In the PERMENANT DENTITION, ALL TWELVE ANTERIOR TEETH have a CINGULUM.
32
435. Cusp ridges are separated from marginal ridges by DEVELOPMENTAL GROOVES.
436. The UNION of facial and lingual TRIANGULAR RIDGES forms a TRANSVERSE RIDGE.
437. The occlusal table of a permenant POSTERIOR TOOTH is RECTANGULAR-SHAPED

and occupies approximately 60% of the total BUCCAL-LINGUAL dimension.
438. The FACIAL/BUCCAL HEIGHT OF CONTOUR for ALL TEETH is located in the
CERVICAL THIRD (except for mandibular molars).
439. The LINGUAL/PALATAL HEIGHT OF CONTOUR for ALL ANTERIOR TEETH is located
in the CERVICAL THIRD.
440. The LINGUAL/PALATAL HEIGHT OF CONTOUR for ALL POSTERIOR TEETH is located
in the MIDDLE THIRD (except mandibular 2nd premolar, which is located in the occlusal
third).
441. All permenant incisors (except mandibular centrals) have their DISTAL CONTACT
MORE APICAL than their mesial contact with the adjacent tooth.
MAXILLARY CANINE
442. The permenant ANTERIOR tooth with the GREATEST CERVICAL PROMINENCE and
GREATEST FACIO-LINGUAL CROWTH WIDTH is the MAXILLARY CANINE.
443. The permenant tooth with the GREATEST OVERALL LENGTH and LONGEST ROOT (not
crown) in the oral cavity is the MAXILLARY CANINE.
444. The maxillary canine has a DISTAL BULGE and greatest F-L dimension of all anteriors.
445. The maxillary canine is the tooth most likely to have a SINGLE ROOT.
446. The clinical crown facial and palatal outline of the maxillary canine is PENTAGONAL.
33
447. The maxillary canine CUSP TIP is slightly FACIAL to the lingual axis, thus from an
incisal view, the lingual aspect is more visible. The cusp tip extends from the middle
facial lobe.
448. From the incisal view, the maxillary canine cusp tip is positioned facial and mesial to the
crown’s center.
449. From the mesial view, a line bisecting the maxillary canine’s root and apex passes
LINGUAL to its cusp tip.
450. From the mesial view, the maxillary canine’s pulpal outline resembles a FISH.
451. The prominent MIDDLE LOBE of the maxillary canine includes its cusp tip.
452. From a proximal view the MAXILLARY CANINE is positioned closest to the VERTICAL
AXIS.
453. The MAXILLARY CANINE has a CENTERED DISTAL CONTACT and is the only tooth
that can potentially contact both an anterior and posterior tooth.
454. The maxillary canine’s mesial and distal contacts are ASYMMETRIC due to its DISTAL
BULDGE.
455. The maxillary tooth LEAST LIKELY to be extracted is the maxillary canine.
456. The incisal morphology of the maxillary canine has a prominent lingual ridge that splits the
lingual fossa into mesial and distal fossae.
457. The maxillary canine’s lingual anatomy typically contains a lingual ridge, cingulum,
mesial and distal fossae and marginal ridges. It does NOT have developmental grooves
or a lingual cusp.
458. The maxillary canine’s cingulum is MORE PROMINENT than the mandibular canine
cingulum.
459. The maxillary canine crown has a PROMINENT FACIAL RIDGE.
460. The maxillary canine’s HEIGHT OF CONTOUR is typically located at the CERVICAL
THIRD on the crown’s facial and palatal surfaces.
461. In MICP, the maxillary canine can contact both anterior and posterior antagonists.
462. The maxillary canine’s MESIAL CONTACT is located at the junction of the crown’s
middle and incisal third, and its DISTAL CONTACT is located at the crown’s MIDDLE
THIRD. *Note: the contacts of all other permenant anterior teeth are incisal to the crown’s
middle third, except the maxillary canine’s distal contact which is located in the middle
third.
463. The maxillary canine is the only permanent anterior tooth with at least one interproximal
contact (distal) located in the crown’s MIDDLE third incisogingivally.
34
464. The largest incisal embrasure is between the maxillary canine and maxillary lateral
incisor.
465. Compared to the mandibular canine, the maxillary canine is WIDER M-D, has a short clinical
crown, more pronounced cingulum, and its cusp tip is centered over the root from the facial
view.
466. The maxillary canine has the LARGEST MESIODISTAL ROOT DIMENSION of any tooth.
467. The mesial slope of the maxillary canine’s cusp is shorter than the cusp’s distal slope.
MANDIBULAR CANINE
468. The tooth with the LONGEST CROWN DIMENSION is the MANDIBULAR CANINE.
469. Compared to the maxillary canine, the mandibular canine has a LESS PROMINENT
CINGULUM and is NARROWER MESIO-DISTALLY.
470. The anterior tooth that most often has a BIFURCATED ROOT is the MANDIBULAR
CANINE.
471. In cervical cross-section, the mandibular canine root is an IRREGULAR OVAL and is
FLAT mesiodistally.
472. From crown tip to root apex, the mandibular canine is C-SHAPED.
473. In cross-section, the mandibular canine CEJ is OVOID and wider M-D from the labial
aspect.
474. The mandibular tooth with the LONGEST ROOT is the MANDIBULAR CANINE.
475. The mandibular contact has GREATER INCISAL CONTACT than the maxillary canine.
476. The mandibular canine’s MESIAL contact is at the INCISAL 1/3 and the DISTAL contact is
at crown’s MIDDLE 1/3 cervico-incisally.
477. The mandibular canine’s facial surface is CONVEX from its incisal to apical end.
478. The incisal edge of the mandibular canine is LINGUAL to its long axis, while the incisal
edge of the maxillary canine is PALATAL to its long axis.
479. The mandibular canine has the STRAIGHTEST MESIAL ALIGNMENT of crown-to-root of
any tooth.
480. From the facial, is mesial outline (from the contact area to root apex) is STRAIGHT.
481. The mandibular canine crown’s MESIAL SURFACE is nearly PARALLEL to it long axis.
482. The mandibular canine is the anterior tooth most likely to resist carious invasion.
35
483. Compared to the maxillary canine, the mandibular canine has a LESS-PRONOUNCED
CINGULUM, straighter mesial border viewed facially, more incisal contacts, and a cusp tip
displaced lingually.
484. The mandibular canine’s lingual surface is SMOOTH and FLAT with a poorly developed
marginal ridge and cingulum.
485. The crown measurement is greater F-L than M-D.
486. The only teeth that have LABIAL RIDGES are the maxillary and mandibular canines.
487. ALL ANTERIOR TEETH AND PREMOLARS HAVE 4 LOBES except premolars with two
lingual cusps (which have 5 lobes).
MAXILLARY LATERAL INCISOR
488. The most common CONGENITALLY MISSING tooth and MICRODONTIA (peg-shaped)
is the MAXILLARY LATERAL INCISOR.
489. The tooth most likely to exhibit TALON CUSPS is the maxillary lateral incisor (lingual
surface).
490. Has the GREATEST VARIATION in crown size and form after third molars.
491. The tooth most likely to have a pronounced developmental lingual fossa (concavity) that
is susceptible to caries development is the MAXILLARY LATERAL INCISOR.
492. The lingual fossa of the maxillary lateral incisor occupies 2/3 of the crown’s lingual
surface and is TRIANGULAR-SHAPED.
493. The maxillary lateral incisor’s occlusal outline is OVAL and proximal outline is
TRIANGULAR.
494. The prominent cingulum of the maxillary lateral incisor is located in the crown’s CERVICAL
THIRD.
495. The maxillary lateral incisor has a prominent DISTOLINGUAL GROOVE that extends from
enamel onto cementum that may complicate root planing.
496. The maxillary lateral incisor has the most anomalies and well-developed lingual anatomy,
and has the only LINGUAL-GINGIVAL GROOVE in the dentition.
497. The maxillary lateral’s mesial contact is near the crown’s middle and incisal thirds, and
its distal contact is at the crown’s middle third. Its contact with the maxillary central incisor
is centered FL and its lingual embrasure is wider than the facial embrasure.
498. The maxillary lateral incisor’s root length is > the maxillary central incisor’s root length
cervicoapically.
36
499. From a proximal view of the mesial, the curvature of the maxillary lateral’s cervical line
(CEJ) points in the direction of the crown’s incisal ridge.
500. The MI and DI crown incisal angles of the maxillary lateral incisor are ROUNDED (not
sharp like the mandibular lateral incisor). The DI angle has the greatest convexity and less
sharp than the MI corner.
501. The largest incisal embrasure in both arches in formed by the MAXILLARY LATERAL
AND MAXILLARY CANINE.
502. The maxillary lateral’s canal shape can be ROUND, OVAL, or TRIANGULAR.
503. The presence of a PALATOGINGIVAL GROOVE may predispose the maxillary lateral and
maxillary central incisors to localized periodontal disease.
MANDIBULAR LATERAL INCISOR
504. The LARGEST EMBRASURE in the mandibular arch is located between the LATERAL
INCISOR and CANINE.
505. The mandibular lateral incisor often has one root with either one or two canals with the
same statistical frequency.
506. The mandibular lateral incisor ROOT is LARGER IN ALL DIMENSIONS compared to
the mandibular central incisor.
507. The MOST reliable criterion to distinguish between a permenant mandibular central
incisor and mandibular lateral incisor is the DIFFERENCE IN CROWN ROTATION ON THE
ROOT as the distal half of the mandibular lateral incisor’s crown appears twisted and curves
LINGUALLY and DISTALLY from an incisal view.
508. The mandibular lateral incisor’s crown TIPS SLIGHTLY DISTAL relative to its root with the
cingulum slightly off-center distally. The mandibular central incisor’s cingulum is in the
center of the lingual surface. BOTH TRUE.
509. From an incisal view, the incisal edge of the mandibular lateral incisor does not form a right
angle with a line bisecting the crown F-L. Rather, it takes an oblique course appearing
TWISTED around the root’s long axis.
510. The mesial and distal contacts of the mandibular lateral incisor are located in the crown’s
INCISAL THIRD with the distal contact slightly more cervical than the mesial contact.
37
MAXILLARY CENTRAL INCISOR

511. The maxillary central incisor ROOT is the only maxillary tooth at its cervix that is the same
thickness both M-D and F-L, making its canal cervix ROUND.
512. The maxillary central incisor has the most frequent root and canal morphology that has ONE
ROOT WITH ONE CANAL (just like the maxillary lateral).
513. The average inciso-cervical length of a maxillary central incisor is 10-11mm and 8-9mm
mesiodistally.
MANDIBULAR CENTRAL INCISOR
514. The smallest permenant tooth in the dentition that also forms the smallest incisal
embrasure in both arches is the mandibular central incisor.
515. The FIRST SUCCEDANEOUS tooth to ERUPT is the mandibular central incisor.
516. The mandibular central incisor is the SMALLEST permenant tooth in the dentition and
forms the SMALLEST INCISAL EMBRASURE of both arches.
517. The most difficult permenant tooth to distinguish between its mesioincisal and
distoincisal aspects because they are bilaterally symmetrical is the mandibular central
incisor.
518. From the facial aspect, the mesial and distal contacts of the mandibular central incisor
are INCISAL to the junction of the incisal and middle thirds (its mesial contact is in the
incisal third).
519. A mid-root cross-section of the mandibular central incisor reveals the pulp cavity is
FLATTENED mesiodistally.
38
MAXILLARY FIRST PREMOLAR
520. The maxillary first premolar is typically the LARGEST premolar.
521. The maxillary first premolar’s crown has a prominent mesial marginal ridge groove that
can inhibit adequate oral hygiene.
522. The maxillary first premolar and maxillary canine form the LARGEST OCCLUSAL
EMBRASURE of both arches.
523. The maxillary first premolar is the LARGEST of all premolars with a prominent buccal
ridge.
524. Maxillary first premolar is WIDER FACIALLY than lingually and the tooth has a F-L
convergence.
525. The occlusal outline shape is HEXAGONAL and is proximal outline shape is
TRAPEZOIDAL.
526. The only premolar with 2 ROOTS/2 CANALS, and a prominent mesial root concavity.
527. The root outline and pulp chamber are often KIDNEY-SHAPED and in mid-section the
root outline appears as a figure-eight with two canals.
528. The only tooth whose crown has a mesial cusp ridge higher than the distal cusp ridge.
529. The distinguishing feature to differentiate a maxillary right vs. maxillary left premolar is the
pronounced MESIAL DEVELOPMENTAL GROOVE.
530. From the palatal view, the maxillary first premolar has a SHORTER LINGUAL CUSP
than the maxillary second premolar. The maxillary second premolar buccal and lingual
cusps are the same LENGTH AND WIDTH. BOTH TRUE.
531. The most difficult surface on the maxillary first premolar to achieve close adaptation of the
matrix band when placing a class II restoration is the MESIAL SURFACE due to the
developmental cervical concavity.
39
532. The maxillary first premolar is the only premolar with a M-B cusp ridge LONGER than its D-
B cusp ridge.
MANDIBULAR FIRST PREMOLAR

533. The mandibular first premolar is the SMALLEST premolar.
534. The mandibular 1st premolar’s MESIAL marginal ridge is MORE CERVICAL than its distal
marginal ridge.
535. The mandibular 1st premolar is the only tooth with a mesial contact that is CERVICAL to
its distal contact.
536. The mandibular first premolar is developed from 4 LOBES.
537. The only tooth in the dentition with a developmental MESIOLINGUAL GROOVE is the
mandibular first premolar.
538. The occlusal outline of the mandibular first premolar is DIAMOND-SHAPED.
539. The mandibular first premolar has a small non-functioning lingual cusp, thus is MOST
similar in masticatory function to the mandibular canine.
MAXILLARY SECOND PREMOLAR
540. The maxillary second premolar has a short, central groove with many supplemental grooves
with a more “wrinkled” appearance.
541. The maxillary second premolar’s occlusal table is more OVOID and SYMMETRICAL than
the maxillary first premolar.
542. Shorter and smaller than the maxillary first premolar.
543. The maxillary second premolar has the HIGHEST crown-to-root ratio in the maxillary arch.
544. The crown outline form of a first or second maxillary premolar from the proximal view is
TRAPEZOIDAL.
40
MANDIBULAR SECOND PREMOLAR
545. The mandibular 2nd premolar (three-cusps) has mesial, distal, and lingual grooves on its
occlusal surface to form a Y-SHAPED groove pattern.
546. The mandibular 2nd premolar is typically developed from 5 LOBES (3 buccal + 2 lingual).
547. Mandibular 2nd premolar (two-cusps) has a single U-SHAPED central groove.
548. The mandibular 2nd premolar mesial and distal contacts are the SAME HEIGHT.
549. The crown form of a first or second mandibular premolar for a proximal view is
RHOMBOIDAL.
MAXILLARY FIRST MOLAR
550. CUSP OF CARABELLI is found on the PALATAL SURFACE OF MAXILLARY FIRST

MOLARS.
551. The LARGEST and LONGEST ROOT on the maxillary first molar is the PALATAL.
552. The LARGEST PERMENANT TOOTH that ALWAYS HAS 3 ROOTS with 3, 4, or 5
canals.
553. The only tooth BROADER LINGUALLY than buccally.
554. The maxillary first molar’s B-L width is greater than its M-D length.
41
555. The SHORTEST root on the maxillary first and second molar is the DISTOBUCCAL (DB).
556. From a lingual view, the maxillary first molar’s PALATAL ROOT lines up with the
midpoint of its MESIO-DISTAL (M-D) diameter.
557. The SMALLEST ROOT on the maxillary first molar is the DISTAL-BUCCAL (DB).
558. The OUTLINE FORM of the maxillary first molar from an occlusal view is RHOMBOIDAL.
559. From an occlusal outline, the maxillary first molar’s MF and DL angles are ACUTE
ANGLES, while the DF and ML angles are OBTUSE ANGLES.
560. The maxillary first molar’s crown has the GREATEST B-L diameter of ANY TOOTH due
to the cusp of Carabelli.
561. From the buccal aspect, the maxillary first molar’s PALATAL ROOT APEX is in line with its
buccal groove.
562. The maxillary first molar root is MOST LIKELY to penetrate through the maxillary sinus
floor during an extraction.
563. The maxillary first molar’s BUCCAL EMBRASURE is LARGER than its lingual embrasure
because the tooth tapers BUCCALLY.
564. LARGEST and LONGEST cusp on the maxillary first molar is the MESIOLINGUAL (ML)
cusp.
565. The maxillary first molar’s DISTOLINGUAL (DL) cusp is the only cusp located OUTSIDE
its molar cusp triangle.
566. The primary cusp triangle is formed by the MB, ML, and DB cusps, and the secondary
cusp triangle is formed by the DL cusp.
567. When a 4th pulp canal is present in the maxillary first molar, it is the MESIOBUCCAL (MB)
canal.
568. The distal boundary of the maxillary first molar’s central fossa is formed by its OBLIQUE
RIDGE.
569. The maxillary first molar is wider M-D towards the buccal then towards the palatal.
570. The DISTAL CONCAVITY of the maxillary first molar can make matrix band placement
difficult when placing restorative materials.
571. The oblique ridge center on a maxillary first molar is at the SAME HEIGHT as its marginal
ridge.
572. The maxillary first molar’s OBTUSE CORNERS of its oblique ridge coincide with direction
of the oblique ridge.
42
573. The maxillary first molars crown has a shorter DL groove than the maxillary 2nd molar.
574. The maxillary first molar’s oblique ridge connects the ML and DB cusps.
575. The maxillary first molar’s ML cusp occludes in the central fossa of mandibular molars.
576. The maxillary first molar is closest in size B-L than M-D to any maxillary posterior tooth.
577. The maxillary first molar’s MESIAL FURCATION is the closest to its cervical line while
its DISTAL FURCATION is farthest from the cervical line. Furcation Distance: M < B < D.
578. The maxillary first molar is mainly innervated by the POSTERIOR SUPERIOR ALVEOLAR
NERVE (PSA), with its MB root sometimes innervated by the MIDDLE SUPERIOR
ALVEOLAR NERVE.
43
MANDIBULAR FIRST MOLAR
579. The occlusal outline of the mandibular first molar is PENTAGONAL.
580. Mandibular first molar has the largest M-D diameter crown dimension of ALL TEETH and
largest B-L crown dimension of any other mandibular tooth.
581. The mandibular first molar has a “Y” occlusal groove or ancestral “Dryopithecus”
pattern.
582. The mandibular first molar has TWO ROOTS and THREE PULP CANALS (MB, ML, + D).
583. The mandibular first molar’s developmental groove between the DB cusp and D cusp is
closer to the DB cusp.
584. The mandibular first molar typically has 5 CUSPS (2 Buccal, 2 Lingual + 1 Distal).
585. The DISTAL CUSP RIDGE on a five-cusp mandibular first molar does NOT connect to
and does not help form a transverse ridge as its distal cusp ridge terminates at the distal
fossa.
586. The mandibular first molar’s SMALLEST cusp is the DISTAL cusp.
587. The mandibular first molar’s LARGEST cusp is the MESIOBUCCAL (MB) cusp.
588. The mandibular first molar’s cusp size ranked from largest to smallest: MB > DL > ML > DB
> D.
589. The mandibular first molar has the LONGEST ROOTS of any posterior tooth and
GREATEST ROOT SEPARATION of any tooth.
590. The LARGEST TOOTH in the mandibular arch is the MANDIBULAR FIRST MOLAR.
591. When the mandibular 1st molar’s MESIAL ROOT is cross-sectioned at its middle third, the
MESIAL root has the greatest F-L dimension of any root to provide room for the MB2
canal.
592. The mandibular 1st molar LINGUAL CUSPS are the ideal position and height to
accommodate WORKING MOVEMENT.
593. The PRIMARY MANDIBULAR FIRST MOLAR has a RHOMBOIDAL occlusal surface
and DOES NOT RESEMBLE ANY OTHER TOOTH. It has two distinct buccal cusps, large
mesial cusp, a groove between the ML and DL cusps, and prominent buccal curve at its
cervical third.
594. The presence of APICAL DELTAS (small, branching accessory canals) is highest in the
FIRST MOLAR’s DISTAL ROOT then its MESIAL ROOT.
44
595. LATERAL CANALS are most likely to present in the FURCATION of the FIRST MOLAR,
followed by the second molar furcation.
596. A TRANSVERSE ANASTOMOSIS is most commonly found in the FIRST MOLAR’s

MESIAL ROOT then its DISTAL ROOT.
MANDIBULAR SECOND MOLAR
597. The DISTOBUCCAL (DB) cusp of the mandibular 2nd molar occludes in the central fossa
of the maxillary molars.
598. The occlusal groove pattern of the mandibular 2nd molar is typically CRUCIFORM
(CROSS +).
599. The occlusal outline of the mandibular 2nd molar closely resembles a RECTANGLE.
600. The mandibular 2nd molars buccal and lingual grooves form RIGHT ANGLES with its central
groove.
601. The greatest BUCCOLINGUAL (BL) diameter of the mandibular 2nd molar occlusally is
the crown’s MESIAL THIRD (this characteristic distinguishes between extracted #18 and
#31).
602. The mandibular 2nd molar has FOUR CUSPS approximately EQUAL in size.
603. A newly erupted permenant mandibular 2nd molar is FOUR PULP HORNS.
604. The ROOTS of the mandibular 2nd molar are more DISTALLY INCLINED and LESS
DIVERGENT (closer together) than the mandibular 1st molar.
605. The mandibular 2nd molar’s crown in its proper position relative to the occlusal plane
inclines MESIALLY and LINGUALLY.
606. The ROOT APICES of the mandibular 2nd molar are located INFERIOR to the insertion of
the MYLOHYOID MUSCLE.
607. The mandibular 2nd molar is the only posterior and mandibular tooth WIDER M-D than B-
L.
608. The mandibular 2nd molar crown inclines MESIALLY and LINGUALLY due to its larger
mesial cusps.
609. The teeth most likely to have LATERAL CANALS are FIRST and SECOND MOLARS.
45
MAXILLARY SECOND MOLAR
610. The maxillary 2nd molar’s DISTOLINGUAL (DL) cusp is the only cusp outside its molar
cusp triangle.
611. The ROOTS of the maxillary 2nd molar have a GREATER DISTAL INCLINATION and are
LESS DIVERGENT than the maxillary 1st molar.
612. When the DISTOLINGUAL (DL) cusp is absent on a maxillary 2nd molar, the occlusal
outline is HEART-SHAPED by the remaining three cusps.
613. In cross-section, the CERVICAL OUTLINE form of the maxillary 2nd molar is
TRIANGULAR.
614. The pulp chamber shape of permenant maxillary molars is generally TRIANGULAR.
615. The maxillary second molar has 3 ROOTS (1 palatal + MB, DB). The LARGEST root is the
PALATAL and smallest root is the DB. (P > MB > DB).
616. The cross-sectional outline of the maxillary second molar at the cervical level is
TRIANGULAR.
617. The occlusal outline of a three-cusp maxillary second molar is HEART-SHAPED.
618. Cusp size from largest to smallest is (ML > MB> DB > DL).
619. The maxillary second molar’s 3 roots are as long as the maxillary first molar’s roots, are
closer together MD and BL, and curve more distally than the maxillary first molar’s roots.
46
620. Compared to the anatomy of the maxillary first molar crown, the maxillary 2nd molar crown
has a SHORTER DISTOLINGUAL AND BUCCAL GROOVES.
621. Compared to the anatomy of the maxillary first molar crown, the maxillary 2nd molar crown
has a SMALLER oblique ridge and MORE VARIED pit and groove occlusal pattern.
622. The maxillary 2nd molar does NOT have a Cusp of Carabelli.
623. The primary cusp triangle on ALL maxillary molars is formed by the ML, MB, and DB
cusps (not the DL cusp).
THIRD MOLARS
624. Maxillary 3rd molar often only has 3 CUSPS and a HEART-SHAPED occlusal outline due
to the absence of a DL cusp.
625. Maxillary 3rd molars are the permanent teeth with the MOST VARIABLE OCCLUSAL
ANATOMY.
626. Maxillary 3rd molar has the greatest variation in ROOT ALIGNMENT, TOOTH MASS, and
CROWN MOROPHOLOGY.
627. Maxillary 3rd molars have the greatest DISTAL ROOT INCLINATION of any tooth.
628. Maxillary 3rd molar is the permenant tooth most likely to show anomalies in RADICULAR
MORPHOLOGY.
629. Maxillary 3rd molars have only one antagonist tooth in intercuspation.
630. The most difficult third molar to extract is a DISTOANGULAR impaction.
631. The maxillary third molar is the SHORTEST permenant tooth.
632. The maxillary third molar and mandibular central incisor each occlude with only one tooth
on the opposing arch.
633. The HIGHEST risk of PARESTHESIA is associated with a third molar that is
MESIOANGULAR IMPACTED because the roots are in close proximity or “saddling” the
mandibular canal.
634. The greatest RISK associated with the PROPHYLACTIC EXTRACTION of THIRD
MOLARS in the absence of pathology or a specific problem is IATROGENIC INJURY.
47
PRIMARY (DECIDUOUS) TEETH
635. Permenant teeth in GIRLS erupt earlier and exfoliate before permenant teeth in boys.
636. ECTOPIC ERUPTION is most common in the mandibular anterior region where
succedaneous teeth erupt lingually relative to their primary precursors. Ectopic eruption of
a permenant first molar is more common in the maxillary arch. BOTH TRUE.
637. Root formation is completed approximately three years after eruption in the permenant
dentition and around one year in the primary dentition.
638. Maxillary and mandibular first molars have a much more pronounced CERVICAL RIDGE
BUCCALLY.
639. Conditions that can cause early eruption of primary teeth are STURGE-WEBER
SYNDROME, HAND-SCHULLER-CHRISTIAN DISEASE, and HYPERTHYROIDISM.
640. The roots of deciduous anterior teeth are NARROWER and LONGER than the roots of
anterior permenant teeth.
641. Compared to permenant teeth, deciduous teeth are LIGHTER, WHITER, and LESS
PIGMENTED.
642. Compared to permenant teeth, deciduous teeth are smaller in overall size and in crown
dimension, and narrower at their CEJ.
643. The ROOTS of primary ANTERIOR TEETH are NARROWER and LONGER compared to
permenant anterior roots.
644. A typical child will have all 20 primary teeth between ages 30-33 months.
645. The FIRST primary teeth to erupt are the MANDIBULAR CENTRAL INCISORS at around
5-7 months of age.
646. A unique characteristic common to both the PERMENANT MANDIBULAR FIRST MOLAR
and PRIMARY CANINE is their mesial contacts are positioned CERVICAL to their distal
contacts.
647. The primary mandibular first molar is unique in that it does not resemble any other
primary or permenant tooth.
648. Eruption of the primary dentition occurs between 6-30 months of age.
649. The period of time that begins with the emergence of the permenant central incisors and is
ends when all primary teeth have exfoliated is the MIXED DENTITION.
650. The presence of 1 or more decayed, missing, or filled tooth surfaces (dmfs) in any primary
tooth in a pre-school aged child is EARLY CHILDHOOD CARIES (ECC).
48
MICROBIOLOGY AND PATHOLOGY
651. All cells in the immune system were derived from PRIMITIVE CELLS IN BONE MARROW.
652. Cellular movement to the site of inflammation in response to chemical signals is

CHEMOTAXIS.
653. The cells FIRST TO RESPOND to an inflammatory reaction via chemotaxis are
NEUTROPHILS (WBCs).
654. IMMUNE COMPLEX is formed by the combination of an ANTIBODY and ANTIGEN.
655. An amorphous gelatinous structure that surrounds the entire bacterium to prevent
phagocytosis, contains antigens, and mediates cellular adhesion is the CAPSULE.
656. A NARROW ZONE of partial hemolysis and greenish discoloration surrounding a bacterial
colony like Streptococcus pneumonia is characteristic of an ALPHA-HEMOLYTIC
REACTION.
657. COMPLETE hemolysis of hemoglobin within the RBC represented by a WIDE, CLEAR
AGAR ZONE around a bacterial colony like Streptococcus pyogenes is a BETA-
HEMOLYTIC REACTION.
658. A condition where the immune system identifies its own cells and tissues as foreign, and
signals antibodies to attack is an AUTOIMMUNE REACTION.
659. The period of HIGHLY RAPID EXPONENTIAL bacterial GROWTH & REPRODUCTION
(cell doubling) is the LOG (EXPONENTIAL) PHASE.
660. The period of initial SLOW BACTERIAL GROWTH, no cell division, and stable metabolic
activity is the LAG PHASE.
661. Bacteria that metabolize substance aerobically if oxygen exists, or anaerobically if

oxygen is absent are FACULTATIVE ANAEROBES.
662. The facultative anaerobe primarily responsible for ROOT CARIES is ACTINOMYCES
NAESLUNDII.
663. The gram (-) facultative anaerobe primarily responsible for AGGRESSIVE
PERIODONTITIS is A. ACTINOMYCETEMCOMITANS.
664. Phagocytic cells that provide a non-specific cellular disease resistance mechanism (start
the immune process) are MACROPHAGES.
665. PLASMA CELLS produce and secrete ANTIBODIES into the blood to fight foreign bodily
substances.
49
666. PLASMA CELLS stem from DIFFERENTIATED B-CELLS to synthesize

IMMUNOGLOBULINS.
667. A protein (antibody) produced by plasma cells and lymphocytes for the immune system
to identify and neutralize pathogens by adherence is an IMMUNOGLOBULIN.
668. Inflammatory mediators produced by B-CELLS and T-CELLS that are critical in cellular
signaling and communication are CYTOKINES.
669. The MOST ABUNDANT and only immunoglobulin (antibody) that CROSSES THE
PLACENTA and BINDS COMPLEMENT is IgG.
670. The LEAST ABUNDANT immunoglobulin (1%) with unknown function, located on the
membrane surface of most circulating B-LYMPHOCYTES is IgD.
671. The PRIMARY SALIVARY secretory immunoglobulin (antibody) that is also present in
MUCOUS SECRETIONS such as SWEAT and TEARS is IgA.
672. The immunoglobulin found on MAST CELLS and BASOPHILS and is responsible for
promoting MOST TYPE I HYPERSENSITIVITY REACTIONS (allergic and anaphylactic)
is IgE.
673. CONTACT DERMATITIS (red, itchy rash) due to a latex allergy or tuberculin skin test is a
T-cell mediated TYPE IV delayed hypersensitivity reaction.
674. ACELLULAR OBLIGATE INTRA-CELLULAR PARASITES that replicate only inside living
cells are VIRUSES.
675. Unique protein agents of chronic disease that infect and cause NERVE TISSUE DAMAGE
with potentially long incubation periods are PRIONS.
676. A chronic hard, non-tender infection of the face and neck caused by FILAMENTOUS,
GRAM+ ANAEROBIC BACTERIA and triggered by an existing dental abscess or prior
extraction is ACTINOMYCOSIS (LUMPY JAW).
677. The normal oral flora bacterium most often responsible for ACTINOMYCOSIS is
ACTINOMYCES ISRAELII.
678. The gram-negative facultative opportunistic anaerobe responsible for pneumonia,

bacteremia, and acute bacterial meningitis is HAEMOPHILUS INFLUENZA.
679. The antibiotic of choice and first-line treatment of ROCKY MOUNTAIN SPOTTED FEVER
caused by RICKETTSIA RICKETTSII is DOXYCYCLINE.
680. Continuous submucosal and mucosal inflammatory disease of the COLON and RECTUM
with characteristic pathologic PSEUDOPOLYPS are clinical features of ULCERATIVE
COLITIS.
681. KELOID formation is primarily due to the formation of EXCESS TYPE III COLLAGEN.
50
682. The oral antibiotic that effectively treats laryngitis, bronchitis, and pneumonia and is highly
resistant to HYDROCHLORIC ACID (gastric acid) in the stomach is PENCILLIN V.
683. INHIBITION of DIHYDROPTEROATE SYNTHASE is the mechanism of action of

SULFONAMIDES.
684. INHIBITION of BACTERIAL TRANSPEPTIDASE is the mechanism of action of BETA-

LACTAM antibiotics.
685. An OBLIGATE ANAEROBE killed in the presence of oxygen is CLOSTRIDIUM species.
686. The bacterial species primarily responsible for FOOD-BORNE SICKNESS is

SALMONELLA.
687. The most DEFINITIVE blood test to detect ACUTE PANCREATITIS is ELEVATED LIPASE
LEVELS.
688. The intense immunologic response with NEISSERIA GONORRHOEAE infections is due its
endotoxin LIPOOLIGOSACCHARIDE (LOS) that stimulates the inflammatory release of
TUMOR NECROSIS FACTOR-ALPHA.
689. CEFTRIAXONE is the antibiotic of choice to combat the gram-negative diplococcic

responsible for the sexually transmitted disease GONORRHEA.
690. A rare autosomal recessive disorder that primarily manifests ORALLY as AGGRESSIVE
PERIODONTITIS and DERMATOLOGICALLY, as dry scaly patches on the palms and
soles is PAPILLON-LEFEVRE SYNDROME.
691. A penicillin-tolerant patient with TETRALOGY OF FALLOT (cyanotic heart defect)

requires 2g ORAL AMOXICILLIN prophylactically one-hour before scaling and root
planning, oral surgery, or root canal therapy.
692. The FIRST antibiotic PRE-MEDICATION ALTERNATIVE for a penicillin-allergic patient

with unpaired cyanotic congenital heart disease and artificial heart valves is
CLINDAMYCIN (600mg before the dental procedure) or CEFAZOLIN.
693. Antibiotic prophylaxis before dental treatment is NOT required for atherosclerosis,
cardiac pacemakers, pulmonary stenosis, or hypertension.
694. Antibiotic prophylaxis is required 1 hour before dental treatment for patients with a
prior history of bacterial endocarditis, unpaired congenital heart disease, prosthetic cardiac
valve, and prior cardiac transplant with valvulopathy.
695. If this same patient cannot take oral amoxicillin prophylactically, then AMPICILLIN is
administered INTRAVENOUSLY.
696. Proteins produced inside pathogenic gram (+) and some gram (-) bacteria as part of their
growth and metabolism that are secreted or released into the cell’s surrounding medium
after lysis are EXOTOXINS.
51
697. Characteristics of EXOTOXINS: polypeptides produced by mainly gram (+) bacteria, are
diffusible, highly toxic, lack enzymatic activity, and damage the host by cellular destruction
or disrupting cellular metabolism.
698. Bacterial species that SECRETE EXOTOXIN include Staphylococcus aureus,

Streptococcus pyogenes, Clostridium botulinum, and Corynebacterium diphtheria.
699. Lipid portions of the lipopolysaccharides (LPSs) located in the outer cell wall of gram (-)
bacteria that are released upon cellular death and cell wall destruction are ENDOTOXINS.
700. Bacterial species that SECRETE ENDOTOXIN include E.coli, Salmonella Typhi, Shigella,
and Vibrio cholera.
701. The gold standard technique to positively serotype and detect swelling of encapsulated
bacteria like Streptococcus pneumonia and Cryptococcus neoformans is the QUELLUNG
REACTION.
702. A positive quelling reaction reveals a bacterial capsule as a sharply demarcated halo
around the dark blue stained cell, while a negative quelling reaction reveals the absence
of a clear, enlarged halo surrounding the stained cell. BOTH TRUE.
703. TRICLOSAN for hand sanitation is a highly effective antimicrobial against both GRAM (+)
and GRAM (-) bacteria, and viruses.
704. A severe, rare life-threatening renal complication of abnormal RBC destruction that
occurs in approximately 10% of individuals infected with Escherichia coli (shiga toxin) or
Shigella dysenteriae is HEMOLYTIC UREMIC SYNDROME (HUS).
705. An individual immunized with an attenuated, killed, or inactive bacteria antigen for
mycobacterium tuberculosis is a classic example of ARTIFICIAL ACTIVE IMMUNITY.
706. Antibodies passed from the maternal blood into the fetus or newborn’s bloodstream during
pregnancy is a classic example of NATURAL PASSIVE IMMUNITY.
707. The best method to test for ACTIVE TUBERCULOSIS is to examine the patient’s sputum
on a smear using the ACID FAST STAIN test for the bacteria MYCOBACTERIUM
TUBERCULOSIS.
708. During the ACID FAST STAIN test, “acid-fast bacteria” RESIST de-colorization with
methylene blue dye and appear BRIGHT RED against a BLUE BACKGROUND under the
microscope.
709. The MOST NUMEROUS circulating white blood cells during ACUTE INFLAMMATION is
the POLYMORPHONUCLEAR NEUTROPHILS (PMNs).
710. The MOST ACTIVE CELL in the periodontal pocket and FIRST TO MIGRATE INTO THE
GINGIVAL SULCUS are POLYMORPHONUCLEAR NEUTROPHILS (PMNs).
711. A chronic, salivary gland disorder that affects the salivary and lacrimal glands in a patient
who presents with XEROSTOMIA, XEROPHTHALMIA, or KERATOCONJUNCTIVITIS
SICCA is SJOGREN SYNDROME.
52
712. The most common pre-cancerous oral lesion that is more prevalent in male smokers,
and is commonly found on the lower lip vermillion border, buccal mucosa, and gingiva is
ORAL LEUKOPLAKIA.
713. A condition triggered by the EPSTEIN-BARR VIRUS (EBV) characterized by irregular hairy,
white corrugated patches on the tongue, and mainly affects people with HIV/AIDS is ORAL
HAIRY LEUKOPLAKIA.
714. The percentage of oropharyngeal cancers potentially caused by HUMAN

PAPILLOMAVIRUS (HPV) is 70%.
715. The most common etiology of SQUAMOUS PAPILLOMA which may occur on the hard and
soft palate, or the tongue’s ventral surface is HUMAN PAPILLOMAVIRUS (HPV).
716. The most common papillary lesion that presents as a painless, pink to white lesion with
a CAULIFLOWER-LIKE surface and finger-like projections is ORAL SQUAMOUS
PAPILLOMA.
717. The strain of human papillomavirus responsible for most oropharyngeal cancers is HPV-16.
718. A type of inflammatory bowel disease that can affect any segment of the GI tract from
the mouth to anus, involves “skip lesions” and is transmural is CROHN’S DISEASE.
719. A rare, MALIGNANT small, round blue cell tumor of bone or soft tissue tumor that mainly
affects adolescents and young adults (10-20 years) is EWING’S SARCOMA.
720. The most common areas affected by EWING’S SARCOMA are the diaphysis of long
bones and the pelvis.
721. The classic lamellated or “ONION-SKIN” periosteal reaction visible radiographically is

characteristic of EWING’S SARCOMA.
722. An increase and greater distribution of LAMININ in the extracellular matrix is highly
correlated with EPITHELIAL CELL MALIGNANCY.
723. The process by which a biological cell stops growing or dividing is CELLULAR
QUIESCENCE.
724. A rare, autoimmune disorder causing inflammation of the blood vessels (vasculitis) that
intra-orally resemble aphthous ulcers on the soft palate and oropharynx, but may also affect
the genitals, eyes, and joints is BEHCET’S DISEASE.
725. Small, round-to-ovoid herpetic lesions 2-4mm in diameter with an erythematous halo found
mainly on non-keratinized buccal and labial mucosa that rarely scar are MINOR
APHTHOUS ULCERS.
726. Systemic diseases associated with APHTHOUS ULCERS include CELIAC DISEASE,
BEHCET SYDNROME, as well as VITAMIN and IgA deficiencies.
53
727. The main bacteria responsible for PREGNANCY GINGIVITIS and hormone-related
periodontal diseases is P. INTERMEDIA.
728. The gram-negative bacterial rod primarily responsible for AGGRESSIVE PERIODONTITIS
is AGGREGATIBACTER ACTINOMYCETEMCOMITANS.
729. Medications that may cause GINGIVAL HYPERPLASIA (ENLARGEMENT) include

PHENYTOIN, CYCLOSPORINE, and CALCIUM CHANNEL BLOCKERS (Verapamil,
Amlodipine, & Nifedipine).
730. The highly regulated process of programmed cell death in multicellular organisms that
involves biochemical cellular changes such as shrinkage, blebbing, chromatin
condensation, and chromosomal DNA fragmentation and nucleus involution is
APOPTOSIS.
731. Protein degrading enzymes that are activated by the intrinsic and extrinsic pathways to
initiate APOPTOSIS are CASPASES.
732. Traumatic cellular death due to acute cellular injury is NECROSIS.
733. The most common oral manifestation of the rare autoimmune disease
GRANULOMATOSIS with POLYANGITIS (formerly Wegener Granulomatosis) is
STRAWBERRY GINGIVITIS.
734. The classic eruptive “TARGET LESIONS” present on the distal extremities due to a TYPE
IV hypersensitivity reaction triggered mainly by HERPES SIMPLEX VIRUS (HSV), and
less commonly NSAIDs and antibiotics is ERYTHEMA MULTIFORME.
735. The CDC recommends that the enzyme-linked immunosorbent assay (ELISA) is the BEST
test to SCREEN for LYME DISEASE, and THEN confirm the results using the WESTERN
BLOT TEST.
736. LYME DISEASE is caused by the bacterial species BORRELIA MAYONII and BORRELIA
BURGDORFERI.
737. A microorganism’s pathogenicity, or its ability to cause disease is VIRULENCE.
738. The ENTEROBACTERIA most often responsible for URINARY TRACT INFECTIONS
(UTIs) is E. COLI. PROTEUS, PROVIDENTIA, and MORGANELLA are other
enterobacteria implicated in UTIs.
739. CROHN’S DISEASE most commonly involves the TERMINAL ILEUM.
740. PSEUDOMEMBRANOUS COLITIS causes acute inflammation of the COLON and small
intestine due to an acquired secondary nosocomial infection from the overgrowth of
CLOSTRIDIUM DIFFICILE from taking certain antibiotics like CLINDAMYCIN,
PENICILLINS, CEPHALOSPORINS and FLUOROQUINOLONES.
741. A gram-positive, aerobic SPORE-FORMING that resides mainly in the human GI tract and
soil is CLOSTRIDIA. Ex: Clostridium difficile.
54
742. A bacterium that produces exotoxin (neurotoxin) causing muscle weakness and paralysis
by blocking the release of acetylcholine at the neuromuscular junction in cholinergic motor
neurons is CLOSTRIDIUM BOTULINUM.
743. A highly contagious skin infection that mainly affects infants and children, causing red
sores around the nose and mouth due to infection by Staphylococcus aureus or
Streptococcus pyogenes is IMPETIGO.
744. The antibiotic of choice for a patient with METHICILLIN-RESISTANT STAPHYLOCOCCUS

AUREUS (MRSA) is VANCOMYCIN.
745. A delayed allergic complication of a STREPTOCOCCUS PYOGENES infection that can

cause fever, joint pain, and permenant heart damage is RHEUMATIC FEVER.
746. A patient has been taking Amoxicillin for several days for a sore throat prescribed by his
physician. The patient also displayed bilateral tender anterior cervical lymph nodes and
enlarged tonsils bilaterally. This patient goes to the dentist two week later for a composite
restoration. At the restorative visit, the patient complains of new pain in multiple joints,
and an epidermal rash on his body trunk. The most likely cause of these new signs and
symptoms is RHEUMATIC FEVER.
747. Most pathogens that inhabit the human body due to its moderate temperature are
MESOPHILES.
748. The most virulent bacteria and initiator of DENTAL CARIES is the gram (+) facultative
anaerobe STREPTOCOCCUS MUTANS.
749. Caries that invades a natural tooth surface is PRIMARY CARIES. Recurrent caries that
occurs at the margin of a previously placed restoration is SECONDARY CARIES. BOTH
TRUE.
750. The sudden appearance of widespread, rapidly burrowing destructive caries with early
pulpal involvement on tooth surfaces that are typically caries-resistant is RAMPANT
CARIES.
751. HIGH RISK factors associated with RAMPANT CARIES are HAVING IN-BETWEEN MEAL
EXPOSURES TO SUGAR > 3 TIMES and WEARING AN ORTHODONTIC APPLIANCE.
752. A visible white or brown spot lesion on a wet tooth surface has demineralized
COMPLETELY THROUGH ENAMEL and potentially into dentin.
753. A malignant VASCULAR TUMOR that presents as painless, red-to-purple, raised patches
on the skin, and frequently associated with AIDS is KAPOSI’S SARCOMA.
754. The most common benign salivary gland mixed tumor that primarily affects the
PAROTID GLAND is PLEOMORPHIC ADENOMA.
755. The primary hemolytic defect and morphologic hallmark of HEREDITARY

SPHEROCYTOSIS is the production of MICROSPHEROCYTES, caused by the loss of
RBC membrane surface area that results in RBC cytoskeleton instability and fragility.
55
756. A patient diagnosed with the hemolytic disorder HEREDITARY SPHEROCYTOSIS had a
splenectomy to treat splenomegaly. This patient is at an increased risk of acquiring
encapsulated bacterial infections like KLEBSIELLA PNEUMONIA, STREPTOCOCCUS
PNEUMONIA, and E.COLI.
757. Amikacin, Gentamicin, Neomycin, and Streptomycin AMINOGLYCOSIDES that bind to the
30S ribosome to inhibit bacterial PROTEIN SYNTHESIS.
758. A MACROLIDE commonly used to treat BACTERIAL CONJUNCTIVIITS and OTITIS

MEDIA by binding to the 50S ribosomal subunit to inhibit bacterial protein synthesis is
AZITHROMYCIN.
759. The primary virus responsible for the COMMON COLD whose primary route of transmission
is the upper respiratory tract (mouth and nose) is RHINOVIRUS.
760. Primary symptoms of RHINOVIRUS include sore throat, nasal congestion, sneezing, non-
productive cough, and muscle fatigue and weakness.
761. ACUTE INFLAMMATION of the MIDDLE EAR and most common cause of an earache is
OTITIS MEDIA.
762. The most predominant bacteria that cause otitis media are STREPTOCOCCUS
PNEUMONIAE, MORAXELLA CATARRHALIS, and non-typeable H. INFLUENZAE.
763. An infant with Vitamin K deficiency would have a decrease in coagulation factors 2,7,9,
and 10.
764. Vitamin K is a cofactor for Factors 2,7,9, and 10.
765. A risk factor for a PULMONARY EMBOLISM is BRADYCARDIA (slower than normal HR).
766. Risk factors that contribute to an ARTERIAL EMBOLISM that can result in a myocardial
infarction include diabetes, smoking, diet high in trans-saturated fat, and tachycardia.
767. AVASCULAR NECROSIS (bone death) is caused by lack of blood supply to bone due to
SICKLE CELL ANEMIA, CHRONIC ALCOHOLISM, CHRONIC STEROID USE, or
TRAUMA.
768. SICKLE CELL DISEASE occurs when VALINE replaces GLUTAMATE in the B subunit of
hemoglobin.
769. The plasma-clotting enzyme produced by STAPHYLOCOCCUS is COAGULASE.
770. An enzyme that lyses FIBRIN is STREPTOKINASE.
771. The fibrous protein that is the main component of blood clots is FIBRIN.
772. An infection of articular tissue and joint destruction by NEISSERIA GONORRHOEAE or

STAPHYLOCOCCUS AUREUS is characteristic of INFECTIOUS ARTHRITIS.
56
773. Acute gingival inflammation characteristic of PREGNANCY GINGIVITIS due to increased

progesterone levels are caused by PREVOTELLA INTERMEDIA.
774. The bacteria involved in dental caries that can be transferred to a child from the caretaker’s
saliva is STREPTOCOCCUS MUTANS.
775. A gram-negative facultative anaerobe that excretes a toxin causing watery diarrhea
especially in children is VIBRIO CHOLEREA.
776. A dormant form of bacteria that is non-reproductive and resistant to desiccation and
chemical disinfectants is an ENDOSPORE.
777. A rod-shaped facultative gram-negative anaerobe that is non-spore forming and non-motile
and is most commonly transmitted via the fecal-oral route of contamination causing
diarrhea, cramping, and emesis is SHIGELLA.
778. SHIGELLA DYSENTERIAE contains SHIGA TOXIN that inhibits protein synthesis by
cleaving an adenine nucleobase from the RNA of the ribosomal 60S subunit.
779. The most common type of HEART FAILURE affects the LEFT-SIDE OF THE HEART.
780. An integral component of GRAM NEGATIVE BACTERIA’s outer cell membrane that
contains lipopolysaccharides (LPS) and are released during cell lysis are ENDOTOXINS.
781. A facultative anaerobe and virulent food pathogen that contains lipopolysaccharide (LPS)
in its outer cell membrane is LISTERIA MONOCYTOGENES.
782. The GRAM POSITIVE COCCI bacteria implicated in TOXIC SHOCK SYNDROME is
STAPHYLOCOCCUS AUREUS.
783. ENTEROCOCCUS FAECALIS most commonly infects the BILIARY and URINARY
TRACTS.
784. A glomerular filtration rate < 5% OF NORMAL is characteristic of END-STAGE RENAL

DISEASE.
785. Potential causes of HAIRY TONGUE include SMOKING, POOR ORAL HYGIENE,
ANTIBIOTIC THERAPY, and RADIATION THERAPY.
786. KERATIN ACCUMULATION and ELONGATION OF FILIFORM PAPILLAE on the tongue

dorsum are associated with HAIRY TONGUE.
787. Small, dark-red papules on the SOFT and HARD PALATES that may be associated with
RUBELLA (GERMAN MEASLES) is the FORCHHEIMER’S SIGN.
788. Clinical signs of inflammation confined to the gingival tissues without clinical attachment
loss is GINGIVITIS.
789. The MOST common form of gingivitis that involves bleeding, gingival enlargement,
edema, and erythema is PLAQUE-INDUCED GINGIVITIS.
57
790. The most prevalent form of adult periodontal disease that may also occur in children is
CHRONIC PERIODONTITIS.
791. Recurrent periodontal disease that does not respond to treatment is REFRACTORY
PERIODONTITIS.
792. The main difference between NUG and NUP is the PRESENCE OF BONE LOSS WITH
NUP.
793. Inflammation of the periodontium that extends beyond the gingiva into underlying bone and
destroys C.T. around teeth is PERIODONTITIS.
794. Gingival inflammation limited to the gingival tissues with a junctional epithelium (JE) intact
and attached is GINGITIVIS.
795. The anticoagulant that inactivates HISTAMINE is HEPARIN.
796. A powerful neurotransmitter and inflammatory mediator that increases capillary permeability
to WBC and proteins and is produced and released by MAST CELLS, BASOPHILS, and
EOSINOPHILS is HISTAMINE.
797. A rare disease involving the proliferation and accumulation of mast cells in the skin, bone
marrow, and internal organs, with the subsequent production of excess histamine is
MASTOCYTOSIS.
798. The H-antigen on gram (-) bacteria are typically associated with FLAGELLA.
799. Membrane transport proteins that serve as water-filled channels to allow the diffusion of
hydrophilic molecules (sugars, ions, and amino acids) to move inside and outside of the
bacterial cell wall are PORINS.
800. Factors that INCREASE membrane permeability include decreased membrane thickness
and solute size, and increasing the oil-water coefficient of the solute.
801. A characteristic of the GRAM NEGATIVE aerobic bacteria PSEUDOMONAS

AERUGINOSA is UNIPOLAR MOTILITY.
802. A patient with clinical manifestations of sudden WEIGHT LOSS, tachycardia, insomnia,
irritability, heat intolerance, tremors, goiter, and exophthalmos (wide-eyed staring gaze)
is most likely experiencing HYPERTHYROIDISM.
803. Multiple Sclerosis (MS), DM-Type I, tuberculosis, and contact dermatitis are all examples
of TYPE IV HYPERSENSITVITY REACTIONS.
804. A TYPE III hypersensitivity reaction involves the production if IgG and IgM antibodies.
805. Immunoglobulins (antibodies) that polymerize and are associated with J CHAINS that hold
the polymerized antibodies together are IgA and IgM.
806. An early-phase antibody secreted from B-cells upon first encountering an antigen is IgM.
58
807. The immunoglobulin commonly found in high concentrations in SALIVA, BREAST MILK,
and mucosal linings like the RESPIRATORY, and GASTROINTESINTAL TRACT is IgA.
808. Immunoglobulins found on the SURFACE OF B-CELLS are IgM and IgD.
809. Characteristics of gingivitis and periodontitis include BLEEDING, BACTERIA,

INFLAMMATION and POCKETING.
810. The most critical ENVIRONMENTAL factor linked to PERIODONTAL DISEASE is

CIGARETTE SMOKING.
811. The cardinal sign of PERIODONTITIS is DESTRUCTION OF ALEVOLAR BONE.
812. Systemic conditions that increase the risk of GINGIVITIS due to an alteration in the gingival
inflammatory response to plaque include PREGNANCY, PUBERTY, MENSES, and
DIABETES.
813. The PLAQUE-HOST INTERACTION that leads to plaque-induced gingival disease is

altered by LOCAL and SYSTEMIC FACTORS, MEDICATIONS, and MALNUTRITION.
814. A chronic C.T. autoimmune disease that involves the overproduction and accumulation
of collagen, particularly in women between 30-50 years, is SCLERODERMA.
815. Adverse effects of high doses of CARBENICILLIN include bleeding and HYPOKALEMIA
due to potassium loss at the kidney’s distal convoluted tubule.
816. An inflammatory mediator and peptide hormone that causes vasodilation and
subsequent reduction in blood pressure is BRADYKININ.
817. Antibodies derived from two different individuals within the same species are ALLOTYPES.
818. Antibodies derived from the SAME individual are AUTOTYPE.
819. The ability to inhibit RNA-dependent DNA polymerase is a mechanism of action of ANTI-
RETROVIRAL MEDICATIONS.
820. A pre-cancerous white patch or plaque that CANNOT BE SCRAPED OFF and cannot be
characterized clinically or pathologically as any other disease is LEUKOPLAKIA.
821. Characteristics of ORAL LEUKOPLAKIA associated with a HIGH RISK of malignant

transformation are verrucous and erythema lesions located on the FLOOR OF
MOUTH,TONGUE DORSUM or LIP VERMILLION. More than 90% with these features
show dysplasia or carcinoma when biopsied. ALL TRUE.
822. A histological characteristic exclusive to MALIGNANT NEOPLASMS is BASEMENT

MEMBRANE INVASION.
823. ERYTHROPLASIA, BLEEDING ON MILD MANIPULATION, and a LESION FIXED TO

ADJACENT STRUCTURES are clinical characteristics consistent with lesion
MALIGNANCY.
59
824. Disorganized cellular death caused by ischemia, trauma, or infection, found in both
MALIGNANT and BENIGN physiological processes is NECROSIS.
825. A LOW NEUTROPHIL COUNT (WBC) in the blood (< 4,000) is characteristic of
LEUKOPENIA.
826. An acute condition of severe and dangerously reduced NEUTROPHILS count causing
immunosuppression that results in an individual’s high susceptibility to serious infections is
AGRANULOCYTOSIS.
827. The primary advantage of ETHYLENE OXIDE is its ability to sterilize rubber and plastic
dental instruments and items due to its ability to STERLIZE AT LOW TEMPERATURES.
828. The process by which microorganisms are KILLED (excluding bacterial spores) is
DISINFECTION.
829. The physical or chemical process that completely destroys all microorganisms to achieve
asepsis and prevent disease transmission is STERILIZATION. STERILIZATION is the
highest achievable level of microbial death that eliminates all spores and microorganisms.
BOTH TRUE.
830. Antimicrobial substances applied to LIVING TISSUE to reduce the potential of infection or
sepsis describes ANTISEPTICS.
831. A potent virucidal agent that reduces the activity of hepatitis B surface antigen (HBsAg) and
the hepatitis B core antigen (HBcAg) is GLUTARALDEHYDE.
832. The most effective penicillin antibiotic derivative against the highly penicillin-resistant
PSEUDOMONAS AERUGINOSA is CARBENICILLIN.
833. The most appropriate antibiotic to treat a severe LISTERIA infection in a non-penicillin
allergic patient is PENICILLIN (AMPICILLIN). Or with Gentamycin.
834. A medical emergency characterized by a rapid rise in blood pressure above 180/120
mm Hg causing blurred vision, chest pain, nausea and confusion is MALIGNANT
HYPERTENSION (ARTERIOLAR NEPHROSCLEROSIS).
835. The most specific test to detect active MYCOBACTERIUM TUBECULOSIS in a

symptomatic patient suspected of having TUBERCULOSIS is the ACID FAST STAIN OF
SPUTUM SAMPLE.
836. The classic symptomatic triad associated with TUBERCULOSIS is WEIGHT LOSS, NIGHT
SWEATS, and HEMOPTYSIS.
837. The mechanism of action of the prodrug ISONIAZID to treat TUBERCULOSIS is the
INHIBITION OF MYCOLIC ACID SYNTHESIS.
838. Bacteria implicated in PLAQUE-INDUCED GINGIVITIS include GRAM (+), GRAM (-),
anaerobic and FACULTATIVE ANAEROBES.
60
839. Electrocardiographic waves that become more prominent as body temperature drops and
are characteristic of HYPOTHERMIA and HYPERCALCEMIA are OSBORN WAVES (J
WAVES).
840. The most common BENIGN bone tumor is OSTEOCHRONDROMA (EXOSTOSIS).
841. A MALIGNANT tumor that affects the diaphysis region of long bones is
CHONDROSARCOMA.
842. The helical-shaped GRAM NEGATIVE bacterium that colonizes in the stomach and is the
primary pathogen responsible for GASTRIC ULCERS and CHRONIC GASTRITIS is
HELICOBACTER PYLORI (Campylobacter Pylori).
843. HUNTINGTON’S DISEASE is an autosomal dominant neurodegenerative brain disorder

causing progressive, uncontrollable movements due to a lesion and atrophy of the forebrain
portion called the STRIATUM.
844. The primary input area for the basal ganglia responsible for coordinating body movements,
fine motor skills, and mediating rewarding experiences is the STRIATUM.
845. DRY HEAT penetrates LESS effectively than moist heat, and requires longer sterilization
times and temperatures.
846. A method of CHEMICAL VAPOR sterilization that uses high pressure and high
temperature, with the main ACTIVE ingredient of 23% FORMALDEHYDE is
CHEMICLAVE.
847. SAFRANIN counterstain turns GRAM NEGATIVE bacteria RED due to their THIN
peptidoglycan layer that cannot trap the crystal violet stain.
848. Rod-shaped, GRAM NEGATIVE bacteria that contains leukotoxin and is present in elevated
levels in patients diagnosed with LOCALIZED AGGRESSIVE PERIODONTITIS is
AGGREGATIBACTER ACTINOMYCETEMCOMITANS (AA).
849. The GRAM NEGATIVE periodontopathogen implicated in CHRONIC PERIODONTITIS and

found in subgingival plaque is BACTEROIDES FORSYTHUS.
850. Gram (+) bacteria will stain BLUE after stained with crystal violet and safranin due to its
THICK PEPTIDOGLYCAN LAYER. Due to their thin peptidoglycan layer, gram (-) bacteria
retain RED or PINK upon staining. BOTH TRUE.
851. The main causative bacteria of INFECTIVE ENDOCARDITIS are STREPTOCOCI and
STAPHYLOCOCCUS AUREUS (80-90%) due to their ability to adhere to fibronectin and
colonize vegetations.
852. A complication of strep throat that may result in valvular scarring and subsequent heart
failure is RHEUMATIC FEVER.
853. The process by which a virus (bacteriophage) inserts and transfers DNA into a bacterium
is TRANSDUCTION.
61
854. The decoding and conversion of an mRNA message into protein by ribosomes is
TRANSLATION.
855. Biologically active substances produced by STREPTOCOCCI include HYALURONIDASE,

