Test 1 Flashcards
(131 cards)
1
Q
When do primary teeth begin formation?
A
6 weeks in utero
2
Q
When does mineralization begin?
A
4 months in utero
3
Q
What germ layers does the teeth formed by?
A
Ectoderm and mesoderm
4
Q
What does ectoderm and mesoderm turn into?
A
Ectoderm: Enamel
Mesoderm: Dentin and pulp
5
Q
What is the tooth germ life cycle?
A
Growth, calcification, eruption, attrition
6
Q
What are the stages of growth?
A
Initiation, proliferation, histodifferentiation, morphodifferentiation, apposition.
7
Q
What is initiation also called? What happens during this stage?
A
Bud stage. Epithelial thickening at 20 sites. They will become primary teeth.
8
Q
What is determined in the initiation, or bud stage?
A
Tooth number! Lack of initiation or arrest results in congenital tooth absence. Continued budding of enamel organ leads to supernumerary teeth.
9
Q
What is proliferation also called? What happens during this stage?
A
Cap stage! Further cell multiplication, creating a cap formation with a dental papilla and dental follicle.
10
Q
Dental Organ
A
The cap-like formation. Precursor of enamel.
11
Q
Dental Papilla
A
Cell growth below and within the cap. Precursor of pulp and dentin.
12
Q
Dental Follicle
A
Mesenchyme around enamel organ and dental papilla. Precursor of cementum and PDL.
13
Q
What is determined in the proliferation or cap stage?
A
Tooth number! Missing tooth is a result of lack of initiation or arrest. Congenital tooth absence. An extra tooth can result from excessive cell proliferation. Epithelial rests may become a cyst and with further differentiation, an odontoma or supernumerary tooth depending on the degree of differentiation.
14
Q
What is stage does histodifferentiation occur in? What happens during histodifferentiation?
A
Bell stage! Epithelium continues to develop and differentiates into odontoblasts and ameloblasts (papilla). Marks the end of the proliferative stage. Cells no longer can proliferate. If there is abnormal development, you have problems with dentin and enamel.
15
Q
What stage does Morphodifferentiation occur? What happens?
A
Advanced Bell Stage! Continued growth of formative cells, that form the ultimate tooth shape.
16
Q
What do disturbances and aberrations in the advanced bell stage result in?
A
Abnormal size and shape of teeth including peg laterals, microdontia and macrodontia.
17
Q
What is Apposition?
A
The layer like deposition of non-vital extracellular tissue matrix secreted by the formative cells, ameloblasts and odontoblasts. Matrix creates definitive pattern and rate.
18
Q
Disturbance or local trauma during apposition can result in what?
A
If injured during enamel formation, it can interrupt or arrest matrix apposition. Enamel hypoplasia is most common and often found with premature infants. Dentin hypoplasia is less common and from severe systemic disturbances.
19
Q
What is calcification?
A
Follows matrix deposition and is the precipitation of inorganic calcium salts. Cusps and goes cervically.
20
Q
What can go wrong in calcification?
A
Sensitive and lengthy process. Disturbances may result in enamel hypocalcification. Interglobular dentin.
21
Q
How many years are needed for the calcification process?
A
4 years!
22
Q
What is the most favorable eruption sequence of primary teeth?
A
Central, lateral, 1st molar, canine, 2nd molar
23
Q
What is the 7 + 4 guideline?
A
From age 7 months, 4 teeth erupt every four months.
24
Q
When is the enamel of primary dentition completely formed?
A
12 months.
25
At what age should all primary teeth be erupted?
2-3 years.
26
At what age should all root structures be formed?
3 years.
27
Why should there idealy be spaces between primary dentition?
Successors are larger.
28
Does spacing ensure successors will erupt without crowding?
NO! But it may reduce crowding during transition from primary to mixed.
29
What are the two types of spacing?
Primate and leeway.
30
What is the primate space?
Space between the MX primary lateral and primary canine and a space between the MN primary canine and primary first molar.
31
Leeway Space
The combined MD widths of 1st, 2nd primary molars and primary canine compared to the corresponding combined MD widths of successor 1st, 2nd premolars and canine. MN is +1.7 mm per side. MX is +.9 mm per side. You can control the leeway space using space supervision to accomodate minor crowding.
32
Genetic factors in permanent tooth eruption?
Familial, gender, race.
33
Environmental factors in permanent tooth eruption?
Local interference (supernumerary tooth), low birth weight, premature birth, trauma.
34
Systemic factors in permanent tooth eruption?
Endocrine
35
What are the eruptive phases?
Pre-eruptive: Root formation begins, tooth moves from bony vault to oral cavity surface. Eruptive: prefunctional. Tooth in oral cavity without occlusal contact. Root length is 1/2-2/3. Eruptive functional: Occlusal contact. Dentition continually has movement.
