Oral Diagnosis, Pathology & Medicine Flashcards
1
Q
When is a panorex indicated?
A
New pt- child with transitional dentition or adolescent with permanent dentition
2
Q
When is a FMX indicated?
A
Adolescent with permanent dentition generalized dental disease or hx of extensive tx
3
Q
When do you take bw in a high risk child/adolescent
A
6-12mo
primary teeth/transitional dentition takes 1 year for caries to progress from outer enamel to inner enamel so 6-12 mos high risk children & transitional dent 12-24 mos low risk children & transitional
Permanent teeth takes 3 years for caries to progress from outer to inner enamel (but immature teeth can have quicker progression) so 18-36 months low risk adolescent 6-18 months high risk adult 24-36 months low risk adult
4
Q
When do you take BWX in a low risk child?
A
12-24 mo
5
Q
When do you take bw in a low risk adolescent?
A
18-36
6
Q
When do you take bw in a high risk adult?
A
6-18mo
7
Q
When do you take bw in a low risk adult?
A
24-36mo
8
Q
Rank in order of highest to lowest radiation dosage:chest xray4 BWXPanoramicupper GI series
A
Upper GI series (2.4 msV) Chest X-ray (.08) Panorex 4 BWX (.038 msV) Panorex is about = to 4 intraoral images CBCT about 5-16x greater than panorex **0.15 mSv for FMX**
9
Q
The safest place to stand (minimum exposure site) is
____ degrees from the primary beam as it (enters/exits) patient.
A
10
Q
Maximum scatter site is ____ degrees from the primary beam (entering/exiting) patient
A
90-180o
entering
11
Q
At what vertical angle should BWX be exposed?
A
+8 to +10 degrees
12
Q
What anomalies result from problems in initiation?
A
tooth #
i.e. supernumerary teeth, anodontia
13
Q
What anomalies result from problems in proliferation?
A
Size (micro/macrodontia), proportion, number, twinning
Handbook says: p. 28
deficient development in proliferation results in:
hypodontia, congenital absence, fusion;
excessive development in proliferation results in:
natal teeth, Epithelial rest, gemination
Prolif in bud, cap, bell, late bell
14
Q
What anomalies result from problems in histodifferentiation?
A
enamel (AI type I hypoplastic),
dentin (DI)
Histo part of cap, bell, late bell
15
Q
What anomalies result from problems in morphodifferentiation?
A
Size and shape
e.g.
Deficient devo:
peg lateral, mulberry molars, Hutchinson incisors, microdontia;
Excessive devo:
Carabelli cusp, macrodontia, tuberculated cusps, taurodontism, dens invaginatus
(morpho part of bud, cap, bell, late bell)
16
Q
What anomalies result from problems in apposition?
A
Enamel hypoplasia,
dentin dysplasia;
hypercementosis,
enamel pearls,
odontoma
ghost teeth (regional odontodysplasia)
hypophosphatasia
17
Q
What anomalies result from problems in mineralization and maturation?
A
AI types II, III, IV
fluorosis
localized hypomineralization
interglobular dentin
sclerotic dentin
18
Q
Hyper and hypodontia are anomalies of what histologic stages?
A
Initiation and proliferation
- hyperdontia
- hypodontia
- hypohyperdontia
19
Q
Generalized fluorosis or hypoplasia is a disorder of what developmental stage?
A
mineralization
20
Q
Twinning/gemination is a disorder of what developmental stage?
A
Proliferation
21
Q
Gemination/fusion occurs with what frequency?
A
- 5 – 2.5% primary
- 5% permanent
22
Q
Anomalies in size and conjoined teeth occur in what stages of histologic development?
A
- *Proliferation and Morphodifferentiation**
- micro/macrodontia
- *Proliferation**
- gemination
- fusion
- twinning
- concrescence
23
Q
Name some anomalies that result from problems in morphodifferentiation?