STREPTOKINASE, STREPTODORNASE, and LEUKOCIDIN.
856. RIGHT-SIDED heart failure is a result of LEFT-SIDED heart failure due to pressure build-
up within the PULMONARY CIRCULATION. The resulting pressure increases stress on the
right side of the heart, eventually leading to right-sided heart failure. BOTH TRUE.
857. Specialized cardiomyocyte fibers that transmit electrical impulses from the bundle of His to
the heart apex are PURKINJE FIBERS.
858. The specialized bundle of cardiac muscle fibers that transmits electrical impulses from the
atrioventricular node (AV) to the ventricles is the BUNDLE OF HIS.
859. The normal intrinsic rate of the bundle of His is < 20 BEATS PER MINUTE.
860. The HEART’S natural “PACEMAKER” that initiates electrical conduction by setting its
pulse is the SINOATRIAL (SA) NODE.
861. The cardiac structure that delays electrical impulses from the SA node to increase pumping
efficiency and regulates signals to the ventricles to prevent atrial fibrillation is the
ATRIOVENTRICULAR (AV) NODE.
862. The heart’s ability to adjust to increasing volumes of inflowing blood is best explained by
the FRANK-STARLING MECHANISM.
863. Cardiac muscle contains BETA-1 ADRENERGIC RECEPTORS that produce EXCITATION
such as increased heart rate and contractility.
864. SMOOTH MUSCLE is involuntary and LACKS STRIATIONS, while skeletal and cardiac
muscle have striations.
865. SMOOTH MUSCLE CONTRACTION, VASOCONTSTRICTION, and INTRACELLULAR

CALCIUM MOBILIZATION are mediated by THROMBOXANE A2 that is produced by
activated platelets.
866. The most common cause of OTITIS MEDIA (ear inflammation/infection) is MORAXELLA
CATARRHALIS, HAEMOPHILUS INFLUENZA, and STREPTOCOCUS PNEUMONIA.
867. The main advantages of the CHEMICLAVE method of sterilization are minimal corrosion
and rusting of instruments, much shorter sterilization cycle time compared to dry heat,
and immediate instrument availability upon completion of the sterilization cycle.
868. The superior portion of the upper airway where nasal hair, turbinates, and mucociliary and
IgA secretions are the primary host defense mechanisms is the NASOPHARYNX.
869. Erythema and spontaneous sloughing of the free and attached gingiva caused by lichen
planus, cicatricial pemphigoid, or pemphigus vulgaris is DESQUAMATIVE GINGIVITIS.
62
870. Sexually transmitted diseases that can manifest in the oral cavity include HSV-I, HIV,
TREPONEMA PALLIDUM (Syphilis), and NEISSERIA GONORRHEA.
871. A chronic autoimmune vesiculobullous disease that affects the basement membrane, can
cause desquamative gingivitis, and often involves the oral cavity, conjunctiva, and genitalia
is MUCUOS MEMBRANE PEMPHIGOID (MMP).
872. VIBRIO CHOLEREA bacterium produces a toxin that continuously stimulates the adenyl
cyclase activity of mucosal cells in the intestine to cause diarrheal illness, vomiting, and
muscle cramping.
873. The intestinal pathogen primarily implicated in TRAVELERS’ DIARRHEA is

ESCHERICHIA COLI spread by the ingestion of contaminated food or water.
874. Dental patients who require prophylactic antibiotics to prevent endocarditis should take their
premedication dose 30-60 minutes before the dental procedure.
875. Hormones synthesized from arachidonic acid when tissue is inflamed or infected to control
pain, regulate inflammation, and stimulate platelet aggregation are PROSTAGLANDINS.
876. SLOW, DULL ACHING PAIN signals are stimulated by chemical stimuli and are transmitted
by unmyelinated C FIBERS, while FAST, SHARP PAIN signals are stimulated by thermal
and mechanical stimuli and are transmitted in peripheral nerves by thinly myelinated A
DELTA FIBERS. BOTH TRUE.
877. When a blood vessel is injured, the prostaglandin that stimulates blood clot formation and
vasoconstriction to control bleeding is THROMBOXANE.
878. The most effective treatment for severe ORAL HERPES (HSV-1) is ACYCLOVIR to inhibit
viral DNA polymerase to cease viral replication, but it does not prevent HSV reactivation.
VISCOUS LIDOCAINE may also be prescribed to relieve oral pain.
879. A common disorder associated with RHEUMATOID ARTHRITIS caused by ligament

inflammation and subsequent laxity is ATLANTO-AXIAL DISLOCATION.
880. A child with springtime symptoms of fever, headache, fatigue, and puffy cheeks due to
enlarged parotid glands, and orchitis (testicular inflammation) are consistent with
MUMPS.
881. The most common cause of ASEPTIC MENINGITIS is ENTEROVIRUSES (MUMPS).
882. A 10-year old infected with PARVOVIRUS B19 and presents with a “SLAPPED CHEEK”
appearance and subsequent rash that spread down the trunk, arms, and legs has FIFTH
DISEASE (ERYTHEMA INFECTIOSUM).
883. The gram (+), rod-shaped, facultative anaerobe and highly virulent foodborne pathogen
with unique TUMBLING MOTILITY under light microscopy is LISTERIA
MONOCYTOGENES.
884. An inflammatory reaction of the oral mucosa caused by irritants, allergens, or food additives
such benzoic acid or cinnamaldehyde, especially in the elderly is CONTACT STOMATITIS.
63
885. A post-menopausal woman who describes a scalding sensation accompanied by dryness

of the oral mucosa (lips, tongue, gingiva) in the absence of objective clinical signs, but
whose symptoms typically improve during meals, is most likely afflicted with BURNING
MOUTH SYNDROME.
886. A patient has LOW PLATELET COUNT with spontaneous and prolonged bleeding, but
normal PT and PTT. This patient’s lab results and symptoms are consistent with
THROMBOCYTOPENIA.
887. A salivary and lacrimal gland disorder most common in women 45-55 years, often due
to a complication from another autoimmune disease such as rheumatoid arthritis or lupus
with histology showing focal lymphoid infiltration in exocrine glands is SJOGREN’S
SYNDROME.
888. An asymptomatic inflammatory condition of the tongue dorsum causing areas of atrophy
and well-demarcated areas of smooth, red depapillation of the lingual papilla that migrate
over time is GEOGRAPHIC TONGUE (BENIGN MIGRATORY GLOSSITIS).
889. An acute, self-limiting inflammatory skin eruption due to a type IV hypersensitivity reaction
to an infection or medication and characterized by BULLS-EYE-SHAPED lesions is
ERYTHEMA MULTIFORM.
890. An autoimmune disorder and type II hypersensitivity reaction causing blistering

ACANTHOLYSIS of the oral mucosa when IgG antibodies are directed against
DESMOSOMES is PEMPHIGUS VULGARIS.
891. A POSITIVE NIKOLSKY’S SIGN is a dermatological indication to differentiate between

pemphigus vulgaris and bullous pemphigoid and is associated with PEMPHIGUS
VULGARIS.
892. An autoimmune skin disease and type II hypersensitivity with a NEGATIVE NIKOLSKY’S
SIGN and sub-epidermal BULLAE from IgG antibodies targeting HEMIDESMOSOMES is
BULLOUS PEMPHIGOID.
893. The common standard sterilization method used in dentistry using mechanical indicators to
ensure proper sterilization is the STEAM AUTOCLAVE.
894. A chronic, multisystem autoimmune inflammatory disorder prevalent in younger women with
manifestations of arthralgia, arthritis, and malaise is SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE).
895. SLE, RHEUMATOID ARTHRITIS, and SERUM SICKNESS are TYPE III
HYPERSENSITIVITY reactions.
64
ODONTOGENIC AND BONE LESIONS

896. Oral manifestations associated with TRISOMY 21 (DOWN SYNDROME) include bull-
shaped molars (TAURODONTISM), some missing teeth (HYPODONTIA), increased
gingivitis and periodontal disease, and DECREASED CARIES.
897. Patient with DOWN SYNDROME (TRISOMY 21) would most likely present with the CLASS
III malocclusion (protruded mandible).
898. The MOST common site for oral cancer is the LATERAL BORDER OF THE TONGUE.
899. Stages of PERIAPICAL CEMENTAL DYSPLASIA when viewed radiographically in a

middle-aged African American female are: RADIOLUCENT (Stage 1), MIXED (Stage 2), &
RADIOPAQUE (Stage 3).
900. Inflammation and fissuring at the corners of the mouth (labial commissures) caused by
CANDIDA ALBICANS, RIBOFLAVIN (B2) DEFICIENCY, or ILL-FITTING DENTURE
(DECREASED VERTICAL DIMENSION) is called ANGULAR CHEILITIS (PERLECHE).
901. A 28-year old pregnant patient presents with a pedunculated, raspberry-like, BENIGN soft-
tissue growth on her INTERDENTAL PAPILLAE. The lesion is ulcerated, smooth, red, and
bleeds easily. The lesion is due to local tissue irritation or injury, but can also occur during
due to progesterone changes. This lesion accurately describes a PYOGENIC
GRANULOMA (PREGNANCY TUMOR).
902. A MALIGNANT tumor of BONE-FORMING tissue is an OSTEOSARCOMA.
903. A BENIGN radiopaque BONY OVERGROWTH or protuberance of pre-existing bone found

at the MIDLINE of the HARD PALATE and/or mandibular lingual surfaces is an
EXOSTOSIS (TORI = OSTEOMA).
904. The panorex of a 30 year-old female reveals a painless, unilocular radiolucency with well-
defined margins around the CROWN of an impacted permanent mandibular 3rd molar. This
is most likely a DENTIGEROUS CYST (FOLLICULAR CYST).
905. The MOST COMMON ODONTOGENIC CYST appearing radiographically as a well-

circumscribed unilocular radiolucency at the apex of a NECROTIC TOOTH is a
RADICULAR/PERIAPICAL CYST.
906. Formation of a RADICULAR/PERIAPICAL CYST is attributed to PULPAL

INFLAMMATION.
907. A periapical radiograph of a 19 year-old reveals an asymptomatic, pure radiopaque and

well-defined < 1 cm lesion around the apices of the MANDIBULAR 1st MOLAR (#30) which
is necrotic. The lamina dura and PDL space are obliterated and there is no bony
expansion. This lesion best describes CONDENSING OSTEITIS.
908. The MOST COMMON TOOTH-ASSOCIATED RADIOPACITY seen on dental radiographs

that represents a focal bony reaction to inflammation from a necrotic tooth is CONDENSING
OSTEITIS (FOCAL SCLEROSING OSTEOMYELITIS).
65
909. A 40-year old male presents with a painless, unilocular, well-defined TEAR-DROP SHAPE
radiolucency between and along the lateral surfaces of the MANDIBULAR CANINE &
PREMOLAR. All teeth are vital. This developmental lesion is a LATERAL PERIODONTAL
CYST.
910. An asymptomatic SWELLING that appears as a HEART-SHAPED radiolucency in the

ANTERIOR MAXILLARY MIDLINE due to the position of the nasal spine is a
NASOPALATINE DUCT CYST (INCISIVE CANAL CYST).
911. During a routine extra-oral examination, a 10-year old child presents with a painless swelling
at the anterior midline of the neck just below the hyoid bone. Your knowledge of pathology
tells you this is the MOST COMMON CONGENITAL, BENIGN NECK CYST that requires
a referral to an ENT physician for further evaluation. This lesion is a THYROGLOSSAL
DUCT/TRACT CYST.
912. The most common primary lesion of carcinoma metastasizing to the MANDIBLE in
females is the BREAST.
913. The MOST COMMON head and neck malformation in humans is CLEFT LIP & PALATE.
914. Defective fusion of the MEDIAL and MAXILLARY NASAL PROCESS results in CLEFT
LIP, while defective fusion of the PALATAL SHELVES results in CLEFT PALATE and a
BIFID UVULA.
915. CLEFT PALATE–occurs in 6th-8th week of embryonic life.
916. TOOTH FORMATION starts as the tooth buds begin to grow within the DENTAL LAMINA
of the fetus during the SIXTH EMBRYONIC WEEK.
917. PAGET’S DISEASE may undergo SPONTANEOUS MALIGNANT TRANSFORMATION.
918. A 62-year old man who complains that “my dentures don’t fit” or “my hat is too tight” with
radiographs that show COTTON WOOL RADIOPACITIES and ROOT
HYPERCEMENTOSIS, most likely has PAGET’S DISEASE.
919. An abnormal invagination of the enamel organ into the dental papilla that appears as a
“tooth within a tooth” on radiographs and most commonly seen in maxillary lateral incisors
is a DENS-IN-DENTE (DENS INVAGINATUS).
920. The MOST COMMON SUPERNUMERARY TOOTH located at the maxillary midline
between the central incisors is a MESIODENS.
921. A type of fusion common in maxillary 2nd and 3rd molars where two adjacent teeth are
connected only by CEMENTUM is CONCRESCENCE.
922. BULL-SHAPED MOLARS with an elongated clinical crown, large pulp chamber, short roots
and an apically positioned furcation best describes TAURODONTISM.
66
923. CONGENITAL SYPHILLIS induced enamel hypoplasia characterized by DWARFED

FIRST MOLARS with cusps covered in globular enamel growths and pitted occlusal
surfaces are called MULBERRY MOLARS.
924. The part of the tooth that has been denuded of its gingiva and projects into the oral
cavity is the CLINICAL CROWN.
925. Small, widely spaced, SCREW-DRIVER SHAPED MAXILLARY INCISORS with deep
incisal notches due to an exposure to a congenital infection by TREPONEMA PALLIDUM
during tooth formation are HUTCHINSON INCISORS.
926. The most common clinical manifestation of a MICRODONTIA is the MAXILLARY PEG
LATERAL.
927. The PHYSIOLOGICAL WEARING AWAY of enamel and dentin due to normal age-related
tooth-to-tooth contact or excessive GRINDING (BRUXISM) or CLENCHING teeth is
ATTRITION.
928. Holding the teeth together and tightening the muscles of mastication is CLENCHING, while
moving the mandible while the teeth are together is GRINDING (BRUXISM).
929. While the PRIMARY cause of BRUXISM is STRESS and ANXIETY, other contributing
factors include SLEEP DISORDERS (sleep apnea), MALOCCLUSION, NEUROLOGICAL
CONDITIONS, SMOKING, and ALCOHOL consumption.
930. Occlusal guards and athletic sport guards are NOT interchangeable. Wearing a sport guard
as an occlusal guard for bruxism can cause TMD. BOTH TRUE.
931. Treatment of SLEEP APNEA with an oral appliance that PROTRUDES THE MANDIBLE
TO OPEN THE AIRWAY involves a multi-disciplinary approach between the dental
professional and sleep specialist.
932. The CHEMICAL LOSS of tooth structure from acidic drinks, GERD, BULMEMIA
NERVOSA, or MORNING SICKNESS is EROSION.
933. The MOST noticeable sign of attrition is POLISHED FACETS.
934. The MOST COMMON odontogenic abscess associated with a non-vital tooth is a
PERIAPICAL ABSCESS.
935. Excessive proliferation of chronically inflamed pulpal tissue in a non-vital tooth that
is clinically visible as a red or pink tissue nodule in a clinical crown with an open large
carious lesion, fractured crown, or due to a missing restoration is CHRONIC
HYPERPLASTIC PULPITIS (PULP POLYP).
936. ORAL BISPHOSPHONATES that treat osteoporosis and are associated with
OSTEONECROSIS (BON) of the mandible or maxilla after oral surgery or periodontal
surgery include FOSAMAX, ACTONEL, and BONIVA.
67
937. An extremely rare, hereditary skeletal disorder marked by INCREASED BONE DENSITY
and ABNORMAL BONE GROWTH causing thickening of cortical bone and cancellous bone
sclerosis is OSTEOPETROSIS (MARBLE BONE DISEASE).
938. The underlying defect implicated in OSTEOPETROSIS is the failure of osteoclasts to resorb
bone due to ABNORMAL OSTEOCLAST FUNCTION.
939. A 62-year old male with PUNCHED OUT RADIOLUCENCIES of the mandible and elevated
levels of BENCE-JONES PROTEINS in his urine due to a malignant tumor of PLASMA
CELLS, is consistent with the findings of MULTIPLE MYELOMA.
940. The MOST COMMON benign, painless, but locally aggressive odontogenic tumor with a
SOAP-BUBBLE or HONEY-COMB radiolucent appearance that typically affects the
POSTERIOR MANDIBLE is an AMELOBLASTOMA.
941. The MOST PREVELANT histological patterns of AMELOBLASTOMA are FOLLICULAR

(islands of epithelium resembling the enamel organ epithelium in a mature fibrous CT
stroma) and PLEXIFORM (long, anastomosing cords of odontogenic epithelium).
942. Chronic EXTREME MUSCLE WEAKNESS due to an autoimmune disorder effecting

NEUROMUSCULAR JUNCTIONS is MYASTHENIA GRAVIS.
943. A developmental CONCAVITY of cortical bone on the lingual surface near the ANGLE OF
THE MANDIBLE that may contain SALIVARY GLAND OR LYMPHATIC TISSUE, but does
NOT require treatment is a STAFNE DEFECT (STATIC BONE CYST).
944. A STAFNE/STATIC BONE CYST appears as a uniloclular, well-circumscribed radiolucency

with corticated borders on a PANOREX and lies INFERIOR to the mandibular canal in the
posterior mandible near the third molars.
68
ENDOCRINE PATHOLOGY
945. Clinical features like GOITER, EXOPTHALMOS, WEIGHT LOSS, and GRAVE’S DISEASE
Exophthalmos) are associated with HYPERTHYROIDISM.
946. The MOST common cause of HYPERTHYROIDISM is an AUTOIMMUNE DISORDER.
947. High basal metabolism associated with HYPERTHYROIDISM is due to EXCESSIVE

THYROXIN (T4) PRODUCTION.
948. PARATHYROID ADEMOMA is the most common cause of HYPERPARATHYROIDISM.
949. The MOST common cause of HYPERPITUITARISM is a PITUITARY ADENOMA.
950. A hormonal disorder where the ANTERIOR pituitary gland produces excess growth
hormone causing Class III malocclusion and macroglossia is HYPERPITUITARISM
(ACROMEGALY).
951. The classic triad of DIABETIC symptoms are POLYDIPSIA (excessive thirst),
POLYPHAGIA (excessive hunger), & POLYURIA (large urine volumes).
952. DIABETES (TYPE 1) is the most common PANCREATIC endocrine disorder and
metabolic disease due to a relative or complete lack of insulin secretion by
PANCREATIC BETA CELLS.
953. A rare genetic polyposis syndrome of numerous PREMALIGNANT POLYPS in the

digestive tract, multiple, well-circumscribed or diffuse radiopaque COTTON-WOOL
OSTEOMAS (EXOSTOSIS) in the mandible, and impacted supernumerary teeth are clinical
features of GARDNER’S SYNDROME.
MUSCOLOSKELETAL AND SKIN PATHOLOGY

954. Oral manifestations common to CEREBRAL PALSY include swallowing difficulty, open
bite, bruxism, and facial asymmetry.
955. A rare genetic disorder of diminished quantity or quality of COLLAGEN PRODUCTION

causing FRAGILE and POROUS BONES and clinical manifestations like BLUE SCLERA
and DENTINOGENSIS IMPERFECTA is OSTEOGENESIS IMPERFECTA (BRITTLE
BONES).
956. A 45-year old female presents with limited opening due to TIGHT facial skin and lips,
widened PDL space on radiographs, and complains of cold and numbness of her digits
due to RAYNAUD’S PHENOMENON. She most likely suffers from the C.T. autoimmune
disorder SCLERODERMA.
69
957. An autosomal dominant disorder characterized by multiple benign tumors of the nerves and
skin and light brown CAFÉ-AU-LAIT MACULES in 90% of patients, is VON
RECKLINGHAUSEN’S DISEASE (NEUROFIBROMATOSIS).
958. An individual with CAFÉ AU LAIT SPOTS, increased production of endocrine hormones,
and polyostotic fibrous dysplasia, has the triad of symptoms consistent with McCUNE-
ALBRIGHT SYNDROME.
959. The classic TRIAD of symptoms FISSURED TONGUE, GRANULOMATOUS CHEILITIS,

and FACIAL PARALYSIS is consistent with MELKERSSON-ROSENTHAL SYNDROME.
960. The classic MALAR RASH (BUTTERFLY RASH) over the cheeks and bridge of the nose
is the most characteristic skin lesion of SYSTEMIC LUPUS ERYTHEMATOSUS (SLE).
961. A rare, severe autoimmune intra-epithelial disorder of oral mucous membranes that
manifests as painful, fluid-filled ulcerations or blisters that reveal a positive NIKOLSKY’S
SIGN due to ACANTHOLYSIS is PEMPHIGUS VULGARIS.
962. The MOST SEVERE form of SKIN CANCER that is relatively uncommon intra-orally, but
may occur on the HARD PALATE and MAXILLARY ALEVEOLAR RIDGES is
MALIGNANT MELANOMA.
963. A small, round erosive lesion with a yellowish-white center and red border that forms on
MOVABLE, NON-KERATINZED ORAL MUCOSA like the tongue, lips, or soft palate in
response to trauma, stress, or food allergies is an APHTHOUS ULCER (CANKER SORE).
964. Two keratinized locations in the oral cavity that will NEVER contain an APHTHOUS
ULCER are the HARD PALATE and ATTACHED GINGIVA.
965. The MOST common malignant soft tissue tumor of the head and neck in CHILDREN and
YOUNG ADULTS that develops in STRIATED SKELETAL MUSCLE is
RHABDOMYOSARCOMA.
966. Clinical features of CLEIDOCRANIAL DYSPLASIA (CCD) include HYPERTELORISM,

FRONTAL BOSSING, PERMENANT SUPERNUMERARY TEETH, AND MISSING
CLAVICLES.
967. A rare, benign, encapsulated salivary gland neoplasm that occurs mainly in the PAROTID
GLAND and is characterized by KERATIN PEARLS histologically is BASAL CELL
ADENOMA.
70
BACTERIAL AND VIRAL ORAL PATHOLOGY
968. The cardinal symptoms of fever, sore throat, and STRAWBERRY TONGUE associated
with SCARLET FEVER are caused by group A Streptococcus.
969. During the intra-oral examination, you detect spontaneous and painful bleeding on probing,
and a gray pseudomembranous film on the punched-out interdental papillae. The patient
has a fetid odor and there is no clinical attachment loss. This evaluation is consistent with
NECROTIZING ULCERATIVE GINGIVITIS (NUG).
970. The bacteria primarily responsible for NECROTIZING ULCERATIVE GINGIVITIS (NUG)
are Spirochetes, (Treponema denticola), Fusobacterium and Prevotella intermedia.
971. The most important oral lesion to help clinically diagnose ERYTHEMA MULTIFORME is
HEMORRAGIC CRUSTING OF THE LIP.
972. A SEVERE and potentially fatal bullous form of ERYTHEMA MULTIFORME that clinically
presents as painful BULL’S-EYE (TARGET)-SHAPED LESIONS of the mucous
membranes of the eyes, oral mucosa, and genitalia is STEVENS-JOHNSON SYNDROME.
973. Multiple small, painful vesicles found on the THUMB OR FINGER of a child, or on the
fingers of a dental provider exposed to oral secretion during a barrier break is HERPETIC
WHITLOW.
974. The LEADING cause of OROPHARYNGEAL CANCERS and most commonly sexually
transmitted infection in the U.S. and worldwide is HUMAN PAPILLOMAVIRUS (HPV).
975. The MOST common BENIGN viral neoplasm of EPITHELIAL TISSUE ORIGIN that
appears as a PEDUNCULATED, WHITE or tissue-colored cauliflower-like mass on the
posterior ventral tongue, lips, or palate is a PAPILLOMA.
976. The MOST COMMON FORM OF RECURRENT HERPES SIMPLEX characterized by

small, painful vesicles (cold sores or fever blisters) on the lip’s vermillion border in response
to stress, fatigue, or exposure to sunlight or extreme temperatures is HERPES LABIALIS.
977. A 55-year old male with a child history of chickenpox presents with UNILATERAL
PAINFUL ORAL VESICLES along the distribution a sensory nerve has manifestations
consistent with HERPES ZOSTER (SHINGLES).
978. The surface protein that plays a key role in the receptor recognition and cell membrane
fusion process in SARS-CoV-2 is the SPIKE (S) PROTEIN.
71
BLOOD PATHOLOGY
979. RED BLOOD CELLS are the cellular component of blood that caries OXYGEN and they
do NOT contain a nucleus.
980. SICKLE-CELL ANEMIA is a genetic condition that primarily affects AFRICAN

AMERICANS due to a HEMOGLOBIN “S” DEFECT.
981. A common oral manifestation commonly in patients with ACUTE MONOCYTIC LEUKEMIA
(AML) is GINGIVAL ENLARGEMENT.
982. A common BENIGN developmental VASCULAR LESION consisting of a soft, smooth blue,
red, or reddish-purple proliferation of blood vessels, most commonly found on the ventral
tongue surface and can cause macroglossia is a HEMANGIOMA.
983. A 54-year old female has a history of profuse gingival bleeding when flossing, palatal
petechiae, and multiple bruises on her arms. She has been taking Warfarin, and her most
recent platelet count was unusually low, and she has prolonged bleeding time. Her
condition is consistent with THROMBOCYTOPENIC PURPURA.
984. A serious, acquired or genetic blood condition causing fever, gingivitis and oral ulcerations
due to an increased susceptibility to infections from a SEVERE REDUCTION IN
NEUTROPHIL COUNT is AGRANULOCYTOSIS.
985. The cell surface protein responsible for initiating blood clotting is TISSUE
THROMBOPLASTIN (TISSUE FACTOR).
986. Coagulation factors involved in the INTRINSIC COAGULATION PATHWAY are

FACTORS XII, XI, IX, VIII .
987. Clotting factors involved in the EXTRINSIC COAGULATION PATHWAY are FACTORS VII
and III.
988. The COMMON PATHWAY includes clotting FACTORS I, II, V, X, and XIII.
989. A calcium ion and clotting factor that plays an important role in the common pathway,
intrinsic pathway, and extrinsic pathway is FACTOR IV.
990. The coagulation factor responsible for the activation of PROTHROMBIN TO THROMBIN is
FACTOR X. This reaction also requires FACTOR V. BOTH STATEMENTS ARE TRUE.
991. The laboratory test used to assess the duration of time until clot formation and the activity
of the EXTRINSIC PATHWAY is PROTHROMBIN TIME.
992. FACTOR X, FACTOR V, PROTHROMBIN AND FIBRINOGEN are shared by both the
INSTRINSIC AND EXTRINSIC coagulation pathways.
72
993. The MOST COMMON inherited coagulopathy involving platelet disfunction is VON
WILLEBRAND DISEASE.
994. An x-linked recessive coagulopathy (cofactor deficiency) that results in EASY BRUSING
AND PROLONGED BLEEDING (PROLONGED PTT) AFTER DENTAL PROCEDURES
due to a dysfunction of FACTOR XIII is HEMOPHILIA A.
995. An x-linked recessive coagulopathy resulting in dysfunction of FACTOR IX due to a

protease deficiency is CHRISTMAS DISEASE (HEMOPHILIA B).
996. Patients with HEMOPHILIA A or HEMOPHILIA B will both have NORMAL PT/INR. TRUE.
997. The blood-clotting precursor proteins that circulate in blood in their inactive, proenzyme
form are ZYMOGENS.
73
ORAL WHITE LESIONS
998. A white lesion that CANNOT BE SCRAPED OFF is LEUKOEDEMA.
999. A BENIGN, WHITE, corrugated, thick but SOFT folding of the BUCCAL MUCOSA
bilaterally is WHITE SPONGE NEVUS.
1000. A 55-year old woman presents with asymptomatic, inter-connected SLENDER-FINE,

LACE-LIKE WHITE LINES (WHICKHAM STRIAE) on her BUCCAL MUCOSA just above
the occlusal plane that does not wipe off. Her benign oral condition is consistent with
LICHEN PLANUS.
1001. A benign, HYPERKARATOTIC WHITE LINE along the BUCCAL MUCOSA at the level of
the occlusal plane caused by traumatic irritants like CHEEK BITING, CLENCHING,
BRUXING, or ORTHODONTICS is LINEA ALBA.
1002. The single BEST method to diagnose LINEA ALBA is by its UNIQUE CLINICAL
APPEARANCE.
1003. The MOST COMMON intra-oral BENIGN neoplasm of C.T. origin that occurs on the
BUCCAL MUCOSA, LATERAL TONGUE BORDER, or LOWER LIP as a smooth, sessile
soft-to-firm tissue-colored nodule is an IRRITATION FIBROMA (TRAUMATIC FIBROMA).
1004. The most common cause of an IRRITATION FIBROMA is CHRONIC IRRITATION OR

TRAUMA.
1005. The most likely cause of an OPPORTUNISTIC infection presenting as a WHITE CREAMY
LESION on the BUCCAL MUCOSA or TONGUE that WIPES OFF is
PSEUDOMEMBRANOUS CANDIDIASIS (THRUSH).
1006. A pre-malignant WHITE THICK and FIRM PATCH or PLAQUE on the oral mucosa that
DOES NOT RUB OFF nor DISAPPEAR WHEN STRETCHED caused by TOBACCO and
CHRONIC IRRITATION is LEUKOPLAKIA.
1007. Due to their ability to undergo malignant transformation, ALL LEUKOPLAKIAS must be
BIOPSIED and COMPLETELY EXCISED.
1008. A 35-year old male presents with chief complaint “I have white stuff on my tongue.” The
patient’s history includes a recurrent low-grade fever and fatigue. The patient sometimes
feels cold and slightly ill. Current findings: a white coating on the tongue that WIPES OFF.
The etiology of this condition is a FUGAL INFECTION.
74
PIGMENTED LESIONS
1009. A painless, BLUE-BLACK or GRAY benign iatrogenic lesion visible clinically and
radiographically on the mandibular gingiva or buccal mucosa is an AMALGAM TATOO
(FOCAL ARGYROSIS).
1010. The MOST COMMON PIGMENTED LESION is an AMALGAM TATOO (FOCAL

ARGYROSIS).
1011. Small (pinhead) REDDISH-PURPLE hemorrhagic dots on the PALATE when tiny
capillaries bleed and leak blood into the oral mucosa due to trauma, infectious diseases,
vitamin C or K deficiency, and certain medications are PETECHIAE.
1012. Medications associated with PALATAL PETECHIAE include WARFARIN, HEPARIN,

NAPROXEN, PENICILLIN, and CARBAMAZEPINE.
1013. A 65-year old female presents with asymptomatic, abnormally dilated superficial veins
(reddish-purple) on the tongue’s VENTRAL and LATERAL surfaces called LINGUAL
VARICOSITIES.
1014. A pre-malignant degenerative skin condition found MAINLY ON THE LOWER LIP due to
chronic exposure to UVB radiation from SUNLIGHT is ACTINIC (SOLAR)
CHEILITIS/KERATOSIS.
1015. The most common intra-oral sites for SQUAMOUS CELL CARCINOMA are the posterior
VENTRO-LATERAL TONGUE BORDERS and FLOOR OF THE MOUTH, while the most
common extra-oral site is the vermillion border of the LOWER LIP.
1016. SQUAMOUS CELL CARCINOMA 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.
1017. An asymptomatic, oval-to-rhomboid shaped, smooth BEEFY-RED lesion on the TONGUE

DORSUM MIDLINE with loss of FILIFORM PAPILLAE due to chronic atrophic
candidiasis is MEDIAN RHOMBOID GLOSSITIS.
75
IMMUNOLOGY
1018. All cells in the immune system were derived from PRIMITIVE CELLS IN BONE
MARROW.
1019. Cellular movement to the site of inflammation in response to chemical signals is

CHEMOTAXIS.
1020. The cells FIRST TO RESPOND to an inflammatory reaction via chemotaxis are
NEUTROPHILS (WBCs).
1021. IMMUNE COMPLEX is formed by the combination of an ANTIBODY & ANTIGEN.
1022. A condition where the immune system identifies its own cells and tissues as foreign, and
signals antibodies to attack is an AUTOIMMUNE REACTION.
1023. The period of HIGHLY RAPID EXPONENTIAL bacterial GROWTH & REPRODUCTION
(cell doubling) is the LOG (EXPONENTIAL) PHASE.
1025. Bacteria that metabolize substance aerobically if oxygen exists, or anaerobically if

oxygen is absent are FACULTATIVE ANAEROBES.
NAESLUNDII.
1027. The gram (-) facultative anaerobe primarily responsible for AGGRESSIVE
PERIODONTITIS is A. ACTINOMYCETEMCOMITANS.
1028. Phagocytic cells that provide a non-specific cellular disease resistance mechanism (start
the immune process) are MACROPHAGES.
1029. PLASMA CELLS produce and secrete ANTIBODIES into the blood to fight foreign bodily
substances.
1030. PLASMA CELLS are derived from DIFFERENTIATED B-CELLS to synthesize

IMMUNOGLOBULINS.
1031. Inflammatory mediators produced by B-CELLS and T-CELLS that are critical in cellular
signaling and communication are CYTOKINES.
1032. The MOST ABUNDANT and only immunoglobulin (antibody) that CROSSES THE
PLACENTA and BINDS COMPLEMENT is IgG.
1033. The MOST ABUNDANT antibody found in CIRCULATION (BLOOD) and

EXTRACELLULAR FLUID with the ability to coat pathogens via OPSONIZATION is
IgG.
76
1034. The LEAST ABUNDANT immunoglobulin (1%) with unknown function, located on the
membrane surface of most circulating B-LYMPHOCYTES is IgD.
1035. The PRIMARY SALIVARY secretory immunoglobulin (antibody) that is also present in
MUCOUS SECRETIONS such as SWEAT and TEARS is IgA.
1036. The immunoglobulin found on MAST CELLS and BASOPHILS and is responsible for
promoting MOST TYPE I HYPERSENSITIVITY REACTIONS (allergic and
anaphylactic) is IgE.
1037. CONTACT DERMATITIS (red, itchy rash) due to a latex allergy or tuberculin skin test is
a T-cell mediated TYPE IV delayed hypersensitivity reaction.
1038. ACELLULAR OBLIGATE INTRA-CELLULAR PARASITES that replicate only inside

living cells are VIRUSES.
1039. A chronic infection of the face and neck caused by FILAMENTOUS, GRAM+
ANAEROBIC BACTERIA and triggered by an existing dental abscess or prior extraction
is ACTINOMYCOSIS (LUMPY JAW).
1040. The best method to test for ACTIVE TUBERCULOSIS is to examine the patient’s sputum
on a smear using the ACID FAST STAIN test for the bacteria MYCOBACTERIUM
TUBERCULOSIS.
1041. During the ACID FAST STAIN test, “acid-fast bacteria” RESIST de-colorization with
methylene blue dye and appear BRIGHT RED against a BLUE BACKGROUND under
the microscope.
1042. The MOST NUMEROUS circulating white blood cells during ACUTE INFLAMMATION is
the POLYMORPHONUCLEAR NEUTROPHILS (PMNs).
1043. The MOST ACTIVE CELL in the periodontal pocket and FIRST TO MIGRATE INTO
THE GINGIVAL SULCUS are POLYMORPHONUCLEAR NEUTROPHILS (PMNs).
1044. The main bacteria responsible for PREGNANCY GINGIVITIS and hormone-related
periodontal diseases is P. INTERMEDIA.
1045. The gram-negative bacterial rod primarily responsible for AGGRESSIVE

PERIODONTITIS is AGGREGATIBACTER ACTINOMYCETEMCOMITANS.
1046. The CDC recommends that the enzyme-linked immunosorbent assay (ELISA) is the
BEST test to SCREEN for LYME DISEASE, and THEN confirm the results using the
WESTERN BLOT TEST.
1047. A microorganism’s pathogenicity, or its ability to cause disease is VIRULENCE.
1048. Most pathogens that inhabit the human body due to its moderate temperature are
MESOPHILES.
77
1050. The respiratory virus implicated in COVID-19 is SARS-CoV-2.
1051. The antibodies that can arise in serum within 2-3 weeks after infection onset with SARS-
CoV-2 are IgM and IgG.
1052. Symptoms of COVID-19 include fever, cough, headache, myalgia, chills, and/or
shortness of breath.
1053. CD8 is a marker of CYTOTOXIC T-CELLS.
1054. CD4 bind to MHC class II on antigen-presenting cells.
1055. The T-cell ligand binding B7 on a professional antigen-presenting cell is CD28.
1056. A genuine nucleotide exchange factor (GEF) that promotes the conversion of Ras-GDP
to Ras-GTP is SOS (son of sevenless).
1057. In the immunological synapse the initial interaction between TCR and MHC is unstable.
1058. A primary function of the immunological synapse is to CEMENT the initially unstable
interactions between TCR and MHC to allow optimal T-cell activation.
1059. Lipopolysaccharide (LPS) from gram-negative bacteria is a POLYCLONAL ACTIVATOR

OF MURINE B-CELLS.
1060. T-cell help for antibody production depends on T-cell recognition of antigen processed
by the B-cell
1061. Activation of resting B-cells by T-helpers depends directly upon costimulatory

interaction between CD40 and CD40L.
1062. The main costimulatory signal for activation of resting T-cells is provided by ligation of
CD28.
1063. T-cell CD40L provides a costimulatory signal to B-cells by ligating CD40.
1064. A cytokine receptor that is a member of the hematopoietin receptor family is IL-2 receptor.
78
BIOCHEMISTRY, PHYSIOLOGY, AND NUTRITION
1065. A person with Phenylketonuria (PKU) is most likely deficient in the NON-
ESSENTIAL amino acid TYROSINE.
1066. A person with Phenylketonuria (PKU) should limit FOODS HIGH IN PROTEIN and
ASPARTAME in their diet due to their high PHENYLALANINE content.
1067. A SIMPLE CARBOHYDRATE formed by hydrolysis of glucose + fructose is SUCROSE.
1068. GLUCOSE, FRUCTOSE, & GALACTOSE are MONOSACCHARIDES, the simplest form
of carbohydrates.
1069. The body’s primary source of cellular energy and metabolism and known as
“BLOOD SUGAR” is GLUCOSE.
1070. DIETARY SUGARS and FERMENTABLE CARBOHYDRATES are converted by

HYDROLYSIS into LACTIC ACID by the enzyme SALIVARY AMYLASE in the dental
biofilm to initiate enamel demineralization.
1071. The metabolic pathway that produces GLUCOSE from non-carbohydrate precursors
like pyruvate, lactate, glycerol, and amino acids is GLUCONEOGENSIS.
1072. The purpose of GLUCONEOGENSIS is to MAINTAIN BLOOD GLUCOSE

CONCENTRATIONS.
1073. The MOST IMPORTANT & ABUNDANT ENERGY SOURCE FOR BODY METABOLISM
are CARBOHYDRATES.
1074. The RDA for digestible carbohydrates is 130 grams/day. The minimum daily adult
digestible carbohydrate intake is 50-100 grams/day to prevent wasting amino acids and
proteins as an energy source.
1075. DIABETES is characterized by ABNORMALLY HIGH BLOOD GLUCOSE LEVELS.
1076. The best clinical indicator to determine if a DIABETIC’S CONDITION is CONTROLLED is

the HbA1c level obtained through the GLYCOHEMOGLOBIN BLOOD TEST, which
provides an average amount of glucose in the blood.
1077. The HbA1c hemoglobin blood test goal for diabetics is between 6.5-7.0%
1078. TYPE II DIABETES is the MOST COMMON FORM of diabetes mellitus (80-90% of DM),
that mainly affects ADULTS, and is strongly associated with OBESITY
1079. OSTEOCLASTS cause CEMENTUM & BONE RESORPTION during orthodontic tooth
movement.
1080. The cell’s primary energy source where CELLULAR METABOLISM and CELLULAR
RESPIRATION takes place is in the MITOCHONDRIA.
79
1081. The organelles responsible for PROTEIN SYNTHESIS (TRANSLATION) in eukaryotes

and prokaryotes are RIBOSOMES.
1082. The internuclear non-membrane bound intranuclear body that is the SITE OF rRNA
SYNTHESIS is the NUCLEOLUS.
1083. The INACTIVE phase during which the cell spends most of its life metabolizing and
copying its DNA in preparation for MITOSIS is INTERPHASE.
1084. The FIRST stage of MITOSIS where chromatids condense is PROPHASE, while the
FINAL stage of MITOSIS where a cell divides into two daughter cells to complete cell
division is TELOPHASE.
1085. Bacterial appendages that ATTACH to surfaces and EXCHANGE GENETIC MATERIAL
are PILI.
1086. Dietary sources of COMPLETE PROTEINS that contain sufficient amounts of all nine
essential amino acids are MEAT, FISH, POULTRY, EGGS, and DAIRY.
1087. The MOST common WORLDWIDE cause of an enlarged thyroid (GOITER) is an

IODINE DEFICIENCY. Treat with iodine supplements in the diet.
1088. A component of many enzymes required for IRON METABOLISM and HEMOGLOBIN
FORMATION obtained from nuts, sees, whole grains, organ meats, and water is
COPPER.
1089. The MOST COMMON CAUSE of a GOITER in the U.S. is from overproduction or
underproduction of THYROID HORMONES or nodules that develop in the thyroid
gland.
1090. THYROID HORMONES (T3 and T4) physiological functions include increasing BMR, the
number of beta adrenergic receptors in the heart, and increases lipolysis and
glycogenolysis.
1091. A bone softening disorder due to a VITAMIN D DEFICIENCY after epiphyseal plate
closure that can also be caused by the anticonvulsant PHENYTOIN (DILANTIN) is
OSTEOMALACIA.
1092. A softening or weakening of BONES IN CHILDREN before epiphyseal plate closure

due to extreme and prolonged VITAMIN D DEFICENCY affecting calcium and phosphorus
absorption is RICKETS.
1093. FAT-SOLUBLE VITAMINS needed in small amounts in the diet for normal function,
growth, and maintenance of body tissues are vitamins A, D, E, K.
1094. The fat-soluble vitamin involved in COAGULATION is VITAMIN K.
1095. A lack of INTRINSIC FACTOR secreted in the stomach that prevents vitamin B12
absorption and decreased production of RED BLOOD CELLS causing weakness,
fatigue, and ATROPHIC GLOSSITIS (burning tongue) is PERNICIOUS ANEMIA.
80
1096. A disease caused by severe THIAMINE DEFICIENCY (B1) and by alcoholism due to poor
thiamine absorption is BERIBERI.
1097. The amount of energy the body burns at REST to maintain vital organs and bodily
functions EXCEPT DIGESTION AND PHYSICAL ACTIVITY is BASAL METABOLIC
RATE (BMR).
1098. BMR DECREASES with AGE and REDUCED MUSCLE MASS.
1099. An ACUTE and SEVERE PROTEIN DEFICIENCY associated with sufficient calorie
intake causing a PITTING EDEMATOUS APPEARANCE (swollen ankles and feet) in
impoverished children over 18 months of age is KWASHIORKOR.
1100. CHRONIC deprivation of CALORIES and ENERGY intake of all nutrients (proteins,
carbohydrates, and lipids), causing SEVERE MALNUTIRTION, EMACIATION, and
MUSCLE WASTING in 6-12 month year-old children of developing countries is
MARASMUS.
1101. A rare dietary deficiency of ASCORBIC ACID (VITAMIN C) resulting in swollen and
bleeding gingival tissues, petechial hemorrhages, delayed wound healing, and muscle
and joint pain is SCURVY.
1102. MOST important nutrient for COLLAGEN SYNTHESIS & WOUND HEALING is VITAMIN
C.
1103. A condition caused by a severe deficiency of NIACIN or TRYPTOPHAN with the classic
triad of symptoms diarrhea, dermatitis, and dementia is PELLEGRA.
1104. Vitamin B12 DEFICIENCY caused by atrophic gastritis, loss of gastric parietal cells, or lack
of intrinsic factor can lead to PERNICIOUS ANEMIA.
1105. A severe deficiency of FOLIC ACID (FOLATE) and VITAMIN B12 can cause
MACROCYTIC ANEMIA and INHIBIT DNA SYNTHESIS.
1106. FDA approved NON-NUTRITIVE SWEETENERS that non-caloric and offer no nutritional
benefits are ASPARTAME, SACCHARIN, SUCRALOSE, NEOTAME, and
ACESULFAME-K.
1107. An ANTICARIOGENIC and CARIOSTATIC NUTRITIVE SWEETENER shown to reduce

the growth of STREP MUTANS and new caries formation is XYLITOL.
1108. The greatest contributing risk factor for DENTAL CARIES is PLAQUE CONTROL.
1109. XYLITOL’s benefits that enable the enamel surface to remineralize are due to its ability
to destroy Strep Mutans, decrease biofilm adhesion, increase salivary flow, and increase
the oral pH.
1110. A person with Phenylketonuria (PKU) is most likely deficient in the NON-
ESSENTIAL amino acid TYROSINE.
81
1111. The non-essential amino acid and precursor molecule that produces epinephrine,
norepinephrine, and dopamine is TYROSINE.
1112. Phenylketonuria (PKU) is due to a genetic deficiency in the enzyme PHENYLALANINE

HYDROXYLASE causing the amino acid phenylalanine to accumulate in the body.
1113. 11 NON-ESSENTIAL amino acids are synthesized by the body and do not need to be
obtained from dietary means are Alanine, Arginine, Asparagine, Cysteine, Glutamic acid,
Glycine, Glutamine, Proline, Serine, and Tyrosine.
1114. Amino acids with acidic side chains are negatively charged and are PROTON DONORS.
Amino acids with basic side chains are positively charged and are PROTON
ACCEPTORS. BOTH TRUE
1115. The linear sequence of amino acids in the polypeptide chain and linkage of carboxyl
groups in the amino acid’s amino group describes the PRIMARY PROTEIN STRUCTURE.
Alpha-helix regions within the polypeptide chains and beta-pleated sheets held in shape
by hydrogen bonds that form between carbonyl O groups on one amino acid and the
amino H of another describes the SECONDARY PROTEIN STRUCTURE.
1116. FORCES that support and stabilize a TERTIARY PROTEIN’S STRUCTURE are ionic
bonding, hydrogen bonding, hydrophobic interaction, and disulfide bridges between
cysteine residues.
1117. Protein rigidity and proteolytic resistance is provided by the covalent cross-linking of
CYSTEINE RESIDUES.
1118. A degenerative disease like Alzheimer’s Disease is due to the deposition and
accumulation of abnormal and insoluble proteins (amyloids) in certain body tissues and
organs by AMYLOIDOSIS.
1119. A disease caused by MISFOLDED PROTIENS resulting in various degenerative diseases

is AMYLOIDOSIS.
1120. Elongated structural filaments comprised of protein polymers that often form microtubules
and are present in elastin, collagen, actin, and myosin are FIBRILLAR PROTEINS.
1121. A person with Phenylketonuria (PKU) should limit FOODS HIGH IN PROTEIN and
ASPARTAME in their diet due to their high PHENYLALANINE content.
1122. A SIMPLE CARBOHYDRATE formed by hydrolysis of glucose + fructose is SUCROSE.
1123. GLUCOSE, FRUCTOSE, and GALACTOSE are MONOSACCHARIDES, the simplest

form of carbohydrates.
1124. When the monosaccharides GLUOSE + GALACTOSE are linked together by glycosidic
bonds, the disaccharide formed is LACTOSE.
1125. One gram of carbohydrate provides 4.1 kcal of energy. One gram of protein provides
4.35 kcal of energy. BOTH TRUE.
82
1126. A monosaccharide that undergoes a condensation reaction or dehydration synthesis to

form lactose is GALACTOSE.
1127. The body’s primary source of cellular energy (fuel) and metabolism and known as
“BLOOD SUGAR” is GLUCOSE.
1128. Direct METABOLIC EFFECTS OF INSULIN are the stimulation of glucose transport and
muscle metabolism, triglyceride synthesis in adipose tissue, and glycolysis and glycogen
synthesis in the liver, as well as glucose uptake from the blood.

1130. The metabolic pathway that produces GLUCOSE from non-carbohydrate precursors
like pyruvate, lactate, glycerol, and amino acids and is critical for homeostatic blood
glucose maintenance is GLUCONEOGENSIS.
1131. The purpose of GLUCONEOGENSIS is to MAINTAIN BLOOD GLUCOSE

CONCENTRATIONS.
1132. The hormone produced by the adrenal cortex that helps the body’s stress response by
regulating gluconeogenesis is CORTISOL.
1133. The powerful inflammation-reduction hormone that stimulates gluconeogenesis and

mobilizes fatty acids from adipose tissue during times of stress is CORTISOL.
1134. The MOST IMPORTANT & ABUNDANT ENERGY SOURCE FOR BODY METABOLISM
are CARBOHYDRATES.
1135. The RDA for digestible carbohydrates is 130 grams/day. The minimum daily adult
digestible carbohydrate intake is 50-100 grams/day to prevent wasting amino acids and
proteins as an energy source.
1136. DIABETES is characterized by ABNORMALLY HIGH BLOOD GLUCOSE LEVELS.
1137. The anabolic hormone secreted by pancreatic beta cells that inhibits glycogenolysis,
promotes protein synthesis from amino acids, and increases glucose uptake from the
bloodstream is INSULIN.
1138. The balance of blood glucose and lipids in the body is controlled by INSULIN.
1139. A partial or complete loss of INSULIN function results in DIABETES MELLITUS,

HYPERGLYCEMIA, and DYSLIPIDEMIA.
1140. The best clinical indicator to determine if a DIABETIC’S CONDITION is CONTROLLED is

the HbA1c level obtained through the GLYCOHEMOGLOBIN BLOOD TEST, which
provides an average amount of glucose in the blood.
1141. The HbA1c hemoglobin blood test goal for diabetics is between 6.5-7.0%
83
1142. The major IRON-STORAGE PROTEIN present in nearly all body cells, but whose greatest
concentration is in liver HEPATOCYTES and RETICULOENDOTHELIAL CELLS is
FERRITIN.
1143. TYPE II DIABETES is the MOST COMMON FORM of diabetes mellitus (80-90% of DM),
that mainly affects ADULTS, and is strongly associated with OBESITY.
1144. The storage form of lipids found mainly in ADIPOSE TISSUE and in blood are
TRIGLYCERIDES.
1145. OSTEOCLASTS cause CEMENTUM & BONE RESORPTION during orthodontic tooth
movement.
1146. After a bone fracture there is an increase in OSTEOBLASTIC ACTIVITY to initiate repair.
1147. A MOTOR UNIT is comprised of ALL MUSCLE FIBERS innervated by one motor
neuron axon and that axon. Smaller, finer control muscles typically have fewer muscle
fibers per motor neuron axon than larger muscles.
1148. The sympathetic and parasympathetic nervous systems consist of EXTRINSIC NERVE
INNERVATION comprised of both AFFERENT (sensory) that carry impulses TOWARD
the CNS and EFFERENT (motor neurons) fibers that carry impulses AWAY from the CNS.
BOTH TRUE.
1149. SYMPATHETIC NERVOUS SYSTEM FIBERS originate between spinal cord segments
T1 & L2.
1150. The SYMPATHETIC nervous system consists of a SHORT preganglionic nerve axon and
originates from T1-T12 and L1-L3. The PARASYMPATHETIC nervous system consists
of a LONG preganglionic nerve axon and originates from cranial nerve nuclei III, VII, IX,
and X.
1151. Motor sensors arranged in parallel with extrafusal muscle fibers that detect static and
dynamic changes in muscle length are MUSCLE SPINDLES.
1152. Structures that comprise the majority of muscle and produce the PRIMARY FORCE for
muscle contraction are EXTRAFUSAL FIBERS.
1153. A proprioceptive sensory receptor organ that detects changes in MUSCLE TENSION
and lies at the origin and insertion of skeletal muscle fibers into the tendons of skeletal
muscle is the GOLGI TENDON ORGAN (GTO). GTO is the sensory component of the
golgi tendon reflex.
1154. Onion-shaped mechanoreceptors distributed throughout muscle fibers and skin to detect
vibration and pressure are PACINIAN CORPUSCLES.
1155. The cell’s primary energy source where CELLULAR METABOLISM and CELLULAR
RESPIRATION takes place is in the MITOCHONDRIA.
84
1156. Dark outer regions of skeletal muscle that contain THIN ACTIN and THICK MYOSIN
FILAMENTS are A-BANDS.
1157. The organelles responsible for PROTEIN SYNTHESIS (TRANSLATION) in eukaryotes

and prokaryotes are RIBOSOMES.
1158. The ribosomal subunit found in prokaryotes that is in integral part of mRNA translation
and is the site of inhibition for tetracyclines and aminoglycosides is the 30S subunit.
1159. The internuclear non-membrane bound intranuclear body that is the SITE OF rRNA
SYNTHESIS is the NUCLEOLUS.
1160. The INACTIVE phase during which the cell spends most of its life metabolizing and
copying its DNA in preparation for MITOSIS is INTERPHASE.
1161. MITOCHONDRIAL DNA is only passed genetically by maternal inheritance, does not
replicate on the cell cycle, and has a higher mutation rate than nuclear DNA. Nuclear DNA
and mitochondrial DNA both regulate mitochondria. BOTH TRUE.
1162. DNA is composed of a DEOXYRIBOSE SUGAR PHOSPHATE BACKBONE

NUCLEOTIDE.
1163. The FIRST stage of MITOSIS where chromatids condense is PROPHASE, while the
FINAL stage of MITOSIS where a cell divides into two daughter cells to complete cell
division is TELOPHASE.
1164. Bacterial appendages that ATTACH to surfaces and EXCHANGE GENETIC MATERIAL
are PILI.
1165. Dietary sources of COMPLETE PROTEINS that contain sufficient amounts of all nine
essential amino acids are MEAT, FISH, POULTRY, EGGS, and DAIRY.
1166. The MOST common WORLDWIDE cause of an enlarged thyroid (GOITER) is an

IODINE DEFICIENCY. Treat with iodine supplements in the diet.
1167. A component of many enzymes required for IRON METABOLISM and HEMOGLOBIN
FORMATION obtained from nuts, sees, whole grains, organ meats, and water is
COPPER.
1168. The MOST COMMON CAUSE of a GOITER in the U.S. is from overproduction or
underproduction of THYROID HORMONES or nodules that develop in the thyroid
gland.
1169. A bone softening disorder due to a VITAMIN D DEFICIENCY after epiphyseal plate
closure (adult) that can also be caused by the anticonvulsant PHENYTOIN (DILANTIN)
is OSTEOMALACIA.
1170. A softening or weakening of BONES IN CHILDREN before epiphyseal plate closure

resulting in bowed legs due to extreme and prolonged VITAMIN D DEFICENCY affecting
calcium and phosphorus absorption is RICKETS.
85
1171. WATER-SOLUBLE vitamins that are absorbed by the sodium cotransport systems are
VITAMINS C and B1-B12.
1172. FAT-SOLUBLE VITAMINS needed in small amounts in the diet for normal function,
growth, and maintenance of body tissues are vitamins A, D, E, K.
1173. FAT-SOLUBLE VITAMINS that A, D, and E behave like HORMONES. The only fat-
soluble vitamin that behaves as a coenzyme is VITAMIN K. BOTH TRUE.
1174. NIGHT BLINDNESS (Nyctalopia), decreased growth and development in children, and
impaired wound healing and tissue regeneration are characteristic of VITAMIN A
DEFICIENCY.
1175. The fat-soluble vitamin involved in BLOOD COAGULATION is VITAMIN K.
1176. Vitamin E deficiency is caused by fat malabsorption disorders such as CYSTIC