36
What is the variation in timing that is within normal limits?
+/- 6 months. Mean age of eruption of permanent teeth does not correlate with physical development.
37
How long does it take for root completion for primary and permanent teeth?
Primary: 18 months post eruption. Permanent: 3 years post eruption.
38
How long is the duration of full eruption for a permanent tooth?
About 5 years.
39
At the time of clinical emergence about how much of the root is formed for a permanent tooth?
3/4.
40
How do you predict premolar tooth emergence?
Erupting premolars generally require 6 months to move through 1 mm of bone as measured on a bite wing.
41
How does bone loss from infection affect eruption?
Accelerates it.
42
What is dental age determined by?
Teeth erupted, resorption of primary roots, degree of successor root development.
43
In anterior dentition, how does premature tooth loss affect successor eruption?
Less than 3 years, delayed. More than 5 years, accelerated.
44
In posterior dentition, how does premature tooth loss affect successor eruption?
Less than 7 years, delayed. More than 5 years, accelerated.
45
Where do the resorption patterns occur?
MX incisors: Diagonal. MN incisors: horizontal. Molars: furcation
46
What is the most favorable eruption sequence of permanent teeth?
1. First molars
2. Centrals
3. Laterals.
4. MN canine and MX 1st premolar.
5. MX 2nd premolar and MN 1st premolar.
6. MN 2nd premolar and MX canine.
7. 2nd molars.
47
MN vs. MX canine eruption?
MN erupts before the premolars. MX erupts after the premolars.
48
Delayed Tooth Eruption DTE
Most common deviation in eruption. Biologic: eruption has not occurred even though there has been formation of 2/3 or more of the root. Chronologic: Characterized by the relationship to expected tooth eruption time. 2 standard deviations from the average. Scar tissue, supernumerary teeth, oral cleft, tumors, enamel pearls, ectopic eruption, eruption hematoma, etc.
49
Transposition
Permanent canine erupted in place of the lateral incisor.
50
Ankylosis
Interrupted eruption, possible space loss from tipped adjacent teeth. Etiology unknown. Possibly familial, common for more than 1 tooth. MN primary molars are the most common. Should exfoliate normally. Want to monitor and not extract as to not damage the successors.
51
Altered sequence
Minor eruption variation is normal. Variation less than 6 months between contralateral teeth is normal. Normal variation +/- 18 months.
52
Which tooth is most likely to become impacted?
Last tooth due to lack of remaining space. 3rd molars, then MX canine.
53
Which teeth most commonly erupt ectopically?
MX 1st permanent molars and MN lateral incisors.
54
What causes eruption with malposition?
Chronic extensive bone loss. Crowding and interference.
55
Eruption Sequestrum
No therapy required unless symptomatic.
56
Neonatal inclusion cysts
Developmental white soft tissue lesions. Asymptomatic and no treatment indicated. Will resolve in 3 mo. No gender predilection. Gingival/dental lamina, palatal
57
Gingival Cysts
Occur in up to 50% of neonates. Solitary or multiple discrete or clustered papules on alveoplar mucosa. Mostly on MX. Smooth, translucent to pearly white. 1-3 mm. Keratin filled remnants of dental lamina.
58
Epstein's Pearls
85% of neonates. Asymptomatic and resolve in first month. Keratin filled cysts that are possible remnants of epithelial tissue trapped in raphe during fetal development. Smooth pearly white pearl like lesion on median palatal raphe. Solitary or multiple discrete.
59
Bohn's Nodules
Same clinical findings as epstein pearls. Remnants of minor salivary gland tissue. Histologically different. Located away from palatal raphe and on the junction of hard and soft palate.
60
When do anomalies in number occur?
Initiation and proliferation.
61
When do anomalies in size/shape occur?
Morphodifferentiation
62
When do anomalies in structure occur?
Histodifferentiation, apposition, calcification (mineralization).
63
When do anomalies in color occur?
Histodifferentiation, apposition, calcification (mineralization)
64
What is the most prevalent craniofacial congenital malformation in humans?
Tooth agenesis! Hypodonita!
65
Hypodontia
1-6 teeth absent, not including 3rd molars
66
Oligodontia
More than 6 teeth missing, excluding 3rd molars.
67
Anodontia and Agenesis
Complete absence of teeth in 1 or both dentitions. Agenesis is in both.
68
What are the most common missing teeth?
Permanent: MN 2nd premolar, MX lateral incisor, MX 2nd premolar.
Primary: Incisors
If primary tooth doesn't develope, permanent tooth won't develop.
69
Sporadic Hypodontia
Common occurance. The missing tooth is the most distal of a given type. Can be environmental or genetic.
70
What are the oral conditions seen in Van der Woude Syndrome?