A
Size & Shape
- dens in dente (dens invaginatus)
- dens evaginatus, talon cusp
- taurodontism
- dilaceration
24
Q
What are the 3 types of dens evaginatus?
A
I (talon)
II (semitalon)
III (trace talon)
25
Dens evaginatus occurs with what frequency?
1 – 8% Dens evaginatus
26
What syndrome exhibits taurodontism in 30% of cases?
Kleinfelter syndrome
| (47,XXY; when male has two or more X chromosomes)
27
What are 8 syndromes that have taurodontism?
1. Klinefelter
2. Trichodento-osseous (PARL w/tth)
3. Orofacial digital II aka Mohr
4. hypohydrotic ED
5. AI IV
6. Down syndrome
7. Williams (cardiac, SOCIAL/HAPPY, elfin; hypodontia/partial anodontia, prominent lips, microdontia, enamel hypoplasia) ;
8. Smith- Magenis (lick and flip, self injurious, reduced pain/temp)
28
Anomalies of Apposition affect what structures?
Dentin and cementum
and enamel
29
Enamel (fluorosis, MIH, enamel hypomineralization)
AI III - hypocalcification
30
Maturation affects what?
Enamel
31
Which is NOT an anomaly of proliferation?
1. Concrescence
2. Dens in dente
3. Fusion
4. Gemination
5. Twinning
Answer: B. Dens in dente- an anomaly of morphodifferentiation
32
The dental anomaly that occurs during morphodifferentiation, is a failure of proper invagination of Hertwig’s epithelial root sheath and is seen in Klinefelter and trichodento-osseuous syndrome is
1. Dens invaginatus
2. Gemination
3. Microdontia
4. Taurodontism
Answer: Taurodontism;
30% in Klinefelter,
orofacialdigital II,
ectodermal dysplasia,
AI type IV and
Down Syndrome
33
What are some syndromes that have macrodontia? (what is the histo anomaly?)
(prolif & morpho)
- hemifacial hypertrophy
- Crouzon (also microd, macrod, hypod, hyperd)
- Otodental syndrome: globodontia, molar fusion
- XYY
- pituitary gigantism
- pineal hyperplasia w/hyperinsulinism
34
What are syndromes associated with microdontia?
1) Ectodermal dysplasia
2) Ellis-van Creveld
3) Hemifacial microsomia
4) Down syndrome
5) Crouzon
6) Pituitary Dwarfism
35
Gemination has what characteristics?
Single root and pulp chamber with bifid crown
36
Fusion has what characteristics?
Dentinal union of 2 tth with separate pulp chambers
Separate or fused canals may appear as one chamber with large bifid crown
Dentin always confluent
37
Concrescence has what characteristics?
Fusion occurs after root formation is complete
(technically not a developmental defect)
\*\*most often in maxillary posterior region
\*\*etiology = trauma, crowding
38
What syndromes have dilaceration as finding?
- Congenital ichtyosis (scaly skin)
- Ehlers-Danlos
- Axenfeld-Rieger (glaucoma, tth, skeletal malformations)
- Smith Magenis (lick and flip, self-injurous)
39
What is a possible etiology of dilaceration?
Trauma to primary tooth, especially intrusion
40
Regional odontodysplasia has what pathognomonic characteristic?
“ghost teeth” – localized arrest in tooth development
shell enamel
large pulp
little dentin
failure of eruption
unknown cause
Site: anterior maxilla (80% central incisors)
single or multiple teeth involved +/- gingival enlargement
affects enamel, dentin and cementum
\*\*occurs in the APPOSITION STAGE of development\*\*
41
Hypophosphatasia affects what dental tissue primarily and during which histologic stage?
Cementum during apposition
42
Anomalies of maturation affect what tissue and include what 2 systemic diseases?