FIBROSIS, PANCREATITIS, BASSEN-KORNZWEIG SYNDROME, and SHORT-
BOWEL SYNDROME with symptoms of hemolytic anemia and neurological deficits.
Vitamin E does NOT produce toxic effects at any dose.
1177. A lack of INTRINSIC FACTOR secreted in the stomach that prevents vitamin B12
absorption and decreased production of RED BLOOD CELLS causing weakness,
fatigue, and ATROPHIC GLOSSITIS (burning tongue) is PERNICIOUS ANEMIA.
1178. The physiological mechanism that occurs with PERNICIOUS ANEMIA is stomach
parietal cells are destroyed by the immune system that stops intrinsic factor
production. Lack of intrinsic factor prevents vitamin B12 absorption to cause an
erythrocyte defect.
1179. A hemoglobin deficiency due to lack of functioning or damaged BONE MARROW

frequently due to cancer treatment is APLASTIC ANEMIA.
1180. A disease caused by severe THIAMINE DEFICIENCY (B1) and by alcoholism due to poor
thiamine absorption is BERIBERI.
1181. A DISULFIRAM-LIKE REACTION characterized by severe flushing, tachycardia, and

hypotension can occur when ALCOHOL is consumed with ingested METRONIDAZOLE,
SULFONAMIDES, or BACRTRIM due to increased acetaldehyde concentration in the
blood.
1182. THIAMINE (B1) deficiency can cause the diseases BERIBERI and KORSAKOFF’S
SYNDROME.
1183. A THIAMINE (B1) is a co-factor for dehydrogenase enzymes, thus a B1 deficiency can
potentially disrupt the KREB’S CYCLE (TCA).
1184. The amount of energy the body burns at REST to maintain vital organs and bodily
functions EXCEPT DIGESTION AND PHYSICAL ACTIVITY is BASAL METABOLIC
RATE (BMR).
1185. BMR DECREASES with AGE and REDUCED MUSCLE MASS.
86
1186. An ACUTE and SEVERE PROTEIN DEFICIENCY associated with sufficient calorie
intake causing a PITTING EDEMATOUS APPEARANCE (swollen ankles and feet) in
impoverished children over 18 months of age is KWASHIORKOR.
1187. The most common form of dementia that does not affect bodily movement that typically
affects patients > 65 years causing memory disturbances, cognitive decline, and
alterations in personality and behavior is ALZHEIMER DISEASE.
1188. Dopaminergic degeneration with neuronal loss in the SUBSTANTIA NIGRA on an MRI,
coupled with ipsilateral resting tremor in an upper extremity, are consistent findings
present with PARKINSON’S DISEASE.
1189. A depressed patient who presents with uncontrollable movements, muscle rigidity,
impaired gait, and genetic test results that reveals excessive cytosine-adenine-guanine
repeats most likely has HUNTINGTON DISEASE.
1190. CHRONIC deprivation of CALORIES and ENERGY intake of all nutrients (proteins,
carbohydrates, and lipids), causing SEVERE MALNUTIRTION, EMACIATION, and
MUSCLE WASTING in 6-12 month year-old children of developing countries is
MARASMUS.
1191. A rare dietary deficiency of ASCORBIC ACID (VITAMIN C) resulting in swollen and
bleeding gingival tissues, petechial hemorrhages, delayed wound healing, and muscle
and joint pain is SCURVY.
1192. The MOST important nutrient for COLLAGEN SYNTHESIS & WOUND HEALING is
VITAMIN C.
1193. The most abundant heterotrimeric protein in the body with high tensile strength properties
and composed of a triple helix of amino acids is COLLAGEN.
1194. Glycogen synthesis occurs in the CYTOSOL and requires ATP and UTP. Glycogen is
mainly found in the LIVER and SKELETAL MUSCLE. BOTH TRUE.
1195. An autosomal recessive glycogen storage disease that prevents the metabolism of
glycogen to glucose in muscles due to a deficiency in the enzyme
MYOPHOSPHORYLASE is MCARDLE DISEASE.
1196. The basic structural unit of a muscle is a SARCOMERE. Muscle contains MYOSIN that
forms THICK filaments and ACTIN that forms THIN filaments.
1197. The area of overlap between myosin and actin that includes the H band and contains the
entire length of a single thick filament is the A BAND.
1198. A condition caused by a severe deficiency of NIACIN or TRYPTOPHAN with the classic
triad of symptoms diarrhea, dermatitis, and dementia is PELLEGRA.
1199. The neurotransmitter derived from the amino acid TRYPTOPHAN that gets converted to
melatonin in the pineal gland is SEROTONIN.
87
1200. The conversion of serotonin into MELATONIN hormone used to help individuals with
sleep disorders occurs in the PINEAL GLAND.
1201. Vitamin B12 DEFICIENCY caused by atrophic gastritis, destruction of gastric parietal cells,
or lack of intrinsic factor can lead to PERNICIOUS ANEMIA and MEGALOBLASTIC
ANEMIA.
1202. A decrease in erythrocytes due to the body’s inability to absorb adequate B12 due to the
destruction of gastric parietal cells (weak stomach lining) or autoimmune condition is
PERNICIOUS ANEMIA.
1203. The hormone that stimulates gastric parietal cells to secrete HCL and intrinsic factor and
stimulates gastric mucosal growth in the colon and small intestine is GASTRIN.
1204. The hormone released from gastrointestinal tract cells that inhibits the release of all other
GI hormones and the secretion of gastric hydrogen ion is SOMATOSTATIN.
1205. A blood disorder that prevents hemoglobin release and inadequate distribution of oxygen
to body tissues with potential brownish-blue skin tone and shortness of breath due to the
absence of NADH-cytochrome b5 reductase enzyme is METHEMOGLOBINEMIA.
1206. A severe deficiency of FOLIC ACID (FOLATE) and VITAMIN B12 can cause
MACROCYTIC ANEMIA, GLOSSITIS, and INHIBIT DNA SYNTHESIS.
ACESULFAME-K.
1208. An ANTICARIOGENIC and CARIOSTATIC NUTRITIVE SWEETENER that inhibits the

growth of STREP MUTANS and new caries formation is XYLITOL.
to destroy Strep Mutans, decrease biofilm adhesion, increase salivary flow, and increase
the oral pH.
1210. The degradation of glycogen in liver and skeletal muscle during muscle contraction yields
the primary product GLUCOSE 1-PHOSPHATE.
1211. A glycogen storage disease caused by a deficiency in glucose-6-phosphatase liver

enzyme that impairs the liver’s ability to produce free glucose from glycogen and
gluconeogenesis is VON GIERKE’S DISEASE.
1212. The metabolic PENTOSE PHOSPHATE SHUNT PATHWAY occurs in the CYTOSOL and
is stimulated by the NADP+ substrate to generate NADPH and pentoses like ribose 5-
phosphate.
1213. The enzyme responsible for maintaining sufficient GLUTATHIONE and NADPH levels to
protect erythrocytes from oxidative damage is GLUCOSE 6-P DEHYDROGENASE.
1214. GLYCOGENESIS is the process that converts glucose-6-P to GLYCOGEN which occurs
in the CYTOSOL and requires ATP and UTP.
88
1215. The pathway that does not require oxygen and converts GLUCOSE into the end
product PYRUVATE by pyruvate kinase in the CYTSOL is GLYCOLYSIS. A deficiency
of pyruvate kinase may cause erythrocyte hemolysis and subsequent hemolytic anemia
since erythrocytes lack mitochondria. BOTH TRUE.
1216. A person deficient in the enzyme PYRUVATE KINASE due to a mutation in the PKLR
gene is at risk for HEMOLYTIC ANEMIA due to the potential of ruptured erythrocytes.
1217. During the initial step of GLYCOLYSIS, the phosphorylation (glycolytic degradation)
of glucose into glucose 6-phosphate to produce ATP is catalyzed by HEXOKINASE.
1218. Three major symptoms of DIABETES MELLITUS are polyuria, polydipsia, and
polyphagia.
1219. Molecules with covalently attached carbohydrates that are formed through the
glycosylation of amino acids at either the hydroxyl or amido group side chains are
GLYCOPROTEINS.
1220. Compounds that consist of different chemical structures, but the same chemical formula
are ISOMERS.
1221. Sterioisomers that are non-superimposable mirror images of each other are
ENANTIOMERS.
1222. HEMOGLOBIN molecules are critical in oxygen transport in blood and bind to 4
OXYGEN MOLECULES because each hemoglobin molecule contains 4 HEME
GROUPS.
1223. The two forms of HEMOGLOBIN molecules are the low oxygen affinity TAUT (Tense)
form and the high oxygen affinity R (Relaxed) form.
1224. Characteristics of the HEMOGLOBIN molecule are it CONTAINS 4 HEME GROUPS,

CARRIES OXYGEN TRANSPORTED BY RED-BLOOD CELLS, AND ARE INVOLVED IN
COOPERATIVE BINDING.
1225. The sensory pathway that relays sensory information from the SKIN to the THALAMUS
about crude touch, pain, temperature, firm pressure, itch, and sexual sensations is the
ANTEROLATERAL SYSTEM (SPINOTHALAMIC TRACT).
1226. The CNS somatosensory pathway that transmits localized sensations from the BODY to
the CEREBRAL CORTEX such as fine touch, vibration, and proprioception from the skin
and joints is the DORSAL COLUMN-MEDIAL LEMNISCUS.
1227. PASSIVE MEMBRANE TRANSPORT SYSTEMS that do NOT require energy to cross
a membrane because they only permit molecules to move down their concentration
gradients are facilitated diffusion, passive diffusion, and channel proteins.
1228. A passive carrier-mediated transport system the moves molecules DOWN their
concentration gradient as with the transport of glucose in fat and muscle cells is
FACILITATED DIFFUSION.
89
1229. Molecular movement across a membrane produced by the energy derived directly
from ATP breakdown that occurs UPHILL and against an electrochemical gradient is
PRIMARY ACTIVE TRANSPORT.
1230. The action of the SODIUM-POTASSIUM PUMP uses PRIMARY ACTIVE TRANSPORT.
1231. The POLAR REGIONS of the phospholipid bilayer are located at the bilayer surfaces and
are HYDROPHILIC. The NON-POLAR REGION is oriented toward the bilayer interior
shielded from water and is HYDROPHOBIC. BOTH TRUE.
1232. The mitochondrial enzyme that catalyzes the cleavage of Pyruvate into Acetaldehyde is
PYRUVATE DECARBOXYLASE.
1233. Carbohydrates are bridged with the TCA cycle and pyruvate is converted into acetyl-CoA
via the multi-enzyme PYRUVATE DEHYDROGENASE COMPLEX (PDC).
1234. A deficiency of pyruvate dehydrogenase during the Citric Acid Cycle (TCA) can result
in difficulty breathing, nausea, and CNS and neurological defects; symptoms consistent
with LACTIC ACIDOSIS due to lactate build-up.
1235. The metabolic pathway by which electrons are transferred from electron donors to electron
acceptors in redox reactions to release energy to form ATP is OXIDATIVE
PHOSPHORYLATION.
1236. The metabolic pathway of oxidative phosphorylation to produce ATP occurs in eukaryotes
in the MITOCHONDRIAL INNER MEMBRANE. The site of oxidative phosphorylation in
prokaryotes occurs on the ELECTRON TRANSPORT CHAIN. BOTH TRUE.
1237. The ELECTRON TRANSPORT CHAIN (ETC) exists in the inner mitochondrial
membrane of EUKARYOTES and in the plasma membrane of PROKARYOTES.
1238. The electron transport chain uses electron shuttles for redox reactions to OXIDIZE
NADH that is vital for energy production.
1239. A short-lasting occurrence during which the cell’s membrane potential rises and falls that
occurs in cells and in voltage-gated ion channels is ACTION POTENTIAL.
1240. The resting membrane potential of a cell in DORMANCY is -70mV.
1241. The opening of ion channels and inward flow of SODIUM IONS inside the cell resulting in
a less negative charge (more positive charge) inside the cell is DEPOLARIZATION.
1242. The waste product excreted in urine and formed mainly in the LIVER and in smaller
amounts in the kidneys and brain is UREA (CARBAMIDE). Urea is the product of
PROTEIN METABOLISM.
1243. An acid-base homeostatic mechanism that balances carbonic acid (H2CO3), bicarbonate
(HCO-3), and carbon dioxide (CO2) to maintain pH in the blood and body tissues to ensure
proper metabolic function is the BICARBONATE BUFFER SYSTEM.
90
1244. The BICARBONATE BUFFER SYSTEM is the most powerful extracellular buffer in the
body that contains a WEAK ACID (H2CO3) and a BICARBONATE SALT (NaHCO3). BBS
depends on carbonic anhydrase to form its weak acid, and it is at max capacity when
the pH is between 5.1 and 7.1.
1245. The product of oxidative deamination is AMMONIA.
1246. Urea cycle disorders due to HYPERAMMONEMIA (elevate serum ammonia) are
caused by deficiencies of Arginosuccinate lyase, Ornithine transcarbamylase, Carbamyl
phosphate synthetase I, and N-acetyl glutamate synthetase.
1247. A mitochondrial enzyme used in the citric acid cycle to carry acetyl groups into the cycle
is COENZYME A.
1248. Enzyme inhibition that occurs when the inhibitor and substrate bind at different
enzymatic sites is NON-COMPETITIVE INHIBITION.
1249. The aerobic pathway that transfers FOUR ELECTRON PAIRS during a single turn and
ultimately produces CARBON DIOXIDE waste product upon consuming acetate and
water is the CITRIC ACID (KREBS) CYCLE.
1250. A single turn of the CITRIC ACID (KREBS) CYCLE yields 3 NADH, 1 FADH2, 1 GTP,
and 2 CO2.
1251. The major fuel source for the CITRIC ACID (KREBS) CYCLE is ACETYL CoA.
1252. The liver’s metabolic pathway that recycles excess acetyl CoA to produce ketone
bodies during periods of starvation is KETOGENESIS.
1253. The oxidation of one ACETYL CoA molecule produces a total of 12 ATP.
1254. During the Kreb’s Cycle, the oxidation of one NADH by the ETC produces 3 ATP.
1255. The kidney’s functional unit that filters blood into urine, reabsorbs critical ions from
filtrate, and directs filtrate to renal cycles where it is converted into urine is the NEPHRON.
1256. The nephron portion that has principal cells that are stimulated by aldosterone and ADH
and intercalated cells that are stimulated by aldosterone is the LATE DISTAL TUBULE.
1257. The nephron structure impermeable to water that resorbs 8-10% of sodium ions filtered
out of the glomerulus is the EARLY DISTAL TUBULE.
1258. The nephron structure that resorbs MOST filtered sodium ions and water (68%) out of
the glomerulus is the PROXIMAL TUBULE.
1259. The hormone produced in the ZONA GLOMERULOSA of the adrenal cortex that
increases renal potassium secretion and renal sodium reabsorption (renal sodium
excretion) to produce an increase of extracellular fluid and blood volume is
ALDOSTERONE.
91
1260. The network of capillaries at the beginning of the nephron in the kidney that initially filters
blood passing through the capillaries into the lumen of Bowman’s capsule is the
GLOMERULUS.
1261. The cup-like sac that surrounds the glomerulus and performs ultrafiltration of blood to
form urine is BOWMAN’S CAPSULE.
1262. A critical cell membrane waxy component that produces all bodily steroids and vitamin D
and is. synthesized from 6 isopentyl pentophosphates and requires 18 acetyl CoA is
ESTEROL.
1263. Adrenergic neurons release the neurotransmitter NOREPINEPHRINE and cholinergic

neurons release the neurotransmitter ACETYLCHOLINE (released from ganglions of both
sympathetic and parasympathetic nervous systems).
1264. The neurotransmitter released from the ADRENAL MEDULLA that stimulates adrenergic
and dopaminergic receptors of the sympathetic nervous system to cause pupil dilation,
increased BP, decreased salivation and digestion during the fight or flight response is
NOREPINEPHRINE.
1265. The conversion and synthesis of cholesterol into steroid hormones in humans occurs in
the TESTES, OVARIES, and ADRENAL CORTEX.
1266. The rate-limiting and irreversible step in cholesterol synthesis and site of action for
STATINS is the production of MEVALONATE.
1267. A competitive enzyme and potential target for cholesterol lowering STATINS in plasma
is HYDROXYMETHYLGLUTARYL-CoA REDUCTASE to prevent the initial step in
cholesterol synthesis.
1268. The tetracyclic compound from which all animal and fungi cholesterol are derived is
LANOSTEROL. BILE, STEROID HORMONES, and CHOLESTEROL are then all derived
from CHOLESTEROL. BOTH TRUE.
1269. The enzyme that catalyzes LACTATE into PYRUVATE via an oxidation-reduction
reaction is LACTATE DEHYDROGENASE.
1270. During anaerobic glycolysis PYRUVATE is converted into the final end product
LACTATE. Lactate is present in RBCs, WBCs, ocular structures, and kidney. BOTH
TRUE.
1271. Star-shaped glial cells in the CNS responsible for biochemical support of endothelial that
form part of the blood-brain barrier (BBB) and aids in neuronal migration during
development are ASTROCYTES.
1272. The conduction of nerve impulses to the FOREBRAIN occurs through the PONS,
MEDULLA OBLONGATA (MYENCEPHALON), and MIDBRAIN brainstem divisions.
1273. A hormone that forms in the hypothalamus and is secreted by the posterior pituitary
gland to stimulate uterine contractions during labor and breast milk secretion during
suckling is OXYTOCIN.
92
1274. A hormone produced by the anterior pituitary gland that stimulates breast development
and breast milk production and is inhibited by dopamine is PROLACTIN.
1275. Cell bodies of the posterior pituitary gland that are located in nuclei of the hypothalamus
and secrete vasopressin and oxytocin hormones are called MAGNOCELLULAR
NEURONS.
1276. The region of the forebrain that regulates body temperature, hunger, thirst, and circadian
rhythms is the HYPOTHALAMUS.
1277. The primary plasma protein synthesized by the liver that transports hydrophobic fatty acids
in the blood and acts as a protein reserve during times of nutritional deficiency is
ALBUMIN.
1278. ALCOHOL DEHYDROGENASE is found in BLOOD VESSELS and the CYTOSOL to

break down potentially toxic alcohols.
1279. The hormonal system that regulates plasma sodium concentration, arterial blood
pressure, and vascular tone is the RENIN-ANGIOTENSIN SYSTEM (RAS).
1280. The RAS may be activated during hemorrhage or dehydration by baroreceptors with the
CAROTID SINUS.
1281. The primary function of RENIN hormone secreted from kidney JUXTAGLOMERULAR
CELLS is to INCREASE BLOOD PRESSURE to restore renal perfusion pressure.
1282. y-globulins are produced by PLASMA CELLS and differentiate from B-lymphocytes.
1283. Hydrophobic amino acids with a NON-POLAR side chain and do not donate protons are:
Alanine, Glycine, Isoleucine, Leucine, Methionine, Proline, Phenyalanine, Tryptophan,
and Valine.
1284. Amino acids with an uncharged POLAR side chain are: Asparagine, Cysteine, Glutamine,
Serine, Threonine, and Tyrosine.
1285. The air volume that can be inspired above and beyond the tidal volume during exercise is
INSPIRATORY RESERVE VOLUME (IRV).
1286. The measurement of air in the lungs after maximal inspiration and sum of TV + IRV +
ERV + RV is TOTAL LUNG CAPACITY (TLC).
1287. The air volume remaining in the lungs after maximal expiration capacity is RESIDUAL
VOLUME (RV).
1288. The air volume expired during a forced maximal expiration is TIDAL VOLUME (TV).
1289. The air volume remaining in the lungs after tidal volume is expired is FUNCTIONAL
RESIDUAL CAPACITY (FRC).
93
1290. The air volume that can be forcibly expired after a maximal inspiration calculated by IRV
+ ERV + TV is VITAL CAPACITY (VC). VC is the measurement of air expired after
maximal inspiration.
1291. Lung volumes that cannot be measured with SPIROMETRY are FRC and TLC because
they contain residual air volume.
1292. Functions of SALIVA include the formation of a food bolus, acting as a buffer to
maintain oral pH, washing away bacteria and food debris, destroying bacteria via
proteolytic enzymes, and carbohydrate metabolism.
1293. Anatomical structures lined with the distinctive fuzzy microvilli BRUSH BORDER are the
SMALL AND LARGE INTESTINES and PROXIMAL TUBULE.
1294. The primary function of the microvilli BRUSH BORDER is to INCREASE CELLULAR
SURFACE AREA TO AID IN ABSORPTION.
1295. The period of time immediately after the firing of a nerve fiber during which no action
potential is produced regardless of how intense the stimulus is the ABSOLUTE
REFRACTORY PERIOD.
1296. A GI peptide hormone secreted from duodenum and jejunum I cells that acts as a
hunger suppressant and stimulates the secretion of pancreatic enzymes and bicarbonate
ions is CHOLECYSTOKININ (CCK).
1297. CHOLECYSTOKININ (CCK) release stimulates gallbladder contraction and sphincter

of Oddi relaxation.
1298. A digestive hormone released from S cells of the duodenum that stimulates pancreatic
acinar cells to secrete water and bicarbonate to dilute HCL secreted by the stomach and
inhibits the secretion of gastrin is SECRETIN.
1299. The HUNGER HORMONE produced in the lining of the STOMACH that increases
appetite, initiates the release of growth hormone, and modulates the distribution and rate
of energy used in metabolism is GHRELIN HORMONE (LENOMORELIN).
1300. The “satiety hormone” comprised of adipose cells that circulates in the bloodstream and
travels to the brain to help regulate energy balance by INHIBITING HUNGER and opposes
the action of ghrelin is LEPTIN.
1301. A neuropeptide hormone released from neurons in the GI tract mucosa that
increases bowel motility by stimulating the secretion of electrolytes and water into
pancreatic juice and bile, and may communicate with postsynaptic targets to regulate
circadian rhythm is VASOACTIVE INTESTINAL PEPTIDE (VIP).
1302. The predominant neurotransmitter in the brain and used at neuromuscular junctions to
activate muscles and is concentrated in vesicles prior to its release in synapses is
ACETYLCHOLINE.
1303. An unspecialized afferent nerve fiber ending of a sensory neuron found in the skin that
detects painful stimuli is a FREE NERVE ENDING.
94
PHARMACOLOGY
PHARMACOKINETICS
1304. DOSE-RELATED adverse drug reactions include TOXICITY & SIDE-EFFECTS, NOT a
drug allergy.
1305. DRUG EFFICACY (CEILING EFFECT) is a drug’s ability to produce a desired therapeutic
effect REGARDLESS OF DOSAGE and is NOT RELATED to drug potency.
1306. If a drug has a half-life of 4 hours. Upon discontinuing the drug 94% will be eliminated in
16 hours.
1307. If 100mg of a drug with a half-life of 60 minutes is taken, after 60 minutes of being
administered, 50mg remains. After 120 minutes 25mg remains, and after 180 minutes,
12.5mg remains.
1308. The time required to reduce the concentration of a drug in the body by exactly 50% is:
HALF-LIFE (T ½.)
1309. The formula for a drug’s half-life is: (T ½ = 0.693 x Volume Distribution/Clearance)
1310. Patient variables that can affect a drug’s half-life: AGE, BLOOD CIRCULATION, DIET,
GENDER, HISTORY OF DRUG USE, KIDNEY and LIVER FUNCTION, SMOKING, and
OBESITY.
1311. To improve the patient’s withdrawal process, a patient with a history of prior drug use and
addiction or dependence potential is most appropriately prescribed a medication with a
LONG HALF-LIFE.
1312. The LOWEST DRUG CONCENTRATION NECESSARY to consistently produce

adequate anesthesia is POTENCY.
1313. The adverse drug reaction that is GENETICALLY related is an IDIOSYNCRATIC

REACTION.
1314. THE MAJOR EXCRETION ROUTE TO ELIMINATE FLUORIDE FROM THE BODY IS
URINE.
1315. The KIDNEY is the MAJOR organ responsible for drug EXCRETION and
ELIMINATION.
1316. Regulating potassium and sodium levels, releasing hormones, and eliminating
waste from the blood are all functions of the KIDNEY.
95
1317. The KIDNEY’S main functional component is the NEPHRON.
1318. THE MAJOR SITE OF DRUG METABOLISM is the LIVER by P-450 enzymes.
1319. The ENTERAL route of drug administration includes ORAL, RECTAL, and
SUBLINGUAL.
1320. A drug’s DISTRIBUTION across biologic membranes depends on drug type, patient
weight/age, blood flow to the organ, plasma-protein binding capacity, and the presence
of certain blood-brain barriers.
1321. FIRST-PASS EFFECT occurs with the ORAL ROUTE of drug administration where
the LIVER (PORTAL CIRCULATION) metabolizes some of the active drug before the
drug reaches the circulatory system to produce an effect.
1322. The SMALL INTESTINES are the MOST CRITICAL ABSORPTION SITE during the oral
route of drug administration.
1323. The PARENTERAL route of drug administration includes, INHALTION, INJECTIONS

(IV, IM, subcutaneous, intra-dermal, and intra-arterial).
1324. The parenteral route of administration with the MOST RAPID drug response and
best for an EMERGENCY situation is INTRAVASCULAR (IV).
1325. The MAJOR DISADVANTAGE of the INTRAVASCULAR (IV) route of drug

administration is the POTENTIAL FOR OVERDOSE.
1326. THE only amide local anesthetic metabolized in the BLOOD is ARTICAINE
(SEPTOCAINE).
1327. SURFACE AREA RULE is the MOST accurate method using WEIGHT IN KG to
determine the proper drug dose to safely administer to children.
1328. Medications that may cause GINGIVAL HYPERPLASIA (ENLARGEMENT) include

PHENYTOIN, CYCLOSPORINE, and CALCIUM CHANNEL BLOCKERS (Verapamil,
Amlodipine, & Nifedipine).
1329. Drugs that DO NOT cause gingival hyperplasia (ENLARGEMENT) are DIGOXIN,
BETA BLOCKERS, and TEGRETOL.
1330. PANS drugs (cholinergics and muscarinics) are CONTRAINDICATED for ASTHMA,
PEPTIC ULCERS, GI or URINARY OBSTRUCTIONS, and CARDIACE DISEASE.
1331. PANS drugs treat XEROSTOMIA, URINARY RETENTION, and GLAUCOMA.
1332. PANS (Parasympathetic Autonomic Nervous System) allows the body to REST &
DIGEST using the neurotransmitter ACETYLCHOLINE.
96
1333. The PRIMARY neurotransmitter for the SANS (Sympathetic Autonomic Nervous
System) is NOREPINEPHRINE, however ACETYLCHOLINE is present at SANS pre
and post ganglionic synapses.
1334. SANS FUNCTIONS include VASOCONSTRICTION, PUPIL & BRONCHIOLES

DILATION, and INCREASED HEART RATE.
1335. SANS is responsible for the “FIGHT or FLIGHT response via EPI and
NOREPINEPHRINE.
1336. ADRENERGIC DRUGS are CONTRAINDICATED for ANGINA, UNCONTROLLED

HYPERTENSION & UNCONTROLLED HYPERTHYROIDISM.
1337. ADRENERGIC DRUGS are INDICATED for COLDS (decongestant), anaphylactic

shock, ASTHMA, cardiac arrest, GLAUCOMA, and ADHD.
1338. ADRENERGIC DRUGS include ALBUTEROL, EPI, DOPAMINE, CLONIDINE, &

ADDERALL.
1339. ADRENERGIC drug that treats SHOCK, LOW BLOOD PRESSURE, and
PARKINSON’S DISEASE is DOPAMINE.
1340. EPINEPHRINE is CONTRAINDICATED in an abuser of methamphetamine or

COCAINE (the only anesthetic with vasoconstriction properties) who has used
either drug within 24 hours.
1341. ADRENERGIC drug that helps decrease withdrawal symptoms from OPIATES &
BENZODIAZEPINES is CLONIDINE.
97
RESPIRATORY DRUGS (BRONCHODILATORS)
1342. The BRONCHODILATOR and drug of choice for ACUTE ASTHMA is ALBUTEROL.
1343. INHALED CORTICOSTEROIDS like Budesonide (Pulmicort) or Fluticasone (Flovent)

are the drugs of choice for CHRONIC ASTHMA.
1344. A patient taking THEOPHYLLINE for CHRONIC ASTHMA or COPD should not be
prescribed ERYTHROMYCIN for a bacterial infection due to an increased chance of
SERUM TOXICITY.
1345. Drugs that are CONTRAINDICATED with asthmatics taking THEOPHYLLINE include
aspirin, NSAIDs, barbiturates, narcotics, and erythromycin.
1346. ASPIRIN is contraindicated in asthmatics taking THEOPHYLLINE due to aspirin’s

tendency to produce excess leukotrienes that may cause BRONCHOCONSTRICTION.
1347. The BEST analgesic for oral pain in an ASTHMATIC is ACETAMINOPHEN.
1348. COMMON SIDE EFFECTS of ALUBTEROL are tremor, anxiety, XEROSTOMIA,

headache, tachycardia, and INSOMNIA.
1349. 100% oxygen is contraindicated in patients with Chronic Obstructive Pulmonary

Disease (COPD), thus nitrous oxide should NOT be administered.
1350. ANTICHOLINERGICS like IPRATROPIUM (Atrovent) is the first drug of choice for long-
term COPD management.
1351. PREDNISONE (a synthetic glucocorticoid) can treat autoimmune disorders,

Addison’s Disease, COPD, and allergies.
1352. Significant adverse effects of PREDNISONE include adrenal gland suppression,

Cushing’s Syndrome, weight gain, increased blood glucose, peptic ulcers,
OSTEOPOROSIS, glaucoma, depression, anxiety, and insomnia.
98
ANTI-COAGULANTS AND ASPIRIN (SALICYLATES)
1353. The most common anticoagulant administered via injection (parenterally) to a

hospitalized patient is HEPARIN.
1354. Warfarin inhibits blood clotting by affecting the coagulation pathway to PREVENT
FIBRIN FORMATION. It prevents the conversion of inactive vitamin K to its active
form.
1355. An alcoholic taking WARFARIN may present clinically with PALATAL PETECHIAE.
1356. ASPIRIN’s MECHANISM OF ACTION is to INHIBIT PROSTAGLANDIN SYNTHESIS

by INHIBITING the enzyme CYCLOXYGENASE.
1357. PROSTAGLANDINS are FATTY MOLECULES derived from arachidonic acid involved in
inflammation, pain, and fever.
1358. ASPIRIN produces ANALGESIA, ANTIPYRETIC, and ANTI-INFLAMMATORY

EFFECTS.
1359. ASPIRIN is NOT used for patients with BLEEDING DISORDERS, ASTHMA,
CHILDREN WITH VIRAL INFECTIONS, PEPTIC ULCERS, nor during PREGNANCY.
1360. ASPIRIN inhibits BLOOD CLOTTING to cause PROLONGED BLEEDING by inhibiting

platelet aggregation.
1361. A potentially FATAL SYNDROME associated with CHILDREN taking ASPIRIN for a
viral infection like the chickenpox or flu is REYE’S SYNDROME.
1362. Classic features of REYE’S SYNDROME are RASH, VOMITING, and LIVER DAMAGE.
1363. IBUPROFEN and ASPIRIN are NSAIDs that INHIBIT PROSTAGLANDIN SYNTHESIS.
1364. IBUPROFEN (Motrin or Advil) is contraindicated if your patient takes LITHIUM for
bipolar disorder.
1365. ACETAMINOPHEN (TYLENOL) is an ANALGESIC AND ANTIPYRETIC, but is NOT an

anti-inflammatory (NSAID) and DOES NOT AFFECT PLATELET AGGREGATION
(CLOTTING).
1366. For a patient on anticoagulants (Coumadin/Warfarin) or with Peptic Ulcer Disease,

who has a headache and fever, the drug of choice is ACETAMINOPHEN (TYLENOL),
NOT IBUPROFEN or ASPIRIN.
99
1367. The best medication to manage DENTAL PAIN are NON-STEROIDAL ANTI-
INFLAMMATORY MEDICATIONS (NSAIDs like IBUPROFEN) because NSAIDs reduce
the inflammatory response responsible for most dental pain.
1368. For mild-to-moderate post-operative pain after a periodontal debridement or SRP

in a patient taking anticoagulants or with GI disease is ACETAMINOPHEN
(TYLENOL).
1369. The TOXICITY LIMIT of ACETAMINOPHEN is 15-25 grams. At levels ~ 20 GRAMS,

overdose reaches toxicity potentially causing hepatotoxicity and LIVER DAMAGE. BOTH
STATEMENTS TRUE.
1370. The recommended daily dose of ACETAMINOPHEN for adults is 650mg-1000mg

every 4-6 hours (not to exceed 4g/day). The recommended daily dose of
ACETAMINOPHEN for children is 15mg/kg every 6 hours (not to exceed 60mg/kg/day).
In adults, the minimum TOXIC DOSE as a single ingestion is 7.5-10g/day.
1371. ACUTE INGESTION of > 150mg/kg or 12g ACETAMINOPHEN for an ADULT is

considered a toxic dose and carries a HIGH RISK of LIVER DAMAGE.
1372. WARFARIN (COUMADIN) inhibits blood clotting by decreasing VITAMIN K synthesis

to PREVENT FIBRIN FORMATION.
1373. The MOST IMPORTANT test to determine if a patient taking anticoagulants is an

SRP or SURGICAL RISK due to potential prolonged bleeding is PROTHROMBIN
TIME (PT).
1374. NSAIDs DECREASE the effectiveness of MUSCLE RELAXANTS like Carisoprodol

(Soma).
100
ANTIHISTAMINES AND PROTON-PUMP INHIBITORS (PPIs)
1375. ANTIHISTAMINES mechanism of action BLOCKS natural histamine in the body at H1 &
H2 receptor sites to treat MILD ALLERGIC REACTIONS.
1376. An ALLERGIC REACTION is a drug effect that is UNPREDICTABLE and NOT DOSE-
RELATED.
1377. The MOST COMMON H1 antihistamine that treats mild allergic reactions and seasonal
allergies by blocking vasodilation, bronchi constriction, and capillary permeability is
BENEDRYL (Diphenhydramine).
1378. H2 antihistamines such as Pepcid, Tagamet, Zantac are important in blocking

GASTRIC ACID (HCL) SECRETION to treat duodenal ulcers, GERD, and Zollinger-
Ellison Disease.
1379. Common adverse effects of antihistamines are DROWSINESS, IMPAIRED THINKING,

XEROSTOMIA, and DIZZINESSS.
1380. H2 ANTIHISTAMINES (Tagamet), PROTON-PUMP INHIBITORS (Omeprazole

(Prilosec), and ANTACIDS (sodium bicarbonate), treat GERD and ulcers, after diet
and lifestyle changes are ineffective.
1381. H2 ANTIHISTAMINES ARE CONTRAINDICATED WITH ANTACIDS due to inhibited

absorption.
1382. GASTRIC ULCERATIONS do NOT cause gingivitis (gingival bleeding).
OPIOID ANALGESICS (NARCOTICS)
1383. The MOST COMMON OPIOD used in dentistry is CODEINE, prescribed as TYLENOL
3 when combined with Acetaminophen to treat MODERATE pain.
1384. OPIOIDS work by BLOCKING BRAIN PAIN RECEPTORS without loss of consciousness.
1385. The cardinal sign of an OPIOID OVERDOSE (HEROIN, MORPHINE, CODEINE) is

PINPOINT PUPILS (MIOSIS).
1386. The most appropriate analgesic for HEROIN ADDICTS are NSAIDs because they do
not alter consciousness.
1387. COCAINE users (NOT AN OPIOID and ILLEGAL) exhibit increased heart rate and
BP, sweating and DILATED PUPILS (MYDRIASIS).
101
1388. COCAINE or METHAMPHETAMINE abusers may present clinically with

GENERALIZED, ACTIVE DARK and RAMPANT CERVICAL CARIES (BUCCAL or
FACIAL sides).
1389. The most dangerous symptom of OPIOID overdose is RESPIRATORY

DEPRESSION, which can result in DEATH.
1390. An OPIOID ANTAGONIST administered IV, IM, or IN to reverse an ACUTE OPIOID

OVERDOSE is NARCAN (NALOXONE).
1391. A synthetic opioid used medically to treat NARCOTIC WITHDRAWAL and OPIOID
DEPENDENCE is METHADONE.
1392. METHADONE does NOT treat METHAMPHETAMINE ADDICTION.
1393. An ALLERGIC REACTION or ADVERSE EFFECT to NARCOTICS may include

DIZZINESS, DROWSINESS, CONSTIPATION, GI UPSET, NAUSEA, and
XEROSTOMIA.
ANTIBIOTICS AND ANTIFUNGALS
1394. The penicillin derivative when combined with clavulanic acid that is MOST EFFECTIVE
against bacteria that produce the beta-lactamase enzyme is AMOXICILLIN.
1395. PENICILLINS kill bacteria by competitively inhibiting TRANSPEPTIDASE ENZYME to

disrupt bacteria cell-wall synthesis. Penicillins are BACTERIOCIDAL. BOTH
STATEMENTS TRUE.
1396. The antibiotic of choice in DENTISTRY for non-penicillinase producing oral

infections in a pregnant woman who denies allergies is PENICILLIN VK.
1398. If penicillinase is cultured from an infection, AUGMENTIN (amoxicillin + clavulanic

acid) should be given NOT just Amoxicillin.
1399. PENICILLINS are effective against bacteria by INHIBITING CELL WALL SYNTHESIS
BY LYSIS.
1400. The prophylactic antibiotic of choice and dosage in a non-penicillin allergic patient
one-hour before dental treatment to prevent bacterial endocarditis is AMOXICILLIN
(2 grams).
1401. AMOXICILLIN and AMPICILLIN are contraindicated in patients with INFECTIOUS

MONONUCLEOSIS due to the increased risk of MACULOPAPULAR EXANTHEMS.
102
1402. A MAJOR disadvantage of penicillin compared to other antibiotics is its high

incidence of ALLERGIC REACTIONS.
1403. The FIRST antibiotic PRE-MEDICATION ALTERNATIVE for a penicillin-allergic

patient with congenital heart disease and artificial heart valves is CLINDAMYCIN
(600mg before the dental procedure).
1404. A 62-year old male with no allergies presents for root planing. He had bilateral hip
replacement surgery nearly two years ago without complication, has mitral valve
prolapse with regurgitation, and has a cardiac pacemaker. The appropriate antibiotic
prophylaxis is PRE-MEDICATION IS NOT REQUIRED.
1405. Antibiotic prophylaxis to prevent infective endocarditis is REQUIRED for patients with
PROSTHETIC HEART VALVES, HISTORY OF ENDOCARDITIS, or TETROLOGY OF
FALLOT.
1406. A rare, but dangerous adverse effect of taking CLINDAMYCIN is

PSEUDOMEMBRANOUS COLITIS (overgrowth of Clostridium difficile that produces a
toxin causing colitis).
1407. TETRACYCLINES (Minocycline & Doxycycline) can concentrate in GINGIVAL

CREVICULAR FLUID (GCF) thus may be inserted into the gingival sulcus to treat
periodontal disease.
1408. The MOST COMMON topical antifungal in DENTISTRY to treat CANDIDIASIS is

NYSTATIN.
1409. NITROMIDAZOLES such as Metronidazole (Flagyl) are antibiotics that treat infections
only caused by OBLIGATE ANAEROBES.
1410. ALCOHOL (and alcohol-containing mouth-rinse) are contraindicated with

METRONIDAZOLE (Flagyl) due to its abuse-like adverse effects such as abdominal
pain, nausea, vomiting, high BP, rapid heart rate, and liver damage.
1411. COMBINATION DRUG THERAPY (MULTI-DRUG THERAPY) with an antibiotic like

RIFATER or RIFAMATE is the standard to treat tuberculosis (TB).
1412. DO NOT PROVIDE DENTAL TREATEMENT ON an ACTIVE TUBERCULOSIS (TB)

patient and consult their treating physician.
1413. The Tuberculin Purified Protein Derivative (PPD) TB skin test is a DELAYED
HYPERSENSITIVITY test.
1414. Due to its rapid excretion by the kidney via tubular secretion, PENICILLIN “G” has a half-
life of 0.5 hours.
103
ANTIVIRALS AND VIRUSES

1415. ANTIVIRAL DRUGS treat viral infections by INHIBITING VIRAL DNA SYNTHESIS.
1416. The drug of choice to treat COLD SORES caused by HSV-1 is ACYCLOVIR
(ZOVIRAX) or VALTREX.
1417. HEPATITIS A, C, D, E are RNA viruses, while HEPATITIS B is a DNA virus.
1418. The infectious particle found in a HEPATITIS B POSITIVE patient is the DANE
PARTICLE.
1419. HEPATITIS virus HAS THE HIGHEST RESISTANCE to chemical and physical agents
(greater than HERPES, AIDS, MEASLES, or INFLUENZA).
1420. The major cellular defect caused by HIV infection is DEPLETION OF HELPER CD4+ T-
LYMPHOCYTE CELLS that lead to opportunistic infections.
1421. HIV is a RETROVIRUS (LENTIVIRUS) responsible for the fatal illness AIDS. A
“retrovirus” has RNA as its nucleic acid.
1422. Potential oral pathology caused by opportunistic infections in an HIV + individual are
HAIRY LEUKOPLAKIA, ORAL CANDIDIASIS, & KAPOSI’S SARCOMA.
1423. The MOST common oral manifestation found in an HIV + patient is ORAL CANDIDIASIS
due to immunosuppression.
1424. INFECTIOUS MONONUCLEOSIS and HAIRY LEUKOPLAKIA are both caused by the
EPSTEIN-BARR VIRUS (EBV).
1425. The classic triad of symptoms with INFECTIOUS MONONUCLEOSIS are FEVER,
PHARYNGITIS, and LYMPHADENOPATHY.
1426. The virus responsible for both CHICKENPOX and SHINGLES is VARICELLA
ZOSTER.
1427. The virus that causes HAND-FOOT-AND-MOUTH DISEASE and HERPANGINA is

COXSACKIE VIRUS.
1428. An acute COXSACKIE virus affecting YOUNG CHILDREN that begins with flu-like
symptoms and oral ulcerations/vesicles on the POSTERIOR PALATE & TONSILS, and
typically resolves within one week with palliative treatment is HERPANGINA.
1429. An RNA virus caused by the RUBELLA VIRUS via air droplets from coughing is the
GERMAN MEASLES.
1430. Small, irregular red macules with bluish-white necrotic centers on the BUCCAL
MUCOSA and SOFT PALATE in a patient diagnosed with the RNA MEASELS
(RUBEOLA) VIRUS are called KOPLIK SPOTS.
104
LOCAL ANESTHETICS
1431. Allergic reactions to amides are RARE, but if they occur, are most likely caused by the
PRESERVATIVE (SODIUM BISULFATE or SODIUM METABISULFATE) in the
anesthetic solution.
1432. The purpose of SODIUM BISULFITE in an anesthetic that contains a vasoconstrictor is

to serve as a PRESERVATIVE BY PREVENTING OXIDATION.
1433. An ALKALIZING AGENT added to local anesthetics is SODIUM HYDROXIDE, which

makes the anesthetic solution BASIC.
1434. The MECHANISM OF ACTION of local anesthetics is to BLOCK PERIPHERAL NERVE

CONDUCTION by decreasing the permeability or uptake of Na+ (sodium ion)
channels.
1435. The effects of INFLAMMATION that DECREASE A LOCAL ANESTHETIC’S EFFECTS

are decreased tissue pH, edema, and increased vascularity.
1436. During local anesthetic administration, SMALL, NON-MYELINATED “C” FIBERS are
blocked FIRST and regain sensation LAST.
1437. Local anesthetics inhibit the INFLUX of SODIUM IONS by competing with CALCIUM
IONS for binding sites.
1438. Local anesthetics DO NOT PREVENT POTASSIUM (K+) EFFLUX into the nerve cell.
1439. Local anesthetics DECREASE DEPOLARIZATION RATE but INCREASE the

REPOLARIZATION RATE.
1440. MOTOR is the LAST function lost, but first function regained with local anesthetics.
1441. ESTERS (BENZOCAINE) are mainly used for TOPICAL APPLICATION, have a greater
potential for allergic reaction, and are metabolized in the BLOOD.
1442. LIDOCAINE (XYLOCAINE) is the most common local anesthetic used in dentistry,
may be found in topical anesthetic agents, and is an IV ANTI-ARRHYTHMIC AGENT
to treat life-threatening ventricular arrhythmias.
1443. The current recommended dosage of 2% LIDOCAINE with 1:100K EPI is 7mg/kg for
ADULTS and 4.4 mg/kg for CHILDREN.
1444. The amide local anesthetic safe during PREGNANCY and LACTATION is
LIDOCAINE.
1445. Symptoms of SEVERE LOCAL ANESTHETIC TOXICITY are SEIZURES,

RESPIRATORY DEPRESSION, COMA and DEATH.
105
1446. PRILOCAINE is not used for patient with HYPOXIC CONDITIONS (oxygenation
problems), Hepatic (liver) disease, or patients with METHEMOGLOBINEMIA (iron in
hemoglobin does not effectively carry oxygen).
1447. PRILOCAINE has a LONGER DURATION but LOWER epinephrine content

(1:200,000) than lidocaine.
1448. BUPIVACAINE (MARCAINE) has the LONGEST DURATION OF ACTION of any dental
local anesthetic available.
1449. The amide local anesthetic best for extended procedures and when post-operative
pain is expected is BUPIVACAINE due to its long duration of action.
1450. MEPIVACAINE (CARBOCAINE) has the SHORTEST DURATION OF ACTION of all

amides.
1451. ARTICAINE (SEPTOCAINE) is the only amide local anesthetic metabolized in the
BLOOD.
1452. All amide local anesthetics except articaine (septocaine) are metabolized in the LIVER.
1453. All amides are INACTIVATED by the enzyme MONOAMINE OXIDASE.
1454. A patient with a history of ischemic heart disease and congestive heart failure (CHF) is
taking sympatholytic medications (monoamine oxidase inhibitor and nonselective
beta blocker) to manage his condition. When this patient presents to the dental office for
a dental procedure requiring local anesthesia, AVOID ADMINISTERING LIDOCAINE 2%
WITH 1:50,000 EPI (best practice is DO NOT USE HIGH CONCENTRATIONS OF EPI).
1455. MAXIMUM recommended dose of Articaine (Septocaine) recommended in one

appointment for children and adults 7mg/kg (490mg). Therefore, the maximum
recommended amount of Articaine for a 70kg adult in one appointment is 490mg.
1456. EPINEPHRINE is a VASOCONSTRICTOR that may be added to local amide anesthetics

to PROLONG THE DURATION OF ANESTHESIA, decrease bleeding and anesthetic
toxicity, and delay vascular absorption.
1457. EPINEPHRINE is CONTRAINDICATED in an UNCONTROLLED HYPERTENSIVE

PATIENT.
1458. HEADACHE, HYPERTENSION, TACHYCARDIA, & PALPITATIONS are OVERDOSE

EFFECTS OF EPINEPHRINE.
1459. LOCAL ANESTHETICS are a MIXTURE of local anesthetic agent, antioxidant,

alkalizing agent, sodium chloride, and a preservative.
1460. Local anesthesia occurs by blocking INTRACELLULAR SODIUM CHANNEL

RECEPTORS in the neuron to prevent nerve impulse conduction in the presence of a
painful stimulus.
106
1461. Local anesthesia is achieved when SODIUM CHANNELS are engaged by CHARGED
RNH+ INTRACELLULAR CHARGED MOLECULES.
1462. The MANIDBULAR FORAMEN is the terminal landmark to deposit local anesthetic
during an INFERIOR ALVEOLAR NERVE BLOCK.
1463. The anesthetic technique that provides anesthesia to the INFERIOR ALVEOLAR NERVE,
BUCCAL NERVE, MYLOHYOID NERVE, and LINGUAL NERVE is the GOW-GATES
MANDIBULAR BLOCK.
1464. Specialized SENSORY nerves that detect painful stimuli during a local anesthetic
injection and initiate a signal to the CNS are NOCICEPTORS.
1465. The anatomical landmark located on the mandible’s EXTERNAL (LATERAL) surface
that serves as the EXIT for the inferior alveolar nerve’s superficial terminal branch is the
MENTAL FORAMEN.
1466. Penetrating the needle too far posteriorly and injecting into the PAROTID GLAND during
an inferior alveolar nerve block can result in BELL’S PALSY (FACIAL NERVE
PARALYSIS).
1467. When administering a POSTERIOR SUPERIOR ALVEOLAR (PSA) nerve block OVER-
INSERTING the needle may cause a HEMATOMA by piercing the PTERYGOID VENUS
PLEXUS or MAXILLARY ARTERY.
1468. To decrease the chance of systemic toxicity and PREVENT an INTRAVASCULAR

INJECTION, it is best practice to ASPIRATE THE SYRINGE during an injection to
ensure there is no blood present in the anesthetic cartridge.
1469. An accidental rapid intravascular injection of a vasoconstrictor-containing local

anesthetic can induce RESPIRATORY DEPRESSION, SYNCOPE, CONVULSIONS, and
PALPITATIONS.
1470. A local anesthetic indicated for LONG-LASTING anesthesia during complex periodontal
surgery that can also provide lingering anesthesia is BUPIVICAINE 0.5%:1:200K EPI.
1471. The best needle gauge to REDUCE ASPIRATION RISK in highly vascularized intra-oral
areas is a 25 GAUGE NEEDLE.
107
ANTI-ANXIETY AGENTS AND GENERAL ANESTHESIA

1472. BARBITURATES are contraindicated in patients with respiratory disease, during
pregnancy and alcoholics.
1473. Two main classes of anti-anxiety agents, BENZODIAZEPINES and BARBITURATES,

both produce SEDATION to relieve anxiety, but DO NOT PRODUCE ANALGESIA.
1474. Benzodiazepines and Barbiturates produce their calming effects by DEPRESSING THE
CNS LIMBIC SYSTEM & RETICULAR FORMATION via the central inhibitor
neurotransmitter (neurons) gamma-amino-butyric acid (GABA).
1475. BARBITURATES are ABSOLUTELY contraindicated in patients with a family history

of PORPHYRIA (enzyme deficiency) since they induce P450 enzymes which contain
heme.
1476. CYTOCHROME P450 INDUCERS include ANTICONVULSANTS (PHENYTOIN &

TEGRETOL), BARBITURATES (Phenobarbital), and ST. JOHN’S WART.
1477. BARBITURATES are CONTRAINDICATED with RESPIRATORY DISEASE and

PREGNANCY.
1478. The benzodiazepine ANTAGONIST used to REVERSE the residual effects of a

benzodiazepine OVERDOSE is FLUMAZENIL (MAZICON).
1479. A BENZODIAZEPINE that REVERSES STATUS EPILEPTICUS & SEIZURES

associated with local anesthetic overdose is VALIUM (DIAZEPAM).
1480. A BENZODIAZEPINE such as DIAZEPAM (VALIUM) may be given BEFORE GENERAL

ANESTHESIA.
1481. The General Anesthesia stage where most MAJOR SURGERY is performed is
STAGE III.
1482. The Stage of General Anesthesia where NITROUS OXIDE is used in dentistry is
STAGE I.
1483. NITROUS OXIDE (N2O) works by ELEVATING THE PAIN THRESHOLD.
1484. NITROUS OXIDE is contraindicated in the 1st Trimester of Pregnancy, COPD, cystic
fibrosis, sickle-cell anemia, upper respiratory infections, and patients with
EMOTIONAL or BEHAVIORAL INSTABILITY.
1485. NITROUS OXIDE is NOT contraindicated with ASTHMATICS, DIABETES, or

HYPERTENSION.
1486. N2O can effectively REDUCE OROFACIAL MUSCLE TONE IN CEREBRAL PALSY
PATIENTS during dental treatment.
108
1487. The color of NITROUS OXIDE storage cylinder tanks are BLUE.
1488. The color of OXYGEN storage cylinder tanks are GREEN.
1489. NITROUS OXIDE has a RAPID ONSET and RAPID RECOVERY (about 5 minutes).
1490. Always administer 100% oxygen for 3-5 minutes after the procedure when using
NITROUS OXIDE-OXYGEN (N2O-O2) to prevent DIFFUSION HYPOXIA.
1491. Vomiting and nausea are adverse effects of a NITROUS OXIDE OVERDOSE.
ANTI-HYPERTENSIVES
BETA BLOCKERS
1492. BETA BLOCKERS TREAT: HEART ATTACK, ANGINA, CARDIAC ARRHYTHMIAS,
MIGRAINES, GLAUCOMA, HYPERTHYROIDISM, and STAGE FRIGHT.
1493. NON-SELECTIVE BETA BLOCKERS are CONTRAINDICATED in patients with

ASTHMA or REACTIVE AIRWAY DISEASE.
1494. A patient with asthma or COPD should NOT take a non-cardioselective beta blocker
like Propranolol to treat hypertension because it can block the dilation effects of drugs like
Albuterol which can lead to bronchoconstriction.
1495. To prevent a severe vasopressor response, TRY TO AVOID EPINEPHRINE with

patients taking non-selective beta blockers like Propranolol or Timolol.
1496. The FIRST LINE drug to treat congestive heart failure (CHF) are BETA BLOCKERS (not
Digoxin).
1497. BETA 1 RECEPTORS are mainly in the HEART and KIDNEYS, while BETA 2
RECEPTORS are located mainly in the LUNGS, GI TRACT, LIVER, MUSCLES, and
ARTERIOLES.
1498. MOST COMMON and FIRST DEVELOPED NON-SELECTIVE beta blocker is

PROPRANOLOL.
1499. The non-selective BETA BLOCKER to treat OPEN-ANGLE GLAUCOMA by reducing

AQUEOUS HUMOR production is TIMOLOL.
1500. MOST SERIOUS SIDE EFFECTS of TIMOLOL are CARDIAC ARRHYTHMIAS &
BRONCHOSPASMS.
1501. TIMOLOL is NOT USED in patients with ASTHMA or COPD, severely slow or rapid
heart rate, heart blockage, or heart failure.
1502. According to the AHA, a hypertensive crisis occurs when the patient’s systolic
pressure is > 180 mm Hg OR diastolic pressure is > 110 mm Hg.
109
1503. Oral manifestations of Calcium Channel Blockers such as Nifedipine and Verapamil
are GINGIVAL HYPERPLASIA and XEROSTOMIA.
DIURETICS
1504. DIURETICS decrease BLOOD PRESSURE & BLOOD VOLUME by promoting sodium
and water excretion.
1505. THIAZIDES ARE THE MOST WIDELY USED diuretics to treat hypertension, specifically
HYDROCHLOROTHIAZIDE (HCTZ) in patients with NORMAL KIDNEY FUNCTION.
1506. DIURETICS-the first therapy of choice for HYPERTENSION (high BP).
1507. The first line diuretic for a hypertensive patient with IMPAIRED KIDNEY FUNCTION is
the LOOP DIURETIC LASIX (Furosemide).
ACE INHIBITORS AND STATINS
1508. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE INHIBITORS) such as

Lisinopril treat HYPERTENSION and CHF by “inhibiting” the conversion of inactive
Angiotensin I→Angiotensin II to lower blood pressure.
1509. A relatively common oral side effect of ACE inhibitors such as Lisinopril is DYSGEUSIA
(altered taste sensation).
1510. The effectiveness of ACE inhibitors is decreased if the patient takes NSAIDs
(IBUPROFEN).
1511. STATINS lower BLOOD LDL CHOLESTEROL (increases LDL catabolism) and lower
triglycerides by BLOCKING the key enzyme responsible for cholesterol synthesis
in the liver called HMG-CoA Reductase.
1512. STATINS like LIPITOR (Atorvastatin) may cause adverse effects such as GI upset,
muscle and joint pain.
1513. STATINS like LIPITOR (Atorvastatin) are contraindicated in pregnant woman and
patients taking anticoagulants like Warfarin (Coumadin) since statins may increase the
anticoagulant effect.
110
ANTI-ANGINAL DRUGS
1514. Nitroglycerin/Nitrostat (Amyl Nitrate) is the single most effective drug of choice for an
ACUTE ANGINA PECTORIS ATTACK.
1515. Nitroglycerin is fast-acting and effective within 2-4 minutes if administered

SUBLINGUALLY for angina attacks (must be present in the dental emergency kit).
1516. Alcohol (Ethanol) combined with NITROGLYCERIN can cause dangerously low
blood pressure (hypotension).
ANTI-CONVULSANT DRUGS
1517. The anti-seizure medication mainly used to treat TRIGEMINAL NEURALGIA in
dentistry is Carbamezepine (Tegretol).
1518. Multiple Sclerosis is a complex and progressive autoimmune disorder that damages the
myelin sheaths of nerve cells. A potential early symptom of MS in a person under 60-
years of age is TRIGEMINAL NEURALGIA.
1519. A common oral manifestation found in patients taking the anticonvulsant PHENYTOIN
(DILANTIN) is gingival enlargement due to a folate deficiency.
HYPOGLYCEMICS (ANTI-DIABETICS) AND

ENDOCRINE IMBALANCE DRUGS
1520. HYPOGLYCEMIA is the most serious and common complication of INSULIN

INJECTION therapy for Diabetes Mellitus Type 1 causing sweating, weakness,
confusion, slurred speech, & blurred vision, but NOT shortness of breath.
1521. In the event of a hypoglycemic reaction (insulin shock), promptly administer

concentrated glucose (orange juice) or simple carbohydrate source to relieve mild
hypoglycemia.
1522. If untreated, hypoglycemia can lead to a seizure or unconsciousness, in which case a

GLUCAGON INJECTION should be administered.
1523. The first-line oral hypoglycemic of choice to treat DIABETES MELLITUS TYPE 2
(Non-Insulin Dependent) when exercise and diet have failed is METFORMIN
(GLUCOPHAGE).
1524. METFORMIN functions mainly by DECREASING BASAL HEPATIC

GLUCONEOGENESIS and secondarily by IMPROVING PERIPHERAL INSULIN
SENSITIVITY.
111
1525. METFORMIN benefits include regulating blood glucose, weight control and loss,
decreased LDL and triglycerides, and increased HDL.
1526. The most common cause of HYPOTHYROIDISM in the U.S., affecting more women
than men is the autoimmune disorder HASHIMOTO’S DISEASE (THYROIDITIS).
1527. A rare, but life-threatening sequela from suddenly discontinuing SYNTHROID

(Levothyroxine) for HYPOTHYROIDISM is MYXEDEMA COMA.
1528. If a hypothyroid patient’s SYNTHROID dosage is too low, they may become COLD
INTOLERANT.
1529. An adrenal gland disorder causing CORTISOL and ALDOSTERONE DEFICIENCIES

with BRONZING OF THE SKIN is characteristic of ADDISON’S DISEASE.
1530. Chronic use of prescribed corticosteroids or CORTISOL HYPERSECRETION resulting in

MID-SECTION WEIGHT GAIN, BUFFALO NECK HUMP, and MOON FACE is CUSHING
SYNDROME.
1531. SYSTEMIC CORTICOSTEROIDS are indicated to therapeutically treat auto-immune

related conditions like RHEUMATOID ARTHRITIS, LUPUS, CROHN’S DISEASE, and
PSORIASIS.
1532. Use caution when administering local anesthetics containing EPINEPHRINE to a patient
taking SYNTHROID for hypothyroidism.
1533. ESTROGEN-REPLACEMENT THERAPY is the most effective treatment to relieve hot

flashes and night sweats due to menopause, but can cause adverse effects like
GINGIVITIS, breast cancer, stroke, and heart attack. NOT OSTEOPOROSIS or
XEROSTOMIA (dry mouth).
1534. The primary and MOST POTENT estrogen-steroid sex hormone produced in females
is ESTRADIOL (E2) used to treat infertility, menopause and menstrual disturbances, and
post-menopausal osteoporosis.
1535. PREMARIN and ESTRADERM are effective ESTROGEN-REPLACEMENT THERAPY

medications for post-menopausal women who experience adverse symptoms of
menopause.
1536. During PREGNANCY, there is an increase in ESTROGEN during the first trimester
and an increase in PROGESTERONE which may lead to GINGIVITIS.
1537. The MOST COMMON adverse effects of ESTRADIOL: upset stomach (nausea and
vomiting), headache, or weight changes.
1538. Drugs that are SAFE during pregnancy include: local anesthetics with or without EPI,
acetaminophen, Penicillin VK, Amoxicillin, Cephalosporins, Clindamycin, and Nystatin.
1539. Local anesthetics administered during dental treatment DO NOT AFFECT A NURSING
INFANT.
112

PERIODONTICS
1540. GINGIVA + PDL + CEMENTUM + ALVEOLAR BONE are collectively the

PERIODONTIUM.
1541. The distance established by the junctional epithelium and C.T. attachment to the root
surface (the height of the deepest point of the SULCUS BASE and ALVEOLAR CREST
OF BONE is the BIOLOGIC WIDTH.
1542. VIOLATING BIOLOGIC WIDTH leads to pain, gingival inflammation, and alveolar bone
loss. Thus, the all restoration margins must be at least 3 mm from the ALVEOLAR
CREST OF BONE.
1543. The periodontal surgical procedure performed to expose additional tooth structure to
prevent biologic width violations or to correct a “GUMMY SMILE” is CROWN
LENGTHENING.
1544. Oral structure that demarcates the ATTACHED GINGIVA from ALVEOLAR MUCOSA,
separating keratinized and non-keratinized tissue is the MUCOGINGIVAL JUNCTION.
1545. CLINICAL ATTACHMENT LOSS (CAL) is the distance from CEJ to the POCKET
(SULCUS) BASE + GINGIVAL RECESSION.
1546. An indication that gingivitis has progressed to periodontitis is the presence of CLINICAL
ATTACHMENT LOSS.
1547. Periodontitis is ALWAYS PRECEDED by gingivitis, but gingivitis does NOT always
progress to periodontitis.
1548. PERIODONTITIS is marked by APICAL MIGRATION of the JUNCTIONAL EPITHELIUM

from the CEJ, loss of C.T. attachment and PDL, and bone destruction.
1549. The IRREVERSIBLE transition from gingivitis to periodontitis due to lesion extension
from the gingiva into supporting alveolar bone and PDL due to the apical migration of
the JUNCTIONAL EPITHELIUM best describes the ADVANCED PERIODONTAL
LESION.
1550. The FUSION OF ALVEOLAR BONE AND ROOT due to infection or trauma to the
PERIODONTAL LIGAMENT (PDL) is ANKYLOSIS.
1551. PDL fibers FOUND ONLY ON MULTI-ROOTED TEETH are INTERRADICULAR