CL/CP. Lip pits. Adhesions between MX and MN. Taurodontism in 50%.
71
Ectodermal Dysplasia
Variable defects in morphogenesis of ectodermal derivatives includes: hypodontia, anodontia, conical or peg shaped anterior teeth, alveolar ridge deficiency, hypoplastic maxillae, anterior x-bite, decreased vertical dimension.
72
Odonto-ochyno-dermal dysplasia
ED syndrome. Dry hair, severe hypodontia, smooth tongue, nail dysplaisa, hyperhidrosis of palms/soles, hyperkeratosis.
73
Rieger Syndrome
Malformations in eye, umbilical and hypodontia. Affects both dentitions. MN 2nd premolars, then central incisors and MX 2nd premolars. Hyperplastic MX frena, peg shaped or conical inciors, microdontia, enamel hypoplasia, short roots, taurodontism, delayed eruption.
74
Holoprosencephaly
Midline cleavage of the embryonic forebrain. Most severe is cyclopia. Mildest is a single MX central incisor.
75
Solitary Median MX Control Incisor
Single central incisor. HPE will always have SMMCI but not all with SMMCI have HPE.
76
Achondroplastic Dwarfism
Lack of cartilage calcification leads to deficient growth of limbs. Micrognathia, dental crowding, hypodontia, delayed eruption.
77
Cleft lip and palate
Hypodonita in 80%! Increases with severity of cleft. Agenesis, dysmorphology (microdontia), supernumerary teeth. Most frequently missing: MX lateral incisors followed by MX and MN 2nd premolars.
78
Pierre Robin Sequence
Hypodontia, especially in the MN. Micrognathia, glossoptosis, CP.
79
When do disturbances cause hyperdontia?
Initiation and proliferation.
80
What are the two hyperdontia types?
Supplemental: Normal or typical anatomy.
Rudimentary: Dysmorphic anatomy.
81
Is hyperdontia more common in permanent or primary?
Permanent!
82
Where does hyperdontia most often occur?
MAXILLARY! Mesodens!
83
Where do multiple supernumeraries normally occur?
MN. Premolars.
84
Distomolar
Accessory fourth molar.
85
Paramolar
Posteror supernumerary lingual/buccal to molar.
86
What are the two syndromes with hyperdontia?
Apert and Cleidocranial dysplaisa.
87
Apert Syndrome
Hyperdontia! Delayed ectopic eruption. Narrow palate!
88
Cleidocranial Dysplasia
No clavicles. Multiple supernumerary teeth with delayed eruption and high palate.
89
What are the syndromes with both hyper and hypodontia?
Downs, crouzon, oral-facial-digital syndrome, type 1.
90
What is the most common variation in tooth size/shape/form?
Permanent MX lateral incisors and 2nd premolars.
91
What is twinning?
Either fusion or gemination. Need radiographic evaluation to distinguish.
92
Fusion vs. Gemination
Fusion: two roots, one crown.. Macrodontia from dentinal union of 2 developing teeth. Deficient number of teeth. separate or shared pulp chambers.
Gemination: one root, two crowns. Incomplete division. Bifid crown with one pulp chamber. Increased number of teeth.
93
What syndromes are associated with microdontia?
Hemifacial microsomia, downs, ED.
94
What syndromes are associated with macrodontia?
Facial hemihypertrophy, otodental syndrome.
95
Hemifacial microsomia
MICRODONTIA
96
Taurodontism
Constriction of CEJ and elongated pulp chamber with apically displaced pulp. HYPODONTIA associated. Elongated pulp chamber with short stunted roots. Failure of Hertwig's epithelial root sheath.
97
Amelogenesis Imperfecta
Type 1: hypoplastic (secretory defect)
Type 2: Hypomaturation (protein processing and crystalline maturation defect)
Type 3: Hypocalcified (mineralization defect)
Type 4: Hypomaturation, hypoplastic type with taurodontism.
98
Type 1 Amelogenesis Imperfecta
Lack of cell differentiation into ameloblasts during histodifferentiation. Hypoplastic type. Insufficient enamel quality, matrix imperfectly formed, but calcified. Smaller teeth. Thermal sensitivity. Hard, rough, pitted, thiner.
99
AI Type 2
Hypomaturation. Persistence of organic content in enamel rod sheath during apposition. Deficient mineral quantity, normal thickness. Reduced enamel radiodencity. Pourous enamel. Molted enamel with brown-yellow-white collor. Not excessively susceptible to abrasion or dental caries.
100
AI Type 3
Most common type. Matrix normal in thickness, but calcification deficient during mineralization phase leading to soft fragile enamel, lost soon after eruption. Delayed eruption. Rough surface, increased permeability, increased calculus, stains easily. Moth eaten appearance radiographically.