* *AI type II** – hypomaturation
- brown-yellow-white/porous, chips
- normal thickness
- poorly mineralized
**AI type IV** – hypomaturation-hypoplastic with taurodontism
(histo also involved)
- mottled yellow-brown/pits
- taurodont molars
43
Prevalence of ankyloglossia
0.1-10.7% of the population (comprehensive review)
male predilection
\*\*manual states 4-10.7%
44
Epstein’s pearls are found in ___ % of newborns
75-80%
COMMON
median palatal raphe
from trapped epithelial remnants along the fusion of the palatal halves
45
Lesions of the newborn:
locations for
Epstein’s pearls,
Bohn’s nodules,
dental lamina cysts,
congenital epulis
Epstein’s pearls – median palatal raphe
Bohn’s nodules – buccal and lingual ridge (lateral alveolar mucosa); away from midline, junction of hard and soft palate. Remnants of salivary gland epithelium
dental lamina cysts – crests of dental ridges
(most commonly seen bilaterally in first primary molar region), alveolar mucosa (aka gingival cyst)
\*above three usually asymptomatic, 1-3 mm smooth white nodules filled with keratin. No tx required, disappear within
first 3 months of life.
Gingival cysts occur in 50% neonates, palatal cysts 75%
congenital epulis – gingival mucosa (anterior maxillary ridge)
46
Which gender has marked predilection for congenital epulis of the newborn?
Female (8-10:1)
aka granular cell tumor, **Neumann’s tumor**
rare benign tumor seen only in newborns
protuberant mass arising from gingival mucosa
-nontender, firm, pink/red polypoid mass with smooth surface
ANTERIOR MAXILLARY RIDGE
10% are multiple
Tx: surgical excision, may regress
47
Neonatal alveolar lymphangioma – how is it different from congenital epulis?
\*Male predilection – 2:1 M:F
Site: Alveolar ridge; \*mandible \> maxilla
4% of black male neonates
S/S: translucent to pink, \*fluctuant swelling; single or multiple
\*Tx: none; resolve
\*different from congenital epulis
48
Natal and neonatal teeth occur at what frequency?
Very rare – varies between 1:1000 to 1:30,000 (incidence)
Handbook: 1:2000-3500
49
Natal teeth are present at birth T/F
T.
Neonatal teeth erupt within the first 30 days of life
3:1 natal to neonatal teeth
Most commonly affected are mandibular primary incisors
may be associated with systemic condition like Pfieffersyndrome or histiocytosis X , also chondroectodermal dysplasia (Ellis Van Creveld)
Child should be at least 10 days old to avoid bleeding complications/risk of hemorrhage
50
What % of natal / neonatal teeth are true primary teeth?
90%
51
What is an associated pathologic finding of natal / neonatal teeth?
Riga-Fede disease (ventral tongue trauma)
Tx: conservative (create round smooth incisal edges)
if conservative tx does not correct condition, ext is the tx of choice
52
Most common location for eruption cysts
**Mandibular molar region**
soft tissue cyst that results from **separation of the dental follicle from the crown of an erupting tooth**. Fluid accumulation occurs within this created follicular space. Color ranges from normal to blue-black or brown, depending on the amount of blood in the cystic fluid (note: blood secondary to trauma)
aka eruption hematomas, soft tissue extension of **dentigerous cyst**
no tx necessary, but may be opened surgically if cyst does not spontaneously rupture or if lesion becomes infected
53
A mucocele is caused by rupture of ________ which leads to leakage of _______ into the surrounding tissues that may later be surrounded by a fibrous capsule
Minor salivary glands
mucin
Mucoceles most common on the lower lip, usu lateral to midline
Caused most often by local mechanical trauma to the SG
May burst spontaneously (leaving shallow ulcers that heal w/I a few days) or require treatment to minimize risk of recurrence
54
What are AI types I, II, III, IV ?
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55
What is the definition of amelogenesis imperfecta?
Developmental disturbance that interferes with normal enamel formation in the absence of a systemic disorder.In general, it affects all or nearly all of the teeth in both the primary and permanent dentitions.