FIBERS.
1552. The best periodontal instrument to detect and diagnose the degree of FURCATION
INVOLVEMENT is the NABER’S 2N (HAMP PROBE).
113
1553. The two MOST CRITICAL FACTORS to determine the prognosis of a periodontally
involved tooth are MOBILITY & ATTACHMENT LOSS (the most critical).
1554. The periodontal defect with the MOST PREDICTABLE response to bone grafting due to
better blood supply and cell source proximity is a THREE-WALL DEFECT.
1555. The most biocompatible and most common material used for DENTAL IMPLANTS is
TITANIUM.
1556. The MOST COMMONLY PLACED implants today are ENDOSTEAL TITANIUM
IMPLANTS.
1557. The best indicator of a FAILED DENTAL IMPLANT is MOBILITY due to failed
osseointegration.
1558. OSSEOUS SURGERY is used to treat periodontal disease, and REQUIRES raising a
GINGIVAL FLAP and SUTURES.
1559. The goal of OPEN FLAP DEBRIDEMENT is to gain ACCESS and VISUALIZATION to
the underlying supporting BONE and ROOT SURFACES for effective scaling and root-
planing.
1560. A periodontal procedure that uses BARRIER MEMBRANES to direct and promote the
growth of new clinical attachment of periodontal tissues to reduce probing depths and
arrest periodontal disease is GUIDED TISSUE REGENERATION (GTR).
1561. A PRIMARY goal of periodontal regenerative procedures is to treat INFRABONY

DEFECTS.
1562. The PRIMARY goal of GINGIVOPLASTY is to RESHAPE the gingiva and papilla to
IMPROVE PHYSIOLOGICAL TISSUE CONTOUR.
1563. Indications for GINGIVECTOMY are SUPRA-BONY POCKETS, GINGIVAL

HYPERPLASIA, and PSEUDOPOCKETS.
1564. The most common surgical procedure to REDUCE POCKET DEPTHS by resecting soft
tissue coronal to the base of the pocket is GINGIVECTOMY.
1565. GINGIVECTOMY contraindications are HIGH CARIES INDEX, INFRA-BONY

ABSCESS, & NARROW ZONE OF ATTACHED GINGIVA.
1566. Operculum inflammation around a partially impacted MANDIBULAR 3rd MOLAR crown
due to plaque accumulation and resulting in pain, erythema, edema, and foul taste is
PERICORNITIS.
1567. Three days AFTER a surgical extraction of tooth #17, a patient presents with dull,
throbbing, radiating pain to the ear and a foul odor and taste. The extraction site is filled
with necrotic tissue. This condition is consistent with DRY-SOCKET (FIBRINOLYTIC
ALVEOLAR OSTEITIS).
114
1568. The MOST likely cause of DRY SOCKET is BLOOD CLOT DISRUPTION often from
negative intra-oral pressure due to SMOKING, SPITTING, or STRAW DRINKING,
exposing alveolar bone and delaying healing.
1569. The appropriate emergency treatment for dry socket is GENTLE SALINE IRRIGATION
and PLACEMENT OF A SEDATIVE DRESSING (EUGENOL-CLOVE OIL) to protect the
exposed bone.
1570. When evaluating an OSSEOUS DEFECT, the ONLY WAY TO DETERMINE the number
of walls left surrounding the tooth is by periodontal EXPLORATORY SURGERY.
1571. A pattern of HORIZONTAL bone loss where the pocket base is coronal to the crest of
alveolar bone is a SUPRABONY POCKET.
1572. A pattern of VERTICAL bone loss characterized by the pocket base positioned APICALLY
to the crest of bone is an INFRABONY POCKET.
1573. The GREATER the number of osseous walls remaining around a tooth with an
INFRABONY POCKET, the BETTER THE PROGNOSIS.
1574. The INFRABONY POCKET with the LEAST FAVORABLE prognosis is a ONE-WALL
HEMISEPTUM or RAMP DEFECT.
1575. A SUPRABONY POCKET due to CORONAL expansion of marginal tissue without

attachment loss is a PSEUDOPOCKET.
1576. A 4-mm probing of the junctional epithelium at the CEJ due to gingival margin hyperplasia
WITHOUT the loss of any supporting periodontal tissues, and no apical migration of the
JE is a PSEUDOPOCKET.
1577. The periodontal procedure that reshapes or recontours NON-SUPPORTING ALVEOLAR

BONE without disturbing PDL fibers is an OSTEOPLASTY.
1578. A true periodontal pocket is distinguished from a “pseudopocket” by the APICAL

MIGRATION OF THE JUNCTIONAL EPITHELIUM.
1579. A WINDOW or OPENING in the solid cortical plate of COMPACT BONE located on the
buccal/facial surface that exposes a tooth root is a FENESTRATION.
1580. An advantage of SYNTHETIC RESORBABLE SUTURES is they do not require the

patient to return for removal.
1581. The MOST effective ANTIMICROBIAL and ANTI-GINGIVITIS rinse due to its high
substantivity CHLORHEXIDINE GLUCONATE (0.12%) PERIDEX which remains
effective for 8-12 hours after rinsing.
1582. The pH of CHLORHEXDINE GLUCONATE is between 5.5-6.0.
1583. The correct CHLORHEXIDINE GLUCONATE REGIMEN is 0.12% in 15ml dose for 1
minute TWICE DAILY at least 30 minutes AFTER brushing for two weeks.
115
1584. A drawback of prolonged CHLORHEXIDINE GLUCONATE or STANNOUS FLUORIDE

use is YELLOWISH-BROWN STAINING of teeth.
1585. The chemical responsible for extrinsic YELLOWISH-BROWN STAIN from STANNOUS
FLUORIDE (SnF2) is the TIN ION.
1586. CHLORHEXIDINE GLUCONATE’S mechanism of action DESTROYS THE BACTERIAL

CELL MEMBRANE (WALL).
1587. The PRIMARY nutrient source of minerals in SUPRAGINGIVAL CALCULUS is from

SALIVA.
1588. The PRIMARY nutrient source of minerals in SUBGINGIVAL CALCULUS is from the
secretion of GINGIVAL CREVICULAR FLUID (GCF).
1589. During gingival health, gingival crevicular fluid (GCF) FLOW into the sulcus DECEASES,
while plaque biofilm accumulation and gingival inflammation causes GCF INCREASES.
The purpose of GCF is to transport inflammatory mediators and antibodies to the
periodontal pocket.
1590. The PROTEIN FILM that allows SUPRAGINGIVAL calculus to attach to smooth enamel
surfaces is the SALIVA PELLICLE.
1591. The ACQUIRED ENAMEL PELLICLE forms within MINUTES after exposure of enamel
surfaces.
1592. The SALIVA PELLICLE is a barrier that PROTECTS & LUBRICATES ENAMEL from
attrition and abrasion and is an attachment medium for bacteria.
1593. A 38-year old male presents with a localized purulent infection that extends apically
and adjacent to the periodontal pocket on tooth #19. Radiographically, the patient has
alveolar bone loss, widened PDL, mobility, and a 7mm pocket on the direct buccal aspect.
The tooth is tender to palpation and percussion, but tests vital with the EPT. This patient’s
condition best describes a PERIODONTAL ABSCESS.
1594. The source of a PERIODONTAL ABSCESS is from a bacterial infection of the

PERIODONTIUM.
1595. The purpose of a PERIODONTAL DRESSING is to maintain PATIENT COMFORT and

PROTECT TISSUE adaptation and contour from post-surgical trauma. IT DOES NOT
PROMOTE HEALING.
1596. The BEST CRITERION to determine the success of SCALING & ROOT PLANNING is
the tissue’s response that demonstrates the ABSENCE OF BLEEDING ON PROBING.
1597. A patient presents with a narrow width of attached gingiva in the area of tooth #22 and
around adjacent teeth. To successfully augment the gingival tissue and increase the
amount of attached gingiva in this area, the most predictable surgical procedure is a FREE
CT AUTOGRAPH HARVESTED FROM THE PALATE.
116
1598. SMOKING is the most significant risk factor on implant success. Smokers who receive
dental implants have a much higher risk of implant failure, postoperative infection, and
greater marginal bone loss than non-smokers. BOTH STATEMENTS ARE TRUE.
117

ENDODONTICS
1599. A highly-effective root canal irrigant due to its antimicrobial action, substantivity, low
toxicity, and because it does not interfere with the bond strength of resin cement to
root dentin and a fiber post is 2% CHLORHEXIDINE GLUCONATE (CHX).
1600. The least effective endodontic treatment for primary teeth with extensive caries is the
DIRECT PULP CAP. Pulp-capping should be limited to small exposures produced by
mechanical means or pin-point caries. BOTH TRUE.
1601. The most widely used endodontic irrigant that is bactericidal, dissolves organic pulp and
collagen, but does not remove the smear layer is NaOCl (SODIUM HYPOCHLORITE).
1602. CBCT 3D imaging should be used only when the patient’s history and clinical exam
demonstrate the patient benefits outweigh the potential risks. CBCT should not be used
routinely for endodontic diagnosis or for screening purposes in the absence of clinical
signs and symptoms. BOTH TRUE.
1603. The pulp disinfectant used as an irrigant and chelating agent that kills bacteria by
extracting bacterial surface proteins by combining with metal ions in the bacterial envelops
is EDTA (ETHYLENEDIAMINE TETRA-ACETIC ACID).
1604. The treatment of choice for root fractures in primary teeth with evident coronal
displacement is to only remove the coronal root segment and leave the root apex to
prevent damaging the permenant tooth bud.
1605. The access shape outline form of a maxillary molar with four canals is TRIANGULAR
and positioned in the crown’s mesial half.
1606. Cells involved in the inflammatory process of APICAL PERIODONTITIS include

Polymorphonuclear neutrophilic leukocytes (PMNLs), endothelial cells, mast cells, and
macrophages.
1607. The FIRST cells to travel from the bone marrow to the infected and inflamed area in
apical periodontitis are PMNLs.
1608. If the pulpal floor is directly perforated during access preparation while searching for a
canal orifice, the perforation should be immediately repaired with MTA and proceed
with RCT.
1609. The MOST effective therapeutic treatment to relieve the swelling and pain associated with
an ACUTE APICAL ABSCESS is INCISION and DRAINAGE to release exudate and
decompress pressure and swelling.
118
1610. Profound anesthesia is often DIFFICULT when attempting to perform an incision and
drainage on an endodontic abscess due to increased ACIDITY and INFLAMMATION of
the area.
1611. The initial treatment for a permenant anterior with a horizontal root fracture in the coronal
or middle third of the root is REPOSITIONING and STABILIZATION via splinting for
4-6 weeks to allow the periodontal tissues to heal and repair.
1612. Limited field-of-view (FOV) CBCT is the imaging modality of choice for initial treatment of
teeth with potential extra canals and suspected complex canal morphology or dental
anomalies. TRUE.
1613. Direct and indirect pulp capping, pulp capping, and apexogenesis are methods that do not
involve nerve extirpation, thus are considered VITAL PULP THERAPIES.
1614. After a traumatic tooth injury such as a root fracture, the clinical crown is mobile and begins
to discolor bluish-gray due to PULPAL HEMORRHAGE AND NECROSIS.
1615. The prognosis for internal bleaching is favorable when the cause of the discoloration is
due to NECROTIC PULP caused by either bacterial, chemical, or mechanical means.
1616. The best transport medium for an avulsed permanent tooth is HANKS BALANCED SALT
SOLUTION to maintain cell vitality on the root surface/PDL. Other physiologically
acceptable transport mediums are physiological saline, milk, or saliva (not water or
alcohol). BOTH TRUE.
1617. Pulp-capping procedure for a primary tooth with a small, pin-point exposure due to
trauma or from mechanical exposure in an asymptomatic vital primary molar is best
treated with the medicament MINERAL TRIOXIDE AGGREGATE (MTA) due to its
biocompatibility and excellent sealing abilities compared to formocresol or calcium
hydroxide.
1618. The process of maintaining pulp vitality during pulp treatment to permit the continued
development of the entire tooth root is APEXOGENESIS.
1619. Endodontically treated teeth are weakened and more prone to fracture than vital teeth
because tooth structure is removed during the cleaning and shaping process.
Endodontically treated teeth do NOT become brittle due to dehydration within the first 10
years. BOTH TRUE.
1620. Most ACCESSORY CANALS are found in the root’s APICAL THIRD (~75%). The
fewest accessory canals are found in the root’s MIDDLE THIRD.
1621. The most effective method to sterilize gutta-percha points is 5.25% SODIUM
HYPOCHLORITE (NaOCl) FOR 1 MINUTE.
1622. The FIRST step taken before a radiograph is taken by the dental provider when a patient
presents with a dental emergency such a loose tooth from trauma is to GATHER AND
REVIEW THE PATIENT’S COMPREHENISVE MEDICAL and DENTAL HISTORY.
119
1623. A tapered and twisted square or triangular wire most useful to enter and widen root canals
during root canal therapy is a K-FILE.
1624. A stainless steel slow-speed bur with a rounded tip for safety used to shape the coronal
aspect of the canal space is a GATES GLIDDEN.
1625. Desirable properties of a ROOT CANAL SEALER include slow working time, tissue
biocompatibility, adhesiveness, solubility in solvent, radiopaque, absence of staining, and
no shrinkage with setting,
1626. A patient present for an emergency visit and complains of SPONTANEOUS THROBBING
DIFFUSE PAIN that lasts more than 30 seconds and sometimes several minutes. The
pain increases when the patient lays down at night to sleep. The most likely diagnosis is
IRREVERSIBLE PULPITIS.
1627. A clinical diagnosis based on subjective and objective findings that the VITAL
INFLAMMED PULP is incapable of healing, may accompanied by LINGERING
THERMAL PAIN THAT IS SPONTANEOUS and often REFERRED is SYMPTOMATIC
IRREVERSIBLE PULPITIS.
1628. An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset,
little or no discomfort, and an intermittent discharge of pus through an associated sinus
tract with radiographic signs osseous destruction (radiolucency) best describes a
CHRONIC APICAL ABSCESS.
1629. The most effective way to identify the source of a DRAINING SINUS TRACT is to
carefully place a GUTTA PERCHA CONE through the stoma or opening until it stops
and take a radiograph.
1630. Inflammation of the apical periodontium causing severe pain to biting, to percussion
and/or palpation that may or may not accompanied by radiographic changes, but is highly
indicative of a degenerating pulp is SYMPTOMATIC APICAL PERIODONTITIS.
1631. The LEAST accurate diagnostic indicator to test tooth vitality is the ELECTRIC PULP
TEST (EPT) because the exact reading number is insignificant and the EPT does not
detect slight degrees of vitality. The EPT may also produce false negatives and false
positives due to the presence of calcified canals. BOTH TRUE.
1632. Types of pulp vitality tests include: EPT, cold test, heat test, and blood flow test.
1633. An endodontic test used to test periodontal or periapical inflammation around a tooth by
tapping on a tooth’s incisal or occlusal surface with end of a mirror handle is the
PERCUSSION TEST. Mild-to-moderate pain on percussion typically indicates
periodontal inflammation, while sharp, severe pain usually indicates periapical
inflammation.
1634. A positive (painful) response to the percussion test may indicate an ACUTE APICAL
ABSCESS or SYMPTOMATIC APICAL PERIODONTITIS.
120
1635. A long-standing inflammatory lesion of pulpal origin causing a draining abscess to a sinus
tract to provide a route for the infected tissue to escape and is NOT sensitive to percussion
is a CHRONIC APICAL ABSCESS (CAA).
1636. A patient presents for an emergency appointment due to traumatic injury to tooth #9. At
this appointment the dentist should use the EPT to establish a baseline to use for future
vitality. Subsequent EPTs should be repeated at 3 weeks, 3 months, 6, months, 12
months and then at annual intervals from the date of the initial injury per the
American Association of Endodontics trauma guidelines. BOTH TRUE.
1637. The most common two causes of REVERSIBLE PULPITIS are POST-OPERATIVE
SENSITIVITY and HYPEROCCLUSION.
1638. The main cause of pulpal inflammation is from MICROORGANISMS IN DENTAL

CARIES.
1639. The process of enamel demineralization forms a CARIOUS LESION. An infection disease
caused by STREP MUTANS (bacteria) is DENTAL CARIES. Dental caries and a carious
lesion are NOT interchangeable terms.
1640. The best pain management analgesic combination for SEVERE acute endodontic pain is
IBUPROFEN 600-800mg + 1000mg ACETAMINOPHEN.
1641. A patient recently had a large MOD composite placed in tooth #30. The patient presents
and complains of sharp, transient pain that occurs only when breathing in cold air or
drinking hot or cold water. The discomfort lasts approximately 5 seconds. The most likely
diagnosis is REVERSIBLE PULPITIS.
1642. The minimum file length used to determine the radiographic working length during
endodontic therapy is TUGBACK WITH A NUMBER 20 HAND FILE.
1643. Non-odontogenic pain sources that can mimic a maxillary toothache SINUSITIS,
NEURALGIA, NASAL MUCOSAL and NEUROVASCULAR PAIN.
1644. Sudden prolonged sharp pain followed by rapid diffuse swelling around a necrotic tooth
being treated with endodontic therapy is most likely the result of a SODIUM
HYPOCHLORITE ACCIDENT caused by the extrusion of NaOCl into the periapical
tissues.
1645. Treatment for a NaOCl complication is PALLIATIVE with analgesics, reassuring the
patient, and following-up with the patient. Do NOT prescribe antibiotics or initiate surgical
drainage.
1646. The FIRST LINE ANTIBIOTICS to treat PULPAL INFECTIONS are PENICILLINS.
1647. A patient with DIABETES MELLITUS TYPE 1 (INSULIN DEPENDENT) have a greatly
reduced healing rate following RCT due to their decreased ability to initiate and maintain
an appropriate healing response.
1648. Most root fractures are OBLIQUE (occurring buccal to palatal) and difficult to diagnose.
To improve the ability to diagnose a root fracture radiographically, the best method is to
121
take one occlusal film and three periapical films at various angles from the tooth’s vertical
axis. BOTH TRUE.
1649. Vascular hemorrhage of the pulp causing dentinal color changes from extensive caries
removal during an operative dentistry procedure is termed DENTINAL BLUSHING.
1650. The two major causes of VERTICAL ROOT FRACTURES are wedge forces created by
post placement and cementation, and condensation forces of gutta-percha during root
canal obturation
1651. The MOST common signs of VERTICAL ROOT FRACTURE are an isolated
periodontal probing, evidence of radiographic bone loss on digital imaging, and or
history of root canal treatment. ALL TRUE.
1652. Teeth with horizontal root fractures should be splinted for around 4-6 WEEKS to allow
adequate repair of the periodontium.
1653. The complete displacement of the tooth out of alveolar bone is AVULSION.
1654. The partial displacement of the tooth from the socket and increased mobility is
EXTRUSION.
1655. VIRUSES have been identified and reported in the HEALTHY, VITAL PULPS of HIV
patients.
1656. The best method to distinguish between a PERIODONTAL ABSCESS vs.

ENDONDONTIC ABSCESS is VITALITY TESTING with the EPT, hot test, cold test,
and/or blood flow test.
1657. Pulp vitality tests are used to determine a pulpal and periapical diagnosis. Cold testing
provides the clinician with important information regarding a tooth’s periapical health.
FIRST STATEMENT TRUE, SECOND STATEMENT FALSE.
1658. The use of #2 COTTON PELLET WITH ENDO ICE (generic) is the BEST method to
determine pulpal vitality. An AIR WATER syringe is NOT an appropriate cold test to
determine pupal vitality. BOTH STATEMENT ARE TRUE.
1659. A positive response to percussion and an electric pulp test (EPT) reading of 78 provides
a diagnosis of pulpal necrosis with symptomatic apical periodontitis. FALSE because the
tooth is not necrotic if the EPT responds.
1660. Calcium Hydroxide placement after a mechanical pulp exposure during cavity
preparation promotes dentin formation within the pulp by stimulating undifferentiated
pulp cells to differentiate into odontoblasts which lay down reparative dentin.
1661. Prolonged pulpal irritation after restoring a large MODBL composite is most likely
due to a POOR MARGINAL SEAL allowing fluids to leak in at the margin and allow the
ingress of bacteria from the oral cavity into the dentinal tubules.
122
1662. A patient who receives proper local anesthetic prior to RCT to treat irreversible pulpitis
and still feels sharp pain once the dentin and pulp chamber are reached is most likely
experiencing HYPERALGESIA.
1663. Alternative anesthetic techniques to administer during RCT should HYPERALGESIA

occur include INTRAPULPAL INJECTION, PDL INJECTION, AND/OR
INTRAOSSEOUS INJECTION.
1664. Pain provoked by applying a hypertonic solution or cold, or caused by the cutting or
scraping of dentin as described by the HYDRODYNAMIC THEORY of pain is DENTINAL
HYPESENSITVITY.
1665. Contraindications for performing a pulpotomy on a primary tooth PATHOLOGIC

MOBILITY, EXTERNAL ROOT RESORPTION, and DRAINING FISTULA. The best
treatment in these cases is EXTRACTION. BOTH TRUE.
1666. A tooth that is cold and bite sensitive three days after a composite restoration was placed
should first receive an OCCLUSAL EVALUATION WITH ARTICULATING PAPER.
1667. During root canal instrumentation, ENDODONTIC FILES MAY BE USED FOR FILING
AND REAMING. Endodontic files are handled using a SCRAPING, RASPING, or PUSH-
PULL PLANING MOTION during pulpal extirpation. BOTH STATEMENTS TRUE.
1668. Inflammation of the apical periodontium causing pain on BITING, and/or PERCUSSION,
or PALPATION that may or may not be associated with an apical radiolucency is
SYMPTOMATIC APICAL PERIODONTITIS.
1669. A 52 year-old female presents with an apical radiolucency visible on the periapical
radiograph on tooth #21 at her routine check-up. The patient states “nothing bothers me
on that bottom tooth, and everything feels normal.” Six months prior to her checkup, the
patient was advised that she had deep caries invading the coronal pulp and was advised
that root canal therapy was indicated. The tooth does not respond to cold or heat today.
The diagnosis for tooth #21 is PULPAL NECROSIS with ASYMPTOMATIC APICAL
PERIODONTITIS.
1670. Cone beam computed tomography (CBCT) is considered the standard of care in
endodontic diagnosis and treatment. FALSE. CBCT is an important diagnostic tool to aid
in endodontic treatment in certain cases, but is not necessarily the standard of care for
every root canal treatment. TRUE. FIRST STATEMENT FALSE, SECOND STATEMENT
TRUE.
123

ORAL SURGERY
1671. Indications for a posterior maxillary sinus augmentation (lift) prior to placing a dental
implant include severe alveolar resorption due to SINUS PNEUMATIZATION, atrophy, or
trauma.
1672. Arterial blood supply to the maxillary sinus is derived from the INFRAORBITAL,
MAXILLARY, and PSA.
1673. SINUS PNEUMATIZATION leaves a thin layer of bone in the posterior maxilla’s
OCCLUSAL and LATERAL WALLS.
1674. DEGENERATIVE TMJ ANKYLOSIS is most commonly caused by TRAUMA or

FRACTURE to the TMJ.
1675. A patient with severe restriction of opening, deviation to the affected side, and decreased
lateral excursions to the contralateral side most likely has TMJ INTRACAPSULAR
ANKYLOSIS. A patient whose mandible deviates to the left on opening may be due to
intracapsular ankylosis of the LEFT TMJ.
1676. The average volume of the maxillary sinus is 15 mL.
1677. The maxillary sinus cavity lining that is elevated when insufficient bone height is present
prior to dental implant placement is the SCHNEIDERIAN MEMBRANE.
1678. The most common surgical complication during or after sinus augmentation (lift) is
SCHNEIDERIAN MEMBRANE PERFORATION.
1679. The maxillary sinus communicates with the nasal cavity through the OSTIUM.
1680. ASTHMA is NOT a contraindication for the administration of nitrous oxide. Nitrous
oxide should NOT be administered to patients with drug-related dependencies, cobalamin
deficiency, or during the first trimester of pregnancy. BOTH TRUE.
1681. The MOST COMMON pathological condition of the maxillary sinus is INFLAMMATORY
DISEASE.
1682. Diagnostic methods to identify maxillary sinus pathology are CONVENTIONAL and 3D
CONE BEAM CT, PANOREX, and MRI.
1683. Lymphatic drainage of the maxillary sinus occurs via the INFRAORBITAL FORAMEN and
OSTIUM.
1684. Types of SHORT DURATION local anesthetics that provide pulpal anesthesia for < 30
minutes are MEPIVICAINE HCl 3% and PRILOCAINE HCl 4% by infiltration.
124
1685. The most common LONG DURATION local anesthetic that provides pulpal anesthesia for
> 90 minutes is BUPIVACAINE HCl 0.5% + 1:200,000 EPI.
1686. The GOLD STANDARD graft material for sinus augmentation due to its high
biocompatibility is AUTOGENOUS BONE (AUTOGRAFT).
1687. The primary disadvantage of AUTOGENOUS BONE is the need for a secondary
surgical site that can cause donor site morbidity.
1688. Graft material obtained from tissue banks either as mineralized or demineralized bone are
ALLOGENIC GRAFTS.
1689. The ability of a graft to bring NEW BONE-FORMING VITAL CELLS into the bony defect
is OSTEOGENESIS.
1690. The most common ALLOPLASTIC GRAFT materials are composed of

HYDROXYAPATITE.
1691. An example of a type of XENOGRAFT that can be alone or combination with other grafting
materials is DEPROTEINIZED BOVINE BONE.
1692. The ability of a graft to act as a SCAFFOLD for new bone formation is
OSTEOCONDUCTION.
1693. The ability of a graft to induce OSTEOBLASTIC DIFFRENTIATION of a host’s

undifferentiated cells is OSTEOINDUCTION.
1694. Nose blowing, straw sucking, or closed-mouth sneezing are actions that create
NEGATIVE SINUS PRESSURE and should be avoided for at least one week after SINUS
AUGMENTATION.
1695. The TMJ is a GINGLYMOARTHRODIAL JOINT that has ROTATIONAL and

TRANSLATIONAL movement.
1696. During TRANSLATION (SLIDING), the disk and condyle move FORWARD and
BACKWARD.
1697. During ROTATION (HINGE), the mandible is ELEVATED and DEPRESSED.
1698. The TEMPEROMANDIBULAR JOINT (TMJ) has DUAL ARTICULATION between the
MANDIBULAR CONDYLE and GLENOID FOSSA of the temporal bone (skull).
1699. SENSORY innervation to the TMJ is from V3 (trigeminal mandibular branch) and
BLOOD SUPPLY is from the EXTERNAL CAROTID ARTERY (superficial temporal
branch).
1700. MAXIMUM BLOOD SUPPLY is found in RETRODISCAL PAD of the TMJ’s BILAMINAR
ZONE.
1701. The RETRODISCAL PAD contains COLLAGEN, VENOUS PLEXUS, ELASTIC &
NERVE FIBERS, and FAT.
125
1702. The TMJ posterior attachment tissues located between the posterior portion of the TMJ
DISC and CAPSULE that allows the condyle to move forward, is the BILAMINAR ZONE.
1703. SUPERIOR & INFERIOR LAMINAS and RETRODISCAL PAD form the TMJ’s
BILAMINAR ZONE.
1704. The dense, irregular, and saddle-shaped (biconcave) FIBROCARTILAGE that

SEPARATES THE CONDYLE & TEMPORAL BONE to prevent bone-to-bone contact
and provide a smooth articulating surface is the ARTICULAR DISC (MENISCUS).
1705. The ARTICULAR DISC is surrounded and protected by the FIBROUS C.T. JOINT
CAPSULE.
1706. SPACES located above and below the TMJ’s fibrous disk are SYNOVIAL CAVITIES.
1707. The main function of SYNOVIAL FLUID is TMJ LUBRICATION and NUTRITION.
1708. TEMPEROMANDIBULAR, STYLOMANDIBULAR, and SPHENOMANDIBULAR are the

TMJ LIGAMENTS.
1709. The most minimally invasive surgical procedure to treat TMJ derangement where ports or
cannulas are placed into the TMJ to deliver lavage and break up adhesions within the joint
is ARTHOCENTESIS.
1710. TEMPEROMANDIBULAR LIGAMENT provides lateral reinforcement for the capsule &
PREVENTS POSTERIOR & INFERIOR DISPLACEMENT OF THE CONDYLE.
1711. STYLOMANDIBULAR LIGAMENT separates the PAROTID & SUBMANDIBULAR

salivary glands
1712. CLICKING and POPPING when opening is due to DISK DISPLACEMENT WITH
REDUCTION.
1713. SOUNDLESS, PAINFUL, and LIMITED OPENING (< 30mm) is due to DISK
DISPLACEMENT WITHOUT REDUCTION.
1714. When extracting a mandibular tooth, the BEAKS should be placed PARALLEL to the
tooth’s long axis to prevent damage to adjacent teeth and are used to WEDGE THE
TOOTH OUT OF THE SOCKET.
1715. Signs of SEVERE local toxicity after the administration of local anesthetic are SEIZURES,
RESPIRATORY DEPRESSION, COMA and DEATH.
1716. An INCISIONAL BIOPSY should be NARROW and DEEP and is indicated to remove
only part of the lesion that is > 1cm or is in a dangerous anatomical location. The biopsy
should include part of the questionable tissue, normal underlying tissue, and lesion base.
1717. Larger gauge needles are more difficult to deflect/break compared to shorter gauge
needles. The average length for a long needle is 32mm and 20mm for short needles.
BOTH TRUE.
126
1718. SUBLUXATION (slipping of the condyle from its socket) occurs when the condyle
head moves too far ANTERIORLY on ARTICULAR EMINENCE.
1719. The best diagnostic imaging test to examine DISK POSITION and DISK FUNCTION is
MAGNETIC RESONANCE IMAGING (MRI).
1720. CYTOKINES (chemical mediators) that INCREASE PAIN during an inflammatory

response are CGRP, SUBSTANCE P (dilates blood vessels), and BRADYKININ.
1721. The mechanism of action of local anesthetics to provide anesthesia is to BLOCK SODIUM
ION CHANNELS in the nerve membrane which prevents nerve depolarization.
1722. An 8-year old boy with Type I diabetes was hit the mouth with a baseball and he is bleeding
and missing his teeth. The most important question the dentist should ask the parent first
is “Did your son lose consciousness?”
1723. The best radiograph to screen the child to diagnose a mandibular fracture is a
PANORAMIC.
1724. To best way to reimplant the tooth and protect the boy’s permenant teeth after avulsion is
PLACE THE TOOTH BACK IN THE SOCKET AND SPLINT.
1725. The fractured piece of tooth number 10 has not been found. The first step is to ask the
parent if there was a pre-existing fracture of that particular tooth.
1726. A 35 year-old female presents who recently had teeth 19 (MO) and 18 (DO) composites
restored under local anesthesia. A left inferior alveolar nerve block was administered.
Her chief complaint is “I cannot taste on the left side of my tongue for the past 2 days”
When evaluating the specific location on the tongue for loss of taste, the area (s) most
likely affected are the ANTERIOR THIRD AND MIDDLE THIRD OF THE TONGUE ON
THE LEFT SIDE.
127

ORTHODONTICS AND PEDIATRIC DENTISTRY
1727. The most common chronic condition of rampant caries in the primary dentition due
to intake of dietary sugars, nighttime feeding, and inadequate oral hygiene is EARLY
CHILDHOOD CARIES (ECC).
1728. The most effective orthodontic appliance to retract or retrude protruding or flared
maxillary incisors into proper arch alignment is the HAWLEY REMOVALBE
APPLIANCE WITH CLASPS AND LABIAL BOW.
1729. The two major causes of orthodontic relapse are CONTINUED UNFAVORABLE
GROWTH and SOFT TISSUE REBOUND.
1730. The most common congenitally missing permenant teeth (besides 3rd molars) are
MAXILLARY LATERAL INCISORS and MANDIBULAR SECOND PREMOLARS.
1731. It is NOT recommended to attempt to replant an avulsed primary tooth back into its socket.
It is recommended to immediately replant an avulsed permenant tooth with open apices,
clean roots, and that has only been out of the mouth for < 60 minutes back into its socket.
BOTH TRUE.
1732. Continuous and aggressive orthodontic forces can induce pain and PDL necrosis,
alveolar resorption, and loss of tooth vitality due to inadequate time for the body and
blood supply to adapt to the forces placed on the tooth and PDL.
1733. The oral antibiotic prophylaxis regimen for children is AMOXICILLIN 50mg/kg 1 hour
before the dental procedure. For children allergic to penicillin, the oral prophylactic
antibiotic of choice is CLINDAMYCIN 20mg/kg orally 1 hour before the dental
appointment.
1734. The MOST common location of impacted teeth in the MIXED DENTITION is the
MAXILLARY CANINE REGION which often erupt MESIALLY.
1735. Causes of a MEDIAN DIASTEMA include: UPPER LABIAL FRENUM, HYPODONTIA,

SUPERNUMERARY TEETH, and PROCLINATION OF MAXILLARY INCISORS.
1736. The FIRST clinical sign of dental caries characterized by demineralization of the enamel
subsurface layer is the WHITE-SPOT LESION.
1737. In additional to convention orthodontics, the most effective way to manage a CLASS II
MAXILLARY PROTRUSION is with HEADGEAR to limit or redirect maxillary growth.
Maxillary growth is limited because the headgear places a distal force on the maxilla and
maxillary teeth.
128
1738. When determining the appropriate treatment for the initial white-spot lesion associated
with ECC, the dental clinician must first EVALUATE THE CHILD’S CARIES RISK
STATUS AND COMPLIANCE.
1739. The two-dimensional 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 is the CURVE OF
SPEE.
1740. A mixed dentition child with erupted mandibular incisors and poor oral hygiene who
requires a lingual arch appliance should have the PRIMARY SECOND MOLARS banded
as these molars will eventually exfoliate.
1741. The normal skeletal relations SNA = 82 degrees +/- 2 degrees. A patient whose SNA >
82 angle is PROGNATHIC and a patient whose SNA < 82 degrees will be
RETROGNATHIC.
1742. The MEDIOLATERAL U-SHAPED CURVE of the occlusal plane of maxillary and
mandibular posterior teeth is the CURVE OF WILSON.
1743. The HORIZONTAL overlap or protrusion of the maxillary anteriors, common in Class II,
division I malocclusion is OVERJET.
1744. Dental considerations for a child with TRISOMY 21 include: increased periodontal
disease risk, potential need for subacute bacterial endocarditis, and the child’s ability to
cooperate in the dental chair.
1745. The VERTICAL overlap of maxillary anteriors over mandibular anteriors common in Class
II, division II malocclusion viewed anteriorly is OVERBITE.
1746. Indications for CLEAR ALIGNER THERAPY (INVISILIGN) include patient compliancy,
mild spacing or posterior crowding, distally tipping a molar, and the absolute intrusion of
1-2 teeth.
1747. The SIMPLEST form of orthodontic movement is TIPPING produced when a single force
is applied to the tooth crown.
1748. A RETRUDED MANDIBLE with FLARING OF ALL MAXILLARY ANTERIORS is

characteristic of CLASS II, DIVISION I MALOCCLUSION.
1749. A RETRUDED MANDIBLE with FLARING AND RETRUSION OF SOME MAXILLARY

ANTERIORS best describes a CLASS II, DIVISION II MALOCCLUSION.
1750. The line that units the ANTERIOR AND POSTERIOR NASAL SPINES is the MAXILLARY
PLANE. The line that that joins GONION and MENTON is the MANDIBULAR PLANE.
BOTH TRUE.
1751. Lateral misalignment of the arches resulting in the BUCCAL positioning of the mandibular
molars relative to the maxillary molars is POSTERIOR CROSSBITE.
129
1752. Mesial or distal movement best describes SECOND ORDER TOOTH MOVEMENT.
Vertical tooth movement best describes FIRST ORDER MOVEMENT.
1753. The optimal CONDYLAR POSITION when using an occlusal splint is in the GLENOID
FOSSA.
1754. A tissue-borne orthodontic appliance used for ARCH EXPANSION using large buccal
shields and lip pads to reduce cheek and lip pressure on the dentition is the FRANKEL
FUNCTION REGULATOR.
1755. Centric occlusion is a TOOTH-GUIDED POSITION, while centric relation is a LIGAMENT-

GUIDED POSITION.
1756. The habitual or natural condyle position in the fossa when the teeth contact is CENTRIC
OCCLUSION.
1757. CENTRIC RELATION is the non-habitual tooth contact that occurs when the condyle head
is in its most ANTERIOR and SUPERIOR position.
1758. A cephalometric landmark used to measure the mandibular plane angle is GONION
(GoGn).
1759. The most posterior, inferior point on the gonial angle at the junction of the body of the
mandible and ramus is GONION.
1760. The line joining PORION and ORBITALE is the FRANKFORT PLANE.
1761. PRIMATE SPACES are most noticeable between the MAXILLARY LATERAL INCISOR
and CANINE and between the canine and first primary molar in the mandibular arch.
BOTH TRUE.
1762. Oral manifestations associated with MUSCLE WEAKNESS SYNDROMES such as

muscular dystrophy and cerebral palsy are increased anterior facial height, narrowing of
the maxillary arch, and anterior open bite.
1763. The average peak growth age for boys is 14 years old. The average peak growth rate for
girls is 12 years old. BOTH TRUE.
1764. The primary focus of orthodontic treatment for preadolescents should be on CLEAR and
NECESSARY TREATMENT OBJECTIVES.
1765. The best topical anesthetic advised for pediatric dental patients is BENZOCAINE due to
its rapid onset and acceptable taste.
1766. A patient with a posterior crossbite and sufficient palatal width typically has inwardly
inclined maxillary molars. A patient with sufficient palatal width should have molars with a
normal transverse relationship as there is sufficient space for the molars to erupt and
occlude onto the buccal cusps of the opposing mandibular teeth. A posterior crossbite is
skeletal if there is insufficient palatal width for the maxillary molars to span the transverse
dimension. ALL TRUE.
130
1767. Treatment methods to correct an ANTERIOR CROSSBITE include removable

appliances with biteplates or finger springs, or with fixed appliances bonded to maxillary
molars and brackets bonded to incisors. The best course of anterior crossbite treatment
is determined by the patient’s molar relationship. BOTH TRUE.
1768. The percentage of patients in the U.S. with an ANTERIOR CROSSBITE is < 5%.
1769. The movement or VIBRATION of teeth (especially incisors) during occlusal contact is
FREMITUS.
1770. The maximum OPENING (DEPRESSING) distance of the mandible in the average adult
is 50mm.
1771. The fifth CUSP OF CARABELLI is an anatomical feature typically found on the largest
ML cusp of the MAXILLARY FIRST MOLAR.
1772. A WEDGE-SHAPED DEFECT along the gingival margin caused by FLEXURE at the
CEMENTOENAMEL JUNTION (CEJ) during biting, chewing, or grinding is
ABFRACTION.
1773. A HEAVY FORCE that causes undermining resorption and PDL cell death is necessary
to create an ORTHOPEDIC EFFECT.
1774. A widened PDL on radiographs, mobility, wear facets, fremitus, pain on percussion and/or
during occlusal contact, are all signs of OCCLUSAL TRAUMA.
1775. A child with ECTODERMAL DYSPLASIA typically presents with thin, sparse light-colored
hair, lack of sweat glands, and an OVERCLOSED APPEARANCE WITH MANY MISSING
TEETH (most or all of the permanent teeth are missing) due to underdeveloped of the
alveolar processes.
1776. Cusp ridges are separated from marginal ridges by fine enamel DEVELOPMENTAL
GROOVES.
1777. The JOINING of two triangular ridges on POSTERIOR TEETH form TRANSVERSE
RIDGES.
1778. The absence of vertical overlap of the incisors when the buccal segment teeth are in
occlusion possibly due to a digit-sucking habit or mouth breathing is an ANTERIOR OPEN
BITE.
1779. INCISAL PROMINENCES found on newly erupted permenant anterior teeth that often
wear away with age but may last a lifetime in patients with an anterior open bite, are called
MAMELONS.
1780. For cases of treating severe crowding, the goal of SERIAL EXTRACTION is to make
future comprehensive orthodontic treatment easier and more efficient.
1781. The anchorage value of a tooth approximately EQUALS THE ROOT SURFACE AREA
and is the greatest in the MOLAR REGION. The maxillary first molar has the greatest
anchorage value. BOTH TRUE.
131
1782. Serial extraction may create a CLOSED BITE and does NOT result in ideal tooth position.
1783. The preferred method to perform an intra-oral exam on an infant is the KNEE-TO-KNEE
position where the parent and dental provider sit and face one another (the dental chair
is not necessary).
1784. The ideal amalgam cavity preparation depth for a primary molar is 1.5mm into dentin.
1785. An 11-year old presents in pain with a primary mandibular first molar with a deep carious
lesion. Intra-oral exam reveals a large, pale pink polypoid lesion 1.5cm x 1.5cm wide with
a 2mm diameter stalk protruding from and covering the entire carious lesion. This lesion
best describes CHRONIC HYPERPLASTIC PULPITIS (PULP POLYP).
1786. Variation in jaw SIZE and POSITION relative to the cranial base can cause differences in
a patient’s skeletal relationship.
1787. A five-year old child present to the dental office with multiple abscessed deciduous
mandibular molars. The greatest cause of concern for space loss after extracting primary
molars is the MANIDIBULAR RIGHT SECOND PREMOLAR AREA.
1788. The largest primary tooth is the MANDIBULAR PRIMARY SECOND MOLAR.
1789. The appliance that can deliver large amounts of force to correct skeletal constriction is the
RAPID PALATAL EXPANDER.
1790. Two orthodontic appliances used to correct ANTERIOPOSTERIOR SKELETAL

discrepancies are HEADGEAR and the HERBST APPLIANCE.
1791. The MAXIMUM dose of subcutaneous EPINEPHRINE injected to reverse an asthma

attack of an 11-year old child while in the dental chair is 0.5mg. EPI should only be injected
after oxygen and if patient’s inhaler both fail to reverse the bronchospasm caused by the
asthma attack. BOTH TRUE.
1792. A dentist has a profession obligation to report both CHILD ABUSE and CHILD NEGLECT
(failure to seek or follow through on treatment of caries, oral pain, and/or oral infections).
1793. The MOST common traumatic dental injury in the PRIMARY DENTITION is LUXATION.
132

BIOMATERIALS, OPERATIVE DENTISTRY, AND
PROSTHODONTICS
1794. Pit and fissure SEALANTS are generally comprised of FILLED BIS-GMA RESIN, an ideal
material for occlusal surfaces due to their high wear resistance.
1795. The tooth preparation reduction for metal-ceramic restorations is 1.5-2.0mm to allow for
0.5mm metal thickness and 1.0-1.5mm thickness of porcelain.
1796. The most effective etching solution to prepare the enamel surface for dental sealants is
35%-50% PHOSPHORIC ACID.
1797. HYDROCOLLOIDS like ALGINATE are aqueous and HYDROPHILLIC (water-loving),

while ELASTOMERS like POLYVINYL SILOXANES are non-aqueous and
HYDROPHOBIC.
1798. Indications for using ZOE paste are final impressions for removable dentures
(edentulous ridges) and as a surgical dressing after grafting to provide comfort.
1799. The hydrophilic impression material with the BEST WETTABILITY by GYPSUM is
POLYETHER.
1800. When fabricating a denture, impressions taken with alginate hydrocolloid and dental
impression compound should be poured within ONE HOUR to prevent distortion.
1801. A LINGUAL rest is preferred to an INCISAL rest for a REMOVABLE PARTIAL

DENTURE (RPD) because it is closer to the horizontal axis of rotation to better withstand
occlusal forces during biting and chewing and is more esthetic. In RPD design, it is critical
that forces are exerted as close to tooth’s long axis as possible to prevent tipping. BOTH
TRUE.
1802. Elastic impression materials are removed quickly from the oral cavity to PREVENT
PLASTIC DEFORMATION.
1803. The action or property of similar molecules sticking together via mutual attraction is
COHESION. Dissimilar particles or surfaces sticking together is ADHESION.
1804. High noble metal alloys require 60% by weight of noble metal with at least 40% of that
being gold. Noble metals only require 25% noble metal by weight with no gold required.
BOTH TRUE.
1805. The main constituent of dental PLASTER & STONE is CALCIUM SULFATE HEMI-
HYDRATE.
133
1806. A DENTAL IMPRESSION captures a NEGATIVE (REVERSED) reproduction of the oral

structures, while a DENTAL STUDY MODEL or CAST is a POSITIVE reproduction of the
oral structures.
1807. An FPD pontic with a convex tissue surface that fits into a soft-tissue depression and is
ideal for maxillary anteriors and highly esthetic areas is an OVATE PONTIC.
1808. A highly esthetic FPD pontic that completely covers the ridge, but makes proper oral
hygiene extremely difficult, thus is rarely recommended is the SADDLE-RIDGE-LAP
PONTIC.
1809. The minimum ferrule height required for an endodontically treated tooth with a dowel
placed for greater core retention to prevent the dowel from fracturing is 1.5-2.0mm. This
height must be of intact tooth structure ABOVE the crown’s margin for 360 degrees around
the entire prepared tooth. BOTH TRUE.
1810. When loading the impression tray with dental material, start at the tray’s POSTERIOR-
LINGUAL aspect, and continue loading from POSTERIOR TO ANTERIOR. Seat the
impression tray in the patient’s mouth from POSTERIOR TO ANTERIOR.
1811. The purpose of pouring casts of alginate impressions within 10 minutes of taking the
impressions and wrapping the impressions in MOIST paper towels (rather than soaking
them in a water bowl for 30 minutes), is to prevent distortion by expansion due to moisture
absorption, or IMBIBITION.
1812. The component in alginate powder that controls its SETTING TIME is SODIUM
PHOSPHATE.
1813. The SATURATION intensity or strength of a particular color (hue) is CHROMA.
1814. Preparations for all porcelain crowns should have EVEN THICKNESS
CIRCUMFERENTIALLY to provide even bulk of porcelain thickness of 1.0-1.5mm.
1815. UTILITY WAXES used in dentistry are BOXING WAX, BEADING WAX, and STICKY
WAX.
1816. Recurrent caries due to the passage of saliva and bacteria in and out of tooth structure
due to a marginal gap between the tooth surface and restoration from thermal expansion
and contraction is PERCOLATION (MICROLEAKAGE).
1817. A dental material’s internal resistance to an external force is STRESS.
1818. COMPRESSION, TENSION, and SHEAR are common stresses in dentistry.
1819. DENTAL ATTRITION (incisal wear) from BRUXISM is primarily due to SHEAR STRESS.
1820. The change in shape or deformation of a dental material due to any applied stress is
STRAIN.
1821. Examples of HIGH STRAIN materials used in dentistry that can tolerate high stress levels
are RUBBER and LATEX gloves.
134
1822. A dental amalgam has a HIGH COMPRESSIVE STRENGTH and LOW TENSILE
STRENGTH, properties that refer to amalgam’s BRITTLENESS.
1823. The linear coefficient of thermal expansion (LCTE) of AMALGAM is approximately 2.5x
GREATER THAN THE LCTE OF NATURAL TOOTH STRUCTURE.
1824. Dental pain that occurs when an electrical charge is created due to the proximal or
occlusal contact of two dissimilar metal alloys like gold and amalgam in the presence
of saliva is GALVANIC SHOCK.
1825. The measure of a FLUID’S CONSISTENCY and its INABILITY TO FLOW is called
VISCOSITY.
1826. A dental impression material with a HIGH VISCOSITY flows more SLOWLY.
1827. The MAXIMUM STRESS a material can withstand without permenant deformation by
returning to its original shape when the force is removed is its PROPORTIONAL LIMIT
(ELASTIC LIMIT).
1828. ZINC-OXIDE EUGENOL (ZOE) is used in dentistry as a cavity liner or base to sooth and
protect the pulp, as a temporary cement or restorative material, but is
CONTRAINDICATED under COMPOSITES because EUGENOL INHIBITS
POLYMERIZATION.
1829. The MOST COMMON liner or base for PULP CAPPING to prevent thermal shock and
STIMULATE REPARATIVE DENTIN FORMATION are CALCIUM HYDROXIDE (CaOH)
or MTA (MINERAL TRIOXIDE AGGREGATE).
1830. Time-dependent plastic deformation in response to a constant stress responsible for

marginal fractures on amalgam restorations is CREEP.
1831. The minimum ratio of occlusocervical (OC) dimension to the faciolingual (FL) dimension
recommended for all prepped teeth to provide sufficient resistance to dislodging forces is
0.4.
1832. The purpose of ACID ETCHING enamel is to INCREASE THE SURFACE FREE
ENERGY OF ENAMEL by changing the enamel surface from smooth to ROUGH.
1833. FINISHING a resin composite involves SHAPING, CONTOURING, and SMOOTHING the
final restoration.
1834. A composite SHADE SELECTION when restoring a CLASS IV restoration should be

made WITH SALIVARY MOISTURE ON THE TEETH and BEFORE TOOTH
PREPARATION or RUBBER DAM ISOLATION occurs.
1835. The primary goal of POLISHING a resin composite is to obtain a gloss that resembles
the ADJACENT, SOUND ENAMEL.
1836. The SMOOTHEST resin composite surface is obtained by using a MYLAR STRIP.
135
1837. RESIN COMPOSITE MICROHYBRIDS are classified based on FILLER PARTICLE SIZE.
1838. The primary indication for placing MICROFILLED RESINS is in esthetic areas with
CERVICAL CLASS 5 RESTORATIONS and DIRECT COMPOSITE VENEERS.
1839. BENEFITS of a DIRECT COMPOSITE VENEER include more cost-effective treatment

than porcelain, no need to send to a dental laboratory, same day treatment, and minimal
tooth preparation.
1840. MICROFILLED RESINS are indicated in esthetic areas where HIGH POLISHABILITY is
the primary goal and STRENGTH IS SECONDARY.
1841. MICROFILLED RESINS contain fillers with an average particle size range of 0.01-0.05µm.
1842. In posterior restorative areas where STRENGTH is PRIMARY, a MICROHYBRID or

NANOHYBRID RESIN COMPOSITE is the material of choice.
1843. Heavy filled composite resins currently have a 70% MAXIMUM FILLER VOLUME.
1844. MICROFILLED RESINS are composed of submicron INORGANIC FILLERS that average
0.04µm in diameter and PRE-POLYMERIZED PARTICLES.
1845. A facial shoulder margin for a PFM should form a 90 DEGREE angle with the unprepared
tooth to prevent chipping of the porcelain.
1846. The MOST common cause of failure in a composite resin is from RECURRENT
CARIES DUE TO THE MARGINAL GAP CAUSED BY POLYMERIZATION
SHRINKAGE.
1847. SILVER DIAMINE FLUORIDE (SDF) concentrations of 38% are more effective than
other preventive management techniques to arrest dental caries in the primary dentition.
38% SDF concentration may prevent caries in deciduous teeth and permenant first
molars. BOTH TRUE.
1848. Adverse effects of Silver Diamine Fluoride (SDF) applications to arrest dental caries are
pulpal irritation, extrinsic black tooth staining, and reversible oral mucosal
irritation.
1849. Dentures should be REPLACED every 5-7 years.
1850. Toothbrush abrasion of polymerized acrylic resin dentures bases can cause loss of
surface POLISH, MASS, and SURFACE DETAIL.
1851. The MOST common cause of a cast restoration failure is CARIES.
1852. Lithium disilicate ceramic restorations are typically MONOLITHIC which means the
prosthesis full contour is fabricated from a single material and is homogeneous
throughout.
1853. Benefits of lithium disilicate ceramic restorations are LIFELIFE TRANSLUCENCY,

OPALESCENCE and LIGHT DIFFUSION, ability to be fabricated by milling ceramic
136
blocks, and the ability to be stained, glazed, or cut back to layer veneering porcelain to
improve incisal characteristics.
1854. The FLEXURAL STRENGTH of lithium disilicate ceramic ranges from 900 MPa to 1200
MPa.
1855. Acrylic resin properties are influenced by TEMPERATURE, TIME, and

POLYMERIZATION METHOD.
NAESLUNDII.
1858. An ANTICARIOGENIC and CARIOSTATIC NUTRITIVE SWEETENER shown to reduce

ACESULFAME-K.
1860. XYLITOL’s benefits that enable the enamel surface to remineralize are due to its
ability to destroy Strep Mutans, decrease biofilm adhesion, increase salivary flow, and
increase the oral pH.