101
AI Type 4
Defects in apposition and histodifferentiation. Enamel molted with yellow brown color and pitted on facial surfaces. Taurodontism of molars, enlarged pulp chambers.
102
Oculodentodigitaldysplasia
Micropthalmos, microcornea, epicanthal folds, fine sparse hair, enamel hypoplasia, MN with wide alveolar ridge, syndactyly of fingers and toes, muscle weakness, nystagmus.
103
Dentinogenesis Imperfecta
Developmental defect during histodifferentiation causing abnormal matrix common to teeth and bone. Type 1 collagen.
104
Clinical Features of Dentinogenesis Imperfecta
Teeth a red-brown to gray opalescent color. Susceptible to wear, pulpal abcess
105
Radiographic features of DI
Bulbous crowns and slender roots. Pulpal obliteration. Small or absent with ribbon like pulp canals. Root fractures.
106
DI Treatment
Primary: Full coverage restorations to prevent wear of posterior teeth, esthetics, pulp therapy or extractions with severe pulp obliteration.
Permanent: Bleaching, resin/veneer/full coverage. Rootcanals for posterior.
107
Dentinogenesis Imperfecta Shields Type 1
Blue sclera, bone fragility, normal inteligence. Primary more affected than permanent. Occurs with OI.
108
DI Shields Type 2
Same as 1 except permanent teeth equally affected. No osteogenesis imperfecta.
109
DI Shields Type 3
Rare. Brandywine population in Maryland. Shell like teeth with short roots and multible pulp exposures.
110
Dentin Dysplaisa
Group of dentin disorders. Results from apposition phase. Anomalies of circumpulpal dentin and root morphology. Two types.
111
DD Shields Type 1
Primary and permanent: Normal crown morphology. Abnormal crown color with amber translucency. Periapical radiolucencies. No pulp chambers. Blockage of dentinal tubules from calcified masses. Short, contricted roots.
112
DD Shields Type 2
Primary dentition: Amber color similar to DI.
| Permanent: Radiographically normal, thistly shaped pulp chamber and pulp stones. No periapical radiolucencies.
113
Epidermolysis Bullosa
Associated with Cementum disorders.
114
Hypophosphatasia
Associated with cementum disorders. Premature/spontaneous tooth expholiation. Alveolar bone loss in anterior.
115
Tricho Dento Osseus Syndrome
Enamel hypolasia of primary/permanent dentition. Taurodontism. Curly hair, brittle nails. Delayed bone age.
116
Oculofaciocardiodental Syndrome
Canine radiculomegaly. Variable root length. Delayed dental development and eruption. Retained primary teeth. Oligodontia.
117
Which procedures require ABX Prophylaxis?
All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.
118
What indicates the need for ABX prophylaxis?
Prosthetic cardiac valve or prosthetic material used for cardiac valve repair. Previous infective endocardtitis. CHD, Unrepaired CHD, Completely repaired CHD, Repaired CHD with defects, Cardiac transplantation.
119
When is abx prophylaxis required for shunts, catheters, etc.
Only at the time of placement to prevent surgical site infection. Immunocompromised should be considered separately.
120
Prosthetic joints abx prophylaxis
Conflicting recommendations. No prophylaxis for pints, plates, screws or other hardware that is not in the synovial joint. Not routinely indicated for total joint replacement. Consider prophylaxis for high risk.
121
What spacial planes do you use to do the facial examination?
AP, vertical transverse.
122
Classes for Facial Pattern-Draw Line
Bridge of nose to base of upper lip to chin. Class 1: Slightly convex. Class 2: Convex. Class 3: concave
123
How do you evaluate MX and MN jaw for deficiency or excess?
Drop perp line from bridge of nose. Normal is upper lip on or near the line with chin slightly behind.
124
How do you examine vertical face relationship?
Normal relationship is face is divided into equal thirds with the hairline, bridge of nose, base of upper lip and bottom of chin. Lower 3rd can be slightly larger and still be considered well proportioned.
125
In 3-6 year olds where do the lips lie when you draw a line from the tip of the nose to the most anterior point of the chin?
1 mm anterior. older, lip lies behind the line.
126
What happens to nose chin and lips in adolescents?
Growth in nose and chin and thinning of the soft tissue of the lips.
127
How do you assess for asymmetries?
Look down on the patient, drawing a line down the midline with floss. Check for facial midline matching the MX and MN dental midline and check for posterior crossbites?
128
Developmental space
Space between all teeth in primary dentition
129
Primate space
Mesial to MXX canine and distal to MN canine.
130
What is the most commonly missing primary tooth?
MX Lateral.
131
Ankylosis
Tooth is fused to the bone and other teeth continue to erupt leaving the ankylosed tooth behind. Most common are MN then MX. Most exfoliate with eruption of permanent successor.