(Other forms of enamel dysmineralization can exhibit pattern based on time of insult, like fluorosis – but fluorosis tends to spare premolars and second permanent molars). In contrast, AI will affect all teeth similarly and can have a familial history.
56
Hypomaturation-hypoplastic AI with taurodontism is associated with what syndrome?
Tricho-dento-osseous syndrome
AD
kinky (worm-like) hair, AI IV, dense and sclerotic bone
57
Clinical implications of AI
Accelerated tooth eruption, or late eruption
_low caries susceptibility_
rapid attrition
excessive calculus deposition
gingival hyperplasia
Pathologies associated with AI:
enlarged follicles, impacted permanent teeth, ectopic eruption, congenitally missing teeth, crown and/or root resorption and pulp calcification, agenesis of second molars, ankylosis.
58
T/F The incidence of class III malocclusion is greater in pts with AI.
F. Incidence of open bite is increased
I Hypoplastic AI – 50% open bite
II Hypomaturation – 30% open bite
III Hypocalcified – 60% open bite
59
What stages of development are disrupted, resulting in AI, DI, and DD?
Histodifferentiation, apposition, and mineralization
AI Type I and DI – Histodifferentiation
DD – Apposition
AI Type II and IV– Maturation
AI Type III - Mineralization
60
What stage of development is disrupted and results in disturbance in dentin for DI?
Histodifferentiation.
61
What’s the incidence of AI in the US?
1:7000
62
What is the inheritance pattern of AI?
Reference manual says
X-linked or sporadic
Specific mutations proven to cause AI include amelogenin (AMELX), enamelin (ENAM), kallikrein4 (KLK4) enamelysis (MMP-20) and FAM83H
Handbook says “multiple” inheritance patterns including AD, AR, X-linked; most common subgroup of AI Type I hypoplastic – AD
63
What % of pts with AI have an anterior open bite?
I -Hypoplastic 50%
II- Hypomaturation 31%
III- Hypocalcified 60%
64
What is the incidence of DI?
1:8000
65
Which DI is autosomal dominant (AD)?
Type I, II, and Type III
II and III listed as AD in Manual (associated with chromosome 4q12-21; mutated DSPP gene)
Type I and II listed as AD in Handbook
66
What is the incidence of Dentin dysplasia?
1:100,000
67
What is the inheritance pattern of dentin dysplasia?
Dentin dysplasia =
Autosomal dominant
68
Which dental disease results in multiple periapical radiolucencies?
DI type I, II, Dentin dysplasia type I
69
Does DD Type I or Type II have pulps that fill in before eruption?
DD Type I
\*\*also DI Type II (hereditary)
70
What are the 3 main types of DI?
Shields Type – Clinical Presentation (inheritance) – WitkopType
Type I – Osteogenesis imperfecta with opalescent teeth – Dentinogenesis Imperfecta
Type II – Isolated Dentinogenesis Imperfecta (AD) – Hereditary Opalescent Dentin
Type III – Isolated Dentinogenesis Imperfecta (AD) – Brandywine Isolate
71
How does DI Type III differentiate clinically from Types I and II?
shell teeth (normal enamel thickness, thin dentin, large pulps)
bell-shaped crowns (esp. permanent dentition)
multiple pulp exposures
rare
72
What is the general clinical presentation of DI all types?
Blue-gray to yellow-brown discoloration (abnormal colored dentin showing through translucent enamel)
Enamel frequently fractures (due to poor support from poorly mineralized dentin)
leading to rapid wear and attrition → decreased VDO, spontaneous abscess
X-ray: bulbous crowns; pulpal obliteration, short roots
severity of discoloration and enamel fx in all three DI types is highly variable
73
What differentiates DI Type II from DI Type I?
Type II – obliteration of pulp chambers can begin before tooth eruption
Type I – occurs with OI
whereas Type II occurs w/o systemic disease.