1862. The form, shape, and configuration that resists displacement or removal of the restoration
from the cavity preparation under all types of tilting and tipping masticatory forces is
RETENTION FORM.
1863. A patient presents for tooth #19 crown preparation which is a SHORT CLINICAL CROWN.
The greatest advantage to add buccal grooves into the preparation is to INCREASE
RESISTANCE FORM. Increasing resistance will help prevent crown fracture from apical
or oblique forces, and resists crown movement by occlusal forces.
1864. Advantages of isolating the operative field with a rubber dam when performing
operative dental procedures are: maintains a dry and clean operating field, controls
moisture, improves operator access and visibility, and protects the patient and operator.
Isolation does NOT enhance patient breathing. BOTH TRUE.
1865. A junction of two surfaces of different orientations along the line is a LINE ANGLE. There
are EIGHT line angles involved with a Class I cavity preparation of a molar’s occlusal
surface. BOTH TRUE.
1866. To ensure proper RETENTION of a complete maxillary denture at delivery, the

VIBRATING LINE and POSTERIOR PALATAL SEAL must be properly marked and
designed on the denture base.
137
1867. The main disadvantage of fabricating a metal denture base is the metal is DIFFICULT TO
ADJUST AND RELINE.
1868. A MAJOR CONNECTOR on a removable partial denture must be RIGID to allow the
proper distribution of forces to supporting dento-alveolar structures with proper soft tissue
positioning to prevent impingement of anatomical structures.
1869. An ideal denture base should be COLOR STABLE, RESIST SOLUBILITY to prevent
deformation and deformation, and should be HIGHLY ABRASION RESISTANT to prevent
being scratched or damaged.
1870. A valid and reliable direct scaling method where the patient reports their pain intensity by
marking directly on a horizontal scale to quickly assess pain intensity chairside is the
VISUAL ANALOGUE SCALE (VAS).
1871. The main purpose of using a water-coolant when using the high-speed drill is to prevent
heat and friction from DAMAGING PULP. Water coolant also keeps the tooth moist and
prevents desiccation.
1872. The purpose of surveying a master cast to design and fabricate a well-fitted RPD is to
determine the denture’s best path of draw, adequate guideplanes, undesirable undercuts,
and desirable retentive areas.
1873. The most critical factor that produces cariogenic plaque is HIGH FREQUENCY
SUCROSE EXPOSURE. Sucrose and other sugars are metabolized into acid which then
becomes the food source for bacteria.
1874. A resin-composite restorative technique to reduce voids during a Class II cavity

preparation that involves initially placing a layer of uncured flowable composite then
placing a layer of packable composite on top of the flowable and curing both
simultaneously is the SNOWPLOW TECHNIQUE. The packable composite displaces
most of the flowable after it adapts to all of the walls to eliminate voids. BOTH TRUE.
1875. A ROUND BUR is the most effective bur to remove soft, carious dentin at slow-speeds
because it will not cut/remove sound dentin or enamel fast, and because a round bur
resembles the natural round shape of carious dentin.
1876. The lips of a complete denture patient are primarily supported by the CERVICAL
ASPECTS OF MAXILLARY ANTERIOR TEETH.
1877. A Siebert Class III edentulous ridge deformity is the LOSS OF RIDGE HEIGHT and
WIDTH. Class III ridge deformities are the most common ridge defect. BOTH TRUE.
1878. The MINIMUMM axial wall taper of a tooth prepared for a full coverage crown is 6
DEGREES.
1879. A steep condylar eminence will cause the condyle to descend faster than a shallow
eminence as it moves anteriorly. A steep condylar eminence allows posterior restorations
to have LONGER CUSPS, while a shallow condylar eminence requires SHORTER
CUSPS. BOTH TRUE.
138
1880. A CHAMFER margin is indicated for CAST METAL and METAL-CERAMIC

RESTORATIONS because the margin provides a distinct margin with sufficient bulk for
material.
1881. A PFM crown preparation requires a LINGUAL CHAMFER MARGIN AND FACIAL
SHOULDER MARGIN.
1882. The primary constituent of gypsum-based dental plasters and stones is CALCIUM
SULFATE.
1883. That preparation outline form that improves and provides sufficient VISIBILITY, ACCESS,
and EASE OF OPERATION for the dentist during caries excavation is CONVENIENCE
FORM. Convenience form is used when caries extends past the preparation’s external
outline and undermined enamel exists.
1884. Sealants are indicated to be placed on TEETH WITH INCIPIENT CARIES, PRIMARY
TEETH, and in SPECIAL NEEDS CHILDREN to slow or arrest the progression of caries
of non-activated, active caries.
1885. Sealants should not be routinely placed on PERMENANT TEETH OF CHILDREN WITH
A CARIES-FREE DECIDUOUS DENTITION. These permenant teeth should simply be
examined at each recare appointment. BOTH TRUE.
1886. The best treatment for a non-cavitated demineralized lesion on the occlusal surface of
tooth 12 on a 35-year old male is a SEALANT.
1887. The MINIKIN PIN is the pin of choice to REDUCE THE RISK of dentinal craze lines,
external perforation, and pulpal penetration in posterior teeth.
1888. The retention of a SELF-THREADING PIN is NOT increased when the pin’s insertion
depth into dentin or amalgam is more than 2mm deep. Inserting a self-threading pin more
than 2mm deep can compromise the strength of remaining tooth structure and the
amalgam restoration. BOTH TRUE.
1889. A 75 year-old male presents to the dental office with the chief complaint “I am tired of my
teeth, and I just want to get them all pulled and get dentures.” The patient has rampant
caries on his remaining twenty teeth, but his teeth exhibit no mobility and are periodontally
healthy. The best method to manage this patient is to REVIEW ALL OF HIS TREATMENT
OPTIONS AND RECOMMEND A SPECIALIST CONSULTATION. NEVER SIMPLY
JUST DO WHAT THE PATIENTS ASKS IF YOU DO NOT FEEL COMFORTABLE!
139
PROFESSIONAL ETHICS AND PATIENT

MANAGEMENT
ETHICAL AND LEGAL PRINCIPLES, DENTAL PRACTITIONER

RESPONSIBILITY AND INFORMED CONSENT
1890. A hygienist’s professional obligation to be HONEST and TRUTHFUL and provide full
patient disclosure best describes the ethical principal VERACITY.
1891. Written communication that falsely defames one’s character is LIBEL.
1892. Verbal communication that falsely defames one’s character is SLANDER.
1893. A hygienist’s responsibility and duty to DO NO HARM and protect patients during the
course of treatment is NON-MALEFICENCE.
1894. The duty of a dental professional TO DO GOOD with the primary obligation to provide the
highest quality of care and service within one’s capacity to patients and the public is
BENEFICENCE.
1895. EXCEEDING TREATMENT BEYOND what the patient, parent, or guardian has
authorized, such as placing sealants or applying fluoride without consent is TECHNICAL
BATTERY.
1896. The philosophy or science of law is JURISPRUDENCE.
1897. The Dental Hygiene Practice Act and Dental Practice Act are STATUTES enacted to
PROTECT THE PUBLIC.
1898. WRITTEN LAW enacted by the LEGISLATIVE BRANCH of government that specifies the
legal requirements of healthcare professionals are called STATUTES.
1899. Denying treatment because the individual is infected with HIV, HBV, or another blood-
borne pathogen based solely on that fact is UNETHICAL and violates the ADHA’s core
value of JUSTICE.
1900. Providing dental treatment with fairness and equality irrespective of age, race, gender,
handicap, or economic status embodies the principle of JUSTICE.
1901. A dental professional whose treatment, or lack of treatment, falls below the minimum
standard of care when compared to other dental professionals in the same area and
under the same circumstance is NEGLIGENCE.
140
1902. Guaranteeing a patient that placing a locally applied antibiotic in conjunction with scaling
and root planing will decrease clinical attachment loss from 6mm to 3mm is a BREACH
OF CONTRACT.
1903. A new patient arrives for their first dental appointment and receives a comprehensive
examination without verbal or written consent. This is an example of IMPLIED CONSENT.
1904. The process of educating patients of their clinical diagnosis, treatment plan and alternative
treatment options, risks, and benefits of treatment through an expressed contract is
INFORMED CONSENT.
1905. INFORMED CONSENT is permission to treat a patient after discussing the treatment
with the patient. INFORMED CONSENT must be obtained BEFORE starting the dental
procedure. BOTH TRUE.
1906. While it depends on state law, the PATIENT DENTAL RECORD AND RADIOGRAPHS
are the legal property of the DENTIST who created them based on professional knowledge
and expertise.
1907. The governing body that sets forth the RULES and REGULATIONS that determine a
dental hygienist’s SCOPE OF PRACTICE is the STATE BOARD OF DENTISTRY.
1908. The dental hygienist has an ETHICAL and LEGAL responsibility to report suspected or
confirmed cases of child abuse to the appropriate child protective agency to PROTECT
THE CHILD FROM FUTURE ABUSE.
SPECIAL NEEDS AND MEDICAL EMERGENCIES
1909. In PARKINSON’S DISEASE neurons in the BASAL GANGLIA to DEGENERATE,

causing DECREASED DOPAMINE production.
1910. CARBIDOPA-LEVODOPA (Sinemet) is the current MOST EFFECTIVE drug

combination to treat PARKINSON’S DISEASE by replenishing dopamine.
1911. The opioid and CNS stimulant that can produce PARKINSON-LIKE EFFECTS due to
altered dopamine levels is METHAMPHETAMINE (crystal meth).
1912. A 13-year-old child during a routine prophylaxis had a sudden lapse of consciousness
that began with a blank stare and ended quickly within 10-15 seconds with complete and
immediate recovery. This child most likely had an ABSENCE (PETITE MAL) SEIZURE.
1913. A patient undergoing RENAL DIALYSIS for ESRD should schedule their dental hygiene
appointment THE DAY AFTER DIALYSIS.
1914. When treating a pregnant patient, position patient on her LEFT SIDE with a FOLDED
TOWEL or PILLOW UNDER HER RIGHT HIP to elevate the hip and prevent vascular
compression.
141
1915. The best time to provide ELECTIVE dental treatment is during the 2nd TRIMESTER OF
PREGNANCY.
1916. Elective dental treatment should be delayed for at least 6 MONTHS after a STROKE
(CVA).
1917. HYPERTENSIVE PATIENTS SHOULD BE SCHEDULED FOR AFTERNOON

APPOINTMENTS.
1918. CONGESTIVE HEART FAILURE (CHF) clinical signs that the dental hygienist may
observe in a hygiene patient include swollen ankles, pronounced jugular veins, and
cyanosis (bluish skin discoloration due to poor circulation).
1919. Treat and CHF patient in the SEMI-SUPINE/SEMI-RECLINING or UPRIGHT POSITION

in the dental chair (not in the supine position).
1920. ULTRASONIC SCALING is contraindicated with CYSTIC FIBROSIS patients and

patients with UNSHIELDED PACEMAKERS.
1921. Overuse (more than several days) of NASAL DECONGESTANTS can cause REBOUND
NASAL CONGESTION (Rhinitis Medicamentosa = swollen nasal passages). Best
treatment is for patient to quit “COLD TURKEY.”
1922. Treatment modifications for COPD patients (Chronic Bronchitis or Emphysema)

include SHORT-APPOINTMENTS in the upright chair position and refrain from using N2O,
rubber dams, power-driven polishers, and ultrasonic scaling instruments.
1923. The MOST COMMON medical emergency in the dental setting, characterized by
sudden and transient loss of consciousness due to EMOTIONAL STRESS is
VASODEPRESSOR SYNCOPE.
1924. During treatment of syncope, the unconscious patient should be placed in the SUPINE
POSITION WITH THEIR FEET ELEVATED.
1925. SYNCOPE is most likely to occur DURING OR IMMEDIATELY AFTER

ADMINISTRATION OF LOCAL ANESTHESIA.
1926. The most effective preventive measure to enhance enamel remineralization and manage
caries and xerostomia in patients undergoing cancer radiation therapy is daily use of
HOME FLUORIDE TRAYS CONTAINING 5,000 PPM FLUORIDE GEL.
1927. Emergency situations requiring the administration of EPINEPHRINE are ANAPHYLAXIS,

ACUTE ASTHMA ATTACK, and CARDIAC ARREST.
1928. Dental emergencies that require administration of OXYGEN are SYCOPE, COPD,
ASTHMA, and CARDIAC ARREST.
1929. Chemotherapy-induced ORAL MUCOSITIS is a complication that is prevented and

relieved with SALINE and SODIUM BICARBONATE WATER RINSES or a NON-
ALCOHOLIC MOUTHWASH to hydrate and neutralize the oral pH.
142
1930. To prevent the risk of ADRENAL CRISIS during a dental appointment with an anxious
patient taking 5-10mg of PRENISONE chronically for ADDISON’S DISEASE, it is advised
to CONSULT WITH THE PATIENT’S PHYSICIAN TO DETERMINE IF THE STEROID
DOSAGE SHOULD BE INCREASED.
1931. Increasing the steroid dosage may prevent an ADRENAL CRISIS in a nervous patient
with ADDISON’S DISEASE because the additional dosage supplements the patient’s
inability to produce extra CORTISOL in response to stress.
1932. The “5 A’s” smoking cessation are: ASK, ADVISE, ASSESS, ASSIST, and ARRANGE.
1933. When discussing smoke cessation with a patient who vapes with E-cigarettes, an
important factual statement to convey to the patient is that E-cigarette contain VOLATILE
ORGANIC COMPOUNDS AND TOXIC SUBSTANCES.
1934. The nicotine in E-cigarettes can prime the adolescent brain for addiction to other drugs.
E-cigarettes contain nicotine, ultrafine particles, heavy metals, and volatile organic
compounds that can damage the lungs. BOTH STATEMENTS ARE TRUE.
1935. The third step when implementing a smoking cessation program is ASSESS.
1936. METRONIDAZOLE can cause a DISULFIRAM-LIKE REACTION when taken with

ALCOHOL (even alcohol-containing mouthrinse).
1937. SMOKING DECREASES the PLAQUE ACCUMULATION RATE, GINGIVAL

VASCULARITY, gingival inflammation and decreases BOP.
1938. An anti-depressant prescribed for SMOKING CESSATION to alleviate nicotine withdrawal

symptoms, but is CONTRAINDICATED with ANTI-CONVULSANTS, WELLBUTRIN,
and patients with EATING DISORDERS is ZYBAN (BUPROPION).
1939. ADVERSE EFFECTS of long-term tobacco SMOKING include CHRONIC BRONCHITIS,

LUNG CANCER, MYOCARDIAL INFARCTION, and SYSTEMIC ATHEROSCLEROSIS.
1940. An interactive and communicative approach used with apprehensive patients that
establishes patient RAPPORT and gives the PATIENT CONTROL requiring the dental
hygienist to request permission to start and stop is TELL-SHOW-DO.
1941. Eye contact and the TELL-SHOW-DO behavior management technique during dental
treatment are highly effective with ANXIOUS CHILDREN & ADULTS and ADHD.
1942. Patients with AUTISM SPECTRUM DISORDER should receive a few SHORT
ORIENTATION APPOINTMENTS within a ONE-WEEK period that involves the same
dental staff BEFORE the actual dental appointment to relax and familiarize the patient
with the positive dental experience.
1943. The MOST common sleep-related breathing disorder characterized by recurrent upper
airway obstruction from repetitive narrowing or collapse of the pharyngeal airway during
sleep is OBSTRUCTIVE SLEEP APNEA.
143
1944. The strongest and only statistically significant risk factor linked to obstructive sleep
apnea is OVERWEIGHT and OBESITY.
1945. The preferred method to objectively test patients for obstructive sleep apnea is IN-
LABORATORY POLYSOMNOGRAPHY.
RESEARCH METHODS, VARIABLES, AND STATISTICS
1946. The ARITHMETIC AVERAGE of scores, and MOST COMMON measure of central
tendency is the MEAN.
1947. If 10 hygienists scored a total of 950 points out of 1000 possible points on the NBDE
after using the DENTIN study guide, then the MEAN score is 950/10 = 95%.
1948. The measure of central tendency that would locate the midpoint of sample data using a
DATA MATRIX is the MEDIAN.
1949. The DIFFERENCE between high and low scores on a data matrix that is affected by
OUTLIERS is the RANGE.
1950. The number or score that is repeated most often in a data set is the MODE. A
distribution of scores that contains two modes is called BIMODAL.
1951. When sample data is plotted on a BELL CURVE (NORMAL CURVE), the MEAN,
MEDIAN, & MODE are EQUAL.
1952. The MOST COMMON method of DISPERSION in oral hygiene research that represents
the RANGE OF DATA is the STANDARD DEVIATION.
1953. The greater the RANGE (STANDARD DEVIATION) the WIDER the distribution curve.
1954. Conducting a TRIAL RUN of the planned study on a small sample of the population is
the purpose of a PILOT STUDY.
1955. Experimental treatment is withheld from CONTROL GROUPS that receive the PLACEBO.
1956. A continuous and logical process that allows the researcher to make observations and
conduct experiments by initially ASKING A RESEARCH QUESTION is the
SCIENTIFIC METHOD. The scientific method follows a logical and rational order of steps
that allows the researcher to reach a conclusion.
1957. SCIENTIFIC METHOD STEPS: OBSERVATION/RESEARCH, HYPOTHESIS,

PREDICTION, EXPERIMENTATION and CONCLUSION.
1958. An expected level of certain diseases found regularly in a certain population in particular
areas or during particular time periods like the INFLUENZA during winter, or Malaria in
tropical regions, is an ENDEMIC.
144
1959. An infectious disease that spreads across multiple continents in a short time period like
HIV/AIDS or ZIKA VIRUS is a PANDEMIC.
1960. Subjects are RANDOMLY chosen from a previously subdivided population is a

STRATIFIED RANDOM SAMPLE.
1961. RANDOMIZED CONTROL TRIALS provide the STRONGEST FORM OF EVIDENCE.
1962. Prevalence is used to measure dental caries when caries rates are expected to be LOW.
1963. A test’s ability to correctly identify the ABSENCE OF DISEASE is SPECIFICITY.

SPECIFICITY is the percentage of people who do NOT have a given disease. BOTH
TRUE.
1964. A test’s ability to correctly DIAGNOSE the PRESENCE of condition or disease that
exists is SENSITIVITY.
1965. A disease’s past and present CUMULATIVE EFFECT until the time of examination is
PREVELANCE.
1966. The PERCENTAGE of people in a population suffering from a particular disease at a given
point in time is PREVELANCE.
1967. The most important function of the STATE health department is to provide
CONSULTATIVE ASSISTANCE.
1968. A dental health program’s effectiveness is best measured by the EXTENT TO WHICH IT
MEETS PROGRAM OBJECTIVES.
1969. “HEALTHY PEOPLE 2010” was published by the DHHS (DEPARTMENT OF HEALTH &
HUMAN SERVICES.
1970. CDC, DHHS, & NIH are examples of FEDERAL ORGANIZATIONS dedicated to national
health issues.
1971. The primary international organization dedicated to proactively and reactively addressing
global health problems is the WORLD HEALTH ORGANIZATION.
1972. A study where both subjects and researcher are unaware of which subjects belong to the
experimental group or the control group is DOUBLE-BLIND.
1973. The best study to PREVENT BIAS is one that is DOUBLE-BLIND.
1974. An OBSERVATIONAL study that collects data on the same subjects over a long period
of time is a LONGITUDINAL STUDY.
1975. Three types of LONGITUDINAL STUDIES are PANEL, COHORT, and

RETROSPECTIVE.
1976. An observational study that compares the relationship between oral cancer and male
smokers at a SINGLE POINT IN TIME is a CROSS-SECTIONAL STUDY.
145
1977. The best research sample to ELIMINATE BIAS in a study is to use a CONVENIENCE
SAMPLE.
1978. The research sample that yields the GREATEST BIAS POTENTIAL is a JUDGEMENT
SAMPLE.
1979. When more scores fall within the LOWER RANGE the curve skew is POSITIVE.
1980. Most scores in a NORMAL BELL CURVE fall within +1 and -1 from the STANDARD
DEVIATION.
1981. The DEPENDENT VARIABLE in an experiment is the outcome of interest.
1982. The extent that a test or index measures what it is intended to measure is VALIDITY.
1983. The measure of confidence in test results is STATISTICAL SIGNIFICANCE.
1984. The statistic that best helps the researcher determine the SIGNIFICANCE of test results
and weigh the strength of evidence is the P-VALUE.
1985. SMALL p-values (< 0.05) indicate statistically significant results and strong evidence
that the results DID NOT OCCUR BY CHANCE. LARGE p-values (> 0.05) indicate results
OCCURRED BY CHANCE (cannot reject the null hypothesis).
1986. The HIGHER the P-VALUE, the LESS LIKELY a relationship exists between two
variables, and greater chance the relationship occurred merely by chance.
1987. The best test to compare the difference between at least THREE mean scores is ANOVA.
1988. Consistent performance BETWEEN DIFFERENT EXAMINERS refers to INTER-

EXAMINER RELIABILITY.
1989. The CLOSER the CORRELATION CO-EFFICIENT to +1 or -1, the STRONGER

CORRELATION and more probable the CAUSE & EFFECT.
1990. An increase in patient oral hygiene proficiency resulting in a decrease in plaque

accumulation in an example of a NEGATIVE CORRELATION.
1991. An increase in dietary carbohydrates and sugar consumption resulting in increased caries
and obesity is an example of a POSITIVE CORRELATION.
1992. A PRETEST-POSTTEST STUDY DESIGN is the PREFERRED method to compare

participant groups by measuring the DEPENDENT VARIABLE before introducing the
INDEPENDENT VARIABLE. The PRE-POST design uses SUMMATIVE and
QUANTATIVE evaluations to enable the researcher to compare pretest and posttest
scores to MEASURE THE DEGREE OF CHANGE from dental treatment or community
oral health initiatives.
1993. When making decisions about patient treatment, a SYSTEMIC REVIEW STUDY
provides the clinician with the strongest evidence.
146
1994. The process of subjecting a dental author’s scholarly research or work to the scrutiny of
dental experts in the same field before the journal or book is published to improve research
validity is PEER REVIEW (REFEREEING).
1995. The most effective method for the dental professional to promote NEW LEARNING at a
community oral health fair and achieve the highest level of community participation is
through PRACTICAL, HANDS-ON ACTIVITIES that actively engage community
participants.
1996. The MOST effective teaching method for the dental hygienist to evaluate school-aged
children learning the cognitive and psychomotor skills necessary for proper oral hygiene
is through active DISCUSSION, DEMONSTRATION, and ROLE-PLAYING.
ORAL HEALTH INDICES AND PREVENTION
1997. The BEST caries index to use when an epidemiologist’s main purpose of research is to
determine caries susceptibility rather than immediate treatment needs is the DFMT.
1998. The PRIMARY goal in any oral health preventive program is PLAQUE CONTROL.
1999. The only index that is REVERSIBLE & IRREVERSIBLE because it measures both
gingivitis and periodontitis is the PERIODONTAL DISEASE INDEX (PDI).
2000. The BEST dental index to detect EARLY signs of GINGIVITIS is the SULCULAR
BLEEDING INDEX (SBI).
2001. The FIRST clinical sign of GINGIVITIS is BLEEDING ON PROBING.
2002. The probe tip must be WALKED along the entire gingival sulcus in 1 mm increments
because the EPITHELIAL ATTACHMENT DEPTH VARIES.
2003. To prevent penetrating the soft and resilient JUNCTIONAL EPITHELIUM that forms the
sulcus base, the probe tip is inserted and walked using 10-20 GRAMS OF PRESSURE.
2004. The GINGIVAL INDEX (GI) was scored by the technique developed by LOE & SILNESS.
2005. The BEST INDEX to determine the rate of pregnancy gingivitis in a specific population
is the GINGIVAL INDEX (GI).
2006. A unique characteristic of the ROOT CARIES INDEX (RCI) compared to other indices is
that it INCLUDES THE CONCEPT TEETH AT RISK.
2007. The G.V. Black classification implicated in ROOT CARIES is CLASS V.
2008. Caries on the PROXIMAL surfaces of ANTERIOR TEETH without incisal edge
involvement is CLASS III CARIES.
147
2009. The index that selects and examines a combination of SIX permanent teeth is the
RAMFJORD TEETH
2010. Qualities such as VALIDITY, RELIABILITY, UTILITY, SENSITIVE, CLINICALLY

ACCEPTABLE, and QUANTIFIABLE are all characteristic of a DENTAL INDEX.
2011. An evidence-based approach to prevent and manage CARIES by assessing risk levels
that form intervention guidelines before irreversible tooth damage occurs is CAMBRA.
2012. An IRREVERSIBLE oral condition caused by excessive and prolonged ingestion of

fluoride that causes ENAMEL MOTTLING and PITTING is called DENTAL FLUOROSIS.
2013. DENTAL FLUOROSIS is caused by CHRONIC LOW-DOSE, LONG-TERM FLUORIDE

INTAKE DURING THE MINERALIZATION STAGE OF ENAMEL DEVELOPMENT.
2014. WHITE SPOTS on the CORONAL THIRD of anterior teeth are most likely caused by
FLUOROSIS.
2015. FLUOROSIS may result from excessive fluoride intake during the MINERALIZATION
STAGE of tooth development.
2016. During enamel formation, fluoride is initially deposited at the DENTINOENAMEL

JUNCTION (DEJ).
2017. ROOT HYPERSENSITIVITY DECREASES as CELLULAR DENTIN FORMATION

INCREASES.
2018. Professional fluoride application is beneficial after POLISHING because the GREATEST
CONCENTRATION OF FLUORIDE IONS on the outermost enamel layer may be
removed.
2019. Sources of FLUORIDE INGESTION are WATER, FOOD, SUPPLEMENTS, &

DENTRIFICES.
2020. The FIRST sign of ACUTE FLUORIDE TOXICITY is NAUSEA.
2021. The FIRST step taken when a person > 6 years old ingests a toxic amount of fluoride is
INDUCE VOMITING (EMESIS).
2022. Oral administration of ipecac syrup, milk, 1% calcium gluconate, or calcium chloride
are treatments for ACUTE FLUORIDE TOXICITY.
2023. The MINIMUM LETHAL FLUORIDE DOSE for an average adult is 5 GRAMS.
2024. Factors that increase the severity of CHRONIC FLUORIDE TOXICITY are increased
consumption of naturally fluoridated water, increased dietary intake of high-fluoride foods,
and low calcium diet.
2025. Historically, the recommended OPTIMAL natural fluoride concentration in community

drinking water ranged from 0.7 to 1.2 ppm depending on the CLIMATE (AIR)
TEMPERATURE.
148
2026. The OPTIMAL FLUORIDE LEVEL in community water is 0.7 ppm mg/L.
2027. The fluoride concentration in SALIVA ranges from 0.01-0.04.
2028. The most COST-EFFECTIVE and EFFICIENT method to systemically implement a

community fluoride program is through WATER FLUORIDATION.
2029. The fluoridation method that can be ingested both systemically during pre-eruption and
topically during post-eruption is WATER.
2030. SYSTEMIC FLUORIDE during PRE-ERUPTION protects teeth by REDUCING

FLUOROAPATITE SOLUBILITY.
2031. CHEMICAL COMPOUNDS used to fluoridate community water are SODIUM FLUORIDE
(NaF), SODIUM SILICOFLUORIDE (Na2SiF6), and HYDROFLUOROSILICIC ACID
(HFS).
2032. SYSTEMIC FLUORIDE is rapidly ADSORBED in the STOMACH and SMALL

INTESTINE and is EXCRETED through the KIDNEYS.
2033. A 17-year old patient presents with rampant interproximal and occlusal caries.
Appropriate fluoride application methods include USE OF DENTRIFICE, MOUTH RINSE,
& PROFESSIONAL FLUORIDE TREATMENT.
2034. A resident in upstate NY with a water fluoride concentration of 3.4 could be at high risk for
FLUOROSIS.
2035. The percentage of children in the U.S. with some form of DENTAL FLUOROSIS is 20-
25%.
2036. Properties of FLUORIDE are BACTERIOCIDAL, BACERIOSTATIC, and

SUBSTANTIVITY.
2037. FLUORIDE is BACTERIOSTATIC at LOW concentrations, and BACTERIOCIDAL at

HIGH concentrations.
2038. SUBSTANTIVITY describes FLUORIDE’S ability to penetrate and bond to the PELLICLE,
PLAQUE, ENAMEL, and CEMENTUM, be released over time with prolonged potency.
2039. CEMENTUM DEMINERALIZATION occurs when the pH is 6.0-6.7 while ENAMEL

DEMINERALIZATION occurs at 5.5 pH.
2040. The HIGHEST pH where ENAMEL HYDROXYAPATITE DEMINERALIZES is 5.5, which

represents the CRITICAL pH.
2041. ENAMEL (HYDROXYAPATITE) DEMINERALIZATION occurs when saliva and plaque

fluid are no longer saturated with CALCIUM and PHOSPHATE.
2042. Teeth with early subsurface caries CAN BE REMINERALIZED WITH FLUORIDE,
while teeth suffering acid erosion cannot be remineralized.
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2043. The HOTTER the CLIMATE, the LOWER the recommended fluoride concentration
due to increased water consumption (people drink more).
2044. When determining the appropriate dose of systemic fluoride supplement for a child, the
most important factors for the dental professional to consider are the CHILD’S AGE,
FLUORIDE CONCENTRATION OF CHILD’S DRINKING WATER, &
CONSCIENTIOUSNESS OF PARENT.
2045. The MOST EFFECTIVE professional topical fluoride delivery system for patients with
RAMPANT CARIES, GERD, BULEMIA, or BEFORE CANCER RADIATION is the TRAY
METHOD WITH NEUTRAL SODIUM FLUORIDE (NaF).
2046. The best professional fluoride application to prevent damage to composite and
porcelain from etching is SODIUM FLUORIDE (NaF).
2047. The professionally applied fluoride FDA approved as a CAVITY LINER and to reduce
DENTINAL HYPERSENSITIVITY is 5% SODIUM FLUORIDE (NaF) VARNISH.
2048. The pain associated with DENTINAL HYPERSENSITIVITY is TRANSIENT in nature.
2049. Active ingredients in DENTRIFICES to reduce dentinal hypersensitivity due to gingival

recession include POTASSIUM NITRATE, SODIUM CITRATE, and STRONTIUM
CHLORIDE.
2050. The purpose of adding a DETERGENT to a DENTRIFICE is to LOOSEN DEBRISE,

CREATE A FOAMING ACTION, and ACT AS A SURFACTANT.
2051. The BEST fluoride application method to prevent caries is LOW CONCENTRATION,
HIGH FREQUENCY.
2052. A drawback of prolonged CHLORHEXIDINE GLUCONATE or STANNOUS FLUORIDE

use is YELLOWISH-BROWN STAINING of teeth.
2053. The chemical responsible for extrinsic YELLOWISH-BROWN STAIN from STANNOUS
FLUORIDE (SnF2) is the TIN ION.
2054. STANNOUS FLUORIDE is both BACTERIOCIDAL & BACTERIOSTATIC and is effective

against plaque, caries, gingivitis, dentinal hypersensitivity, and breath malodor.
2055. The professional applied solution with the HIGHEST FLUORIDE ION CONCENTRATION
is STANNOUS FLUORIDE (SnF2).
2056. The professional fluoride CONTRAINDICATED on COMPOSITES, PORCELAIN,

SEALANTS, and IMPLANTS, due to its ability to cause corrosion, pitting or etching of
these materials is ACIDULATED PHOSPHATE FLUORIDE (1.23%).
2057. The appropriate amount of DAILY fluoride supplement that should be given to a 6-16
year old patient in an area with a 0.25 ppm fluoride ion concentration in drinking water is
1.00 mg.
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2058. The appropriate amount of DAILY fluoride supplement given to a 6 month-3 year old
child living in an area with a 0.5 ppm fluoride ion concentration in drinking water is NONE.
2059. The most appropriate OTC fluoride rinse is 0.05% NaF, which has the GREATEST
EFFECT on NEWELY ERUPTED TEETH and SMOOTH TOOTH SURFACES.
2060. SYSTEMIC FLUORIDES are LEAST EFFECTIVE on ROOT SURFACES.
2061. The MOST EFFECTIVE practical method to prevent dental caries in communities with
established water systems is FLUORIDATION.
2062. 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.
2063. ENVIRONMENTAL PROTECTION AGENCY (EPA) monitors fluoride concentration in

COMMUNITY DRINKING WATER, while the FDA establishes fluoride limits in BOTTLED
WATER.
2064. The EPA RECOMMENDS water defluoridation when fluoride levels exceed 2 ppm, and
MANDATES defluoridation when fluoride levels exceed 4 ppm.
2065. Government agencies that recommend natural fluoride concentration levels include the
HHS, EPA, and U.S. PUBLIC HEALTH SERVICE.
2066. The INITIAL STEP when planning a COMMUNITY PROGRAM is to conduct a NEEDS
ASSESSMENT.
2067. A critical reason to conduct a needs assessment when planning a community program is
to OBTAIN BASELINE DATA.
2068. During a community preventative oral health initiative, the dental hygienist performs an
intra-oral TYPE IV exam using ONLY a TONGUE DEPRESSOR and LIGHTING.
2069. During another community oral health initiative, the dental hygienist performs an intra-oral
TYPE III exam using ONLY a MIRROR and LIGHTING.
2070. When conducting a needs assessment for a LARGE POPULATION, the most effective
tool to obtain the data is a SURVEY.
2071. The completion and return rate of a well-designed SURVEY are increased when the
survey can be submitted electronically and when an incentive is attached.
2072. The FEDERAL health insurance program for the DISABLED and ELDERLY is
MEDICARE, while the joint FEDERAL and STATE administered health insurance
program for the poor is MEDICAID.
ACESULFAME-K.
151
2074. An ANTICARIOGENIC and CARIOSTATIC NUTRITIVE SWEETENER show to reduce

to destroy S. Mutans, decrease biofilm adhesion, increase salivary flow, and increase the
oral pH.
2076. The first step when placing a dental sealant is to ISOLATE TO OBTAIN A DRY FIELD.
2077. According to the ADA, the MOST EFFECTIVE way to maintain a dry field when placing
sealants is with the teamwork of TWO PROPERLY TRAINED DENTAL OPERATORS.
OSHA AND INFECTION CONTROL
2078. The MOST EFFECTIVE methods to prevent infection and disease transmission are HAND
WASHING and PRACTICING UNIVERSAL PRECAUTIONS.
2079. HANDS should be thoroughly washed IMMEDIATELY after removing gloves to prevent
microbial growth on the hands due to the warm temperature and moisture within the glove.
2080. The MOST common antimicrobial agent present in hand sanitizers for disinfection is
ALCOHOL.
2081. OSHA’S BLOODBORNE PATHOGEN STANDARD establishes requirements for

EMPLOYERS to implement to prevent the transmission of blood-borne diseases to
EMPLOYEES.
2082. The HAZARD COMMUNICATION STANDARD requires DENTISTS to ENSURE

CHEMICAL SAFETY IN THE WORKPLACE by providing training, protective attire,
labeling chemical containers, and maintaining MSDS.
2083. PERSONAL PROTECTIVE EQUIPMENT includes GLOVES, GOWNS, EYE

PROTECTION, FACE SHIELD, & MASKS.
2084. The process by which ALL life forms in an environment are COMPLETELY
DESTROYED is STERLIZATION.
2085. STERILIZATION methods include STEAM UNDER PRESSURE AUTOCLAVE,

CHEMICAL VAPOR, DRY HEAT, and ETHYLENE OXIDE.
2086. A container made of POLYSTYRENE or POLYETHYLENE are NOT heat-resistant thus

should NOT be placed inside an autoclave. Heat-resistant materials that CAN be placed
inside an autoclave include STAINLESS STEEL, POLYCARBONATE,
POLYPROPYLENE, and BOROSILICATE GLASS.
2087. DRY HEAT STERILIZATION destroys microorganisms by causing PROTEIN

COAGULATION.
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2088. The proper TIME and TEMPERATURE for DRY HEAT STERILIZATION is 320°F (160°C)
for 2hrs, or 340°F (170°C) for 1hr.
2089. An appropriate method of COLD STERILIZATION for instruments with heat intolerance is
soaking the instrument in GLUTARALDEHYDE FOR 10 HOURS.
2090. Factors that qualify instruments or devices to be COLD STERILIZED include HEAT
INTOLERANCE, BASED ON MANUFACTURER’S RECOMMENDATIONS, NOT
REGISTERED WITH FDA AS A SINGLE-USE DEVICE, and APPROVED AND
REGISTERED BY FDA or EPA.
2091. An instrument that penetrates SOFT TISSUE cannot be COLD STERILIZED.
2092. The destruction or inhibition of MOST pathogenic bacteria while in their ACTIVE
GROWTH PHASE and inactivation of SOME viruses (not TB or Hepatitis) is
DISINFECTION.
2093. ALCOHOLS, CHLORHEXIDINE, IODOPHORS, PHENOLS, and QUATERNARY

AMMONIUM are all examples of DISINFECTANTS.
2094. DISINFECTANTS are only applied to INANIMATE OBJECTS.
2095. The GREATEST RISK for airborne infection comes from AEROSOLS due to their small
size.
2096. The GREATEST RISK for transmission of blood-borne pathogens comes from
SPLATTER.
2097. UNIVERSAL PRECAUTIONS applies to contact with SKIN, MUCOUS MEMBRANES, &
ALL BODILY FLUIDS (except sweat).
2098. REGULATED WASTE in the dental setting includes EXTRACTED TEETH,

CONTAMINATED SHARPS, EXCISED HARD & SOFT TISSUES, & GAUZE
SATURATED WITH BLOOD.
2099. According to the CDC and OSHA, the safest method to recap a needle after a dental
injection is using the ONE-HANDED SCOOP technique.
2100. DENTAL UNIT WATER LINES and DEVICES that enter the patient’s mouth should be
FLUSHED for 2 minutes at the beginning of each day and for 20-30 seconds after
each patient to remove patient debris that may have entered the turbine, air, or waterlines.
2101. Opportunistic pathogens that inhabit biofilm inside dental unit water lines are
PSEUDOMONAS AERUGINOSA & LEGIONELLA PNEUMOPHILIA.
2102. Methods to reduce biofilm accumulation inside dental unit waterlines include using
INDEPENDENT WATER RESERVOIRS (BOTTLE), CHEMICAL WATERLINE
TREATMENT, POINT-OF-USE-FILTERS, and DAILY DRAIN AND AIR PURGING
PROTOCOLS.
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2103. The purpose of MATERIAL SAFETY DATA SHEETS (MSDS) is to PROTECT and
PROVIDE EMPLOYEES with information about the CHEMICAL HAZARDS OF
DENTAL MATERIALS.
2104. Copies of MSDS sheets MUST BE KEPT ON FILE IN THE DENTAL OFFICE and MADE
READILY AVAILABLE TO EMPLOYEES.
2105. BIOLOGICAL INDICATORS (BI) test the proper functioning of sterilization cycles AT
LEAST WEEKLY.
2106. STERILIZATION INDICATORS such as SPORE STRIPS and INDICATOR TAPE enable
routine monitoring, qualification, and load monitoring of the steam sterilization process.
Indicators reveal if the conditions of steam autoclave cycle were adequate to achieve
defined level of microbial inactivation.
2107. Process indicators and biological indicators during autoclaving are used to ensure
complete sterilization. The MAIN difference between biological monitors and process
indicators is biological indicators PROVE that sterilization was achieved by
showing that bacterial spores were killed. These indicators are required for the
sterilization process because they show that the overall intent of the sterilization process
was successful.
2108. The MOST accepted means of monitoring sterilization to assess the sterilization
process directly by the killing high resistant microorganisms (e.g. Geobacillus or Bacillus
species) are BIOLOGICAL INDICATORS (SPORE TESTS).
2109. If the sterilizer time, temperature, pressure, and chemical indicators suggest it is
functioning properly, but the weekly spore test results is POSITIVE, the sterilization
operator SHOULD REPEAT THE SPORE TEST IMMEDIATELY USING the SAME
CYCLE that produced the positive biological indicators.
2110. Contaminated PPE like SCRUBS and GOWNS should be LAUNDERED IN THE
DENTAL OFFICE following the manufacturer’s instructions, or placed in a biohazard-
labeled, leak-proof bag and sent to a LAUNDRY SERVICE.
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ORAL PATHOLOGY AND DISEASES

METABOLIC AND GENETIC DISEASES
HYPERTHYROIDISM-caused by excessive production of thyroid hormone (THYROXIN).
Thyroxin’s stimulates cellular metabolism, growth, and differentiation of all tissues. In excess, it
leads to high basal metabolism, fatigue, weight loss, excitability, elevated temperature
(heat intolerance, sweating), generalized osteoporosis, fine hair, diarrhea, tremor
(shakiness), tachycardia (rapid heart rate). Oral manifestations are not uncommon, but if the
disturbance starts early in life, premature tooth eruption and loss of deciduous dentition are
common. GRAVES DISEASE and EXOPTHALMOS (bulging eyes). Two types of
Hyperthyroidism:
1. GRAVES DISEASE (Toxic Diffuse Goiter)-most common form that occurs mostly in
WOMEN ages 20-40. Usually arises after an infection or physical or emotional stress.
Typical signs of hyperthyroidism are present plus GOITER (bulging neck) &
EXOPHTHALMOS (bulging eyes).
2. PLUMMER’S DISEASE (Toxic Multinodular Goiter)-caused by the presence of many

toxic thyroid nodules (adenomas) within the thyroid gland. Plummer’s is uncommon in
adolescents and young adults, and increases with age. Exophthalmos (bulging eyes)
is rare.
HYPOTHYROIDISM-a clinical feature is WEIGHT GAIN, cold intolerance, lowered pitch of voice,
mental and physical slowness, constipation, dry skin, coarse hair, and puffiness of face, eyelids,
and hands.
• Myxedema-very severe hypothyroidism in adults, much more common in WOMEN than

men. Characterized by puffiness of face and eyelids, swelling of tongue and larynx. Skin
becomes dry, and rough, and hair sparse. Individual has a low basal-metabolic rate and low
body temperature, poor muscle tone, low strength, tires easily, and are mentally sluggish.
Administering thyroid hormones alleviates myxedema.
• Hashimoto’s Disease (Thyroiditis)-autoimmune disease where the immune system attacks

the thyroid gland causing primary hypothyroidism. It is the most common cause of
hypothyroidism in the U.S., affecting more women than men. Potential causes include
genetics, hormones, excessive iodine, or radiation exposure. Most common symptoms:
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fatigue, weight gain, pale/puffy face, feeling cold, joint or muscle pain, constipation, thin or
brittle hair, depression, slow heart rate.
• Cretinism-severe hypothyroidism in a child, due to lack of thyroid hormone causing

retardation of growth and abnormal bone development. Severe mental retardation is caused
by improper CNS development. If recognized early, Cretinism can be improved with thyroid
hormones.
• Dental findings in a child with hypothyroidism are a LARGE TONGUE, under-developed

mandible, over-developed maxilla, delayed eruption, and longer retained deciduous
teeth.
HYPERPARATHYROIDISM-a common complication is KIDNEY STONES (renal calculi).

Kidney stones form due to an increase in urinary excretion of calcium and phosphate.
Osteoporosis, GIANT CELL GRANULOMAS, and metastatic calcifications are
manifestations of hyperparathyroidism.
• The main cause is an ADENOMA (benign tumor of the gallbladder epithelium). Laboratory
findings include hypercalcemia, decreased serum phosphorus, and increased serum
alkaline phosphatase and serum PTH. Clinical characteristics: cystic bone lesions
(osteitis fibrosa cystica or von Recklinghausen’s Disease of bone), nephrocalcinosis,
kidney stones (renal calculi), and peptic duodenal ulcers. May find well-defined cystic
radiolucencies on a panorex or peri-apical radiograph.
• EXCESS LOSS OF CALCIUM in urine stimulates the parathyroid glands to undergo

hyperplasia because the feedback mechanism that detects low serum calcium elicits
growth of the gland. The resulting metabolic effects are identical to primary
hyperparathyroidism effects.
HYPOPARATHYROIDISM-in rare instances, associated with congenital thymic hypoplasia

(DiGeorge’s syndrome). Most commonly caused by accidental surgical excision during
thyroidectomy.
ACROMEGALY – a hormonal disorder that occurs when the PITUITARY GLAND produces
EXCESS GROWTH HORMONE (HYPERPITUITARISM) due to a BENIGN TUMOR after
adolescence (fusion of long bone epiphyses). Most commonly affects MIDDLE-AGED ADULTS
and can cause serious illness and premature death.
• In > 90% of acromegaly patients, GH overproduction is caused by a BENIGN TUMOR of the

pituitary gland (ADENOMA). Whether or not the epiphyses of the long bones have fused with
the shaft is the main determinant of whether gigantism or acromegaly will occur when there is
over-secretion of GH by the pituitary gland.
• Clinical Signs: soft tissue swelling of the hands & feet (an early feature), with patients noticing
a change in ring or shoe size. Gradually, bony changes alter the patient’s facial features (i.e.
brow & lower jaw protrude, nasal bone enlarges, and teeth spacing increases).
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• Oral Manifestations of Acromegaly & Gigantism: enlarged tongue, mandibular

prognathism, teeth are tipped to buccally or lingually due to an enlarged tongue, and roots may
be longer than normal.
• GIGANTISM-caused by a benign tumor BEFORE adolescence (non-fusion of epiphyses).
DWARFISM (Pituitary Dwarfs) – characterized by arrested growth caused by undersecretion of

GROWTH HORMONE. Dwarfs often have limbs and features not properly proportioned or
formed.
• Oral Manifestations: delayed eruption rate & shedding of teeth, clinical crowns & roots appear
smaller, dental arch is smaller causing malocclusion, and an under-developed mandible.
• MOST COMMON type of Dwarfism is ACHONDROPLASIA. Child is very short (~50 inches),
fingers are stubby, bowed legs, bulging forehead, bossing of frontal bones, saddle-like nose,
and mandibular prognathism.
OSTEOGENESIS IMPERFECTA (“BRITTLE BONES”) –a rare genetic defect/disorder that

affects the COLLAGEN PRODUCTION (major protein of the body’s C.T.). Person either has less
collagen than normal, or poorer quality of collagen than normal causing WEAK BONES THAT
FRACTURE/BREAK EASILY often from little or no cause.
• The main clinical characteristic is EXTREME FRAGILITY & POROUS BONES with a
proneness to fracture due to the effects of inadequate osteoid production.
• Additional Clinical Features: BLUE SCLERA, deafness due to osteosclerosis, loose joints,
low muscle tone, triangular face, and a tendency toward spinal curvature.
• Teeth have bulbous crowns with a cervical constriction, partially or completely obliterated
pulps, and narrower & shorter roots. Deciduous (primary) teeth are more severely affected
than permanent teeth. Teeth are poor and abnormal due to dentin malformation (Type 1
Dentinogenesis Imperfecta); may be linked to DENTINOGENESIS IMPERFECTA.
• Treatment: NO KNOWN CURE. Treatment aims to prevent and control symptoms.
HYPOPHOSPHATASIA –resembles OSTEOGENESIS IMPERFECTA. It’s an inherited

metabolic (chemical) BONE DISEASE that results from LOW LEVELS of ALKALINE
PHOSPHATASE (enzyme essential the calcification of bone tissue). Loosening,
hypocalcification, and premature loss of deciduous teeth are characteristic. Radiographically,
large pulp chambers and alveolar bone loss are present.
Hypophosphatasia’s severity varies greatly. Some patients have blue sclera that resembles
osteogenesis imperfecta. Others have deformity of the arms, legs, and chest and/or frequent
bouts of pneumonia and recurrent fractures.
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PAGET’S DISEASE OF BONE (OSTEITIS DEFORMANS) – a common, chronic, non-metabolic

bone disorder characterized by an INCREASE in serum ALKALINE PHOSPHATASE levels.
Bones become enlarged & deformed, dense, but fragile due to excessive breakdown and
formation of bone. Has potential to undergo “spontaneous” malignant transformation. There is
excessive bone destruction and unorganized bone repair.
• Radiographic Features: “COTTON-WOOL” APPEARANCE ON PANOREX (skull and

jaws). Hypercementosis of roots and loss of lamina dura around roots.
• Effects males & females, but rarely people under 40yrs (affects middle-aged & elderly people).
• Cause is hereditary. Patients are predisposed to developing OSTEOSARCOMAS.
• Signs and Symptoms: PAIN in affected area, bone deformity & susceptibility to fractures in
the affected area, headache, and hearing loss if the affected area is the skull. Symptoms
develop SLOWLY.
• Clinical Features: Patients may give a history of progressively INCREASE IN HAT SIZE OR
NEED FOR NEW DENTURES being made more frequently due to bony changes.
• Bones are warm to touch due to increased vascularity.
• Lab tests show highly increased serum alkaline phosphatase, urinary calcium, &
hydroxyproline; with normal levels of SERUM PHOSPHATE and CALCIUM.
• Treatment: Administer anti-metabolites or CALCITONIN to decrease bone resorption, or treat

with a high-protein & high calcium diet.
PAGET’S DISEASE (ENLARGED ALVEOLAR RIDGES)
OSTEOMALACIA (Adult Rickets) – SOFTENING of bones in adults because osteoid tissue in

bones failed to calcify due to LACK OF VITAMIN D. More common in women, and may be
asymptomatic until a bone fracture occurs.
• STEATORRHEA-one of the most common causes of Osteomalacia due to FAT

MALABSORPTION where the body cannot absorb fats, so fats are passed directly out of
the body in stool causing poor absorption of vitamin D (fat soluble) and calcium. Osteomalacia
affects ALL BONES, specifically at their epiphyseal growth plates.
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• Signs and Symptoms: pain in bones of the arms, legs, spine, and pelvis.
RICKETS (Child Osteomalacia) –causing skeletal deformities, and usually accompanied by

irritability and generalized muscle weakness. Bowlegs, pigeon breast, and protruding stomach
are signs. Teeth are affected by delayed eruption, malocclusion, and developmental
abnormalities of dentin and enamel, with a higher caries rate.
CEREBRAL PALSY – a group of disorders affecting body movement and muscle coordination
due to an insult or anomaly of the brain’s motor control centers. This damage interferes with
messages from brain to the rest of the body. The effects vary greatly among people.
• CP is mainly characterized by SPASTIC PARALYSIS or impairment of control or

coordination over voluntary muscles. Often accompanied by mental retardation,
seizures, & disorders of vision/communication.
• NO ORAL PATHOLOGIC MANIFESTATIONS are present in people with cerebral palsy,

but several conditions are more common, or more severe than in the normal population:
Ø Higher incidence of periodontal disease, caries, bruxism, and malocclusion.
Ø Prone to gingival hyperplasia if Dilantin is used to control seizures.
Ø More susceptible to trauma, especially maxillary anterior teeth.
DOWN SYNDROME – a congenital defect caused by a chromosomal abnormality (TRISOMY

21), marked by various degrees of mental retardation and characteristic physical features (short,
flattened skull, slanting eyes, thickened tongue/fissured, broad hands/feet, etc.)
• Oral Manifestations: mandibular prognathism, increased periodontal disease, thickened or

fissured tongue, delayed teeth eruption, higher incidence of congenitally missing teeth,
malocclusion, & enamel dysplasia.
MUSCULAR DYSTROPHY – a group of genetic diseases marked by progressive weakness &

degeneration of skeletal or voluntary muscles that control movement.
• Oral Manifestations: increase in dental disease if oral hygiene is neglected, weakness in

muscles of mastication causing decreased maxillary biting force, higher incidence of
mouth breathing, and open bite.
ECTODERMAL DYSPLASIA – hereditary condition characterized by abnormal development of

the skin and associated structures (hairs, nails, teeth, & sweat glands). ED involves all
structures derived from ECTODERM, affecting MALES more than females. Manifests orally
as reduced/missing teeth.
• Clinical Signs: hypothrichosis (decrease in hair (fine sparse hair), anhidrosis (no sweat or
sebaceous glands, causing heat intolerance), Anodontia (complete absence of teeth),
Oligodontia (partial absence of teeth), no tooth buds of the primary or permanent dentition
(edentulous), depressed nose bridge, lack of salivary glands, and child appears much older
than their true age.
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• Affects tooth bud development causing congenitally missing teeth (lack of permanent teeth)
and/or peg-shaped or pointed teeth. Enamel may also be defective.
• Treatment: Dentures can be fabricated for young children, but they will need to be replaced
periodically to accommodate the patient’s jaw growth. Implants can be placed once the jaw if
fully developed, or orthodontics to close spaces. Treatment is complex so use a multi-
disciplinary treatment approach.
ECTODERMAL DYSPLASIA
CLEIDOCRANIAL DYSPLASIA (DYSOSTOSIS)-genetic disorder of bone development

characterized by absent or incomplete formed COLLAR BONES, heavy protruding jaw, wide
nasal bridge, and dental abnormalities (malaligned teeth, multiple supernumerary teeth, and
unerupted teeth). Observing a panorex or FMX alone often suggests the diagnosis.
CLEIDOCRANIAL DYSPLASIA (DYSOSTOSIS)
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PIERRE-ROBIN SYNDROME – an inherited disorder with the following findings in the

NEONATE:
• Micrognathia-smallness of the jaws.
• Glossoptosis-downward displacement or retracted tongue.
• Breathing problems and cleft palate.
LATERAL CLEFTING OF THE LIP – results from failure of the MAXILLARY & FRONTAL
NASAL PROCESSES TO MERGE. Cleft lip occurs during the 5th-6th week of embryonic life. It
can be bilateral or unilateral, more common in males, and involves the LEFT SIDE more than the
right side.
CLEFT PALATE – occurs in 6th-8th week of embryonic life. Isolated cleft palates are more
common in females, characterized by a fissure in the midline of the palate due to failure of the
two sides to fuse during embryonic development. The most severe handicap caused by cleft
palate is an impaired mechanism PREVENTING NORMAL SPEECH & SWALLOWING.
Important: Speech problems associated with Cleft Lip & Cleft Palate are usually due to the
inability of the soft palate to close airflow into the nasal area.
CHERUBISM – a BENIGN genetic autosomal dominant disease of the maxilla & mandible,
typically in children by age 5 (affects males 2:1). Most cases occur in the MANDIBLE. The jaws
are firm and hard to palpation, and regional lymphadenopathy may be present. BILATERAL
expansion of the jaws gives the child a very round face, reminding one of cherubs (cupids)
in paintings. The tumors stop growing shortly after puberty. As the patient’s age and size
increases, the deformity is less noticeable.
• Histologically, cherubism lesions closely resemble Central Giant Cell Granulomas.

Histology shows a giant cell lesion with some reactive bone formation. However, perivascular
collagen cuffing is pathognomonic for cherubism.
• Radiographically: lesions appear as multiple, well-defined, multi-locular radiolucencies of the

jaw.
• No associated systemic manifestations. However, the deciduous dentition may spontaneously

shed prematurely, starting as early as age 3. There is often delayed eruption of the permanent
dentition, which is often defective with the absence of numerous teeth and displacement of
those teeth present.
• Treatment: cautious waiting as Cherubism tends to regress in early adulthood. Do not treat
with radiation therapy.
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CYSTIC FIBROSIS – a congenital/genetic metabolic disorder that causes EXOCRINE GLANDS

(glands that secrete fluids into a duct) to produce ABNORMAL SECRETIONS mainly
affecting GI and respiratory systems. CF results in several symptoms (the most important
symptom affects the digestive tract and lungs). In some glands (glands in the pancreas &
intestines), the secretions are thick or solid excessively viscous mucous that can completely
block a gland. Mucous-producing glands in the lung’s airways produce abnormal secretions that
clog the airways allowing bacteria to multiply. CF is the MOST COMMON genetic disease
causing death among white people in the U.S. and is equally common in boys & girls.
• CF is usually characterized by COPD, exocrine pancreatic insufficiency, and abnormally high

sweat electrolytes (sweat glands secrete fluids that have a high sodium & chloride content).
• Oral Manifestations: staining of teeth as patients with CF are usually subjected to large
amounts of tetracycline during childhood. A high % of children have dark-colored teeth
(yellowish gray to dark brown). There is a greatly reduced caries rate in CF patients, probably
due to saliva alterations and long-term use of antibiotics.
• CF Signs & Symptoms: poor growth despite good appetite, malabsorption, and foul, bulky
stools (steatorrhea), chronic bronchitis (COPD) with cough, recurrent pneumonia with
respiratory infections, clubbing of fingers/toes, & barrel-chested appearance.
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INFLAMMATORY JAW LESIONS

OSTEOMYELITIS –inflammation or infection of the bone marrow and adjacent bone, usually
caused by bacteria (Staphylococci) due to trauma or surgery by a direct extension from a nearby
infection, or via the bloodstream.
• Signs and Symptoms: pain, redness, swelling in the infected area, fever, and general
malaise. Radiographically, poorly circumscribed radiolucency with a central sclerotic nidus
may be present.
CONDENSING OSTEITIS (CHRONIC FOCAL SCLEROSING OSTEOMYELITIS) – an unusual

bone reaction to an infection (most often associated with a long-standing periapical infection)
that occurs during instances of extremely high tissue resistance or in cases of low-grade infection.
There may be no signs or symptoms of the disease, other than mild pain associated with an
infected pulp. Mandibular 1st molar is the tooth most commonly involved. Most often occurs
in young patients.
• Radiographic Findings: periapical radiographs show pathognomonic, well-circumscribed

radiopaque mass of sclerotic bone surrounding and extending below the apex of one
or both roots. The entire root outline is always VISIBLE (important feature that
radiographically distinguishes it from a benign cementoblastoma).
• A tooth with a condensing osteitis lesion can be treated with RCT or extracted, since the pulp
is infected, and the infection has spread past the immediate periapical area. The sclerosing
bone constituting the osteomyelitis is NOT attached to the tooth, so it remains after the tooth
is treated or removed.
PERIAPICAL ABSCESS – usually arises from pulpal infection of a tooth due to carious
involvement of the tooth. The cellular debris and/or infection that caused the tooth pulp to become
necrotic, slowly filters out of the root tip, producing an inflammatory reaction around the root tip.
A periapical abscess can also occur after traumatic injury to a tooth, causing pulpal necrosis, and
in cases of irritation of the periapical tissues (either by mechanical manipulation or application of
chemicals) in endodontic procedures.
Clinical Features:
• Acute Periapical Abscess: tooth is extremely painful to percussion (may feel slightly
extruded from its socket), and is MOBILE. Radiograph presents only a slight thickening of the
periodontal membrane (PDL). Not typically seen on periapical film because until it becomes
chronic.
• Chronic Periapical Abscess: presents as a granuloma or cyst (radiolucent area at the root
apex), but there are usually no clinical features or symptoms (asymptomatic).
• Treatment: establish DRAINAGE by opening the pulp chamber (RCT) or extracting the tooth.
If not treated, it can cause serious complications (i.e. osteomyelitis, cellulitis, & bacteremia).
OSTEONECROSIS–bone death or necrosis; a rare complication of cancer patients (radiation and

chemotherapy), patients with tumors or infectious embolic events, or with osteoporosis taking IV
or oral bisphosphonates. May be caused by a defect in bone remodeling or wound healing (defect
in osteoclast function).
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BISPHOSPHONATE-OSTEONECROSIS (BON)-a dental phenomenon that may lead to surgical

complications (bone necrosis) due to impaired wound healing after extractions, periodontal
surgery, or RCT.
• Caution with patients taking IV bisphosphonates (Zometa (zoledronic acid) & Aredia
(pamidronate) for osteoporosis and cancer treatment respectively.
• Caution with patients taking oral bisphosphonates (Fosamax, Actonel, & Boniva). Occurs
more common in patients taking IV bisphosphonates (.05-7%) and < 1% taking oral
bisphosphonates.
OSTEONECROSIS
OSTEOPOROSIS – a reduction of total skeletal mass due to INCREASED BONE RESORPTION,

causing predisposition to pathologic fractures caused by calcium or estrogen hormone
deficiencies over a long time period. BONES BECOME LESS DENSE & BRITTLE.
• Osteoporosis is most common in THIN, ELDERLY WHITE WOMEN. Treatment: estrogen
therapy, calcium & vitamin D supplements, bisphosphonates.
OSTEOPETROSIS (“Albers-Schonberg Disease” or “Marble Bone Disease”) – an

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

VON RECKLINGHAUSEN’S DISEASE (NEUROFIBROMATOSIS) – the most common feature
is NEUROFIBROMATOSIS (multiple tumors of nerve tissue origin). VRD is a relatively common
inherited autosomal dominant trait characterized by multiple neurofibromas, cutaneous café-
au-lait macules, bone abnormalities, & CNS changes.
• Clinical Signs: 6 or more café-au-lait macules > 1.5cm in diameter indicates VRD.
• Treatment: No satisfactory treatment. The lesions run a high-risk of becoming malignant.
• A single neurofibroma presents at any age as a non-inflamed, asymptomatic nodule on the

tongue, buccal mucosa, & vestibule. This single nodule is removed by surgical excision,
and rarely occurs.
SCLERODERMA (SYSTEMIC SCLEROSIS) – a relatively RARE autoimmune disease of dense

collagen deposition within tissues that affects blood vessels and C.T. Characterized by
hardness and rigidity of the skin and subcutaneous tissue. The continuous deposition of
dense collagen in major organs can cause dysfunction and potential organ failure.
• Clinical Features: typically manifests in middle-age (30-50yrs), mainly in females (4:1). The
skin is typically affected first, and becomes indurated with dermal findings that range from
Raynaud phenomenon, to mastlike and “mouse” facies. Lips appear pursed with limited
opening.
• Oral Radiographs: show ABNORMAL WIDENING OF THE PDL AROUND ROOTS (this is
also found in osteosarcomas). The space is created by a thickening of the periodontal-
membrane due to an increase in size & number of collagen fibers. The enlarged space is
almost uniform in width, surrounds the entire tooth root, making the tooth appear as if it is being
extruded rapidly from its socket. Other oral radiographic features may include bilateral
resorption of the angle of the mandible’s ramus, or complete resorption of the
mandibular condyles and/or coronoid process.
• Treatment: focused on limiting further progression, but changes are often irreversible. Range
of motion exercises may improve limited opening.
SCLERODERMA
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ORAL TRAUMATIC NEUROMA- a SOFT TISSUE TUMOR due to trauma to a peripheral nerve,
usually appearing as a very small nodule/swelling (< 0.5cm in diameter) of the mucosa near/over
the mental foramen on the alveolar ridge in edentulous areas, lips, & tongue. MOST COMMON
SITE IS OVER THE MENTAL FORAMEN IN EDENTULOUS PATIENTS, but they can occur
wherever a tooth has been extracted. Extraction sites in the anterior maxilla & posterior
mandible are common sites.
• In the oral cavity, the traumatic neuroma may be due to trauma from a surgical procedure
(i.e. tooth extraction, local anesthetic injection, or accident). A nodule or swelling PAINFUL
WHEN PALPATED, as applied digital pressure elicits a response described as an “electric
shock”.
• Multiple neuromas on the lips, tongue, or palate may indicate the patient may have MEN III
(Multiple Endocrine Neoplasia Syndrome).
• Treatment: surgical excision of the nodule with small proximal portion of the involved nerve.
Recurrence is uncommon.
NEURILEMOMA (SCHWANNOMA) –a rare, benign SOFT TISSUE TUMOR (encapsulated

mass) of Schwann cells around the peripheral nerve sheath that presents as an asymptomatic
lump MOST COMMONLY ON THE TONGUE INTRA-ORALLY. Can also occur on the mouth
floor, gingiva, vestibular mucosa, lips, mental nerve area. Rarely affects the palate. Bony lesions
may cause pain or paresthesia. Derived from a proliferation of Schwann cells of the neurolemma
that surrounds peripheral nerves. Covered by normal mucosa, sessile & does not metastasize
but still do biopsy. Treatment: conservative excision. Recurrence is rare. Refer to ENT.
NEUROFIBROMA-may be derived from the Schwann cell or Perineural Fibroblast and can occur
in two forms:
1. Solitary Neurofibroma-an asymptomatic nodule on the tongue, buccal mucosa, or
vestibule treated by surgical excision.
2. Multiple lesions as part of the Neurofibromatosis syndrome. Removing the lesions is

impractical, but monitor due to the high risk/rate of malignant transformation.
FIBROMA (“IRRITATION FIBROMA OR “TRAUMATIC FIBROMA”)-the most common intra-

oral BENIGN neoplasm of CONNECTIVE TISSUE (soft tissue) origin, that occurs in people of
all ages and with equal frequency in both sexes. It’s the most common tumor in the oral cavity
and is reactive. Fibromas can arise from almost any soft tissue in the mouth, but are most
common on the buccal mucosa, lateral border of tongue, and lower lip. NODBULAR PINK
MORPHOLOGY (pink, fibrous nodule with smooth surface).
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FIBROMA
• Clinical Features: usually pink (same color or lighter than normal buccal mucosa, painless,
smooth, elevated, well-demarcated masses). Smooth, sessile, soft-to-firm nodule on buccal
mucosa, lips, and tongue.
• Microscopic Features: bundles of collagen interspersed (interlacing) with fibroblasts and

small blood vessels.
• Histogenesis: fibrous C.T. (C.T. origin).

• In most cases, the tumor is reported present for months or years with a slow-growing behavior
pattern.
• Some feel “true fibromas” of the oral cavity are rare, and are merely localized
hyperplasia due to long-standing irritation or trauma (“irritation fibroma or “traumatic fibroma”).
These fibrous nodules are comparable to hyperplasias from denture irritation (“epulis
fissuratum”). The only difference between a “true fibroma (a true neoplasm) and “irritation
fibroma” (not a true neoplasm), is the hyperplastic tissue with an irritation fibroma can regress
after removing the irritant, while a true fibroma will not regress. Treatment: conservative
surgical excision. Recurrence is rare.
PERIPHERAL FIBROMA – a well-demarcated focal mass of hyperplastic tissue with either a

sessile or pedunculated base. Similar in color to surrounding C.T., and may be ulcerated.
Treatment: local excision and recurrence is RARE. 3 Forms of Peripheral Fibroma:
1. Peripheral Ossifying Fibroma-a gingival mass with visible characteristic calcified

islands of bone and an ulcerated surface. The gingiva anterior to the permanent molars
is most often affected. Histologically, in its high degree of cellularity, it exhibits bone
formation (in contrast to peripheral fibroma). Vascularity is NOT a prominent feature as it
is with a pyogenic granuloma. POF is a subtype or variant form of a peripheral fibroma,
although both originate from an inter-dental papilla and both occur more frequently in
young adult females (but can occur at any age and are more common in children & young
adults). Usually presents as a well-demarcated focal mass of hyperplastic tissue on the
gingiva with a sessile or pedunculated base. It is usually the same color as normal
mucosa or slightly reddened. May demonstrate bone radiographically and often
demonstrates bone formation histologically. Treatment: Local Excision. POF lesions may
recur (peripheral fibroma lesions rarely recur).
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2. Peripheral Odontogenic Fibroma-gingival mass composed of well-vascularized, non-

encapsulated fibrous C.T.
3. Giant Cell Fibroma-a fibrous hyperplasia composed of multi-nucleated C.T. cells.
GIANT CELL TUMOR – a bone tumor of multi-nucleated giant cells that resemble osteoclasts
scattered in a matrix of spindle cells. May be benign or malignant, and can cause pain, functional
disability, and sometimes pathologic bone fracture.
PAPILLARY FIBROMA – a benign neoplasm of C.T. origin.
LIPOMA – a COMPETELY 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: floor
of mouth, buccal mucosa, and tongue. YELLOWISH MASS covered by normal mucosa. A
biopsy specimen will FLOAT in the formalin. Easier to diagnose than other tumors because it is
yellowish, soft, smooth, & movable, and FLOATS IN FORMALIN.
• Microscopic Features: lobules of mature fat separated by delicate C.T. septae.
• Treatment: conservative excision. Recurrence is rare. Remove surgically only if it becomes

painful, tender, infected, or enlarges to where it becomes bothersome.
LIPOMA
RHABDOMYOMA – a RARE BENIGN tumor of SKELETAL MUSCLE. Tongue is the most

common place in the head & neck. Sessile, non-painful, and covered by normal mucosa.
LEIOMYOMA – an always benign tumor of SMOOTH MUSCLE (smooth muscle neoplasm).

Non-painful, sessile, (covered by normal mucosa). Bundles of spindle-shaped smooth muscle
cells.
LYMPHANGIOMA – a BENIGN YELLOWISH-TAN TUMOR composed of a mass of DILATED

LYMPH VESSELS. Most common site in the oral cavity is the TONGUE, but can appear on the
lips and neck. Derived from endothelial cells, C.T. origin. Clinical Features: painless, nodular,
vesicle-like swelling that equally affects both sexes.
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• Superficial lesions are manifested as grayish-red papillary lesions. On the tongue,

considerable enlargement can occur (macroglossia). The papillary lesions may contain fluid,
and are often present at birth or arise early in life, but are less common than Hemangiomas.
LYMPHANGIOMA (Dilated Lymph Vessels)
• Treatment: SURGERY OR CRYOSURGERY. May recur due to their lack of encapsulation.
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BENIGN EPITHELIAL TUMORS
PAPILLOMA
PAPILLOMA –the most common BENIGN neoplasm of EPITHELIAL TISSUE ORIGIN caused
by HUMAN PAPILLOMA VIRUS (HPV). It appears as a pedunculated (foot-shaped), or sessile
WHITISH cauliflower-like mass on the tongue (posterior border), lips, gingiva, or soft
palate. A papilloma is soft in the oral cavity, but on exposed areas of the lips, are usually rough
and scaly.
• Papilloma-a vital benign cauliflower-like, white lesion with a verrucuous & pedunculated
(foot-shaped) surface. Easy to diagnose. HPV lesion is not covered by normal mucosa and
is a disease of epithelium. Non-ulcerated, small, slow growing, usually non-painful. Lateral
border of tongue, hard or soft palate are common areas. MUST EXCISE SURGICALLY and
recurrence is rare.
• Microscopic Features: finger-like projections of stratified squamous epithelium supported

by thin cores of vascular fibrous C.T. Epithelium may show hyperkeratosis or parakeratosis.
Histogenesis: squamous epithelium.
VERRUCA (Warts)-similar to a papilloma, but is NOT pedunculated caused by a viral

infection. Do excision & biopsy, especially children who have this on their finger and place their
finger in their mouth and spread the infection orally.
Keratoacanthoma-a non-painful crater-formed lesion (VIRAL) growing for 2-3 months in the
SKIN that looks like squamous cell or basal cell carcinoma, and can heal by itself, but must still
do biopsy. Can last up to 6 months. It is usually only in the skin and very rarely inside the mouth.
MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES (MEN SYNDROME) – groups of

syndromes characterized by tumors of various endocrine glands that occur in association with
a variety of other pathologic features. The most important aspect of MEN syndrome is medullary
carcinoma of the THYROID due to its ability to metastasize and cause death. Thus, detecting
mucosal neuromas may alert the clinician for early diagnosis and treatment. MEN is classified
into 3 groups:
1. Men I Syndrome-tumors or hyperplasias of the pituitary, parathyroids, adrenal cortex, and

pancreatic islets (pancreas).
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2. Men II (Sipple’s Syndrome)- parathyroid hyperplasia or adenoma, but NO tumors of the

pancreas. Patients have pheochromocytomas of the adrenal medulla, and medullary
carcinoma of the thyroid gland.
3. Men III Syndrome-mucocutaneous neuromas, pheochromocytomas of the adrenal

medulla, and medullary carcinoma of the thyroid gland. The most constant feature is
neuromas (especially in the oral cavity), most common on the lips, tongue, and
buccal mucosa.
EPULIS GRANULOMATOSUM–soft, non-painful, bleed easily, most often caused by RETAINED

FOREIGN MATERIAL (i.e. bone or tooth fragment) due to an iatrogenic error. Most
commonly found in a post-extraction socket, almost always within 10 days of the extraction.
• TREATMENT: curettage.
• Microscopic Features: granulation tissue in bone, dentin, cementum, or foreign material.
CONGENITAL EPULIS OF NEWBORNS (CONGENITAL GINGIVAL GRANULAR CELL

TUMOR) – composed of cells identical to a granular cell myoblastoma (granular cell tumor).
Usually on the ANTERIOR GINGIVA OF NEWBORNS as a PINK, non-inflammed, pedunculated
or broad-based mass. Maxillary gingiva is involved more than the mandibular gingival. Affects
females more than males.
• Treatment: surgical excision with minimal recurrence.
CONGENITAL EPULIS OF NEWBORNS
GRANULAR CELL MYOBLASTOMA (TUMOR) – an uncommon neoplasm of unknown etiology,

presenting as an uninflamed, asymptomatic mass. TONGUE is the most common location in
the head and neck region. Can affect any age group, but affects females more than males.
Congenital Epulis and Granular Cell Myoblastoma lesions are histologically identical as
they both contain granular cells. However, Congenital Epulis of newborns does not exhibit
pseudo-epitheliomatous hyperplasia of the overlaying epithelium that is often seen in Granular
Cell Myoblastoma.
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GRANULAR CELL TUMOR (TONGUE)
PYOGENIC GRANULOMA (PREGNANCY TUMOR) – an elevated ulcerated mass that bleeds

easily, more common in females (pregnant women), and may recur. Caused by minor trauma
that provides a pathway for non-specific organisms & calculus. Most commonly found on the
gingiva, but also the lips, tongue, & buccal mucosa. TREATMENT: EXCISION (but may recur).
Has exuberant granulation tissue microscopically.
PYOGENIC GRANULOMA (PREGNANCY TUMOR)
• PYOGENIC GRANULOMA is BENIGN. The MOST common site is the INTER-

DENTAL GINGIVA, but may also occur on the lower lip, tongue, & buccal mucosa.
Rarely occurs on other areas of the oral mucous membrane. Arises due to minor tissue
trauma (i.e. cementation of a crown or calculus) that provides a pathway for the invasion
of non-specific types of microorganisms. Pregnant patients are prone to these lesions
(called a “Pregnancy Tumor” in a pregnant patient). May be caused secondarily by
an altered endocrine state (hormone changes) during pregnancy in the 1st trimester.
• Clinical Features: soft, pedunculated (foot-shaped) broad-based growths with a smooth

red surface due to the presence of hyperplastic granulation tissue that contains many
capillaries. They are often ulcerated, bleed easily, and may look RASBERRY-LIKE.
• Treatment: Surgical Excision after pregnancy. May occasionally recur.
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VERRUCAL PAPILLARY LESIONS

VERRUCA VUGLARIS (SQUAMOUS PAPILLOMA) – the common WART of VIRAL etiology
(caused by Papilloma virus) that is a common skin tumor analogous to the oral papilloma. It
has an incubation period of 6 weeks to 1 year. Although it is a primary lesion of the skin, it may
occur in the oral cavity (especially lips & palate). Clinically, it is a sessile, soft,
CAULIFLOWER-LIKE LESION.
• Microscopically: a papillomatous lesion where the epithelium is thrown into folds. The lesion
shows alternating hyperkeratosis, parakeratosis, and long epithelial ridges. If excised, they
usually do not recur, but autoinoculation is possible. Intra-orally, that is how most cases
develop.
INFLAMMATORY FIBROUS HYPERPLASIA (“EPULIS FISSURATUM” OR “PALATAL

PAPILLOMATOSIS”) –found at the area of the denture borders, more common in the maxilla
(hard palate) than mandible caused by ill-fitting dentures and poor oral hygiene.
• Clinical Features: rolls of soft-tissue in the muco-labial fold, RED-PINK, elongated, firm,
ulceration, soft lesion.
• Treatment: SURGICAL EXCISION and re-evaluate the prosthesis or remake or reline the
dentures.
INFLAMMATORY FIBROUS HYPERPLASIA
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NEOPLASMS
LYMPHOEPITHELIOMA – a poorly differentiated squamous cell carcinoma involving lymphoid
tissue in the tonsils & nasopharynx regions. It has a high frequency in young adults of East Asian
descent. The primary lesion is usually very small (often completely hidden). SWELLING OF THE
LYMPH NODES is the most common symptom, followed by sore throat, nasal obstruction,
bloody nose, & headache.
• Lymphoepitheliomas are composed of squamous or undifferentiated cells, with a slight-to-

moderate amount of fibrous stroma that contain numerous lymphocytes. Lymphoepithelioma
shows METASTASIS AT AN EARLY STAGE TO THE CERVICAL LYMPH NODES.
• Treatment of choice is RADIATON, but the complicating factor is the relative inability to treat
the widespread metastases in the various organs. POOR PROGNOSIS (30% 5-year survival
rate).
METASTIC CARCINOMA–the most common malignancy affecting SKELETAL BONES.

However, metastic disease of the mandible and maxilla is unusual (~1%). Most important, a jaw
tumor may be the first evidence of dissemination of a known tumor from its primary site.
Metastases to the jaws most commonly originates from primary carcinomas of the
BREAST, KIDNEY, LUNG, COLON, PROSTATE, & THYROID. Metastatic carcinoma of the jaws
is LEAST likely to originate from the brain.
• Clinical Features of Metastic Jaw Lesions: may be completely asymptomatic, but there is
usually paresthesia or anesthesia of the lip or chin due to involvement of the mandibular
nerve (patient is usually aware of slight discomfort or pain). Teeth in the area are loose or
extruded (the molar region is mainly involved), there can be swelling or expansion of the jaw,
and appears as an asymptomatic radiolucency. Although rare, metastic jaw tumors affect the
mandible MUCH more than the maxilla.
Most common osseous malignancies are OSTEOSARCOMAS, followed by

Chondrosarcomas, Fibrosarcomas, and Ewing’s Sarcoma.
OSTEOSARCOMA (OSTEOGENIC SARCOMA)-a MALIGNANT BONE TUMOR of anaplastic

cells derived from mesechyme. MOST COMMON PRIMARY MALIGNANT TUMOR OF BONE,
arising in LONG BONES which show the greatest longitudinal growth. Joint involvement is rare.
Its PEAK incidence is BEFORE epiphyseal fusion (ages 10-25yrs), but a later peak is
associated with Paget’s Disease, Chronic Osteomyelitis, and previous radiotherapy.
• Radiographic Features: most important EARLY radiographic feature of an osteosarcoma of

the jaw is a SYMMETRICALLY WIDENED PDL SPACE around one or more teeth. Other
radiographic features may be “SUN-BURST” or “SUN-RAY” appearance due to excessive
bone production. Most osteosarcomas have a MIXED appearance radiographically
(radiolucent + radiopaque).
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OSTEOSARCOMAS (SUN-BURST APPEARANCE)
ERWING’S SARCOMA – a MALIGNANT TUMOR developing from BONE MARROW, usually in

long bones or pelvis of adolescent boys (peak ages 10-20yrs). It is an uncommon HIGHLY
LETHAL MALIGNAN NEOPLASM OF BONE of uncertain origin. PELVIS, THIGH, and BODY
TRUNK, are the most common sites.
• Radiographic Characteristics: MOTH-EATEN destructive radiolucencies of the medulla, with

erosion of the cortex with expansion. A variable periosteal “ONION-SKIN” reaction may also
be seen.
EWING’S SARCOMA (MOTH-EATEN APPEARANCE)
• Intermittent pain and swelling of the involved bone are the earliest clinical
signs/symptoms. Fever & leukocytosis are also present.
• Histologically, ES is difficult to distinguish from a neuroblastoma or reticulum cell sarcoma,

but cells of ES contain GLYCOGEN.
• When the jaws are involved, there is predilection for the RAMUS OF THE MANDIBLE
with pain followed by rapid swelling and loosening of the teeth.
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MULTIPLE MYELOMA (“PLASMA CELL MYELOMA”) – a FATAL malignant neoplasm/lesion

of bone marrow & plasma cells. Characterized by elevated blood levels of Bence-Jones
Protein & multiple radiolucent areas in the mandible & skull. The tumor consists mainly of
PLASMA CELLS that destroy osseous tissues (progressive bone marrow destruction occurs
and is replaced with neoplastic plasma cells).
• Most patients are older than 40yrs (40-70yrs) affecting males 2x more than females (2:1). The
vertebrae, ribs, and skull are most often involved. PAIN in the lumbar or thoracic regions
of the spine is a common early symptom.
• Jaws are RARELY a PRIMARY site, but are involved in 70% of cases. Mandibular molar-
ramus area is the most common intra-oral site. Symptoms: swelling, pain, loose teeth, and
paresthesia.
• Radiographic Features: variable, slight demineralization to extensive bone destruction.

Characteristic finding is multiple, small, discreet “PUNCHED OUT” radiolucencies of
involved bones. A LATERAL SKULL RADIOGRAPH best confirms a Multiple Myeloma
diagnosis.
• Treatment: Chemotherapy/Radiation. Poor prognosis, with a median survival time of 2-3

years.
MULTIPLE MYELOMA
ODONTOGENIC MYXOMA–a RARE slow growing, usually asymptomatic MANDIBULAR

TUMOR. Patients are usually < 35yrs of age. Causes localized jaw expansion. Treatment:
Curettage. Not fatal.
ODONTOGENIC MYXOMA
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OSTEOCHONDROMA – a BENIGN tumor of bone & cartilage.
TNM–a method to clinically stage and assess the prognosis and therapy of MALIGNANT
NEOPLASMS (TUMORS) based on the primary tumor’s size (T), presence of regional lymph
node involvement (N), and presence of distant metastases (M). Ex: a carcinoma of the oral
cavity may have a TNM assessment of T2, N1, M0.
• T = SIZE of the primary tumor.
• N = Presence of regional LYMPH NODE involvement.
• M = Presence of DISTANT metastasis
MELANOMA exhibits a “radial” (horizontal) or “vertical” growth phases in the skin:
1. Radial Growth Phase-the INITIAL growth phase of melanoma just above & below the
dermo-epidermal junction in a horizontal plane. It is clinically macular or only slightly
elevated.
2. Vertical Growth Phase-begins when neoplastic cells populate the underlying dermis.
Characterized clinically by an increase in size, change in color, nodularity, & ulceration.
METASTASIS is possible when the melanoma reaches this phase.
MALIGNANT MELANOMA –the MOST SEVERE and potentially serious type of SKIN
CANCER mainly due to excessive exposure to UV sun radiation causing the tanning cells
(melanocytes) in the skin that produce a dark-colored substance (melanin) to undergo
uncontrolled growth. May suddenly appear without warning, but often develops from or near
a MOLE (NEVUS). Common in fair-skin white people, occurring anywhere on the skin.
• SKIN CANCER IS THE MOST COMMON MALIGNANCY IN THE U.S. 1 in 100 people in the
U.S. develop this cancer in a lifetime. Without treatment, it can widely metastasize and cause
death. Linked to excessive SUN EXPOSURE & PAINFULL SUNBURNS during childhood.
• Malignant Melanoma is an uncommon neoplasm of the oral mucosa but exhibits a definite
predilection for the HARD PALATE & MAXILLARY ALEVEOLAR RIDGES. Unfortunately,
oral mucosa melanomas have a poor prognosis (5-year survival rate for oral melanoma tumors
is ~7%). The most common intra-oral site for melanoma is the hard palate.
MALIGNANT MELANOMA (HARD PALATE)
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4 TYPES OF MELANOMA:
1. Superficial Spreading Melanoma-the MOST COMMON form of malignant melanoma
(65%), & most common cutaneous melanoma in Caucasians. The lesion is TAN, BROWN,
BLACK, or ADMIXED on sun-exposed skin (especially BLACK). The cancer begins at
one focus in the skin at the dermo-epidermal junction (DEJ). It initially grows in a horizontal
plane, along and just above & below the dermo-epidermal junction (this is the “radial”
growth phase of melanoma which predominates), and is clinically macular or only slightly
elevated. The “vertical” growth phase is characterized by an increase in size, change in
color, nodularity, and at times ulceration.
2. Nodular Melanoma-much less common (~13% of cutaneous melanomas). THERE IS NO

“RADIAL” GROWTH PHASE (it exists only in the “vertical” growth phase). NM presents
as a sharply defined nodule with degrees of pigmentation (may be pink (amelanotic
melanoma) or black, and occurs more often on the back, head, and neck of men.
3. Lentigo Malignant Melanoma-even less common (~10% of cutaneous melanomas), and

is most common in the ELDERY population. The lesion may grow for years in the “radial”
growth phase before developing into the more aggressive “vertical” growth phase. This
radial growth phase is known as lentigo maligna (melanotic freckle of Hutchinson), while
the vertical growth phase is known as lentigo maligna melanoma.
4. Acrolentiginous Melanoma-occurs on the hands and feet with a reputation for being
ignored by the patient, resulting in the development of metastic disease.
NEVUS (MOLES)-nearly all moles are normal. Atypical (Dysplastic) nevi-unusual moles are
generally larger than normal moles, and are flat or have a flat part, with irregular borders with
variable shades of color (especially brown, but can be a Blue Nevus). The presence of dysplastic
nevi may mark a greater risk of malignant melanoma developing on apparently normal skin.
NEVUS
ACQUIRED NEVI (MOLES) – small, usually dark, skin growths that develop from pigment-
producing cells (melanocytes) in the skin. Fairly common on the skin and intra-orally (much more
common than congenital nevi both intra-orally and extra-orally). When present, they are usually
on the HARD PALATE, or may be on the gingiva and lips. Acquired nevi are microscopically
classified into 5 subtypes:
1. Intramucosal Nevus- MOST COMMON nevus in the oral cavity. Nevus cells are located
in the C.T. or lamina propria of the oral mucosa. Under palpation, these nevi appear SOLID
& SLIGHTLY RAISED over the mucosa surface.
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2. Blue Nevus-the SECOND most common acquired nevus in the oral cavity. Congenital,
painless, color is based on the deep cutaneous or subcutaneous/submucosal deposits of
melanin.
3. Compound Nevus-rare in the oral cavity. Nevus cells are located at the epithelium-lamina
propria interface deep in the dermis. They are raised and solid.
4. Junctional Nevus-rare in the oral cavity. Nevus cells are located at the interface between
the epithelium and lamina propria. They are flat and not detected by palpation. Some
regard as pre-malignant, and may undergo transformation into malignant melanoma.
5. Intradermal Nevus (common mole)-the most common lesion of skin. Nevus cells lie
exclusively in the dermis.
TREATMENT OF CHOICE FOR ORAL PIGMENTATIONS with unknown etiologies is

CONSERVATIVE, EXICIONAL BIOPSY to rule out melanoma. Recurrence of oral nevi is very
rare and malignant transformation has not been reported.
BASAL CELL CARCINOMA – a MALIGNANT epithelial cell tumor that begins as a papule that
enlarges peripherally, forming a central crater that erodes, crusts, & bleeds. Only found on the
skin, and NEVER in the mouth 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. Frequently develops on exposed skin surfaces, face (nose), & 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.
• BASAL CELL CARCINOMASA ARE NEVER IN THE MOUTH (INTRA-ORALLY).
• Common in adult Caucasians with fair complexions due to sun exposure or in patients with
basal cell syndrome.
• Basal Cell Carcinoma has a much better prognosis than squamous cell carcinoma
since it DOES NOT PRODUCE METASTASIS (it is invasive, so if you do not do surgery,
the patient will die, but if treated, the patient will be cured). Ex: Frontal skin lesion in a 72-
year male with two years of evolution.
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). SCC is a malignant
EPITHELIAL TUMOR that is twice as prevalent in males (ages 40-65yrs). 50% of all oral SCC
occurs on the TONGUE LATERAL BORDERS.
• More common on the LOWER LIP than intra-orally. The most common intra-oral site is the
lateral border & ventral surface of the TONGUE (from this site, it often metastasizes to
cervical lymph nodes). Dorsal tongue surface is almost never affected. FLOOR OR
MOUTH is the second most common intra-oral site, with the WORST prognosis.
• Risk Factors: smoking & smokeless tobacco (main risk factor), alcohol, painful & ill-fitting
dentures, and chronic inflammation.
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• INVASION is the most reliable histologic criterion for diagnosing oral SCC.
• Treatment: surgery & radiation to remove lymph nodes in neck.
• Squamous Cell Carcinoma can be RED, irregular, non-painful lesion, or a WHITE lesion
caused by sun exposure. Lasts > 1 month.
• Histology: hyperchromatism, pleomorphism, atypical mitosis, dyskeratosis, alteration of

nuclei-cytoplasm ratio, acanthosis, but NOT sub-epithelial cleft.
• Found MAINLY in posterior LATERAL tongue border (can also be on the ventral
surface), but can be on lower lip and floor of mouth. NOT common on dorsum of tongue.
SQUAMOUS CELL CARCINOMA
Metastasis of SCC occurs via CERVICAL LYMPHATICS. Risk increases with age.
Squamous Cell Carcinoma Occurs in these Head and Neck Areas:

1. Nasopharynx: caused by tobacco & alcohol. Represents < 2% of all cancers in U.S. (the
least common SCC). Affects males ages 30-40yrs. Roof or lateral wall is the most common
site. Signs: cervical mass, earache, sore throat, and nasal obstruction.
2. Palate: uncommon, but caused by tobacco, alcohol, and denture irritation. Represents
10% of all oral carcinomas (soft palate is more common than hard palate). Affects men >
60yrs. Signs: painful ulcer, leukoplakia, exophytic mass.
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3. Oropharynx: caused by tobacco & alcohol. Represents 10% of all head & neck cancers,
affecting men > 50yrs. Signs: sore throat, dysphagia, painful ulcer, cervical mass.
4. Maxillary Sinus: etiology unknown. Represents 30% of all head & neck cancers. Affects men
> 40yrs. Signs: chronic sinusitis, bulging palate, teeth loosening, paresthesia in the cheek.
5. Tongue: most common site is the LATERAL BORDER, but also occurs on the ventral surface
(under the tongue) (dorsum is the least likely involved). Tongue cancer causes more deaths
than any other malignant lesion in other regions of the head & neck because the tongue
is the MOST COMMON INTRAORAL SITE OF CANCER because it is a highly mobile organ
richly endowed with lymphatics & blood vessels that facilitate metastasis (most commonly
metastasizes to the CERVICAL LYMPH NODES). It very RARELY gives rise to skeletal
metastasis.
• Etiology: tobacco, alcohol, syphilis, Plummer-Vinson Syndrome.
• Mostly effects men > 60yrs. on the posterior lateral border and middle third of the
tongue. Presents as a painless ulcer with leukoplakia and erythroplakia.
6. Lips: THE MOST COMMON SITE 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
occurs in MALES 60+ due to chronic sun exposure & pipe smoking. This location (lips) is
etiologically related to race, complexion, pipe smoking, sunlight. It is a PAINLESS ulcer and
keratotic plaque.
7. Floor of Mouth: SECOND MOST COMMON INTRA-ORAL SITE FOR CANCER, occurring
mainly in the ANTERIOR SEGMENT on either side of the midline near salivary gland
orifices. Caused by tobacco & alcohol. Pre-malignant lesions of squamous epithelium most
often occur here. VERY POOR PROGNOSIS. Typically, effects men 40-60yrs. It is a painless
ulcer with leukoplakia and erythroplakia.
8. Buccal Mucosa: generally occurs along the PLANE OF OCCLUSION, midway

anteroposteriorly. Represents 10% of all oral carcinomas, caused by tobacco, alcohol, and
denture irritation. A painless ulcer and exophytic mass with leukoplakia.
9. Gingiva and Alveolar Mucosa: more common in the POSTERIOR MANDIBLE than maxilla,
with posterior sites affected more than anterior sites. Represents 10-15% of all oral
carcinomas, caused by tobacco and alcohol. Mainly effects men 60+ years. Common on the
mandibular mucosa as a painless ulcer and plaque-like or exophytic mass.
Squamous Cell Carcinoma 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.
• 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.
• SCC of the TONGUE is the most common INTRA-ORAL malignancy. The most common
location is the posterior lateral border, then the posterior 1/3 (tongue base). SCC is
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uncommon on the dorsum or tongue tip. These lesions metastasize early, and the prognosis
is not as good as lip lesions.
• MOUTH FLOOR is the 2nd most common INTRA-ORAL location of SCC. It occurs mainly
in older men (especially alcoholics and smokers). These lesions metastasize early with a poor
prognosis.
• Treatment of choice for ORAL CANCER (SCC) IS SURGERY.
SQUAMOUS CELL CARCINOMA (3 TYPES):
1. VERRUCOUS CARCINOMA- RARE form of squamous cell carcinoma (MALIGNANT) that

DOES NOT METASTASIZE, but occurs in oral cavity soft tissues (mandibular mucobuccal
fold, alveolar mucosa, & palate), or laryngeal cavity due to tobacco chewing, smoking, or snuff
dipping. Mostly effects men 60+ years. The tumor mass has a characteristic WHITISH-
CAULIFLOWER or CORAL-LIKE papillary appearance. Typically, develops on the vocal
cords of an elderly male who has been a heavy cigarette smoker. It is known for its slow
growth pattern and well-developed hyperkeratotic epithelial boundaries.
VERRUCOUS CARCINOMA
Pathologically, it is a well-differentiated squamous cell neoplasm that may invade or infiltrate the
borders of adjacent structures, but does not metastasize. It can transform into an invasive form
of carcinoma, or co-exist with other squamous cell carcinomas. Often misdiagnosed histologically
as a benign lesion.
Treatment: SURGERY. Prognosis: 60-70% have 5-year survival rate.
Verrucous Carcinoma is a non-aggressive, very well-differentiated tumor that DOES NOT

METASTASIZE. COMMON IN THE ELDERLY. Can present as a diffuse, WHITE, well-
demarcated, painless papillary surface mass on the UPPER (MAXILLARY) ALVEOLAR RIDGE,
measuring 6x4 cm, and can be present 2-3 years before a definitive diagnosis is made. Better
prognosis than carcinoma invasive. Can destroy the bone.
2. CARCINOMA IN SITU: located only inside epithelium (intra-epithelium), atypical mitosis,

hyperchromatism, all epithelial layers are affected, BUT IT DOES NOT INVADE C.T. (basal
membrane is intact). Better prognosis than carcinoma invasive, but must treat.
Carcinoma in situ is MALIGNANT, BUT CANNOT metastasize due to lack of blood or
lymphatic vessels in epithelium. Located ONLY in the epithelium which does not have
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blood or lymphatic vessels so it cannot produce metastasis. Ex: 60-year-old alcoholic female
with red FLAT area in the mouth floor. Area is flat, asymptomatic, present for 4 months,
increasing in size, but not painful. Her medical history is non-contributory.
3. CARCINOMA INVASIVE-Ex: 60-year-old alcoholic female with red area in the mouth floor.
Area is flat, asymptomatic, present for 4 months, increasing in size, but not painful. Her
medical history is non-contributory.
Characteristics of Malignant Lesions:

• Erythroplasia: lesion is totally red or speckled red and white. Red, non-ulcerated area
on a mucous membrane. The texture can be normal or rough, and its size varies (some
are so small and may go undetected, while large areas are conspicuous to casual
inspection). There are usually no symptoms, being neither elevated nor depressed,
presenting as quiet, unpretentious lesions The border may be sharp, or blend
imperceptibly into surrounding normal mucosa. Important: early carcinoma often
appears as an area of erythroplasia. There are certain areas of the oral mucosa that
are more prone to malignancy. Additionally, oral cancer is more often seen in people
over age 40yrs. Because of this, an area of erythroplasia in a cancer prone area in a
patient over 40yrs is highly suspicious of malignancy and should be biopsied on the day
it is seen (especially lesions whose duration exceeds 2 weeks).
• RAPID GROWTH that is often an ulcerated fixed lesion that bleeds on gentle
manipulation. The lesion and surrounding tissue are firm to touch. On physical
examination, PAINLESS induration of soft tissue suggests an invasive malignant
lesion.
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ODONTOGENIC ABNORMALITIES
ABRASION – abnormal, PATHOLOGIC WEARING AWAY (LOSS) of tooth structure.

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

drinking acidic liquids (soda) or eating acidic foods. Common in BULIMCS due to regurgitated
stomach acids. Affects smooth surfaces and occlusal surfaces of teeth.
EROSION
INTRINSIC STAINING: can be caused by the following except DIABETES MELLITUS.

• Dentinogenesis imperfecta-causes a translucent or opalescent hue, usually gray to
bluish-brown.
• Erythroblastosis fetalis- causes intrinsic stain that is bluish-black, greenish-blue, tan, or
brown.
• Porphyria-causes an intrinsic stain that is red or brownish.
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• Fluorosis-causes white opacities, or light brown to brownish-black.

• Pulpal injury- intrinsic stain starts pink, then becomes orange-brown to bluish-black.
• Internal resorption-causes a PINKISH intrinsic stain.
• Tetracyclines-intrinsic stain from light-gray, yellow, tan, or shades of gray. Risk to 7
years old.
ANKYLOSIS –fusion of surrounding alveolar bone to a tooth root. May be initiated by an

infection or trauma to the PDL. The ankylosed tooth has lost its PDL space, and is actually
fused to the alveolar process of bone. There is change in the continuity of the occlusal plane
caused by the continued eruption of non-ankylosed teeth & growth of the alveolar process.
GEMINATION (TWINNING)–a division of a single tooth germ by invagination causing incomplete

formation of two teeth (usually the incisors). Incomplete splitting of a tooth germ.
GOMPHOSIS – a type of fibrous joint where a conical process is inserted into a socket-like portion
(i.e. styloid process in the temporal bone, or the teeth inserted into the dental alveoli).
FUSION-the joining of two normally separated tooth buds to form A SINGLE, LARGE, WIDE
CROWN (results in one less tooth in the arch). Most commonly affects ANTERIOR INCISORS
and can occur in the primary or permanent dentition.
CONCRESCENCE – a condition where only the CEMENTUM of two or more teeth are joined.
DILACERATION-a sharp bend or curve in a root due to trauma during tooth development.
TAURODONTISM (“BULL-LIKE”)-found usually in MOLARS; the tooth body and pulp chamber
are enlarged vertically at the root’s expense causing an apical shift of the pulpal floor and
tooth furcation down the tooth root (large pulp chambers and short roots) causing teeth to
look “bull-like”. Caused by failure or late invagination of Hertwig’s epithelial root sheath that is
responsible for root formation.
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DENS-IN-DENTE (Dens Invaginatus)-“tooth within a tooth”, caused by a deep invagination of

the enamel organ Hertwig’s epithelial root sheath during formation. Most commonly associated
with a MAXILLARY LATERAL INCISOR.
DENS-IN-DENTE (TOOTH WITHIN A TOOTH)
MESIODENS – the most common SUPERNUMERARY TOOTH (extra tooth) usually appearing
singly, or in pairs as a small tooth with a cone-shaped crown and short root visible between
vital PERMANENT MAXILLARY CENTRALS on a radiograph. It may be erupted, impacted, or
inverted. Appears situated in the maxilla near the midline and almost always posterior to
normal central incisors. Thus, many mesiodens are bypassed by the permanent incisors still
erupt into their normal position in the arch regardless.
MESIODENS (SUPERNUMERARY)
If the mesiodens does not interfere with the normal eruption of the permanent maxillary central
incisors, you can wait until the child is 6-8 years old to extract the mesiodens non-surgically if it
erupts, or surgically if it does not erupt.
HYPERCEMENTOSIS – excessive (abnormal) CEMENTUM FORMATION around or on root

surface after tooth eruption (often confined to the apical half of the root, but may involve the entire
root). THICKENING OF CEMENTUM (ROOT TISSUE). Caused by trauma, metabolic
dysfunction, chronic periapical inflammation, or when a tooth has lost its antagonist.
Hypercementosis is merely a dental anomaly, but can be seen in ACROMEGALY & PAGET’S
DISEASE.
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• Mainly affects VITAL teeth (MAINLY PREMOLARS), then first & second molars.
• Produces no significant clinical signs or symptoms, but seen radiographically as a BULBOUS

ENLARGEMENT with a surrounding continuous/unbroken periodontal membrane space
and normal lamina dura. Radiographically, with Paget’s Disease, there is complete absence
of the periodontal membrane space & lamina dura that surrounds the hyperplastic cementum.
HYPERCEMENTOSIS
ENAMEL HYPOPLASIA–enamel developmental defect due to INCOMPLETE FORMATION of

the enamel matrix. ENAMEL IS HARD, BUT, THIN & DEFICIENT IN AMOUNT, resulting in
incomplete formation of the enamel matrix with a deficiency in the cementing substance. EH
affects deciduous (primary) and permanent teeth, and is usually caused by illness or injury
during tooth formation, or due to a genetic disorder (genetic forms of EH are considered types
of amelogenesis imperfecta). If only one permanent tooth is affected, it is usually caused by
physical damage to the replaced primary tooth. WHITE & BROWN DEFECTS ON TOOTH
SURFACE.
• Clinical Features: lack of contact between teeth, rapid breakdown of occlusal surfaces,
yellowish-brown stain that appears due to EXPOSED DENTIN.
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ENAMEL HYPOCALCIFICATION-a hereditary dental defect where the ENAMEL IS SOFT &
UNDERCALCIFIED, yet normal in quantity due to defective maturation of ameloblasts (a
defect in the mineralization of the formed matrix). Teeth are chalky, surfaces wear down rapidly,
and a yellowish-brown stain appears due to underlying EXPOSED DENTIN. Affects deciduous
& permanent teeth.
ENAMEL HYPOCALCIFICATION
AMELOGENESIS IMPERFECTA – an inherited hereditary ECTODERMAL DEFECT transmitted

as a dominant trait that affects the deciduous & permanent dentition, causing enamel to be soft,
thin, and yellow due to EXPOSED DENTIN through the thin enamel layer. Teeth are easily
damaged and susceptible to decay. Crowns may or may not show discoloration. If discoloration
is present, it varies depending on the type of disorder, ranging from yellow to dark brown.
• Open contacts between teeth and occlusal surfaces/incisal edges are often severely abraded.
• Radiographic findings are often distinctive & pathognomonic. When enamel is totally
absent, the radiographic appearance makes the diagnosis obvious. When some enamel is
present, thin radiopaque coverings on the proximal surfaces are visible. When anatomic crown
forms are normal or near normal, the softness of the defective enamel may not be easily
distinguished from dentin.
• Dentin, pulp, & cementum are NOT affected by AI (unlike dentinogenesis imperfecta).
Exception: AI will only show pulp obliteration if there is advanced abrasion with secondary
dentin formation.
AMELOGENESIS IMPERFECTA
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OPEN CONTACTS & SQUARE CROWNS (AI)
3 TYPES OF AMELOGENESIS IMPERFECTA:

1. (Type 1) Hypoplastic AI: enamel has not formed to full normal thickness, or may be
completely absent on newly erupted developing teeth due to defective formation of the
enamel matrix.
2. (Type 2) Hypomaturation AI: enamel can be pierced by an explorer tip under firm pressure
and chipped away from normal-appearing dentin. Characterized by IMMATURE
CRYSTALLITES.
3. (Type 3) Hypocalcified AI: quantity of enamel is normal, but so soft it can be removed
during a prophylaxis due to the defective MINERALIZATION of the enamel matrix.
DETINOGENESIS IMPERFECTA (HEREDITARY OPALESCENT DENTIN)– RARE disorder

found in only 1:7,000 children. An inherited/hereditary MESODERMAL DEFECT OF DENTIN that
only affects deciduous & permanent teeth. Teeth have an OPALESCENT HUE.
• Clinical Features: teeth have amber, gray, or purple opalescence/translucence or

discoloration, pulp chambers may be completely obliterated due to continued
deposition of dentin, crowns are short & bulbous, with narrow roots. Enamel can chip away
within 2-4yrs after eruption, exposing the dentin which is soft and wears away rapidly. Enamel
is structurally and chemically normal. DI is usually easily detected and identified, as
teeth exhibit a translucent or opalescent appearance. Abnormal constriction at the CEJ is
another clinical feature detected by exploration.
DENTINOGENSIS IMPERFECTA
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DENTINOGENESIS IMPERFECTA (3 TYPES):

1. Type 1: dentin abnormality occurs in patients with Osteogenesis Imperfecta, characterized
by blue sclera or history of bone fractures.
2. Type 2: the most common; only a dentin abnormality exists. NO BONE INVOLVEMENT.
3. Type 3 (Brandywine Type): like Type 2, only a dentin abnormally exists. There are clinical
& radiographic variations that include multiple pulp exposures in the deciduous (primary)
dentition.
DENTIN DYSPLASIA (ROOTLESS TEETH) – a hereditary disease transmitted as an

autosomal dominant trait. Clinical Features: normal enamel, atypical dentin, pulpal
obliteration, defective root formation, tendency toward multiple periapical radiolucencies
and early exfoliation of teeth. Not associated with any systemic C.T. disorder. 2 Types of
Dentin Dysplasia:
1. Type I (Radicular)-the more common type involving both dentitions. Normal morphology
and color (deciduous & permanent teeth). Mobile teeth, premature exfoliation, short roots
(rootless teeth), obliterated pulp chambers (deciduous), crescent-shaped pulpal remnant
(permanent), periapical radiolucencies, coronal dentin is normal, but root dentin is
disoriented. PULPAL OBLITERATION BY EXCESS DENTIN “chevron” shaped pulp
chambers.
2. Type II (Coronal)-involves both dentitions (but coronal dentin is normal). Deciduous teeth
exhibit bluish-gray opalescent appearance, obliterated pulp chambers, amorphous and
atubular dentin in the radicular portion of the teeth. Permanent teeth exhibit a normal
clinical appearance, thistle-tube pulp chambers & stones, and true denticles. Pulpal
obliteration of primary teeth, and pulp stones in permanent teeth.
ANODONTIA –developmental abnormality characterized by TOTAL ABSCENSE of teeth. Two

Forms:
1. Complete/True Anodontia-a rare condition where ALL TEETH are missing. May involve
the primary and permanent dentitions. Usually associated with hereditary Ectodermal
Dysplasia.
2. Partial Anodontia (Congenitally Missing Teeth)-common condition usually affecting

maxillary & mandibular 3rd molars (affects mainly maxillary 3rd molars), maxillary laterals,
& mandibular 2nd premolars. Rule: if only one or a few teeth are missing, the absent tooth
is the MOST DISTAL tooth (if a molar, then the 3rd molar is missing; if a premolar, then
the 2nd premolar).
OLIGODONTIA – congenital absence of MANY (but not all) teeth.
HYPODONTIA – absence of only a FEW teeth
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WHITE LESIONS
ORAL CANDIDIASIS (“THRUSH” OR “MONILIASIS”) – a FUNGAL infection of the oral cavity

or vagina caused by a Candida species (usually Candida albicans) causing an inflammatory,
pruritic infection with a thick, white discharge. Appears diffuse, curly or velvety white mucosal
plaques on the cheeks, palate, and tongue that CAN BE WIPED OFF, leaving a red, raw, or
bleeding surface. The most common symptoms are discomfort and burning of the mouth &
throat, and altered taste.
• Candida is a yeast-like fungi and normal inhabitant of the oral cavity & vaginal tract, but
is normally held in check by indigenous bacteria of these areas. Factors that stimulate Candida
growth are extended use of antibiotics (antibiotics prescribed for a dental infection),
steroids, diabetes, pregnancy, or vitamin deficiency (iron, folate, B12, zinc).
• Very common in patients on long-term antibiotic or chemotherapy, and immunosuppressed

patients (AIDS).
• Treatment: topical with LOZENGES (Trouches) & mouth rinses (NYSTATIN is most widely
used).
ACUTE PSEUDOMEMBRANOUS CANDIDIASIS – the most common oral candidiasis,

usually found on the buccal mucosa, tongue, and soft palate. Oral cytology smears diagnose
acute pseudomembranous candida by revealing budding organisms with branching
pseudohyphae.
ANGULAR CHEILITIS (PERLECHE) – any chronic inflammatory lesion that occurs at the labial
commissure (corners of mouth) due to unknown cause. Generally associated with LOSS OF
VERTICAL DIMENSION in elderly patients. Mouth corners are painful, irritated, red, cracked,
and scaly. Candida albicans fungus (Thrush) may grow in the corners of the mouth, keeping them
sore.
• Predisposing Factors: Candida albicans infection, loss of inter-maxillary distance (decreased

vertical dimension), trauma to the labial commissure due to prolonged dental treatment, &
vitamin deficiencies (especially riboflavin or thiamine).
• Treatment: NYSTATIN and TRIAMCINOLONE (Mycolog-II) cream.
ANGUAL CHELITIS (PERLECHE)
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ACTINIC CHEILITIS (SOLAR CHEILITIS/FARMER’S LIP) – a PRE-MALIGNANT condition

caused by chronic and excessive exposure to the UV sunlight radiation. A counterpart of actinic
keratosis of the skin, and can also develop into squamous cell carcinoma. There is thick,
WHITISH discoloration of the lip at the border of the lip and skin, and loss of the usually sharp
demarcation between the red of the lip and normal skin (vermillion border). May lead to SCC, so
it must be treated.
ACTINIC CHEILITIS
LEUKOEDEMA – a condition that mimics leukoplakia as it appears to be a WHITE PATCH, but

is a just a VARIANT OF NORMAL MUCOSA. Varies from a filmy opalescence of the mucosa
in the early stages, to a more definite grayish-white cast with a coarsely wrinkled surface in
later stages. Usually occurs BILATERALLY and along the occlusal line in the bicuspid and
molar region. Diagnostically, one can stretch the tissue and the white disappears
(Important: Leukoplakia DOES NOT DISAPPEAR WHEN STRETCHED). NO TREATMENT
REQUIRED.
LEUKOEDEMA
• Leukoedema’s white appearance is caused by water inside spinous cells, causing light to
reflect back as whitish.
• Differential Diagnosis: leukoplakia, white sponge nevus, and benign intraepithelial

dyskeratosis.
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WHITE SPONGE NEVUS (FAMILIAL WHITE FOLDED DYSPLASIA)–an often genetic and
benign BUCCAL MUCOSAL ABNORMALITY (often mistaken for leukoplakia. Characterized by
WHITE (pearly or opalescent), CORRUGATED THICK SOFT FOLDING OF THE BUCCAL
MUCOSA (bilaterally). Can also occur on the labial mucosa, alveolar ridge, and floor of mouth.
Almost NEVER found on the gingival margin & dorsal of tongue. NO TREATMENT
NECESSARY.
WHITE SPONGE NEVUS
LEUKOPLAKIA – a PREMALIGNANT LESION WHITE PATCH or plaque on the oral mucosa

that DOES NOT RUB OFF (UNLIKE CANDIDA) and cannot be assigned as any specific disease.
Possible etiologic factors are tobacco (PIPE SMOKING), alcohol, oral sepsis, and chronic
irritation. Most often due to TOBACCO and chronic irritation (ill-fitting denture, rough
filling, cheek biting). May be present for many months in a heavy pipe-smoker. Pipe-smoking
is the most important predisposing etiologic factor in leukoplakia. More common in elderly
men, and DOES NOT DISAPPEAR WHEN STRETCHED. Mouth floor, tongue, and lower lip are
the regions at greatest risk for carcinoma occurring in leukoplakia. Speckled Leukoplakia-has
mixed red and white areas.
• Leukoplakia is a slow developing change in a mucous membrane characterized by thickened,

white, firmly attached patches, that are slightly raised & sharply circumscribed. Lesions
on the mouth floor and base of the tongue are the most aggressive. Most display no dysplasia,
but can be pre-malignant so MUST BIOPSY.
• Treatment: BIOPSY due to the chance of malignant transformation, ALL LEUKOPLAKIAS

MUST BE BIOPSIED AND COMPLETELY EXCISED (if untreated, some progress to
carcinoma). Although less common than leukoplakias, erythroplakias have a much greater
malignant potential. Incisional Biopsy is indicated for a 3cm area of leukoplakia of the soft
palate. Biopsy are not required for papillary fibroma, exostosis, Fordyce’s granules, or
Hemangiomas as these are benign.
• Any white or red lesion that does not disappear itself in 2 weeks must be re-evaluated and
considered for BIOPSY to obtain a definitive diagnosis.
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LEUKOPLAKIA
LEUKOPLAKIA
• Carcinoma in situ is a term applied to mucosal lesions that resemble leukoplakia in all
respects except dysplasia is very pronounced and involves almost all epithelial layers. It shows
no tendency to invade or metastasize to other tissues. Exhibits all of the histologic
characteristics of malignancy (pleomorphism, hyperchromatism, abnormal mitoses,
anaplasia), but DOES NOT show invasiveness or extension into adjacent structures.
• Clinical Differential Diagnosis of White Patch: leukoplakia, lupus erythematosus,

leukoedema, white sponge nevus, chemical or thermal burn, candidiasis, lichen planus, &
migratory glossitis/stomatitis.
HAIRY LEUKOPLAKIA-an unusual BENIGN form of leukoplakia seen mainly in people with
HIV/AIDS or the immunocompromised caused by EPSTEIN-BARR VIRUS (HSV-4). Fuzzy,
hairy white patches mainly on the tongue (may resemble THRUSH caused by Candida).
Treatment: systemic anti-viral therapy (Acyclovir) or topical therapy with retinoic acids (tretinoin),
or ablative therapy.
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HAIRY TONGUE–HYPERTROPHY of FILIFORM PAPILLAE (NO TASTE BUDS). A BENIGN

condition of the tongue dorsum which is FURRY due to elongated filiform papillae. Color varies
from yellowish-white to brown or black. This is not Hairy Leukoplakia, but is just
DISCOLORATION of the DORSUM tongue surface, elongation & hyperkeratosis of FILIFORM
PAPILLAE ON TONGUE’S DORSUM SURFACE. 4 Types of Tongue Papillae: taste buds are
present only on fungiform, circumvallate, & foliate papillae.
1. Filiform papillae-the most numerous. Small cones in “v”-shaped rows paralleling the sulcus
terminalis, characterized by no taste buds and increased keratinization. NO TASTE BUDS.
2. Fungiform papillae-scattered among filiform papillae. Flattened, mushroom-shaped, and

found mainly at the tongue tip and lateral margins. HAVE TASTE BUDS.
3. Circumvallate papillae-the LARGEST, LEAST NUMEROUS papillae. Circular-shaped

arranged in an inverted “v”-shaped row toward the back of the tongue. Associated with
ducts of Von Ebner’s glands. HAVE TASTE BUDS.
4. Foliate papillae-found on the lateral margins as 3-4 vertical folds. HAVE TASTE BUDS.
CIRCUMVALLATE PAPILLAE
Hairy tongue can be WHITE, GREEN, BROWN, OR BLACK completely covering the tongue
dorsum as filiform papillae are stained and discolored with DEBRIS the patient eats or
smokes. Ex: dorsal surface of tongue of a smoker exhibits elongated, brownish filiform papillae.
Can present as a bright green, flat area on the tongue dorsum, with very poor dental status & oral
hygiene. The green area is probably DEBRIS. Etiology: overgrowth of fungal microorganisms
due to smoking or poor oral hygiene (brush tongue).
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BENIGN MIGRATORY GLOSSITIS (GEOGRAPHIC TONGUE) OR (ERYTHEMA MIGRANS) A

HARMLESS, USUALLY PAINLESS (maybe slight burning), COMMON condition due to
desquamation of FILIFORM papillae (no taste buds). One or more irregular-shaped patches
on the tongue exist. The center area is redder than the rest of the tongue, and edges of the
patch are whitish color. These patches appear and remain for a short time, heal, then reappear
at another site. The patches usually do not respond to treatment, but disappear
spontaneously. Geographic Tongue often occurs with Fissured Tongue.
GEOGRAPHIC TONGUE
FISSURED TONGUE (“SCROTAL TONGUE”) –a DEEP, usually asymptomatic (maybe painful

if infected with Candida Albicans) MEDIAN FISSURE with laterally radiating grooves that vary
in number, but are usually symmetrically arranged across the DORSUM (TOP) OF THE
TONGUE. Rare in children, but incidence increases with age. Found in Melkersson-Rosenthal
Syndrome (along with Cheilitis Granulomatosum & Facial Nerve Paralysis).
FISSURED TONGUE
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STOMATITIS NICOTINA (“PIPE-SMOKER’S PALATE” OR NICOTINIC STOMATITIS): the

initial clinical response is generalized palatal erythroplakia then becomes a white
hyperkeratotic area with small red dots. Related to pipe smoking (tobacco), occurs ONLY ON
THE PALATE, and mainly affects males. The palate is initially red & inflamed, then develops a
diffuse, grayish-white, thickened, multi-nodular popular appearance with a small red “spot” in the
center of each tiny nodule. This “spot” corresponds to orifices of palatal salivary gland ducts.
Treatment: None, except to stop smoking. Not usually premalignant.
• Found ONLY in the palate (palate is leathery white and full of keratin (hyperkeratosis with RED
DOTS (inflamed minor salivary glands). The only lesion produced by tobacco that is not
cancerous. Usually a white, generalized area with red dots on the hard palate that are
PAINLESS & non-indurated. White areas with multiple red dots (inflamed salivary glands in
the palate).
NICOTINIC STOMATITIS (PIPE-SMOKER’S PALATE)
LICHEN PLANUS – oral lesion mainly on the BUCCAL MUCOSA appearing as white or
grayish-white striae arranged in a lace-like pattern (Wickman’s Striae) often bilaterally &
symmetrically distributed, and usually asymptomatic, but may sometimes cause a burning
sensation. A fairly common inflammatory disease, of unknown cause, but may be autoimmune.
It usually affects the skin, mouth, or both. May also be on the tongue, lips, hard palate, & gingiva,
but MAINLY BUCCAL MUCOSA.
• Microscopic Features: hyperparakeratosis with thickening of the granular cell layer,

development of a “saw-tooth” appearance of rete pegs, degeneration of the basal cell layer,
and infiltration of inflammatory cells into the sub-epithelial layer of C.T.
LICHEN PLANUS
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• Affects women slightly more than men, and occurs most often in middle-aged adults.
• Treatment: intra-oral lesions respond to TOPICAL STEROIDS.
TWO ADDITIONAL FORMS OF LICHEN PLANUS:

1. Bullous Lichen Planus-fluid-filled vesicles project from the buccal mucosa surface.
2. Erosive Lichen Planus-intensely red or raw-appearing lesions that resemble desquamative

gingivitis when they involve the gingiva.
FORDYCE’S GRANULES (ECTOPIC SEBACEOUS GLANDS)– found in the oral mucosa,

present in > 75% of adults. Usually appear as yellow or yellow-white submucosal clusters that
are normal. Rice-like or cauliflower-like whitish-yellow or white asymptomatic papules 1-3mm
usually found BILATERALLY on the buccal mucosa, upper lip vermillion, mandibular
retromolar pad, and tonsillar area (but can be on any oral surface). Surrounding mucosa looks
normal, but they can remain constant throughout life.
FORDYCE GRANULES
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BLOOD DISEASES
PURPURA –HEMORRHAGES in the skin & mucous membranes that cause the appearance of
purplish spots or patches. Tooth extractions are contraindicated due to potential excessive
bleeding.
THROMBOCYTOPENIC PURPURA (Werlhof’s Disease)-a bleeding disorder characterized by

a deficiency in the number of platelets, resulting in multiple bruises, PETECHIAE, &
hemorrhage into the tissues. May be caused by heparin (warfarin) therapy. Oral manifestations
are severe/profuse gingival hemorrhage, & palatal petechiae. Petechie can also be caused by
streptococcus.
PETECHIAE
THROMBOCYTOPENIA-dominated clinically by PETECHIAE cutaneous bleeding, intra-cranial

bleeding, and oozing from mucosal surfaces. Characterized by decreased platelet count
causing prolonged bleeding time. THE MOST COMMON CAUSE OF BLEEDING
DISORDERS.
IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)-a bleeding disorder due to a deficiency

in the number of platelets causing multiple bruises, petechiae, & hemorrhage into the tissues.
ITP is a common complication of Leukemia, Aplastic Anemia, & Aggressive Cancer
Chemotherapy.
• Bleeding Time is abnormally prolonged in ITP.
THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)-a severe and frequently fatal form

characterized by thrombocytopenia, hemolytic anemia, renal insufficiency, fever, and neurologic
abnormalities. Low platelet count in the blood and thrombosis in the terminal arterioles and
capillaries of many organs.
• Purpura-a condition characterized by hemorrhages in the skin and mucous
membranes that result in the appearance of purplish spots or patches.
• Petechiae-small pinpoint hemorrhages flush with the skin surface.
• Ecchymosis (bruise)-a discoloration of an area of skin or mucous membranes due to

the extravasation of blood into the subcutaneous tissues due to trauma or hemorrhage.
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PROLONGED BLEEDING TIME (Thrombocytopenia) CONDITIONS:

• A patient taking Dicumarol-inhibits formation of prothrombin in the liver.
• A patient taking Heparin-acts as an antithrombin by preventing platelet aggregation.
• Idiopathic Thrombocytopenic Purpura (ITP)-often associated with leukemia; a
decrease in the number of platelets.
• Von Willebrand’s disease-deficiency of vWF (von Willebrand’s factor); results in
impaired platelet adhesion.
• Long-term treatment with aspirin; aspirin is a cyclooxygenase inhibitor; results in
impaired production of thromboxanes, important in platelet aggregation.
AGRANULOCYTOSIS – an abnormal blood condition due to a severe reduction in the number

of granulocytes (NEUTROPHILS) caused by ingesting a drug. It is an acute toxic
effect/condition characterized by pronounced LEUKOPENIA with a severe reduction in the
number of polymorphonuclear leukocytes (PMNs). It is a toxic effect of certain anti-thyroid
drugs (propylthiouracil, methimazole, carbimazole). Can occur at any age, but is more common
in adult females.
• WBC count is < 2,000 with almost complete absence of PMN neutrophils
(polymorphonuclear leukocytes). Normal WBC count is 4,000-10,000 and neutrophils are
usually 50-70%.
• Agranulocytosis begins with a high fever, chills, and sore throat. The patient suffers from
malaise, weakness, and prostration. Skin appears pale and anemic. The most characteristic
feature is the presence of an INFECTION IN THE ORAL CAVITY. Signs and symptoms
develop very rapidly (within a few days), and death may occur soon after.
• Oral lesions (necrotizing ulcerations) are an important phase of the clinical aspects, appearing
as necrotizing ulcerations of the oral mucosa of the GINGIVA & HARD PALATE. These
lesions are ragged necrotic ulcers covered by a gray membrane. One important aspect is that
there is little or no apparent inflammatory cell infiltration around the lesions. Histologically, the
ulcerated lesions do not exhibit polymorphonuclear reaction due to the bacteria in the tissues.
• Treatment: ELIMINATE THE CAUSATIVE DRUG. Administer antibiotics to control the

infection.
SICKLE-CELL ANEMIA (SICKLE-CELL DISEASE) – a chronic, usually fatal inherited form of

anemia marked by crescent-shaped red blood cells, characterized by fever, leg ulcers,
jaundice, and episodic pain in the joints due to the production of abnormal hemoglobin
(Hemoglobin S) due to a genetic defect. N2O administration is CONTRAINDICATED.
• Primarily affects African-Americans (especially females), and usually manifests before age
30yrs.
• SCA Signs: (patient is weak, short of breath, easily fatigued, and muscle and joint pain are
common).
• Dental radiographs show ENLARGED BONE MARROW (MEDULLARY) SPACES because

of loss of many bony trabeculae (but the trabeculae that are present are abnormally
prominent). Occasionally, osteosclerotic areas are noted in the midst of large radiolucent
marrow spaces. However, the lamina dura and teeth are unaffected.
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SICKLE-CELL ANEMIA (Enlarged Bone Marrow Spaces)
LEUKEMIAS-cancers of mainly WHITE BLOOD CELLS with most of unknown cause.