Both:
- amber color common
- affects both dentitions (BUT most severe in primary for Type I, then FPM/incisors \>\>\>2nd and 3rd molars; dentitions equally affected type II)
- bulbous crowns
- cervical constriction
- thin roots
- early obliteration of root canal/pulp chambers due to excessive dentin production
- PARL & root fractures
74
What is defective in OI/DI Type I, that is important in dentin formation?
Collagen Type I
- the most abundant dentin protein
- COL1A1 and COL1A2 gene mutations cause DI type I
DI types II and III may have defects with dentin phosphoprotein and dentin sialoprotein (chrom 4q12-21, DSPP gene mutations)
75
How many main types of Dentin Dysplasia are there? Is it more common or less common than DI?
Two types – less common
AUTOSOMAL DOMINANT
76
What are the types of Dentin Dysplasia?
Type I – Radicular dentin dysplasia, “rootless teeth”
- crowns mostly normal (occasional amber translucency)
Ranges from: **roots short/absent** w/no pulp, to roots shortenedwith chevron - pulp chambers, to **pulp stones** & normal pulp chamber
- **Affects both primary and permanent dentition**. Variability most profound in the permanent dentition.
- **Pulp obliteration prior to eruption in primary teeth**
- **Multiple PARLs in both dentitions** – secondary to caries or spontaneous exposure of pulpal remnants in defective dentin
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Type II - coronal dentin dysplasia
- normal root lengths
- amber colored primary teeth resemble DI – bulbous crowns, thin roots, cervical constrictions, early pulp obliteration
* *- thistle-tube pulp chambers
- pulp stones
- NO PARLs**
77
What are some similarities and differences between DD types I and II and DI?
78
An unrelated disorder with pulpal findings similar to DD Type II is…
Pulpal dysplasia
Teeth clinically normal w/ radiographic thistle-tube shaped pulp chambers and multiple pulp stones, both primary and perm dentition
79
Class III malocclusion with high incidences of posterior crossbites and open bites occur in \_\_\_\_\_.
DI Type I
80
What are some treatment considerations for child with OI?
Worried about pathologic bone fracture
- Contraindication to medical immobilization
- careful when pushing on jaws
- careful with surgical procedures & positioning
81
What are 2 important considerations for restorative options for DD?
1. Poor crown:root ratios in DD Type I – means that prosthetic replacements are the only practice course of dental rehab
2. Pulp necrosis even with shallow restorations because of pulpal vascular channels that extend close to the DEJ
3. Endo can be successful but difficult.
4. Due to shortened roots and PA lesions, the prognosis for prolonged tooth retention is poor! Early loss of teeth from periodontitis is frequent.
82
3 reactive gingival lesions known as 3 P’s
PG (pyogenic granuloma)
PGCG (peripheral giant cell granuloma)
POF (peripheral ossifying fibroma)
POF and PGCG resorb alveolar bone and may displace teeth (cause diastema), may recur following surgery
83
What are the common sites of a pyogenic granuloma?
Gingiva \> lips \> tongue \> buccal mucosa
painless, soft nodule, red/ulcerated, bleeds easily
F\>M
exuberant response to local irritation
Tx: excisional biopsy, remove local irritation
84
Most common “tumor” of oral cavity
Irritation fibroma
Cause: reactive fibrous hyperplasia in response to local irritation
Site: buccal mucosa, tongue, gingiva
S/S: painless, pink firm nodule with smooth surface; may be white or pigmented
Tx: excisional biopsy; removal local irritation
Some arise from pyogenic granuloma
Variant: frenal tag
85
What is a fibrous hyperplasia of unknown cause that occurs in children and young adults?