LEUKEMIA involves uncontrolled proliferation of leukocytes causing a diffuse and almost total
replacement of the red bone marrow with leukemic cells. Leukemia is classified by the dominant
cell type and by duration from onset to death. It can modify the inflammatory reaction. While the
cause is unknown, these agents are closely associated with leukemia development:
1. Ionizing radiation: increased incidence of leukemia among atomic bomb survivors &
radiologists, usually myelogenous.
2. Viruses: shown to cause leukemia in fowl and rodents. Herpes-like viral particles have
been cultured from patients with various types of leukemia and leukemic patients have
high antibody titer to the Epstein-Barr Virus.
3. Genetic Mutations: Philadelphia chromosome (translocation of chromosome material

between chromosomes 22 and 9) is present in 90% of patients with Chronic Myelogenous
Leukemia (CML). Also higher incidence of acute leukemia in patients with Down
Syndrome (Mongolism) in which there is Trisomy 21.
4. Other: chronic exposure to benzol, aniline dyes, and related chemicals.
All LEUKEMIAS occur in an ACUTE or CHRONIC form, but 50% are ACUTE. Acute Leukemia
is the most common malignancies of the pediatric age group (under 20 years).
ORAL MANIFESTATIONS OF LEUKEMIA:

• Acute and chronic leukemias all cause ORAL LESIONS. The most common is seen in
acute monocytic leukemia (a subtype of acute myeloid leukemia), where 80% of patients
exhibit GINGIVITIS, GINGIVAL HYPERPLASIA, PETECHIAE, & HEMORRHAGE.
Spontaneous gingival bleeding in acute leukemia is due to THROMBOCYTOPENIA.
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CLASSES OF LEUKEMIA: All Leukemia occurs in an ACUTE or CHRONIC form:
1. Myelogenous Leukemia-involves granulocytes & megakaryocytes. Philadelphia

Chromosome and low levels of leukocyte alkaline phosphatase are common findings.
Massive splenomegaly is characteristic. CML is one of a group of diseases called
myeloproliferative disorders. Other diseases in this class are Polycythemia Vera,
Myelofibrosis, & Essential Thrombocythemia. CML is characterized by uncontrolled
proliferation of immature granulocytes (but is the least malignant leukemia). CML accounts
for 20% of all adult leukemias (typically affects middle-aged individuals). Although uncommon,
CML may occur in younger individuals.
• CML Clinical Signs: spongy bleeding gums, fatigue, fever, weight loss, moderate
splenomegaly, joint/bone pain, and repeated infections.
• Leukemic cells in 95% of CML patients have a Philadelphia Chromosome which is the
result of a reciprocal translocation between chromosomes 9 and 22 which result in a
shortened chromosome 22.
• Mean survival time with CML is 4 years with death due to hemorrhage or infection.
2. Lymphocytic Leukemia-involves lymphocytes. Chronic Lymphocytic Leukemia runs a

variable course (older patients may survive years even without treatment). Lymph node
enlargement is the main pathologic finding. May be complicated by autoimmune hemolytic
anemia.
• Acute lymphocytic (lymphoblastic)-is largely confined to children (the most

common leukemia in children). Lymph node enlargement is common. In 75% of cases,
the lymphocytes are not B nor T cells, but are “null” cells. Bone and joint pain are
common.
3. Monocytic Leukemia-involves monocytes. ORAL LESIONS ARE COMMON and may be

the initial manifestations of the disease. Gingivitis, gingival hemorrhage, generalized gingival
hyperplasia, petechiae, ecchymosis, and ulcerations. Chronic Monocytic Leukemia is
VERY RARE.
Chronic Leukemia (Clinical Features):

• Insidious onset (slow) with weakness and weight loss. May be detected during an examination
for another condition (i.e. anemia, unexplained hemorrhages, or recurrent intractable
infections).
• Organ involvement is similar to acute leukemia: skin is often involved, and may manifest as
petechiae or ecchymosis, recurrent hemorrhages and bacterial infections are common
(anemia).
ACUTE LEUKEMIA – has an abrupt onset of a few months (not insidious) with fever, weakness,
malaise, severe anemia, and generalized lymphadenopathy. Untreated patients dies within 6
months (usually due to brain hemorrhage or superimposed bacterial infection). With intensive
chemotherapy, radiation, and marrow transplants, remissions lasting up to 5 years may be
obtained.
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• Clinical Features: severe anemia, hemorrhages, and slight enlargement of the lymph nodes
or spleen. Primary organs involved are bone marrow, spleen (splenomegaly), & liver
(hepatomegaly). Petechiae & ecchymosis in skin and mucous membranes, hemorrhage from
various sites, and bacterial infections are common.
• Lab Findings: leukocytosis 30,000-100,000/mm3 with immature forms (myeloblasts &

lymphoblasts) predominating; anemia and thrombocytopenia, prolonged bleeding and
coagulation times, tourniquet test is usually positive.
ACUTE MYELOID/MYELOGENOUS LEUKEMIA (AML)-malignant BONE MARROW disease

where hematopoietic precursors are arrested in an early stage of development (has an abrupt
onset). AML is distinguished from other related blood disorders by the presence of > 30%
MYELOBLASTS in the blood and/or bone marrow that contain AUER RODS in their cytoplasm.
THE MOST MALIGNANT LEUKEMIA. More common in adults.
POLYCYTHEMIA VERA (PRIMARY ERYTHEMIA):

A CHRONIC myeloproliferative condition of TOO MANY ERYTHROCYTES (RBC) produced in
the circulation due to tumorous abnormalities in tissues that make RBC, making BLOOD TOO
THICK to pass easily through small blood vessels in the body. This leads to CLOT FORMATION
& BLOCKAGE of vessels causing a STROKE (cerebrovascular accident). Usually accompanied
by leukocytosis. Splenomegaly, due to vascular congestion, occurs in 75% of patients. Usually
occurs within in ages 20-80yrs., with age 60yrs being the mean age of onset.
• PV Clinical Features: headache, weakness, weight loss, pruritus, hemorrhage and

thrombosis.
• PV Oral Manifestations: oral mucous membranes (especially gingiva & tongue) appear deep
purplish-red, gingiva is swollen and bleeds easily, and submucosal petechiae (purplish spots),
ecchymosis (petechiae, but bigger), and hematomas are common.
• Secondary Polycythemia-an increase in the total number of erythrocytes (RBC) due to

another condition (i.e. chronic tissue hypoxia of advanced pulmonary disease, high altitude
(Osker’s Disease), or secretion of erythropoietins by certain tumors.
PLUMMER-VINSON SYNDROME - a rare disorder associated with severe and chronic iron-
deficiency ANEMIA occurring mainly in women ages 30-40yrs. Due to the predisposition to
develop carcinoma of the oral mucous membranes, it is essential to diagnose early, so
treatment can be given ASAP (administer iron, vitamin B complex, and a high protein diet).
• Systemic Symptoms: weakness, pallor, difficulty swallowing (dysphagia) due to esophageal

stricture or web, and difficulty breathing (dyspnea).
• Oral Symptoms: angular stomatitis, smooth, red, painful tongue with papillae atrophy.
APLASTIC ANEMIA – a form of anemia where bone marrow’s capacity to produce RBCs is
defective. THE MOST SERIOUS & LIFE-THREATENING blood dyscrasia associated with
drug toxicity.
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1. Primary Anemia-unknown etiology that affects young adults; usually fatal. Symptoms: pallor,
weakness, malaise, dyspnea (difficulty breathing), headache, and vertigo. Oral symptoms:
spontaneous bleeding, bruising (petechiae), and gingival infections.
2. Secondary Anemia-caused by exposure to toxic agents (i.e. radiation, chemicals, or drugs

like Chloramphenicol). Occurs at any age, with the same symptoms as primary anemia.
Prognosis is good after the cause is removed.
PERNICIOUS ANEMIA-a disease caused by an inability to absorb adequate amounts of

vitamin B12 from the digestive tract. A relatively common, chronic, progressive megaloblastic
anemia, caused by the lack of secretion of INTRINSIC FACTOR in normal gastric juice
(intrinsic factor is necessary for adequate vitamin B12 absorption, which is required for erythrocyte
maturation). As a result, fewer than normal RBC are produced. The lack of intrinsic factor
causes poor B12 absorption and leads to low RBC production. Diagnosed by the Schilling
Test to determine the body’s ability to absorb an oral dose of B12.
• Characterized by a Triad of Symptoms: weakness, SORE PAINFUL TONGUE (ATROPHIC

GLOSSITIS), and tingling of extremities.
ATROPHIC GLOSSITIS (Pernicious Anemia)
THALASSEMIA MAJOR & MINOR –hemolytic anemias caused by a genetic defect,

characterized by a low level of erythrocytes & abnormal hemoglobin. Oral Manifestations:
oral mucosa may exhibit anemic pallor, flaring of maxillary anterior teeth with malocclusion.
ERYTHROBLASTOSIS FETALIS (HEMOLYTIC DISEASE OF NEWBORN) – a severe

hemolytic disease of the fetus or newborn caused by the production of maternal antibodies for
fetal RBC. It usually involves Rh factor incompatibility between the mother and fetus.
Characterized by excessive destruction of erythrocytes due to an antigen-antibody reaction in
the infant’s bloodstream resulting from the placental transmission of maternally formed antibodies
against the incompatible antigens of the fetal blood. In Rh factor incompatibility, the hemolytic
reaction only occurs when the mother is Rh (-) and infant is Rh (+).
• Oral Manifestations: teeth have a green, blue, or brown hue due to deposition of blood
pigment in enamel and dentin. ENAMEL HYPOPLASIA may occur, affecting the incisal
edges of anterior teeth and middle portion of the deciduous canine and first molar crown.
204
ERYTHROCYTE SEDIMENTATION RATE (ESR)-a non-specific test that only monitors the
PROGRESSION OF DISEASE. ESR is the rate at which RBC settle out in a tube of unclotted
blood, expressed in mm/hour. Blood is collected in an anticoagulant and allowed to sediment
in a calibrated glass column. At the end of one hour, the lab measures the distance the
erythrocytes have fallen in the tube. The speed that the RBC fall to the bottom of the tube
reflects the degree of inflammation
• Elevated sedimentation rates are not specific for any disorder, but indicate the presence of
inflammation. Inflammation causing an alteration of blood proteins that make RBC aggregate,
becoming heavier than normal. ESR rises during inflammation, tissue degeneration,
suppuration, and necrosis. Certain non-inflammatory conditions (i.e. pregnancy) are also
categorized by high sedimentation rates.
WISKOTT-ALDRICH SYNDROME – affects ONLY BOYS and causes eczema, low platelet
count, and a combined deficiency of B and T lymphocytes that lead to repeated infections.
Children who survive past age 10 usually develop cancers (lymphoma and leukemia).
EMBOLUS-a mass (detached BLOOD CLOT = thrombus), an air bubble or a foreign body that
moves within a blood vessel to lodge at a site distant from its place of origin. The danger
from an embolus is it can lodge in vascular beds of vital organs, occluding blood flow and causing
infarction.
• The most common source of a Pulmonary embolism is thrombophlebitis (a thrombus

formed within a vein). Femoral vein is the common source of origin of the thrombus
which then occludes a blood vessel in the lung.
GINGIVAL HYPERPLASIA: diffuse soft tissue overgrowth affecting both jaws with a pink-to-red
color and firm consistency from the mucogingival junction to the free gingival margin.
• Local Factors: can be caused by poor oral hygiene, malocclusion, tooth malformations,
caries, faulty restorations, allergens, chronic mouth breathing.
• Systemic Factors: diabetes, hormone changes (puberty and pregnancy),

immunoincompetence, gingival fibromatosis, Wegener Granulomatosis, aplastic anemia,
leukemia, scurvy (vitamin C deficiency), and drugs PHENYTOIN (DILANTIN), VALPROIC
ACID, CYCLOSPORINE, and CALCIUM CHANNEL BLOCKERS (CCBs) (ex:
NIFEDIPINE for hypertension and cardiovascular diseases). Other CCB that can cause
gingival hyperplasia (Amlodipine, Felodipine, Verapamil, and Diltiazem).
• Develops 1-9 months after Calcium Channel Blocker administration.
• A biopsy of constant hyperplasia can rule out a systemic disease like

LEUKEMIA.
• Gingivectomy can treat, but it will recur with continued use of most CCBs.
Discontinuing the CCB usually restores the gingiva to normal size within one
month.
• Histologic Examination: epithelial hyperplasia with acanthosis, parakeratosis, and

elongated, slender epithelial RETE PEGS and dense C.T. with foci of chronic
inflammation.
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NEUROLOGIC AND MUSCLE DISORDERS

TRIGEMINAL NEURALGIA (Tic Douloureux) – an excruciating, PAINFULL illness where the
person feels sudden stab-like pains in the face that usually last only moments, but are among
the most severe pain humans can feel. This pain is provoked by touching a “trigger zone” near
the nose or mouth, caused by degeneration of the trigeminal nerve or by applying pressure to
the nerve. Can affect any of the trigeminal’s three branches (V1, V2, or V3). The momentary bursts
of pain recur in clusters, lasting many seconds. Paroxysmal episodes of the pains may last
hours.
• Drug Treatment: drug of choice is Carbamazepine (Tegretol), an analgesic and

anticonvulsant that usually relieves the pain within 48hrs. Tegretol is also prescribed to treat
certain seizure disorders.
MULTIPLE SCLEROSIS (MS)-a chronic, often disabling disease that randomly attacks the CNS
(brain and spinal cord) due to an autoimmune response where the immune system attacks a
person’s own tissues. Women are affected 2x more than men, with the onset of symptoms
occurring usually between ages 20-40yrs (tingling, numbness, paralysis, and blindness).
Patients with MS may have facial and jaw weakness, and Bell’s Palsy & Trigeminal Neuralgia
may develop more frequently in MS patients.
GLOSSOPHARYNGEAL NEURALGIA – pain similar to trigeminal neuralgia that arises from the
glossopharyngeal nerve (CN 9). It is not as common as trigeminal neuralgia, but the pain may be
as severe. Occurs in both sexes (middle-aged and elderly). Sharp, sudden, shooting almost
always UNILATERAL pain in the ear, pharynx, nasopharynx, tonsils, or posterior tongue.
POSTHERPETIC NEURALGIA-a persistent burning, aching, itching, and hyperesthesia along

distribution of a cutaneous nerve after an attack of HERPES ZOSTER. May last a week or many
months. Involves FACIAL NERVE (CN 7) & geniculate ganglion that produces Ramsey Hunt
Syndrome (facial paralysis & otalgia/earache).
MYASTHENIA GRAVIS – a chronic condition of EXTREME MUSCLE WEAKNESS due to an

autoimmune disorder where the body creates antibodies against its own nicotinic ACh
(acetylcholine) receptors in the neuromuscular junctions. The muscles are quickly fatigued
with repetitive use. It is typical for the patient to have a flattened smile and DROOPY EYES with
slow papillary light responses (double vision). XEROSTOMIA & RAMPANT CARIES may be
present because acetylcholine needed for proper transmission of nerve impulses is destroyed,
so salivary glands do not receive adequate stimulation.
• Immune system produces autoantibodies that attack Acetylcholine receptors that lie on
the muscle side of the neuromuscular junction causing dysfunction of the myoneural
junction (the neuromuscular junction functions abnormally causing muscle weakness).
This decreases the responsiveness of the muscle fibers to acetylcholine released
from motor neuron endings. Difficulty speaking and swallowing, and weakness of the
arms and legs are common (muscles of the face, neck, arms, and legs are affected).
• 10% of people develop a life-threatening weakness of the breathing muscles (a condition

called myasthenic crisis).
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• Drugs that increase the level of acetylcholine (e.g. pyridostigmine or neostigmine) may
be given for treatment.
EATON-LAMBERT SYNDROME – similar to myasthenia gravis in that it is an autoimmune

disease causing weakness, but due to the inadequate RELEASE of acetylcholine rather than
by abnormal antibodies that attack acetylcholine receptors as in Myasthenia Gravis.
FREY’S SYNDROME (AURICULOTEMPORAL SYNDROME)–an uncommon phenomenon due

to damage to the auriculotemporal nerve and subsequent re-innervation of the sweat glands
by parasympathetic salivary fibers. Can occur after surgery (i.e. removal of a parotid tumor,
ramus of the mandible, or infection of the parotid that has damaged the auriculotemporal nerve
(branch of V3). Gustatory sweating is the chief complaint. Patient exhibits flushing and
sweating of the involved side of the face during eating.
BELL’S PALSY –facial paralysis from damage to the FACIAL NERVE (CN7). Can occur at
any age, but disproportionately attacks pregnant women, diabetics, and people with
influenza, cold, or other upper respiratory infection.
• Clinical Signs: unilateral paralysis of all facial muscles with loss of eyebrow & forehead
wrinkles, drooping of eyebrows, flattening of the nasiolabial furrow, sagging of the mouth
corner, and inability to frown or raise the eyebrows. The upper and lower lips may also be
paralyzed on the affected side. Drooping mouth on one side with a watering eye, loss of
taste sensation on the anterior portion of the tongue may occur.
• Sudden onset, but paralysis begins to subside in 2-3 weeks, and gradual, complete
recovery occurs in > 85% of patients.
• Important: While giving an inferior alveolar block, if you inject anesthetic solution into the
parotid gland capsule, you may cause a Bell’s Palsy-like feeling by anesthetizing the
facial nerve.
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NON-ODONTOGENIC CYSTS
CONGENITAL CYSTS:
1. Branchiogenic Cyst-arises from the persistence of the second branchial arch cleft. This
cyst is located along the anterior border of the sternocleidomastoid muscle at any level
in the neck. The cyst is lined with ciliated and striated squamous epithelium, and contains a
milky/ mucoid fluid. Treatment: complete surgical excision.
2. Dermoid Cyst-relatively uncommon cyst in the oral cavity. This cyst often contains hair,
sebaceous and sweat glands, and tooth structures. The most common site is the MOUTH
FLOOR. Treatment: complete surgical excision.
3. Thyroglossal Duct Cyst-may arise from any part of the thyroglossal duct. Found in a midline
position and is usually dark colored, and may be vascular resembling a hemangioma.
Hemorrhage into the mouth is a common and important symptom caused by rupturing
of the overlying veins. Treatment: complete excision of the tract to the base of the tongue
(often including part of the hyoid bone).
NON-ODONTOGENIC FISSURAL CYSTS (DEVELOPMENTAL CYSTS): (Nasopalatine,

Nasoalveolar, Median Palatal, and Globulomaxillary cysts).
NASOPALATINE DUCT CYST (Incisive Canal Cyst)-a “HEART-SHAPED” radiolucency in the

midline of the hard palate. Most common non-odontogenic/developmental/fissural cyst.
Usually asymptomatic (but patient may complain of tender swelling of the palate), or may produce
an elevation in the anterior part of the palate. Teeth are vital. Treatment: surgical
excision/enucleation. Prognosis is excellent. Occurs in bone (intra-osseous).
• Radiographic Features: a circular (round) well-demarcated oval or heart-shaped

radiolucency between and above the MAXILLARY CENTRAL INCISORS (rarely just
lateral to the midline) on a radiograph clinically seen as a marked swelling in the region of
the palatine papilla, situated distal to the roots of the central incisors. The pulps of the
anterior teeth are vital. The lesion crosses the midline. Do not confuse with an enlarged
palatine foramen.
• Cysts that arise from epithelial remnants in the incisive canal are the most common
type of maxillary developmental cyst. Histologically, its walls are lined with vessels,
nerves, and mucous glands (remnants of nasopalatine ducts within bone). They most
often remain limited in size and are asymptomatic. Some however, become infected or
have a tendency to grow extensively. When this occurs, surgical intervention is indicated.
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NASOPALATINE DUCT CYST (Incisive Canal Cyst) = HEART SHAPED
Palatine Papilla Cyst-the soft tissue (and much less common) variant of the Nasopalatine Duct
Cyst.
NASOLABIAL CYST (Nasoalveolar Cyst)-a soft tissue cyst of the UPPER LIP (extra-osseous
cyst) superficially located in soft tissue of the upper lip that histologically develops from
epithelial remnants from the inferior and anterior portion of the nasolacrimal duct.
• Clinical Features: swelling below or inside the NOSTRIL that may present in the canine
region. CANNOT SEE THIS CYST ON A RADIOGRAPH, but may produce “cupping” of
underlying bone. NOT WITHIN BONE (extra-osseous) so not visible on a radiograph.
Treatment: Enucleation (surgical excision). Excellent prognosis.
GLOBULOMAXILLARY CYST-an inverted “PEAR-SHAPED” radiolucency in bone between

the roots of the maxillary lateral & canine (often causes roots of the involved teeth to
DIVERGE).
• Clinical Features: usually asymptomatic, but occasionally produces swelling with or

without pain. All regional teeth are vital. Occurs within bone (intra-osseous).
• Histologic Features: consists of epithelial remnants where the globular & maxillary
processes are fused.
• Radiographic Features: inverted PEAR-SHAPED radiolucency between the maxillary

lateral & canine roots. Teeth are vital, but roots may be divergent. Do not confuse with a
Lateral Periodontal Cyst.
• Treatment: Enucleation without disturbing the teeth. Excellent prognosis.
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MEDIAN PALATAL CYST-rare, but may occur anywhere along the MEDIAN PALATAL RAPHE,
usually in the HARD PALATE MIDLINE, posterior to the pre-maxilla (occurs in bone; intra-
osseous). May produce swelling on the palate. Clinically, this lesion presents as a firm,
painless swelling. This cyst may represent a more posterior version of a Nasopalatine Duct Cyst,
rather than a separate cystic degeneration of epithelial rests at the line of fusion of the palatine
shelves.
• Histologic Features: epithelial remnants in the line of fusion between the palatine
processes. Appears as a soft, fluctuant or crepitant swelling in the hard palate midline.
• Radiographic Features: well-demarcated radiolucency in the midline of the hard palate.
• Treatment: Enucleation with an excellent prognosis.
MEDIAN ALVEOLAR CYST-rare, but occurs in the bony alveolus (intraosseous) between the
central incisors. Distinguished from a periapical cyst by the fact that the adjacent teeth are vital.
Treatment: enucleation.
ODONTOGENIC CYSTS
LATERAL PERIODONTAL CYST-a painless unilocular, well-defined TEAR-DROP SHAPE

radiolucency (with opaque margins) that occurs 95% of the time between and along the lateral
surfaces OF VITAL MANDIBULAR CANINE & PREMOLAR ROOTS. DO NOT PROBE THE
AREA. Affects middle aged males > than females. Developmental cyst treated by surgical
enucleation. Histologic Features: thin lining of non-keratinized epithelium.
LATERAL PERIODONTAL CYST
RADICULAR CYST (APICAL PERIODONTAL CYST OR PERIAPICAL CYST)-the MOST COMMON

ODONTOGENIC CYST, mainly found at the ROOT APEX. It develops within a pre-existing periapical
dental granuloma. Increased osmotic pressure in the cyst lumen is important in its pathogenesis. Clinical
Features: asymptomatic, tooth is NECROTIC; can be sensitive to percussion.
• Radiographic Features: well-circumscribed radiolucency at the tooth apex.
• Histologic Features: exhibits a lumen (true cyst) invariably lined by stratified squamous epithelium.
The cyst wall is condensed C.T. with plasma cells, lymphocytes, and PMN leukocytes.
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• Treatment: RCT with apicoectomy, or extraction with socket curettage.
RADICULAR CYST (PERIAPICAL CYST)
RESIDUAL CYST-occurs when a tooth with a radicular (periapical) cyst is extracted, but the
radicular cyst is left undisturbed and persists within the jaw now as a residual cyst. To
prevent a residual cyst, you must CURETTE the radicular cyst out of the tooth socket after
extraction. Equally affects males and female at any age. Usually asymptomatic, and is found in
EDENTULOUS areas. It is a radicular cyst left in the jaw after a tooth extraction.
• Radiographic Features: well-defined radiolucency not associated with a tooth. Usually

solitary.
• Histological Features: same as a radicular cyst (apical periodontal cyst), has stratified
squamous epithelium lining the lumen.
DENTAL GRANULOMA –the MOST COMMON SEQUELAE OF PULPITIS AT THE ROOT

APEX. Only distinguished from a radicular cyst histologically.
• Clinical Features: asymptomatic, NECROTIC TOOTH, but may be percussion sensitive.
• Radiographic Features: circumscribed radiolucency at the tooth apex.
• Histologic Features: lined by stratified squamous epithelium. Cyst wall is fibrous C.T. with
macrophages, lymphocytes, cells, and capillaries.
• Treatment: RCT or extraction of the involved tooth.
DENTIGEROUS CYST (FOLLICULAR CYST) –an odontogenic cysts always associated with
the crown of an UNERUPTED or DEVELOPING tooth or dental anomaly (ex: odontoma). Most
commonly found with a developing 3rd molar. Can cause marked displacement of teeth due to
pressure of accumulated fluid that usually displaces the tooth apically. If a tooth with a dentigerous
cysts begins to erupt, the bulging the cyst produces on the ridge is an eruption cyst.
ATTACHED TO CEJ.
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• Clinical Features: found in children & teenagers in mandibular 3rd molar & maxillary canine
area (70% in the mandible). Associated with impacted or unerupted teeth. The 2nd most
common odontogenic cyst.
• Radiographic Features: well-defined, unilocular radiolucency.
• Histologic Features: lined by non-keratinized, stratified squamous epithelium with NO rete-

pegs.
• An ameloblastoma is most likely to develop in the wall of a dentigerous cyst.
ERUPTION CYST – a soft-tissue variant of the dentigerous cyst, invariably associated with an
erupting tooth (usually primary, but occasionally permanent teeth). Mainly effects gingival tissues,
not bone.
• Clinical Features: usually a smooth-surface lesion that is REDDISH-PINK or BLUISH-

PINK-BLACK, fluctuant, localized swelling of the ALVEOLAR RIDGE over the crown
of an erupting primary or permanent molar. The intense bluish color is due to
accumulation of blood. Due to this appearance, it can be mistaken for a hemangioma or
hematoma.
ERUPTION CYST
• Treatment: usually NO treatment is necessary. In rare cases, incision or removal of the

overlying tissue may be required due to pain or tenderness associated with the cyst.
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PRIMORDIAL CYST (FOLLICULAR CYST) –well-defined, oval radiolucent lesion that differs
from periodontal and dentigerous cysts since it contains no calcified structures. Located in the
MANDIBULAR 3rd molar space. It may be locular, multilocular, or multiple. This cyst is found in
place of a tooth rather than directly associated with a tooth. Equally affects males and
females under 25yrs.
• Histologic Features: lined by stratified squamous epithelium; no rete pegs (arises from
epithelium of the enamel organ).
ODONTOGENIC KERATOCYST (OKC) – follicular & dentigerous cysts that contain

keratinizing material, and differs from other odontogenic cysts due to their microscopic
appearance & clinical behavior. Keratocysts may resemble periodontal, primordial, or
follicular cysts, and usually CANNOT be distinguished radiographically. The most
remarkable feature is their GREAT TENDENCY TO REOCCUR (over 30% reoccur). Usually
occurs between ages 10-30yrs. Often associated with an impacted tooth. 50% are found in the
mandibular 3rd molar area. HIGH RECURRENCE RATE.
• Keratocysts increase in size mainly by a process of epithelial cell multiplication.
• Radiographic Features: well-circumscribed radiolucency with smooth margins, and thin

radiopaque borders.
• Histologic Features: thin layer of corrugated parakeratin. Uniform thin stratified squamous
lining. Distinct cuboidal to columnar basal layer with varying amounts of keratin debris in the
lumen.
• Treatment: excision of the overlying mucosa in the area where the cyst wall is adhered.
TRAUMATIC (IDIOPATHIC) BONE CYST – may be completely devoid of solid or liquid material
(but may contain blood, fluid, debris, or be completely empty). It is most commonly found in
younger people with no sex predilection, in the MANDIBLE BETWEEN THE CANINE &
RAMUS. Regional teeth are VITAL.
• Clinical Case: a large radiolucent area on the mandible apical to the premolars and
molars on a panorex. No clinical symptoms. Teeth are not carious and respond normally
to vitality tests. Medical history is unremarkable. No fluid or tissue is evident.
TRAUMATIC BONE CYST
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GINGIVAL CYST (GC)–a rare, benign, developmental odontogenic cyst that presents as a painless,
minimally elevated firm papule with a sessile base and pink-red or bluish hue. Derived from remnants of
the dental lamina RESTS OF SERRES. GC has an insidious growth rate, and is a circumscribed swelling
of the free or attached gingiva, usually found in the mandibular canine and premolar areas. Larger GC
may erode underlying bone. Treatment: excision.
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NON-ODONTOGENIC TUMORS
FIBROUS DYSPLASIA – a rare, GENETIC abnormal condition that affects young people (15-30
years) characterized by the fibrous replacement of the osseous tissues in affected bones. The
cause is unknown. Demonstrates typical “GROUND GLASS” appearance of bone, thus if this
appearance is seen, additional tests like a skull radiograph and blood chemistries are
performed to help diagnose. Characterized by normal bone replaced by fibrous tissue. Three
types exist depending on the extensiveness of bone involvement:
1. Monostotic-involves one bone.
2. Polyostotic-involves more than one bone.
3. McCune-Albright’s Syndrome-disorder that affects the bones, skin, and several hormone-
producing (endocrine) tissues. Polyostotic fibrous dysplasia (scar-like fibrous tissue in the
bones) may be present with endocrine disturbances. There is a typical triad of clinical signs.
50% affected produce excess THYROID HORMONE. Patient must have at least 2 of the 3
symptoms: Early puberty, café-au-lait spots, and fibrous dysplasia
FIBROUS DYSPLASIA (GROUND-GLASS)
Fibrous Dysplasia is a symptomatic alteration of bone (SWELLING MASS OF BONE

OCCURS). Normal bone is replaced by fibrous tissue & non-functional bony trabeculae
(teeth may look like they are moving or displaced due to bone growing tissue). Panorex
shows typical “GROUND-GLASS” BONY APPEARANCE. Thus, ground-glass is seen, perform
additional diagnostic tests (skull radiograph & blood chemistries) to confirm the diagnosis.
• Fibrous Dysplasia Treatment: SURGERY to remove the area when the lesion stops growing.
Benign osseous lesions were treated with radiotherapy, but this may produce osteogenic
sarcoma (bone cancer), so do not want to radiate benign bone.
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• Radiographic: when mature it has a radiopaque “GROUND-GLASS” appearance

(diffuse/not well-defined, mixed radiopaque-radiolucent areas). MAIN CHARACTERISTIC is
you never see the lesion’s borders (it blends with the bone).
THREE TYPES OF FIBROUS DYSPLASIA:

1. Monostotic Fibrous Dysplasia-the most common form of fibrous dysplasia (80%) that
affects children & young adults (both sexes equally). This form affects one bone (ribs & femur
are common sites). The jaws are also commonly affected (mainly the maxilla, presenting as
a painless swelling/bulge). A panorex reveals a radiopaque mass/lesion with irregular borders
(poorly defined margins) with “ground/frosted glass” appearance. When several adjacent
bones are affected, it is called “Craniofacial Fibrous Dysplasia”.
• A differential diagnosis of fibrous dysplasia of the jaws is Ossifying Fibroma.

However, radiographically, an ossifying fibroma has a well-circumscribed appearance.
• Often causes expansion and deformity of the jawbone and tooth displacement.
There is radiographic characteristic thickening at the skull base. The lesion is usually
diffuse and radiopaque with “GROUND-GLASS” appearance radiographically.
Malignant transformation is possible if treated with radiation therapy, so treatment
usually consists of SURGICAL removal when possible. However, since these
lesions are not well-circumscribed, surgical recontouring is done to remove the portion
of the lesion causing the facial deformity.
2. Polyostotic Fibrous Dysplasia-usually displays a segmental distribution of the involved

bones (multiple bones). Occurs during childhood (mainly females who reach puberty
prematurely). Affects long bones, face, clavicles, and pelvic bones. Initial signs may be a
limp, pain, or fracture on the affected side.
3. Albright’s Syndrome (McCune-Albright Syndrome)-a disease of unknown cause

affecting the bones (bone disease), skin pigmentation (irregular brown spots/skin
pigmentation), and causing premature sexual development (endocrine problems). The
extent of these problems varies depending on the individual. Hallmark sign is FEMALE
PREMATURE PUBERTY (early sexual development in the male is less common). Affects
young people (males & females equally). Albright’s is THE MOST SEVERE form of
polyostotic fibrous dysplasia (involves multiple bones) with endocrine involvement.
• Triad of Symptoms: polyostotic fibrous dysplasia, Café-au-lait brown skin spots,

and endocrine abnormalities (most common is precocious sexual development in
females), and pathologic bone fractures. Malignant transformation potential of
polyostotic (mainly) & monostotic fibrous dysplasias into osteosarcomas is an
additional complication.
• Treatment: No treatment. Drugs that inhibit estrogen production (Testolactone)

have been used with some success.
GARDNER’S SYNDROME – a polyposis syndrome inherited in a dominant manner. The most

serious complication of is multiple (thousands) of POLYPS that affect the large intestine,
duodenum, colon, and stomach. The polyps usually appear around age 15yrs. and eventually
become malignant eventually causing COLON CANCER.
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• Oral Findings: MULTIPLE ODONTOMAS, multiple impacted & supernumerary teeth (like
Cleidocranial Dysostosis), and multiple jaw osteomas giving a “COTTON-WOOL” (LIKE
PAGET’S DISEASE) appearance to the jaws by appearing as dense, well-circumscribed
radiopacities. Associated with bony tumors in the jaw and skull. When GS is suspected based
on oral findings, refer the patient to a Gastroenterologist.
• Multiple desmoid tumors (fibromatosis), and epidermoid skin cysts may also occur.
GARDNER’S SYNDROME: Multiple Jaw Osteomas with “Cotton Wool” Appearance
GARDNER’S SYNDROME (GI POLYPS)
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CENTRAL GIANT CELL GRANULOMA – a BENIGN tumor (accounts for < 7% of all benign jaw
tumors). Occurs almost exclusively in the JAWBONES after TRAUMA (fall, blow, or tooth
extraction). Occurs mainly in children or young adult ages 0-20yrs (more common in females),
and either jaw may be involved (but affects the mandible more).
• Most common in ANTERIOR SEGMENT (SYMPHYSIS OF MANDIBLE) of females during

0-20 years of age. May sometimes cross the midline.
• Pain is not a main feature of this lesion. Slight to moderate bulging of the jaw due to
expansion of the cortical plates occurs in the involved area depending on the extent of bone
involvement.
• Radiographic Findings: unilocular or multi-locular radiolucencies of bone with well-defined

margins (similar to ameloblastoma & odontogenic keratocyst).
• Histologically, has loose fibrillar C.T. Multi-nucleated giant cells are prominent throughout the
C.T.
• Treatment: Curettage or surgical excision. These lesions fill in with new bone after excision.
CENTRAL GIANT CELL GRANULOMA
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CENTRAL GIANT CELL GRANULOMA

Well-demarcated radiolucent lesion between teeth 22 & 23
MANDIBULAR TORI (TORUS MANDBULARIS) –bony exophytic growths that occur along the
lingual surface of the mandible, superior to the mylohyoid ridge. Mandibular tori most often appear
on the LINGUAL SURFACE of the mandible, usually in the PREMOLAR REGION.
• Mandibular tori may occur singly, but there is a marked tendency toward bilateral
occurrence, and the lesion is not always confined to the premolar region. Unlike palatal tori,
mandibular tori are more readily demonstrated radiographically.
• Maxillary (palatal) & mandibular tori are NOT pathologic, and are rarely of clinical significance
while teeth are still present. However, if a complete denture must be made, tori should be
carefully removed.
EXOSTOSIS (TORI) – slow-growing, BENIGN BONY KNOTS on the hard palate or lingual aspect
of the mandible (usually symmetrical in the mandible). Exostosis are the most common exophytic
lesions.
TORI (EXOSTOSIS)
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CONDYLAR HYPERPLASIA – a rare, UNILATERAL enlargement of the condyle of unknown

cause. May be due to mild, chronic inflammation that stimulates the growth of the condyle or
adjacent tissues. Afflicted patients usually exhibit a unilateral, slowly progressive elongation
of the face with deviation of the chin AWAY from the affected side. The affected TMJ may
or may not be painful, and there is usually severe malocclusion.
CONDYLAR HYPOPLASIA & APLASIA – can occur unilaterally or bilaterally. If unilateral,

there is obvious facial asymmetry, which may alter occlusion and mastication. If unilateral, the
mandible shifts TOWARD the affected side during opening. In bilateral cases, there is no shift.
CENTRAL OSSIFYING FIBROMA –SLOW-GROWING, PAINLESS, BENIGN, asymptomatic

neoplasm (tumor)/lesion that may occur in the MAXILLA or MANDIBLE. Due to its slow growth,
the cortical plates of bone and overlying mucosa or skin are almost always invariably intact. Most
commonly involves only ONE bone (Paget’s Disease, however, involves multiple bones).
• May occur at any age, but is far more common in YOUNG ADULTS. It has an extremely
variable radiographic appearance depending on its stage of development. However, despite
the stage of development, the lesion is always WELL-CIRCUMSCRIBED and
demarcated from surrounding bone (in contrast to fibrous dysplasia). In its early stage,
it is a RADIOLUCENT area, but as it matures, it becomes a uniform radiopaque mass.
• Early Clinical Feature: TEETH DISPLACEMENT.
• Amazing similarity clinically exists between a Central Ossifying Fibroma & Central
Cementifying Fibroma (a tumor of odontogenic origin). These are two separate benign
tumors, identical in nature except for the cell undergoing proliferation (the osteoblast with
bone formation in COF, and cementoblast with cementum formation in the CCF).
Treatment: conservative excision. Recurrence is rare.
CENTRAL OSSIFYING FIBROMA
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HISTIOCYTOSIS X–disorders where abnormal scavenger immune system cells histiocytes

(macrophages), and eosinophils proliferate in the bone and lungs, CAUSING SCARS TO
FORM. Three diseases are grouped under the generic term Histiocytosis, and occur due to
metabolic defects in the reticuloendothelial system, and are characterized by proliferation of
histiocytes (macrophages) of loose C.T.
1. EOSINOPHILLIC GRANULOMA- the MOST BENIGN FORM of Histiocytosis X more

common in males ages 20-40yrs. It may be totally asymptomatic, but there may be local
pain or swelling, especially if a bone fracture occurs. In the mouth, the mandible is most
likely affected with teeth on the affected side being loose and gingivitis. When the LUNGS
are affected, the symptoms may include coughing, shortness of breath, & weight loss.
Pneumothorax is a common complication. Radiographic Features: lesion appears as
irregular radiolucent areas involving superficial alveolar bone. Jaw lesions usually appear as
single or multiple radiolucencies that may be so well-circumscribed, as to resemble cysts or
periapical granulomas.
o Treatment: bone lesions often resolve spontaneously, and do not require treatment
unless they cause symptoms. Curettage provides diagnostic biopsy material and is
curative.
2. LETTERER-SIWE DISEASE (Acute Disseminated Form)-starts before age 3yrs and is

usually FATAL without treatment. Histiocytes damage the lungs (pneumothorax may
occur), skin, lymph glands, bone, liver, and spleen. Oral lesions are uncommon.
3. HAND-SCHULLER-CHRISTIAN DISEASE (Chronic Disseminated Form)-a form of

Langerhans cell disease that usually begins in early childhood (more common in boys). Triad
of Symptoms: exophthalmos, diabetes insipidus, and “punched-out” bone destruction (skull
and jaws). Oral signs: halitosis, sore mouth, mobile teeth.
Treatment: people with Hand-Schuller-Christian Disease or Eosinophilic Granuloma may recover

spontaneously. All three disorders may be treated with corticosteroids & cytotoxic drugs
(ex: Cyclophosphamide). Use radiation therapy if there is bone involvement. Death usually
results from respiratory or heart failure.
LANGERHANS CELL HISTIOCYTOSIS-mainly a disease of children (but can affect adults) that
involves abnormal monoclonal proliferation of antigen-presenting cells. Premature loss of
deciduous teeth and alveolar bone may occur. Oral Findings: hard palate ulcerations, halitosis,
gingivitis, and ulcerated nodules. Teeth may appear to be “FLOATING IN AIR” due to
periodontitis-associated bone loss.
VERRUCIFORM XANTHOMA (“HISTIOCYTOSIS Y”) – a benign soft tissue tumor that

presents as a normal or white colored verrucous lesion. Its cause is UNKNOWN, as it is not
associated with any systemic condition. In adults, the alveolar and palatal mucosa are the
common sites.
• Histologic Features: verrucous, hyperparakeratotic surface with parakeratotic plugging.

Large “foam” cells in C.T. papillae between elongated rete ridges.
• Treatment: simple excision; no recurrence.
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ODONTOGENIC TUMORS
AMELOBLASTOMA-tumors of odontogenic epithelial origin and MOST COMMON EPITHELIAL
(ECTODERMAL) ODONTOGENIC TUMOR! (its occurrence equals the frequency of all other
odontogenic tumors combined). Consists entirely of odontogenic epithelium that shows the
differentiation of the familiar, histologic layers of the enamel organ at sites. Enlargement of the
tumor may expand the buccal, lingua cortical plates of bone, or palatal bone plates. Root
resorption of teeth adjacent to the tumor is common, and in many cases an UNERUPTED,
MANDIBULAR 3rd MOLAR is associated with the radiolucent defect. Ameloblastomas are
slow-growing, locally invasive tumors that usually run a benign course (do not infiltrate). Often
asymptomatic, a painless swelling or expansion of the jaw is the usual clinical
presentation. Ameloblastomas occur in three different clinical-radiographic situations with
different treatments & prognosis:
AMELOBLASTOMA
AMELOBLASTOMA-often associated with unerupted teeth mainly in the posterior body

and angle of the mandible (but can be in the maxilla). Looks like a multi-loculated “SOAP-
BUBBLE” appearance on a panorex. BENIGN TUMOR of ODONTOGENIC ORIGIN that is
usually painless. Can cause severe facial/jaw abnormalities due to its growth potential which
destroys surrounding bone. Treatment: SURGICAL EXICISION.
• Histogenesis: may arise from rests of the dental lamina, epithelial lining of a dentigerous cyst,
basal cells of the oral epithelium (mucosa), developing enamel organ, and possibly remnants
of Hertwig’s sheath. Consists entirely of odontogenic epithelium that shows the
differentiation of the histologic layers of the enamel organ at sites.
• Clinical Features: most often seen in adolescents in the mandibular (retro) molar area. THE
MOST AGGRESSIVE ODONTOGENIC TUMOR that is usually benign, but often shows a
highly expansive and locally invasive mode of growth.
• Ameloblastoma Radiographic Features: multi-locular or uni-locular RADIOLUCENT lesion

on vital teeth with a “soap bubble” appearance when the radiolucent loculations are large
& honeycombed when the loculations are small. Has irregular-scalloped margins. Appears
similar to a Central Giant Cell Granuloma in the mandible.
• Microscopic Features: various microscopic patterns of the tumor include the follicular (most
common pattern of multiple islands with reverse polarity) & plexiform (also the most common
pattern of large anastomosing cords), cystic, acanthomatous (extensive squamous
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metaplasia, keratin formation in central portions of epithelial islands), granular cell (cells with
prominent granular cytoplasm), desmoplastic (thin cords), & basal cell (islands of
hyperchromatic basaloid cells) patterns. All are non-encapsulated.
• Treatment: varies depending on the subtype. Recurrence is common (50-90%) if inadequately

treated. Very rarely metastasizes.
ADENOMATOID ODONTOGENIC TUMOR (ADENOAMELOBLASTOMA) – a BENIGN tumor

of ectodermal origin (purely epithelial) representing 3-7% of all odontogenic tumors. Limited to
CHILDREN & TEENAGERS (10-19yrs), and uncommon in patients older than 30yrs. Not a
variant of ameoloblastoma (best classified as a hamartoma; benign, not a true neoplasm).
Occurs mainly in the ANTERIOR MAXILLA (2x more common in maxilla than mandible) and
affects females 2x more than males. Affects 2nd decade (teenagers). Asymptomatic or painless
swelling.
• Clinical Features: most are small (< 3cm diameter). Clinically looks like a gingival fibrous
lesion. Often asymptomatic, circumscribed, unilocular radiolucency associated with the
crown of an UNERUPTED tooth (mostly canines). Radiolucency sometimes extends
apically along the root past the CEJ (helps distinguish it from a dentigerous cyst). May be
completely radiolucent, but often contains fine snowflake calcifications (tiny radiopaque foci).
• Histology: well-defined lesion surrounded by a thick, fibrous capsule. Enamel organ, lining of
dentigerous cyst, reduced enamel epithelium, Rests of Malessez. Derived from ectoderm
(epithelial) enamel organ and remnants of dental lamina. Tumor is composed of spindle-
shaped epithelial cells that form sheets, strands, or whorled masses of cells in a scant fibrous
stroma.
• Treatment: completely benign, and its capsule allows it to enucleate easily from bone
(enucleation). Recurrence is rare, and is not aggressive.
CALCIFYING EPITHELIAL ODONTOGENIC TUMOR (“PINDBORG TUMOR”) – a rare

lesion/tumor (< 1% of all odontogenic tumors) derived purely from ECTODERM (epithelial).
Found in patients mainly 30-50 years old, no sex predilection (30% are 4th decade). Uncommon
in children and adolescents. 2/3 of cases occur in MANDIBLE (molar-premolar area). Painless,
slow-growing swelling is the most common clinical sign. Rarely extra-osseous. Radiolucent-
radiopaque areas associated with an unerupted tooth and amyloid production.
• Radiographic Features: unilocular or more often multi-locular radiolucent defect. Scalloped

margin. Tumor is often associated with an impacted tooth (mandibular 3rd molar).
Calcifications within the tumor are often most prominent around the crown of an impacted
tooth.
• Histology: reduced enamel epithelium, has discrete islands, strands, or sheets of polyhedral
epithelial cells in a fibrous stroma.
• Treatment: conservative local resection to include a narrow rim of surrounding bone. 15%
recurrence rate (tumors treated by curettage have highest recurrence rate if inadequately
treated). Good prognosis.
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SQUAMOUS ODONTOGENIC TUMOR – rare benign odontogenic tumor/neoplasm derived

purely from ECTODERM (epithelial). Found in patients ages 8-75yrs (average 38yrs). Randomly
distributed throughout the alveolar processes of maxilla and mandible with no site or sex
predilection. Most common complaint is painless or mild painful gingival swelling associated
with tooth mobility.
• Clinical Features: may be asymptomatic, painless swelling associated with mobile teeth.
• Radiographic Features: triangular or circumscribed radiolucency LATERAL to the roots of

an unerupted or erupted tooth. May be an ill or well defined area with sclerotic margins. Most
are small lesions that rarely exceed 1.5cm diameter. Histogenesis: Rests of Malassez.
• Treatment: conservative local excision or curettage, and close follow-up. Recurrence is rare.
CEMENTOMA (PERIAPICAL CEMENTAL DYSPLASIA) – BENIGN odontogenic tumor that

occurs most frequently in the ANTERIOR MANDIBLE (periapical region), and often affects
multiple VITAL teeth. Cementoma is an unusual response of the periapical bone to some
local factor (i.e. traumatic occlusion or infection). While it appears to arise from teeth, the lesions
arise within bone. Age, gender, location, radiographic appearance, and tooth vitality are
important diagnostic criteria. Histogenesis: PDL. Do not mistake this as a need to do RCT (it is
not a periapical abscess). Do a pulp vitality test to diagnose. If the pulp is vital, then NO
TREATMENT IS REQUIRED.
• Clinical Features: occurs at the apex of vital anterior teeth, affecting women over age
30yrs (especially BLACK women) more than men. Asymptomatic, usually multiple, small
periapical radiolucent areas in the mandibular incisor area. Depending on its stage, a
cementoma may appear radiolucent, mixed-radiolucent, or completely radiopaque. Three
Cementoma Stages:
• Stage 1: lesion is a periapical RADIOLUCENCY.

• Stage 2: lesion begins to calcify and become more radiopaque (MIXED).
• Stage 3: well-defined RADIOPACITY bordered by a thin radiolucent line.
Radiographic Features: small sharply circumscribed radiopacity attached to, or adjacent to

apices of teeth. Early lesions are radiolucent, then have a central opacity, and are densely
radiopaque when mature. The opacities are not cementum, but are BONE.
PERIAPICAL CEMENTAL DYSPLASIA (STAGE 1)
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PERIAPICAL CEMENTAL DYSPLASIA (STAGES 2 & 3)
BENIGN CEMENTOBLASTOMA (TRUE CEMENTOMA)–usually affects males under 25yrs.

Mandibular premolars or molars. Usually solitary, and may cause expansion of the cortical
plates. Tooth is vital. Histogenesis: PDL.
• Radiographic Features: well-demarcated, mottled or densely radiopaque mass with

radiolucent periphery attached to the root, causing the root resorption.
• Microscopic Features: cementum-like tissue with conspicuous reversal lines, variable

amounts of fibrous C.T. with sheets of uncalcified “cementoid” especially at the periphery.
• Treatment: EXTRACT THE INVOLVED TOOTH.
CEMENTOBLASTOMA
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GIGANTIFORM CEMENTOMA (FAMILIAL MULTIPLE CEMENTOMAS) –affects middle-aged

black women. Multiple, often symmetrical, and may cause jaw expansion. Histogenesis: PDL.
• Radiographic Features: large, dense lobulated radiopaque masses.
• Microscopic Features: large sheets of tissue that resemble secondary cementum.
• Treatment: conservative excision.
ODONTOGENIC MYXOMA – an AGGRESSIVE tumor derived from the papilla, dental sac, or
PDL. Occurs in adults 30-40yrs as a painless swelling in the mandible.
• Radiographic Features: poorly-defined, multi-locular radiolucency that may be associated

with an unerupted or displaced teeth.
• Treatment: curettage with cautery. High rate of recurrence if inadequately treated.
ODONTOGENIC FIBROMA – derived from dental papilla, dental sac, or PDL. Occurs as a
painless swelling in the mandible of children & young adults. Radiographically, it is a multilocular
or unilocular radiolucency that may be associated with unerupted or displaced teeth. Treatment:
Enucleation. Recurrence is rare.
CEMENTIFYING FIBROMA – a well-defined radiolucency with scattered radiopaque foci. Occurs

in the mandible of adults as a painless swelling. Histogenesis: PDL. Treatment: curettage.
Recurrence is rare.
ODONTOMA (Hamartoma)-ANY odontogenic tumor often associated with an unerupted tooth.

The average age of people found with an odontoma is 14-years old. Remove with oral surgery.
ODONTOMA (HAMARTOMA)
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COMPLEX ODONTOMA- amorphous RADIOPAQUE mass with a thin, radiolucent rim at the
junction of surrounding bone (has varying densities). Most common in the POSTERIOR mandible.
Derived from ectodermal & mesenchymal components of tooth germ. Affects ages 20-30yrs, and
found in the mandibular premolar-molar area. Asymptomatic, but may delay eruption of
permanent teeth.
• Radiographic Features: well-defined, radiopaque mass surrounded by a narrow
radiolucent zone. May or may not be associated with an erupted tooth.
• Histologic Features: conglomerate mass of dental tissues (dentin, enamel, cementum).

Characterized by the formation of calcified enamel and dentin in an abnormal arrangement
because of lack of morphodifferentiation. Treatment: Surgery. DOES NOT RECUR.
COMPLEX ODONTOMA
COMPOUND ODONTOMA – a tumor of enamel and dentin common in the ANTERIOR

MAXILLA (incisor-canine area) derived from ectodermal & mesenchymal components of tooth
germ. It is arranged in the form of anomalous MINIATURE TEETH (several small abnormal teeth).
Affects ages 20-30yrs. May also appear in the mandible canine-premolar area, and can cause
delayed eruption or prevent eruption of permanent teeth.
• Radiographic Features: groups of small radiopacities (multiple small tooth-like

structures with a thin radiolucent rim at the junction with surrounding bone.) Common
between the maxillary premolar and central incisor on a panorex.
• Microscopic Features: multiple, small malformed teeth of dentin, enamel, and cementum.
• Treatment: Enucleation (Surgery), and does not recur.
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COMPOUND ODONTOMA (TOOTHLETS)
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PIGMENTED LESIONS
PEUTZ-JEGHERS SYNDROME (HEREDITARY INTESTINAL POLYPOSIS SYNDROME) – an
autosomal dominant inherited disorder, characterized by MULTIPLE INTESTINAL POLYPS
distributed through the entire intestine (especially the jejunum) and intra-oral MELANIN
pigmentations of the lips and oral mucosa at birth or early age (often during the first decade
of life), and at this time is restricted to the oral region.
• Intra-orally, the pigmentations can be found anywhere on the mucosa, but are most common
on the BUCCAL MUCOSA, GINGIVA, and HARD PALATE. The mucosal surface of the
LOWER LIP is almost always involved. These spots or macules vary in intensity, and range
in shades of BROWN, BLUE, and BLACK. The tongue seldom shows this melanin
pigmentation. The oral pigmentations are harmless, but their presence is important to
determine if multiple polyposis exist in the intestines and colon which may be harmful.
There is a strong tendency for the multiple polyps of the colon to undergo malignant change.
• During succeeding decades of a patient’s life, pigmentations may arise on the skin’s
extremities. Pigmentations of Peutz-Jeghers Syndrome may occur without polyps, and
multiple polyps may be present without any pigmentations.
• When Peutz-Jegher Syndrome is suspected based on oral pigmentations, other conditions to

consider in the differential diagnosis are Addison’s Disease & Albright’s Syndrome.
ADDISON’S DISEASE (“Chronic Adrenocortical Insufficiency” or “Hypocorticolism)-a rare

endocrine disorder caused by ADRNEAL CORTEX HYPOFUNCTION of CORTISOL
(GLUCOCORTICOID)—not enough cortisol is produced. The hyposecretion is either due to
an adrenal gland disorder (primary adrenal insufficiency), or inadequate secretion of ACTH by the
pituitary gland (secondary adrenal insufficiency). CAUSES BRONZING OF THE ENTIRE SKIN.
Cortisol’s most important function is to help the body respond to STRESS. Occurs in all
age groups, affecting men and women equally. MAIN DENTAL CONCERN during dental
procedures is this patient’s adrenal cortex has no capacity to produce extra cortisol in
response to stress, which may result in ADRENAL CRISIS.
• Clinical Signs: usually start gradually and include weight loss, loss of appetite, muscle
weakness, low BP, darkening (hyperpigmentation) of the skin in both exposed &
unexposed parts of the body (most visible on scars, skin folds, pressure points like elbows,
knees, knuckles, toes, and oral mucous membranes). Also nausea, vomiting, diarrhea.
• Oral Signs: diffuse pigmentation of the gingiva, tongue, hard palate, & buccal mucosa.
Although cutaneous pigmentation will usually disappear, after therapy, pigmentation of the
oral tissues tends to persist.
• Lab Tests: show low blood concentrations of Na+ and glucose, increased serum K+, and
decreased urinary output of certain steroids.
ALBRIGHT’S SYNDROME (McCune-Albright Syndrome)-a severe form of polyostotic fibrous

dysplasia that causes lesions of nearly all skeletal bones, brown patches of cutaneous
pigmentation (café-au-lait spots), and endocrine dysfunction (especially precocious puberty in
girls). There is also an increased incidence of osteosarcoma.
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AMALGAM TATTOO – a common finding sometimes mistaken for a melanin-pigmented

lesion. Most common on the gingiva, buccal mucosa, and alveolar mucosa.
AMALGAM TATTOO
ASPIRIN BURN-occurs when patients place an aspirin tablet against an aching tooth, allowing
the cheek or lip to hold it in position, while it dissolves slowly. Within a few minutes, a burning
sensation of the mucosa is noted, and the surface becomes blanched or white (ORAL
MUCOSA NECROSIS), with subsequent sloughing of the necrotic epithelium.
ASPIRIN BURN
• Heavy Metal Bismuth Ingestion-used to treat some dermatologic disorders and various
other diseases. Bismuth pigmentation appears as a “bismuth line” (thin, blue-black line in
the marginal gingiva that is sometimes confined to the gingival papilla).
Most pigmented skin tumors are composed of NEVUS cells due to a developmental
anomaly of MELANOCYTES, and are RARE in the oral cavity. The initial flat, raised lesion can
become nodular, with an increase in consistency. Spontaneous involution may occur, and
malignant transformation is a rare complication. When found intra-orally, pigmented skin
tumors are most often on the HARD PALATE, but may appear on the gingiva and lips. If a
pigmented lesion shows ulceration, increase in size, color darkening, a biopsy is performed to
determine if malignant transformation is occurring.
CONGENITAL NEVI (BIRTHMARK) – are usually larger (> 10cm) but as time passes, it can
change from a flat, pale-to-tan macules into elevated, verrucous, hairy lesions. ~15% occur on
the head & neck skin. Have a higher incidence of malignant transformation than acquired
nevi. Most common intra-oral location is the HARD PALATE.
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FOCAL MELANOSIS – may occur at any age and presents as a single or multiple small, FLAT
BROWN asymptomatic lesion found mainly on the LOWER LIP. Focal melanosis describes two
similar lesions that differ in their location and size:
1. Labial Melanotic Macule-a lesion on the lips (MAINLY LOWER LIP), and almost always
near the midline. Most lesions are 5mm or less in diameter.
LABIAL MELANOTIC MACULE
2. Oral Melanotic Macule intra-oral lesion found on the gingiva, buccal mucosa, and palate.
Most lesions are under 1.0 cm in diameter.
ORAL MELANOTIC MACULE
Treatment: melanotic macules with a short history are EXCISED and BIOPSIED to rule out the
possibility of malignant melanoma. Lesions present > 5 years without a change in size or
color, are followed unless the patient requests removal.
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RED-BLUE LESIONS
MEDIAN RHOMBOID GLOSSITIS –often affects MIDDLE-AGED ADULTS. Once thought to be
a congenital abnormality related to the persistence of the tuberculum impar, but is now believed
to be a permanent end result of a CHROINC CANDIDA ALBICANS INFECTION. Diabetics,
immunosuppressed patients, and patients on long-term antibiotic therapy are most susceptible.
• Clinical Features: smooth, denuded, BEEFY-RED LESION devoid of filiform papillae.

Mainly found on the MIDLINE of TONGUE DORSUM, just anterior to circumvallate papillae.
Generally asymptomatic, and NO TREATMENT is usually necessary, but may need to
prescribe NYSTATIN.
MEDIAN RHOMBOID GLOSSITIS
ERYTHROPLAKIA – a persistent, VELVITY-RED PATCH that cannot be characterized clinically

as any other condition. Like “leukoplakia”, it has no histologic connotation, but most
erythroplakias are histologically diagnosed as severe epithelial dysplasia, carcinoma in-
situ, or invasive squamous cell carcinoma. May be located anywhere in the mouth, but are
MOST likely found in the mandibular mucobuccal fold, oropharynx, and floor of the mouth.
Equally affects males and females, especially over 60yrs.
ERYTHROPLAKIA
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BURNING TONGUE SYNDROME – patients usually do not exhibit clinically detectable lesions,
but symptoms of intense pain and burning. BTS is frustrating for the patient and clinician
because there is usually no clear-cut cause and no uniformly successful treatment. Typically
affects MIDDLE-AGED FEMALES (it affects men too, but usually at an older age). Rare in
children & teenagers.
• Possible Etiologic Factors: anemias (pernicious anemia & iron deficiency anemia), diabetes
mellitus, gastric disturbances (i.e. hyperacidity or hypoacidity), psychogenic factors
(emotional conflict, cancerphobia), trigeminal neuralgia, microorganisms (especially Candida
Albicans & Streptococci), xerostomia (dry mouth) associated with Sjogren’s Syndrome,
anxiety, & drugs. Local irritation (tobacco, spices), and vitamin deficiency (especially B
complex).
PERIPHERAL GIANT CELL GRANULOM-relatively uncommon, pedunculated broad-based

growths with a smooth surface (usually). Always on GINGIVA (between 1st permanent molar
& incisors) or ALVEOLAR PROCESS. Mandibular gingiva is affected more than maxillary
gingiva. It represents an unusual hyperplastic C.T. response to injury of gingival tissues.
REDDISH-BLUE in color, sometimes lobulated, and bleed easily. Most patients are older than
age 20yrs (Central Giant Cell Granuloma occurs mainly before age 20yrs). Affects females 2x
more than males. Radiographs are usually negative. Clinically, it may resemble a fibroma or
pyogenic granuloma.
• Histologically: identical to Central Giant Cell Granuloma. Consists of a non-encapsulated

tissue mass composed of a delicate reticular & fibrillar C.T. stroma with multi-nucleated giant
cells.
• Treatment: COMPLETE SURGICAL EXCISION.
PERIPHERAL GIANT CELL GRANULOMA
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HEMANGIOMA – BENIGN tumor consisting of a mass of BLOOD VESSELS. It can range

from a small mass, to very large sacs of unsightly red, purple, or blue blood vessels (they can
enlarge to very alarming sizes). Present at birth, childhood, or arise later in life (enlarges as
the child grows). In certain locations, large hemangiomas can interfere with proper organ
development and function.
• Clinical Features: a common BENIGN tumor of a PROLIFERATION OF BLOOD

VESSELS, affecting females 2x more than males (2:1). It is a soft, smooth, blue, red, purple,
or purplish-red mass that most commonly affects the TONGUE, BUCCAL MUCOSA, LIPS,
PALATE.
• Microscopic Features: capillary, cavernous, and a hemangioendothelioma of stratified

squamous epithelium covering of loose, fibrous C.T. that contains many thin-walled engorged
vascular spaces.
• Treatment: laser therapy or surgery. May regress spontaneously. DO NOT INCISIONAL

BIOPSY.
HEMANGIOMA
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PSEUDOCYSTS (“NOT TRUE CYSTS”)

NO EPITHELIAL LINING
TRAUMATIC BONE CYSTS (PSEUDOCYSTS)–non-cysts found in the MANDIBLE (between
canine & ramus) of mainly TEENAGERS due to trauma. PAINLESS, WELL-DEFINED
SCALLOPED RADIOLUCENCY between teeth. Although sometimes asymptomatic, it may
produce jaw enlargement. Regional teeth are vital.
• AKA: simple bone cyst, hemorrhagic bone cyst, unicameral bone cyst, extravasation bone
cyst, idiopathic bone cyst, and solitary bone cyst.
• Treatment: open the lesion, curettage, and suture. It may contain blood, serosanguineous
fluid, debris composed mainly of a blood clot, or may be completely devoid of solid material.
ANEURYSMAL BONE CYST– a BENIGN bone lesion generally regarded as a “reactive

process” (not a neoplastic or cystic process). A RARE expansile, osteolytic bone lesion
consisting of a proliferation of vascular tissue that forms a lining around blood-filled cystic
lesions. Most occur equally in males and females under age 20yrs, and is UNCOMMON
AFTER AGE 30yrs.
• Involves the proximal humerus, femur, tibia, and pelvis (uncommon in jaws, but
usually appears in the mandible). Lesions are usually tender or PAINFULL on motion of
the affected bone. Upon entering the lesion surgically, excessive bleeding occurs, and the
tissue often resembles a “blood-soaked” sponge.
• Histology: has no epithelial lining (thus is a “pseudocyst”). Consists of fibrous C.T. stroma
with many cavernous or sinusoidal blood-filled spaces. Fibroblasts & macrophages
(histiocytes) line the sinusoids. Multi-nucleated giant cells (similar to cells of a giant cell
granuloma) are dispersed throughout.
• Radiographic Features: bone is expanded and appears CYSTIC with a “HONEYCOMB

or SOAP-BUBBLE” appearance. Treatment: surgical curettage or excision, with little
chance of recurrence.
ANEURYSMAL BONE CYST (BENIGN)
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BENIGN SALIVARY GLAND TUMORS
BENIGN SALIVARY GLAND TUMORS CLINICAL FEATURES–normal mucosa, painless,

nodular, localized, movable, firm, slow-growing, well-differentiated, & encapsulated/well-
circumscribed.
• Radiographically, a benign neoplasm in bone may be distinguished from a malignant

neoplasm in because with a benign lesion, the CORTEX REMAINS IN-TACT, but may be
thinned and the part involved may be expanded. In addition, benign margins are usually
defined and demarcated from surrounding bone.
PLEOMORPHIC ADENOMA (Mixed Tumor)- MOST COMMON BENIGN salivary gland tumor.
MONOMORPHIC ADENOMAS: Basal Cell, Canalicular, Myoepithelioma, Sebaceous, Papillary

Cystadenoma Lymphomatosum (Warthin’s Tumor), Onocytoma (oxyphilic/acidophilic adenoma).
The most common site of intra-oral MINOR salivary gland neoplasms/tumors is the PALATE.
The
most common site of intra-oral MAJOR salivary gland neoplasms is the PAROTID GLAND.
NECROTIZING SIALOMETAPLASIA – a benign lesion of MINOR salivary glands,

characterized by necrosis of the glandular parenchyma with associated squamous metaplasia &
hyperplasia of the ductal epithelium. Its etiology is unknown, but may be related to vascular
insufficiency and infarction of the glands. HARD PALATE is the most common site.
• NS benign lesion shows no racial or sex predilection, with most patients > 40yrs of age.
Clinically, it presents as a tender deep ulcer with sharply demarcated margins.
Histologically, there is lobular necrosis of the glandular parenchyma, with squamous
metaplasia & hyperplasia of the ductal epithelium. Clinically and histologically, the lesion
may stimulate a malignancy. In the past, the lesion was misdiagnosed as a squamous cell
carcinoma or mucoepidermoid carcinoma.
• After performing a BIOPSY and establishing a diagnosis, additional treatment is usually not
recommended since healing usually occurs within 6-12 weeks.
MUMPS -most common VIRAL DISEASE of the SALIVARY GLANDS caused by RNA-
Paramyxovirus. Clinically, 90% of cases occur before age 14yrs. A major sign is sudden
salivary gland swelling without purulent discharge from the duct. PAROITID GLAND is
involved 90% of the time, and is bilaterally involved in 2/3 of cases. Patient presents with mild
fever, malaise, and anorexia. Most cases are self-limiting.
• Complications: orchitis (inflammation of the testis) and epididymitis can occur in post-
pubertal males, and may cause sterility. CNS disturbances causing meningitis & encephalitis.
Deafness, myocarditis, pancreatitis, oophoritis, and pyelonephritis.
• Serum amylase may be elevated during the acute phase. Prevent by administering a live,
attenuated vaccine which is 95% effective for a least 5 years. However, in non-inoculated
patients, it can still cause acute non-suppurative salivary adenitis.
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MEASELES (RUBEOLA)-an RNA Paramyxovirus spread by nasopharyngeal secretions.

Characterized by KOPLIK SPOTS (small, irregular red dots with bluish-white centers on the
soft palate or buccal mucosa opposite the 1st and 2nd molars, near each STENSON’S DUCT).
Measles can cross the placenta.
MEASELES (KOPLIK SPOTS)
MUCOCELES (MUCOUS RETENTION CYST)- fluid-filled sac under the mucosa usually on the
LOWER LIP (rarely on the upper lip) usually due to trauma (biting lip or tongue). It involves
the MINOR salivary glands and their ducts (ex: trauma to the salivary duct by lip biting or
pinching). A COMMON LESION that may also appear on the palate, cheek, tongue, and mouth
floor. Treatment: Surgical Excision.
• Clinical Features: may lie deep in tissue or be very superficial. Depending on its location, its
clinical appearance varies: Superficial mucocele- a raised, circumscribed vesicle, several
millimeters to 1cm in diameter with a bluish-translucent cast. Deeper mucocele-appears as a
fluctuant swelling also, but the tissue is normal in color.
MUCOCELES
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RANULA (“TRUE RETENTION CYST”)- a fluctuant & painless cyst (swelling) that presents as
a translucent, bluish, well-rounded, smooth-surfaced bulge that protrudes from ONE SIDE of
the MOUTH FLOOR. It characteristically occurs UNILATERALLY in the floor of the mouth.
Caused by an obstruction of either the SUBMANDIBULAR or SUBLINGUAL GLANDS, due to
a salivary stone or soft organic substance. A history of increased size just before or during a
meal, and decrease in size between meals is of diagnostic significance.
• Treatment: COMPLETE SURGICAL EXCISION of the cyst roof or gland.
RANULA
MIKULICZ’S DISEASE (“BENIGN LYMPHOEPITHELIAL LESION”) –rare salivary gland lesion,

closely related to Sjogren’s Syndrome. A progressive, asymptomatic enlargement of the
PAROTID & SUBMANDIBULAR glands. Appears initially unilateral, but over time becomes
BILATERAL. Unknown etiology, but evidence suggests that both Mikulicz’s & Sjogren’s
Syndrome are autoimmune diseases where the patient’s own salivary gland tissue becomes
antigenic. Occurs most often in MIDDLE-AGED WOMEN.
• Histologic Features: replacement of gland parenchyma by lymphocytic infiltrate that

contains scattered epimyoepithelial islands within (this is the histologic cornerstone for the
diagnosis).
• Most are BENIGN, but malignant transformation of the epimyoepithelial islands may
occur.
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MALIGNANT SALIVARY GLAND TUMORS

Clinical Features of MALIGNANT Salivary Gland Tumors: PAINFUL, ulcerated mucosa,
nodular, firm, fixed, rapid growth, invasion, immovable, metastasis, and not well-differentiated
(anaplastic). Metastasis is the most important characteristic that distinguishes a malignant
tumor from a benign tumor. PARASTHESIA suggests metastatic disease.
• Histologic Features of Malignancy: anaplasia, abnormal mitosis, pleomorphism,

hyperchromatism, increased nuclear-cytoplasmic ratio.
• Host response to a malignancy is best reflected by lymphocytic infiltration at the edge of a

tumor. The most characteristic feature of a malignancy rather than an inflammatory lesion
is the malignancy will grow after the causative agent is removed. The most important
characteristic of malignant neoplasms that distinguishes them from benign neoplasms
is their ABILITY TO METASTASIZE.
• Histologic Grading of Malignant Neoplasms: attempts to estimate the aggressiveness or

degree of malignancy of a malignant neoplasm based on the degree of differentiation of
the component cells and number of mitoses. Grading mainly applies to squamous cell
carcinomas, and is of limited clinical use. Most pathologist use three grades, and designate
SCC as well-differentiated, moderately well-differentiated, or poorly differentiated.
• Grade 1 = well-differentiated.
• Grade 2 = moderately, well-differentiated.
• Grade 3 = poorly undifferentiated.
• Grade 4 = undifferentiated.
ADENOCARCINOMA-affects MAJOR salivary glands (50%) & MINOR glands (50%). Its
frequency is 25% minor glands, 5% submandibular glands, and 3% of parotid tumors. Usually
presents as an asymptomatic mass. 80% survival rate for low-grade carcinoma, and 40% survival
rate for high-grade carcinoma.
ADENOID CYSTIC CARCINOMA-a malignant salivary gland tumor that usually affects MINOR
salivary glands of the PALATE (70%), parotid gland (15%), & submandibular gland (14%).
Represents 31% of minor salivary gland tumors, 14% of submandibular gland tumors, and 2% of
parotid gland tumors. Patient presents with pain and/or nerve dysfunction in 25%-33% of
patients. Facial weakness or paralysis is common. A slow, but relentless tumor progression,
with a 20% twenty-year survival rate.
239
ADENOID CYSTIC CARCINOMA
ACINIC CELL CARCINOMA-a malignant salivary gland tumor most likely associated with the
parotid gland (96%), submandibular gland (2-3%), and minor salivary glands of the palate (1-
2%). 2-4% of parotid tumors are acinic cell carcinoma. Patient presents with swelling, pain, or
tenderness, and may have facial weakness or paralysis. 90% cure rate.
MUCOEPIDERMOID CARCINOMA-usually occurs in the parotid gland (60%), palate (13%), &
submandibular gland (6%). Represents 10% of minor salivary gland tumors, 6% of parotid tumors,
and 5% of submandibular tumors. Patient usually has asymptomatic swelling, with a peak
incidence in the 3rd decade of life (30s). Patient may have facial weakness or paralysis. Low-
grade carcinomas have an 85-100% 5-year cure rate, while high-grade carcinomas have a 20-
45% 5-year cure rate.
Metabolic Conditions & Chronic Salivary Gland Enlargement: Diabetes Mellitus, chronic
alcoholism, malnutrition (anorexia & bulimia), obesity, hypertension, & hyperlipidema. PAROTID
GLAND is most frequently enlarged (either unilaterally or bilaterally).
Other Conditions Associated with PAROTID GLAND Enlargement:

1. Sjogren’s Syndrome & Sarcoidosis
2. Warthin’s Tumor (Papillary Cystadenoma Lymphomatosum)
3. Infections (mumps, actinomycosis, tuberculosis)
4. Benign Lymphoepithelial Lesion (Mikulicz’s Disease)
5. Acute Epidemic Parotitis
6. Malnutrition
SJOGREN’S SYNDROME – a salivary gland disorder of unknown cause, but is AUTOIMMUNE.

Marked mainly by chronic inflammation of the salivary and lacrimal glands, that usually
progresses to fibrosis and atrophy of these glands. Mainly affects post-menopausal women who
present with dry eyes, dry mouth. ~50% of cases, have BILATERAL enlargement of the parotid
& submandibular glands.
• Symptoms: rheumatoid arthritis, xerostomia (dry mouth), & keratoconjunctiva sicca

(dryness of the eyes). However, all 3 symptoms rarely occur in one patient. The decrease
in salivation may cause rampant caries reminiscent of radiation caries.
240
• Histologic Features: histological features of the salivary gland lesions in Sjogren’s Syndrome
& Benign Lymphoepithelial Lesion (Mikulicz’s Disease) are identical.
• Treatment: treat the symptoms. Keratoconjunctivitis is treated with ocular lubricants, and
xerostomia is treated with saliva substitutes (artificial saliva). Biopsy of the labial or
palatal salivary glands, sialograms, salivary flow rate tests, and blood work may help establish
a diagnosis. However, radiation, surgical excision, and chemotherapy are NOT used as
treatment.
• Malignant lymphomas & “Pseudolymphomas” (“Atypical Benign Lymphoid Hyperplasia”)

develop in some patients diagnosed with Sjogren’s Syndrome. Thus, close follow-up of
patients is required.
XEROSTOMIA (DRY MOUTH) –not a disease, but a SYMPTOM of certain diseases and
medications. Xerostomia is caused by sialadenitis (insidious inflammatory disease of the major
salivary glands), Sjogren’s syndrome, medications (anti-cholinergic drugs (Atropine &
Scopolamine) & anti-psychotics (Phenothiazines: Chlorpromazine & Prochlorperazine), cancer
therapy, nerve damage, Alzheimer’s, stroke, bone marrow transplants, endocrine disorders,
stress, anxiety, depression, and nutritional deficiencies. Xerostomia is often caused by failure
of the salivary glands to function normally, but it may also occur in people with normal
salivary glands. Xerostomia can cause health problems by affecting nutrition, and psychological
health. Extreme cases can cause rampant tooth decay and periodontal disease. TREAT
WITH PILOCARPINE.
SIALOLITHS (salivary calculus or stones) in Wharton’s Duct (Submandibular Duct) are often
found with OCCLUSAL RADIOGRAPHS. Calculus deposition in the salivary ducts and glands is
more common in middle-age. The most common symptoms of duct obstruction are an increase
and decrease in swelling of the gland (especially at mealtime). The swelling may or may not
be painful, and may also occur in children. Transillumination of the soft tissue is useful to
detect sialolithiasis in children.
• Rate of occurrence in the SUBMANDIBULAR GLAND & DUCT is much higher than in the
parotid or sublingual glands due to the submandibular saliva’s tenacity, and long, irregular duct
shape.
• Treatment: surgical extirpation of the sialolith. Salivary stones located in the glandular
parenchyma also usually require surgical removal of the gland.
• OCCLUSAL RADIOGRAPHS are NOT useful for identifying sialoliths in STENSON’S

DUCT, the mental foramen, or hyoid bone.
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SIALOLITHS
ONCOCYTOMAS (“OXYPHILIC/ACIDOPHILIC ADENOMA”) – a small, benign RARE

glandular tumor composed of large cells with a granular & eosinophilic cytoplasm due to the
presence of many mitochondria. Can occur in the kidney, salivary glands, & endocrine glands. Its
development may be related to the AGING PROCESS. Treatment: surgical excision;
recurrence is rare.
• Clinical Features: most commonly seen in the PAROTID GLANDS of patients over age 50
(slightly more common in women). Slow growth, and they rarely reach any significant size.
• Histologic Features: the tumor is an encapsulated mass composed of relatively large cells
(arranged in sheets, cords, or form tubular or acinar structures). Cells have BRIGHT PINK
CYTOPLASM and small, round nuclei.
SIALOSCINTIGRAPHY-a simple, non-invasive procedure that SEPERATES BENIGN TUMORS

(ex: Warthin’s tumor & Oncocytoma) of the salivary glands from MALIGNANT TUMORS,
and greatly affects the course of treatment.
WARTHIN’S TUMOR (“PAPILLARY CYSTADENOMA LYMPHOMATOSUM”)-BENIGN

PAROTID tumor (almost exclusively in the PAROTID GLAND), arising from heterotopic ductal
epithelium within lymph nodes or near the parotid gland. Strong association with cigarette
smoking.
• Clinical Features: most patients are older 60-70 years (affects males 5:1). 95% are unilateral.
The tumor most often arises in the tail of the parotid gland as a painless, non-tender, slow
growing, firm-to-fluctuant nodule over the ANGLE or RAMUS OF THE MANDIBLE.
• Histologic Features: tumor is encapsulated and composed of CYSTIC SPACES surrounded

by two uniform rows of cells with centrally placed pyknotic nuclei. The lining epithelium
(papillary infoldings) of the cystic spaces protrude back into the spaces. The papillary foldings
have lymphoid stroma aggregates with a geminal center formation that are interspersed.
• Treatment: SURGERY. Recurrence is uncommon and highly unlikely to become malignant.
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PLEOMORPHIC ADENOMA (“BENIGN MIXED TUMOR”)–the MOST COMMON tumor of the

major & minor salivary glands. The term “mixed tumor” is used because it is of both ectodermal
& mesenchymal origin.
• Clinical Features: MOST COMMON SALIVARY GLAND NEOPLASM. Affects more women
than men (most patients between 40-60yrs). ~93% arise in MAJOR salivary glands (these
are almost exclusively PAROTID tumors (84%), but can also affect the submandibular gland.
Present as firm, painless lumps below and anterior to the ear. ~7% arise in the oral cavity
with the PALATE being by far the most common intra-oral site (firm, painless swelling). In most
cases, it does not cause ulceration of the overlying mucosa.
PLEOMORPHIC ADENOMA (BENIGN MIXED TUMOR)
• Histologic Features: epithelial (ectodermal) component consists of round, polyhedral,

elongated, or stellate cells that are relatively small and stain uniformly. The mesenchymal
component varies from areas of myxomatoid tissue, to areas of dense, hyalinized C.T.,
pseudocartilage, or bone.
• Treatment: SURGICAL EXCISION with a generous margin of normal tissue is the

treatment of choice. Inadequate initial removal of the mixed tumor in major salivary glands
may cause recurrence. ~25% of benign mixed tumors undergo malignant transformation
untreated for an extended period.
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ULCERATIVE CONDITIONS
STEVENS-JOHNSON SYNDROME –a SEVERE bullous form of ERYTHEMA MULTIFORME
where systemic symptoms are severe, and lesions are extensive, involving multiple body areas
(especially mucous membranes). SJS is characterized by the acute onset of fever, and
eruptive, ulcerative lesion on the skin, oral mucosa, and eyes. Frequently, genitalia, lungs,
and joints are affected, and it can be fatal. Blindness can occur due to a secondary infection.
• Clinical Features: typical “BULL’S-EYE-SHAPED” LESIONS with the classical triad of eye
lesions, genital lesions, & stomatitis. The lesions are severe and often vesicular or bullous,
with hemorrhage after denudation.
• Treatment: IV fluids, systemic steroids, palliative rinses and antibiotics.
ERYTHEMA MULTIFORME-allergic hypersensitivity reaction in response to MEDICATIONS

(sulfonamides, penicillins, barbiturates, & phenytoin), infections, or illness. Associated
infections include herpes simplex & mycoplasma infections. The exact cause is unknown, but is
believed to involve DAMAGED SKIN BLOOD VESSELS with subsequent damage to skin
tissues.
EM occurs mainly in children and young adults, and its diagnosis is based on the classic target
OR “BULL’S-EYE-SHAPED” SKIN LESION that appears as a central lesion surrounded by
concentric rings of pallor and redness over the dorsal (top) of the hands and forearms.
ERYTHEMA MULTIFORME
• Low-grade fever, general malaise, and headache usually precede the lesions by 4-7 days.
• Oral lesions appear as red macules, papules, or vesicles that may become eroded and
painful, covered by a yellowish-white membrane after rupturing.
• Treatment: topical palliative rinses and sometimes low-dose systemic steroids.
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RECURRENT APHTHOUS ULCERS (ULCERATIVE/APHTHOUS STOMATITIS “CANKER

SORES”) –may be associated with STRESS, a bacterial infection, trauma (self-inflicted, oral
surgery procedures, routine dental procedures), endocrine conditions (menstrual cycle), allergic
factors (certain foods or drugs), immunologic abnormalities, iron, vitamin B, or folic acid
deficiencies. Cause is unknown, but they may be caused by an autoimmune reaction.
1. Recurrent Aphthous Minor (Minor Aphthous Ulcer)-the MOST COMMON form (“canker
sore”). Occurs more often in women, starting as a single or multiple superficial erosion
covered by a gray membrane (1-5 lesions). Looks like an erythematous halo with yellow-
grayish color with a red border). The lesion can be VERY PAINFUL, and varies from 2-10mm
in diameter. Generally last for 7-14 days, and heal gradually with LITTLE OR NO SCARRING.
Occurs on cheeks, lips, tongue, roof of mouth.
2. Recurrent Aphthous Major (Major Aphthous Ulcer) large, usually > 10mm, VERY
PAINFUL ulcers that occur frequently. Patients usually get more than one ulcer at a time.
Unlike minor aphthous ulcers, major aphthous ulcers can last up to 6 weeks and LEAVE A
SCARE UPON HEALING. Occurs on non-keratinizing tissue (LIPS, TONGUE, CHEEKS),
but their border can extend onto keratinized tissue.
3. Recurrent Herpetiform Ulcerations-the MOST SEVERE aphthous ulcer, characterized by

crops of multiple, small, shallow ulcers, often in cluster of up to 100 (1-3mm lesions), and may
occur in any area of the oral cavity. These lesions are present almost continuously for 1-3
years, with relatively short remissions. More common in adult FEMALES, and usually heal
within a month and DO NOT LEAVE SCARRING.
MAJOR & MINOR APHTHOUS ULCERS (CANKER SORES)

ULCERATIVE/APHTHOUS STOMATITIS
*Exact cause is unknown, but citrus, stress, allergies, immune reactions, and B12, iron, zinc,
and folic acid deficiencies may contribute (manifestation of Behcet’s Disease & Crohn’s
Disease)
Some Treatments: Non-alcoholic mouthwash, steroids.
Important: vesicular lesions (vesicles) DO NOT PRECEDE the formation of these ulcers.
This is a distinctive diagnostic feature. When an ulcer heals, the epithelium that will eventually
cover the defect is derived from intact epithelium at the ulcer margin.
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ACTINOMYCOSIS – a subacute-to-chronic bacterial infection with Actinomyces (A. israelii)

which are gram (+) filamentous bacteria that are normal inhabitants of the oral cavity and GI tract,
characterized by contiguous spread, suppurative & granulomatous inflammatory reaction,
and formation of multiple abscesses and sinus tracts that discharge SULFUR GRANULES.
This infection is most likely to cause CHRONIC SUPPURATIVE LESION about the jaws. The
most common clinical forms are cervicofacial actinomycosis (LUMPY JAW), thoracic, and
abdominal actinomycosis.
CERVICOFACIAL ACTINOMYCOSIS (“LUMPY JAW”) –the most common manifestation of

Actinomycosis. Infection typically occurs in patients with poor dental hygiene or after
surgery. In the initial stages, there is soft tissue swelling of the perimandibular area. Direct
extension into the adjacent tissues occurs over time, along with the development of fistulas that
discharge purulent material containing yellow sulfur granules (these granules are actually
colonies of bacteria).
HISTOPLASMOSIS – disease caused by the FUNGUS Histoplasma Capsulatum. The symptoms

vary greatly, but this disease primary affects the LUNGS. Sometimes affects other organs
(Disseminated Histoplasmosis). Histoplasmosis infection is usually asymptomatic, but may
produce a benign, mild pulmonary illness (the primary form of the disease).
• Oral Manifestations: nodular, ulcerative, or vegetative lesions on the buccal mucosa,

gingiva, tongue, palate, or lips usually covered by a non-specific indurated gray
membrane.
SYPHILIS – a sexually transmitted disease caused by a spirochete Treponema Pallidum

that occurs in 3 stages (primary, secondary, & tertiary). Syphilis is usually treated with a
PENICILLIN injection.
1. Primary Syphilis-the first symptom is a non-painful ulcer (“canker”) that appears 2-6
weeks after exposure/infection. Found on the body part exposed to the partner’s ulcer (i.e.
penis, vulva, or vagina). It can also develop on the cervix, tongue, lips, or other parts of
the body. The chancre disappears within a few weeks even without treatment. If not
treated during the primary stage, ~33% of people will progress to chronic stages.
PRIMARY SYPHILIS
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2. Secondary Syphilis-a highly infectious stage that occurs 6 weeks after non-treatment
of primary syphilis. Often marked by a skin rash characterized by brown “penny-sized”
sores. Widely disseminated spirochetes cause mucous membranes to exhibit a reddish-brown
maculopapular cutaneous rash and ulcers covered with a mucoid exudates (mucous patches).
Condylomata lata (elevated broad-based plaques) are also seen on the skin and mucosal
surfaces.
3. Tertiary Syphilis-occurs in infected people many years after non-treatment of secondary

syphilis. A GUMMA (a focal nodular mass) typifies this stage. Most commonly occurs on the
PALATE & TONGUE. Bacteria damages the heart, eyes, brain, nervous system, bones,
joints, or almost any other part of the body. In this late stage, untreated syphilis, although not
contagious, can cause serious heart abnormalities, mental disorders, blindness, other
neurologic problems, and death. Headache, stiff neck, and fever are symptoms of
neurosyphilis.
CONGENITAL SYPHILIS – caused by an infection by the spirochete bacteria Treponema

Pallidum during the fetal period. Expectant mothers with syphilis can transmit the disease
through the placenta to the unborn infant. Nearly 50% of all infants infected during gestation
die shortly before or after birth. The severity of congenital syphilis depends on the time the
organisms pass the placental barrier (protected up to the 16th week), the mother’s stage of
syphilis, and the fetus’s immunologic response. If treated by the 4th or 5th month of pregnancy,
95% show no manifestations. However, if untreated, fetal sepsis may result in stillbirth or visceral
& mucocutaneous manifestations.
CONGENITAL SYPHILIS & HUTCHINSON’S INCISORS
• Newborn Symptoms: irritability, blood discharge from nose, early rash (small blisters or flat
or bumpy rash on the face, palms, and soles), failure to thrive, later rash (copper-colored
vesicles on the palms and soles), saddle nose, frontal bossing, short and high maxilla.
• Infant/Child Symptoms: bone pain, joint swelling, abnormal teeth (HUTCHINSON’S

INCISORS) peg-shaped WIDELY SPACED permanent incisors, and notched at the end
with a centrally placed crescent-shaped deformity. Gray, mucous-like patches on the anus
and vulva (Condyloma lata), saber shins (bone abnormality of the lower leg), visual loss, CN
VIII nerve deafness & intestinal keratitis, and scarring of the skin around earlier lesions of the
mouth, genitalia, and anus (“rhagades”).
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• Manifestations of congenital syphilis: large frontal bone, Saddle nose, Hutchinson’s

teeth (very wide incisor crowns), & MULBERRY MOLARS (look like a mulberry). Not all people
with mulberry molars have syphilis. There is NO chancre in congenital syphilis.
PYOSTOMATITIS VEGETANS-rare oral lesions strongly associated with INFLAMMATORY

BOWEL DISEASE (IBD) and CROHN’S DISEASE.
• Oral Manifestations: lesions have a “SNAIL TRACK APPEARANCE” appearing as

multiple exophytic, yellow pustules that are tender, and have an erythematous base that
may cover the gingiva and buccal and vestibular mucosa.
• Treatment: incisal biopsy and refer to GI physician to treat the underling GI condition.
• Histology: intraepithelial clefting and acantholysis. Accumulation of eosinophils within

the spinous layer (intraepithelial abscesses).
PYOSTOMATITIS VEGETANS
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VESICULO-BULLOUS DISEASES
HERPES SIMPLEX VIRUS – always a vesicle (small virus filled with fluid) that breaks and the
crust forms due to dried fibrin. Related to viruses that cause Mononucleosis, Chickenpox, and
Shingles (not Mumps). HSV is one of the most common viral diseases of man.
HERPES SIMPLEX VIRUS TYPE 1 – oral herpes (affects outside of lips, face, skin, & oral
mucosa) TRANSMITTED BY DIRECT CONTACT. HSV-1 includes herpetic gingivostomatitis
(primary & secondary, and herpes labialis). It is labial & intra-oral herpes that are groups of
small ulcerations in the hard palate, outside of lips, gingiva, or hands and fingers.
• HSV Treatment: “SUPPORTIVE” focused on relieving the acute symptoms so that fluid
and nutritional intake can be maintained. Treatment involves analgesics, topical anesthetics
before eating, maintaining electrolyte balance, and anti-viral agents. NO CORTICOSTEROIDS
(contraindicated)!
PRIMARY HERPETIC GINGIVOSTOMATITIS (Acute Herpetic Gingivostomatitis)-the

primary herpes infection (HSV-1) that mainly affects YOUNG CHILDREN (under age 5), but
may also affect young adults (15-25yrs). It usually occurs in a child who has not had any
contact with HSV-1, and who thus has no neutralizing antibodies. Nearly all primary infections
are of the sub-clinical type that may only have flu-like symptoms, with 1-2 mild sores in the
mouth that go unnoticed by parents. In other children, the primary infection may be manifested
by acute symptoms (acute herpetic gingivostomatitis) these prodromal symptoms are (fever,
malaise, irritability, headache, dysphagia, vomiting, cervical lymphadenopathy) 1-2 days
prior to local lesions. Then, fiery red gingival tissues and small yellowish vesicles form that
rupture quickly, causing painful shallow, round, discrete ulcers with an erythematous (red) halo
on the FREE & ATTACHED MUCOSA. Thus, the primary HSV-1 infection ranges from sub-
clinical (asymptomatic) to severe systemic infections. Dehydration is the most serious
potential problem due to the child not wanting to eat or drink because of the pain. A generalized
marginal gingivitis may precede the ulcers.
ACUTE HERPETIC GINGIVOSTOMATITIS
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PRIMARY HERPETIC GINGIVOSTOMATITIS most commonly occurs in CHILDREN &

YOUNG ADULTS. Patients develop FEVER, irritability, regional lymphadenopathy, and
headache. Within days, the gingiva is intensely inflamed. Any part of the oral mucosa and lips
may become involved. Vesicles then form and rupture shortly later to leave shallow VERY
PAINFUL ulcers covered with a GRAY MEMBRANE and surrounded by a RED HALO. Ulcers
resolve on their own in 7-14 days.
• Treatment: fluid intake, good oral hygiene, and gentle debridement of the mouth. In
healthy individuals, the lesions heal in 7-14 days, and the ulcers heal WITHOUT
SCARRING.
• After recovery from primary HSV, the virus is not cleared from the body, but lies dormant
in a non-replicating state in the sensory nervous system (trigeminal ganglion).
Periodically, latency reactivates and allows the virus to return to the skin or mucous
membranes, where it causes a recurrent infection.
• Primary herpes occurs only in YOUNG PATIENTS (baby, children, adolescents).

Fever, malaise, pain, or could be CHICKENPOX (varicella zoster virus) in a 6yr old child.
Multiple vesicles, sick for one week.
• AFTER the initial primary attack during early childhood, HSV-1 remains inactive in the
TRIGEMINAL GANGLION (sensory nerve ganglia), but often reappears as the familiar
“cold sore” on the OUTSIDE of the lips (“Recurrent Herpes Labialis”). Emotional stress,
trauma, and excessive sun exposure may cause recurrent herpetic lip lesions. Acyclovir
5% ointment (Zovirax) can successfully reduce the duration and severity of these
lip sores.
SECONDARY (RECURRENT) HERPETIC STOMATITIS-generally occurs in ADULTS, triggered

by trauma, fatigue, RTI (respiratory tract infection), stress, allergy, or UV exposure that causes
the release/reactivation of the latent HSV-1 virus. This reactivation causes a recurrent infection
(i.e. cold sores) on the lips (that is bound to periosteum), hard palate, attached gingiva, and
alveolar ridge. Site-specificity is a characteristic manifestation.
• Recurrent Herpes Simplex Virus-COLD SORES on the lips are the most common
manifestation of infection. Some factors often associated with a recurrent outbreak are
sunburn, fatigue, emotional upset, trauma, upper respiratory tract infection, or
menstruation. Often one day before the vesicles form, tingling or itching of the skin or
mucosa occurs. Vesicles ulcerate and resolve just like in primary herpes.
• Remains LOCALIZED on the lower lip or inside the mouth. Lasts about 2 weeks then
heals by itself, but recurrent herpes virus always lays dormant in the trigeminal nerve
ganglion. May or may not have fever, malaise. May present with vesicles in hard palate.
HERPES LABIALIS (Fever Blisters/Cold Sores)-extremely common HSV-1 disease.

Characterized by an eruption of small, usually PAINFULL blisters on the skin of the lips,
mouth, gingiva, or skin around the mouth. The reason most patients suffering from Recurrent
Herpes Labialis rarely give a history of having had acute herpetic gingivostomatitis is the primary
infection was sub-clinical. HSV-1 lesions (cold sores) are found more forward in the mouth
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(tongue, gingiva, buccal mucosa) appearing as vesicles (small, clear, ulcerated, and crusty
blisters) around the mouth and lips.
HERPES LABIALIS (COLD SORES/FEVER BLISTERS) HSV-1
Histological Features: cytopathic effect (CPE) takes the form of BALLOONING

DEGENERATION of epithelial cells with loss of cohesion to adjacent cells. The nuclei are often
multiple, with margination of the chromatin around the intra-nuclear inclusions called Lipschultz
Bodies. These changes are seen in Tzanck smear scrapings taken from an unroofed vesicle.
HERPES SIMPLEX VIRUS TYPE 2 (“HERPES GENITALIS” OR “GENITAL HERPES”)–

transmitted via SEXUAL CONTACT, and affects the mucosa of the genitalia and anal regions,
but may also occur in mouth. Not as common as HSV1. “Genital Herpes” may have serious
consequences in pregnant women because the virus can be transmitted to the infant during
vaginal delivery, and can damage the infant’s CNS and/or eyes.
HERPES SIMPLEX VIRUS TYPE 3 (HSV-3) –caused by Herpes VARICELLA-ZOSTER virus

(DOES NOT CROSS THE MIDLINE). Produces recurrent herpes (adult shingles/herpes zoster),
& chickenpox (primary herpes). Occurs after activation of varicella virus, the affected skin has
VERY PAINFULL ulcerated redicule vesicles, and the lesion follows the path of the trigeminal
nerve. May occur in an elderly patient with a history of leukemia (compromised immune system).
VARICELLA VIRUS – can cause Herpes Zoster lesions along sensory nerve roots in later life. It
is a member of the herpes virus group that causes chickenpox (varicella) & shingles (herpes
zoster). Varicella virus is highly contagious and may be spread by direct contact or droplets.
The histology of chickenpox and shingles shows the same cytopathic effect as herpes simplex.
• Chickenpox-primarily a disease of CHILDREN that peaks at school-age in winter and

spring, characterized by the appearance on the skin and mucous membranes of
successive crops of typical pruritic vesicular lesions that break easily and scab.
Usually accompanied by mild constitutional symptoms (fever, malaise), and is very
contagious 1 day before the rash’s onset and until all of the vesicles have crusted.
It is relatively benign in children, but adult infection may be complicated by pneumonia
and encephalitis. ZIG (Zoster Immune Globulin) reaches morbidity in high-risk children.
• Shingles (Herpes Zoster)-caused by the reactivation of a LATENT varicella-zoster

virus that may have remained in the body from a childhood chickenpox. The virus
reaches sensory ganglia of the spinal and cranial nerves, producing an inflammatory
response. Characterized by painful vesicles on the skin or mucosal surfaces along
the distribution of the sensory nerve.
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• Shingles (Herpes Zoster) Example: 16-yr old male with fever & malaise, DOES NOT
CROSS THE MIDLINE, and is very painful. Can also be in a 65-year old male with a
history of leukemia (weak immune system) who had chickenpox as a child. The
affected skin shows vesicles and lesions follow the path of the nerve due to activation
of varicella virus.
HERPES SIMPLEX VIRUS TYPE 4 –caused by EPSTEIN-BARR VIRUS (EBV) a member of the
herpes virus group that causes Infectious Mononucleosis (Kissing Disease), Hairy
leukoplakia, Chronic Fatigue Syndrome, and two cancers (Burkitt’s Lymphoma &
Nasopharyngeal Carcinoma).
1. HAIRY LEUKOPLAKIA-this is NOT hairy tongue. Appears 99% of time in HIV+ patients.
ALWAYS white furry lesions on LATERAL tongue borders (bilateral) caused by
EPSTEIN-BARR VIRUS. Can usually diagnose without biopsy. Anti-viral medication
removes the lesion, but it reappears when patients stops taking medications. Only treat if the
patient requests with anti-viral medication. Presents as a WHITE extensive area in the
LATERAL border of the tongue, present for 4 months, asymptomatic. The surface lesion is
irregular, bluish areas on the gingiva, candida, and recurrent herpes infection may coexist.
99% occurs in HIV+ patients, so patient should get an HIV test.
2. INFECTIOUS MONONUCLEOSIS (HSV-4)-no specific oral manifestations, but secondary

lesions occur and neck swellings, which are also characteristic of Hodgkin’s Disease and
Tuberculosis.
BURKITT’S LYMPHOMA (HSV-4)-cancer caused by EPSTEIN-BARR VIRUS. High-grade Non-

Hodgkin’s Lymphoma (cancer)/neoplasm with a viral etiology endemic in AFRICA, but occurs
sporadically in North America. There are significant differences between the African & Non-
African forms, but BOTH are histologically identical. One manifests most often as a large
osteolytic jaw lesion (African Form), the other as an abdominal mass (Non-African Form).
• Jaw lesions usually present as expanding intra-oral masses with mobility of the involved
teeth. Radiographically: “MOTH-EATEN” appearance with poorly marginated bone
destruction.
• Non-African Burkitt’s Lymphoma patients are generally older (ages 9-12yrs), with no
gender predilection. Presents most often as an ABDOMINAL MASS involving mesenteric
lymph nodes or Peyer Patches in the ileocecal region, often with intestinal obstruction.
Involvement of the gonads, retroperitoneum, and other viscera are less common.
• Burkitt’s lymphoma is the FIRST HUMAN CANCER WITH STRONG EVIDENCE OF

VIRAL ETIOLOGY. Epstein-Barr virus (herpes-type virus) as these patients have high
titers of antibodies against EBV. Important: Epstein-Barr is also associated with
infectious mononucleosis, & orally hairy leukoplakia.
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BURKITT’S LYMPHOMA
African Burkitt’s Lymphoma (African Jaw Lymphoma)-affects younger patients (age 3-8yrs)
than the non-African form. Affects males more than females (2:1), and typically involves the
mandible, maxilla, & abdomen. Extra-nodal involvement of the retroperitoneum, kidneys, liver,
ovaries, and endocrine glands may be affected.
HERPES SIMPLEX VIRUS TYPE 5 – cytomegalovirus that affects salivary glands.
HERPES SIMPLEX VIRUS TYPE 8–associated with Kaposi’s Sarcoma-AIDS/HIV. Kaposi

Sarcoma: 34-year old male with AIDS, common on palate. Can have Kaposi Sarcoma without
AIDS, but in U.S. it is usually with AIDS. It’s a superficial cancer on the skin, multiple, made
of blood vessels, & is NEGATIVE to pressure test (so don’t confuse with Hemangioma
which is pressure test positive +). Kaposi’s Sarcoma is very common on the PALATE.
Mostly associated with HIV, but can have Kaposi’s sarcoma even without AIDS. (-) to pressure
test. RED LESIONS on the hard palate.
KAPOSI’S SARCOMA–an oral manifestation most commonly associated with AIDS. A

MALIGNANT vascular NEOPLASM originating in the skin, characterized by abnormal vascular
proliferation (cancer of the lining of the blood vessels). It occurs on multiple sites, especially
lower extremities. The initial lesions are small, red papules that enlarge and fuse to form purple-
to-brown spongy nodules. It spreads to lymph nodes and internal organs.
• HARD PALATE is the most common intra-oral location of KAPOSI’S SARCOMA, followed
by the gingiva and buccal mucosa. Oral Findings: non-pigmented, violet, or brown-red
plaques or tumors of the tongue, palate, and gingiva.
• Important: AIDS is caused by an RNA retrovirus (HIV = HTLV-III) acquired by sexual

contact (homosexual and heterosexual), or contaminated blood products.
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KAPOSI’S SARCOMA
TESTS TO DIAGNOSE HERPETIC LESIONS:

1. Tzanck Smear-a cytologic examination of fluid harvested from an unopened vesicle
stained with giemsa, and viewed by the light microscope. Pathologist looks for
LIPSHULTZ BODIES (epithelial cells with intra-nuclear inclusions).
2. Fluorescent Staining-cells show (+) fluorescence when stained with fluorescent labeled
HSV immune serum and globulin. Used to distinguish between herpes zoster & herpes
simplex.
3. Isolation in Tissue Culture
4. Antibody Titers (Anti-HSV Ab Titers)-a test for complement fixing or neutralizing

antibody in acute and convalescent sera, and on tissue sections (begins in 1 week, and
peaks at 3 weeks).
5. Biopsy-shows intra-epithelial cleft covered by exudates of fibrin and PMN leukocyte.

The epithelium exhibits degenerative cells that include bizarre giant cells, and cells with
displaced chromatin with perinuclear halos and inclusions. *Arthrogram is NOT a test to
diagnose herpetic lesions.
HERPANGINA–an acute infectious disease (stomatitis/mouth inflammation) affecting YOUNG

CHILDREN caused by a Group A Coxsackie Virus. It is differentiated clinically from HSV-1 (cold
sore virus) as herpangina oral ulcerations/vesicles usually occur in the BACK OF THE THROAT
around the tonsils and posterior palate. Herpangina may also appear on the tongue.
• Clinical Features: are mild and of short duration compared to HSV-1. Herpangina begins
with a sore throat, fever, headache, and sometimes vomiting & abdominal pain. Papules
or vesicles soon form in the pharynx, and evolve into shallow ulcers that heal spontaneously.
Herpangina usually runs its course in less than 1 week. Treatment: PALLIATIVE.
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HERPANGINA (GROUP A COXSACKIE VIRUS)
HAND, FOOT AND MOUTH DISEASE (HFMD)-COXSACKIE VIRAL INFECTION (usually

Coxsackie A) that usually affects infants and children. Produces red-erythematous
lesions/macules/vesicles areas in the mouth, foot, & hands. Oral lesions/vesicles appear on the
buccal mucosa, tongue, gingiva, & lips.
• Patient has fever, malaise, vomiting, fatigue (may be confused with a cold). HFMD is self-
limiting, disappearing by itself in < 15 days, & does not return. Erythematous macules develop
central vesicles. A very mild disease that is often not diagnosed. No treatment, but symptoms
may be eased with analgesics.
BENIGN MUCOUS MEMBRANE PEMPIGOID (BMMP)–a chronic self-limiting mucocutaneous

autoimmune disease, usually limited to oral and ocular mucous membranes (conjunctival
involvement may cause blindness). Usually effects women over age 50yrs. More common in the
oral cavity, but much less severe (better prognosis) than Pemphigus. Occurs more often than
realized due to improper diagnosis.
• A vesiculobullous disease where auto-antibodies act against basement membrane

components (below epithelium = sub epithelial vesicle), between epithelium & C.T. so
destruction is below the epithelium. Usually shows nice epithelium since the epithelium is
complete & C.T. is separated (not seen in Pemphigus).
• Oral lesions usually present as a “desquamative gingivitis” in which vesicles form, rupture,
and leave gingival erosions. Found in all mucous membranes, but is less severe than
Pemphigus.
• Treatment: Biopsy and systemic STEROID therapy. PAINFUL ORAL ULCERS.
Important: MAJOR histological difference between BMMP & Pemphigus Vulgaris is BMMP
vesicles are sub epidermal with no acantholysis, while with Pemphigus Vulgaris, there is
acantholysis and supra-basilar vesicle.
255
PEMPHIGUS VULGARIS – a chronic RARE SKIN DISEASE characterized by the formation of

vesicles & bullae produced by dyhesion (acantholysis) of epidermal cells due to an autoimmune
mechanism where antibodies attack the intracellular junction of epithelium. Usually occurs after
age 30yrs (usually ages 30-50yrs), and occurs more frequently in JEWISH people.
• Oral lesions are often the FIRST MANIFESTATION. Intact bullae are rarely seen in the oral
cavity, rather, large areas of ulceration and erosions covered by a 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 apparently normal epithelium may be separated
at the basal layer and RUBBED OFF when pressed with a sliding motion. Pemphigus is
often fatal without treatment, which includes high-dose systemic steroids or
chemotherapy (Methotrexate).
PEMPHIGUS VULGARIS
• Histologic Features: vesicles and bullae are formed entirely intra-epithelially, just ABOVE the
basal layer of cells (suprabasilar vesicles). There is intercellular edema and loss of
intercellular bridges with loss of cohesiveness (acantholysis or dyhesion). Clumps of cells
are often found floating free in the vesicle space (Tzanck cells).
• Pemphigus Vulgaris is the most common form, and is more severe than Pemphigoid
(BMMP). With Pemphigus, the patient has auto-antibodies produced against epidermal cell
surface glycoprotein (a component of desmosomes that attaches epithelial cells together)
causing painful oral ulcers. More common in older females (> 50yrs). Intraepithelial vesicle.
A very bad disease whose only treatment is STEROIDS. Patient has vesicles on the skin.
GINGIVA is red, inflamed and is the most common location in mouth.
• MUST DO BIOPSY TO DIAGNOSE using 2 small portions of tissue (one in a vile, the other
goes into a vile of Michel solution (the fixative to do the immunofluorescence). If bullae is
intraepithelial then its Pemphigus Vulgaris. If bullae are between epithelial and C.T. it is
256
Pemphigoid. Produce Ab against desmosomes (attach one epithelial cell to another), so

desmosomes are destroyed and the epithelium is broken causing gingival ulcerations.
Tissue in the “Michel solution” shows yellowish fluorescence areas show where the antibodies
are against desmosomes.
RUBELLA VIRUS–causes German Measles (Rubella). Characteristic RASH (flat, pink spots on
the face that spreads to other body parts). Oral manifestations may include swollen and
congested tonsils, and red macules.
HEPATITIS A (VIRAL OR INFECTIOUS HEPATITIS) –caused by an RNA Enterovirus usually

transmitted by the FECAL-ORAL ROUTE. An infectious disease of the LIVER that most often
occurs in young adults and is prevalent in areas with inadequate sewerage. SHELLFISH from
contaminated waters is also a prime source. Initial symptoms (fever, abdominal pain, nausea,
then jaundice) appear after an incubation period of 3-6 weeks. Vaccination exists.
• Damage to liver cells causes increased serum levels of enzymes like transaminases,
normally active in liver cells. The detection of the increased serum levels of transaminases
helps diagnose the disease. In most Hepatitis A cases, the infection is self-limiting, and
recovery occurs within 4 months.
HEPATITIS B (“SERUM HEPATITIS”) – an infectious LIVER DISEASE caused by a DNA virus

that produces liver inflammation and necrosis. Main method of transmission is exposure to
contaminated blood or serum (but can be transmitted sexually or via blood transfusions). There
is a high rate of transmission among drug addicts who may use contaminated needles.
Vaccination exists.
• Signs & Symptoms: similar to Hepatitis A (fever, abdominal pain, nausea), but it has a longer
incubation period of 2-3 months. Symptoms develop slower, but last longer. Most patients
fully recover, but some develop chronic liver disease.
• Hepatitis B transmission is a MAJOR CONCERN to the dental profession, which have at

least 3x higher risk than the general population to acquire this virus. Thus, ALWAYS USE
UNIVERSAL PRECAUTIONS. Hepatitis D is found ONLY in patients with acute or chronic
episodes of Hepatitis B.
• Hepatitis B vaccine is recommended for all health care personnel. A series of 3 doses is
required (the 2nd and 3rd doses are given at 1 & 6 months after the 1st dose. The injection is
given IM (in the deltoid muscle). Important: hepatitis B vaccine also treats hepatitis D.
• The presence of SURFACE ANTIGEN (A or B) in a patient’s serum indicates the patient is

potentially infected with Hepatitis (“carrier state”). Hepatitis viruses are HIGHLY HEAT
RESISTANT (even more than AIDS virus). However, autoclaving properly kills them.
HEPATITIS C-an infectious liver disease that can cause liver scarring and cirrhosis. Spread
mainly via blood-to-blood contact associated with IV drug use, poorly sterilized medical
equipment, and transfusions. Hepatitis C virus persists in the liver and can be treated with
medication (Peginterferon and Ribavirin). There is no vaccine, and liver transplantation may be
required for severely damaged livers.
257
IMPORTANT DIAGNOSTIC TERMS:

• BIOPSY – the MOST RELIABLE technique to diagnose soft tissue lesions. Scalpel is the
instrument of choice since it cleanly removes tissues without dehydrating them as cautery or
a high-frequency cutting knife may. FORMALIN (10%) is the fixative of choice. The rationale
for surgical removal and biopsy of a large periapical lesion suspected to be of inflammatory
origin is that a clinical diagnosis can be confirmed microscopically. Biopsy is the only way
to distinguish between a granuloma and a cyst.
• EXCISIONAL BIOPSY –involves TOTAL EXCISION of a small lesion for microscopic study.
This is preferred if the lesion size is such that it may be removed along with a margin of normal
tissue, and the wound can be closed primarily (ex: a 1cm exophytic mass-a lesion that grows
outward from an epithelial surface on the cheek).
• INCISIONAL BIOPSY (DIAGNOSTIC BIOPSY)–removes only a SMALL SECTION of tissue

for examination. Done when lesions are too large to excise initially without having established
a diagnosis, or are of such a nature that excision would be inadvisable.
258
RADIOGRAPHIC PATHOLOGY
MOST TO LEAST COMMON LESIONS
1. PERIAPICAL (RADICULAR) ABSCESS—well-defined ovoid-shaped radiolucency at root

apex.
2. DENTIGEROUS CYST—large, well-defined unilocular radiolucency associated with

unerupted molar clinical crown.
259
3. INCISIVE CANAL CYST (Nasopalatine Duct Cyst)-heart-shaped well-circumscribed

radiolucency of midline of hard palate:
4. LATERAL PERIODONTAL CYST-well circumscribed unilocular radiolucency lateral to the

roots of the premolars (between roots of lower premolars). Teeth are usually VITAL.
260
5. RESIDUAL CYST-large, round radiolucency of mandible in the area of a previously

extracted molar.
6. TRAUMATIC BONE CYST (Aneurysmal Bone Cyst)-well-defined radiolucent lesion with

projections between the roots of the vital premolar and molar teeth producing a SCALLOPED
appearance.
261
7. AMELOBLASTOMA-large, multilocular radiolucent lesion of the posterior body and ramus

of the mandible.
8. ODONTOGENIC KERATOCYST (OKC)-large well-delineated radiolucent lesion of the body

of the mandible. HIGH RECURRENCE RATE.
262
9. CENTRAL GIANT CELL GRANULOMA-large radiolucent lesion with scalloped borders of

the body of the mandible—root resorption often accompanies. Almost exclusively in mandible.
Common in women 20-30 years old.
10. OSTEOMYELITIS-poor defined radiolucenies of the body and ramus of mandible.
263
11. PERIAPICAL CEMNTO-OSSEOUS DYSPLASIA-a well circumscribed mixed radiolucent and

radiopaque lesions at the apical area of the mandibular anteriors. TEETH ARE VITAL.
Common in middle-aged African American women.
12. TORI-bilateral mandibular tori superimposed on the canine roots appearing as round, smooth-
surfaced radiopaque structures on mandibular lingual alveolar ridge bilaterally in premolar
areas:
13. ROOT TIP: radiopaque area of the alveolar ridge with the structural appearance of the portion
of a tooth root. A thin periodontal ligament may be visible:
264
14. CONDENSING OSTEITIS-localized area of increased radiodensity of alveolar bone from the
apical portion of the root into the underlying bone forming a bulbous appearing as a radio-
dense mass. Faint outline of the root is visible within the bone showing the increased radio-
density.
15. OSTEOSCLEROSIS: localized irregular-shaped area of bone with increased radiodensity in

the area of a missing tooth.
16. COMPOUND ODONTOMA-dome shaped radio dense mass above the crown of an unerupted
tooth composed of numerous small tooth-like structures, surrounded by a radiolucent zone.
265
17. COMPLEX ODONTOMA-large, irregular shaped radiodense mass preventing tooth eruption.
The radiodensity of the mass resembles the adjacent teeth.
STUDY HARD
TEST WITH CONFIDENCE
www.dentin.co
266

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DENTIN INBDE STUDY GUIDE (2020-2021) www.dentin.

INTEGRATED NATIONAL BOARD DENTAL

INBDE CONTENT INBDE

INTRODUCTION: THE DENTIN INBDE STUDY METHOD:

INBDE PATIENT BOX

BACKGROUND AND/OR PATIENT HISTORY

Medications: Warfarin (Coumadin)

CURRENT CLINICAL FINDINGS

White coating on tongue that wipes off.

Tongue ............................................................................................................................................ 1-26

DENTAL ANATOMY AND OCCLUSION

Dental Anatomy and Occlusion ................................................................................................ 286-441

MICROBIOLOGY AND PATHOLOGY

Biology of Microorganisms and Disease .................................................................................. 651-895

Pigmented Lesions ............................................................................................................... 1009-1017

BIOCHEMISTRY, PHYSIOLOGY, AND NUTRITION

Biochemistry, Physiology, and Nutrition ............................................................................... 1065-1303

Pharmacokinetics ................................................................................................................. 1304-1341

PROVISION OF DENTAL CARE

Periodontics .......................................................................................................................... 1540-1598

PROFESSIONAL ETHICS, PATIENT MANAGEMENT, OSHA

2. EXTRINSIC TONGUE MUSCLES are named based on their ORIGIN.

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

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

18. ATROPHY (areas of erythema) of FILLIFORM PAPILLAE may be due to GEOGRAPHIC

27. A calcification or obstruction to WHARTON’S DUCT can result in SIALOLITHIASIS (Salivary

35. STENSONS’S DUCT drains the PAROTID GLAND.

47. WHARTON’S DUCT drains the SUBMANDIBULAR GLANDS.

48. Most SALIVARY GLAND TUMORS originate from DUCTS.

51. The SMALLEST salivary gland is the SUBLINGUAL GLAND.

SOFT AND HARD PALATES, THROAT AND SINUSES

64. Rapidly adapting encapsulated MECHANORECEPTORS of LIGHT PRESSURE,

67. The LARYNX is evaluated by being moved gently side-to-side by BIMANUAL

68. The PARANASAL SINUSES drain through the NASAL MEATUSES.

73. MAXILLARY SINUSITIS may often accompany a TOOTHACHE.

75. All muscles of mastication are innervated by TRIGEMINAL NERVE (MANDIBULAR

80. The GREATEST MASTICATORY FORCE is produced by the MASSETER MUSCLE.

84. Mandibular movements produced by the LATERAL PTERYGOIDS are OPENING

MUSCLES OF FACIAL EXPRESSION

100. The MOUTH FLOOR is formed mainly by the MYLOHYOID MUSCLE.

103. THYROHYOID, OMOHYOID, STERNOHYOID, & STERNOTHYROID (TOSS), are all

NECK MUSCLES AND NECK TRIANGLES

108. The neck’s ANTERIOR TRIANGLE consists of the CAROTID, SUBMANDIBULAR,

CRANIAL NERVES AND BLOOD VESSELS

125. The ABDUCENS NERVE’S NUCLEUS is located in the PONS.

126. Cranial nerves III (OCULOMOTOR), IV (TROCHLEAR), and VI (ABDUCENS) innervate

140. GLOSSOPHARYNGEAL NERVE provides TASTE sensation to the TONGUE’S

150. The HYPOGLOSSAL NERVE (CN-XII) is responsible for TONGUE MOVEMENT.

156. BLOOD PRESSURE is HIGHEST in ARTERIES and LOWEST in VEINS.

166. Lymph node enlargement due to infection, inflammation, or cancer is

168. The SIMPLEST LYMPHATIC TISSUE presenting clinically as a MUCOSA SWELLING

169. LYMPHOID TISSUE comprise lymph nodes, is COMPOSED OF RETICULAR C.T.,

177. LYMPHATIC CAPILLARIES are MORE PERMEABLE than BLOOD CAPILLARIES.

179. The LYMPHATIC SYSTEM drains into the VENOUS SYSTEM.

182. LYMPHOCYTES become IMMUNOCOMPETENT due to THYMIC HORMONES.

187. The THYMUS is located in the SUPERIOR MEDIASTINUM.

188. Lymphocytes that DO NOT reach the thymus become B-CELLS.

OSTEOLOGY AND TEMPEROMANDIBULAR JOINT

190. During TRANSLATION (SLIDING), the disk

191. During ROTATION (HINGE), the mandible is ELEVATED and DEPRESSED.

193. The TEMPEROMANDIBULAR JOINT (TMJ) has DUAL

194. SENSORY SUPPLY:V3(Post: Auriculotemporal branch of V3 and Ant: Deep temporal

195. MAXIMUM BLOOD SUPPLY is found in RETRODISCAL PAD of the TMJ’s