Giant cell fibroma
Site: 50% gingiva; tongue and palate
Oral: pink nodule with papillary or smooth surface, nontender
Tx: excision
Cause: unknown, not related to trauma
Developmental lesion: Retrocuspid papilla
86
A benign tumor of neural (Schwann cell) origin that usually occurs on the tongue:
Granular Cell Tumor
asymptomatic, firm mass, 1-2 cm, pink to yellow, infiltrative, separation of papilla
tx: excise, no recurrence
87
The common wart is known as V\_\_\_\_ V\_\_\_\_ and is caused by which HPVs?
Verruca Vulgaris
HPV 2, 4, 6, 40
can recur, but no malignant potential
88
Genital warts (Condyloma Acuminatum) is caused by which HPVs?
HPV 6, 11, 16, 18\* and others
Age: adolescents and young adults
Incubation period: 1-8 months
Site: Anogenital and oral mucosa (usually nonkeratinized – lips, FOM, lateral & ventral tongue, buccal mucosa, soft palate; rarely gingiva)
pink nodules with short, blunted projections; painless; usually multiple
Tx: excision, laser ablation, other
Prognosis: recurs, malignant potential
\*Gardasil protects against these HPV types; cause 70% of cervical caner and 90% of genital warts
89
Which HPVs cause oral cancer?
16 and 18
90
What is Heck’s Disease, and which HPV causes it?
1) Focal or multifocal epithelial hyperplasia; caused by HPV 13 and 32
2) benign neoplastic condition; multiple white to pinkish papules that occur diffusely in oral cavity
91
Prevalence of geographic tongue
1-3% of population
increased in children
unknown cause; hypersensitivity rxn
predisposition: atopic kids, genetics
site: primarily dorsal tongue
s/s: oval or semicircular red patches (desquamation of filiform papillae), white border, burning sensation, changes patterns, chronic condition
92
What is the usual site for sialolithiasis?
```
Submandibular gland (Wharton’s duct)
due to tortuous path and thick secretions
```
S/S: episodic pain or swelling, hard yellowish mass if close to surface
Tx: gentle massage, saliva stimulants, surgery
93
What am I?
Bilateral, symmetrical white wrinkled thickened plaques on the buccal and labial mucosa and tongue.
No treatment required and ADinheritance.
White sponge nevus
No treatment required, could use antibiotics to decrease thickness of lesion
Mimics cheek biting, leukoedema\*, candidiasis
becomes more prominent with age
Extends where child cannot bite
\*leukoedema – variation of normal – most prominent in AA, bilateral, filmy white adherent wrinkled patches on buccal and labial mucosa. Extensive intracellular edema of epithelium. Stretching causes lesion to disappear.
94
What is the most common mass of the soft palate?
Squamous papilloma
caused by HPV 6,11
occurs on tongue, labial mucosa, and soft palate
solitary pink or white nodule w/ fingerlike projections
no tx required
95
Atypical gingivitis (non-plaque induced) is seen in this autoimmune disease of connective tissue.
Lupus erythematosus
Oral lesions mimic lichen planus
Prevalence of oral lesions: 25%
atypical gingivitis, bleeding
skin lesions: scaly red annular patches, butterfly rash, photosensitivity
Tends to affect females, second decade
Tx: steroids +/- antifungal agents
96
Which is not true re: aphthous stomatitis?
A. T-cell mediated immunologic rxn
B. Prevalence 20-30% of US children
C. Affects keratinized tissue
D. Single or multiple painful ulcers; sudden onset; recurrent
C.
Aphthous stomatitis affects nonkeratinizedoral mucosa
Associated diseases: GERD, Bechet’s disease, Crohn’s and UC, celiac disease, neutropenia, immunodeficiencies, nutritional deficiencies
97
Ramsay Hunt syndrome is caused by what?
Varicella-Zoster virus
shingles infection near the ear – facial palsy, vertigo, external auditory canal involvement
98
Oral manifestations of epidermolysis bullosa
Enamel hypoplasia, microstomia, ankyloglossia, caries, gingivitis
inherited blistering mucocutaneous disorder; blistering of hands, feet, mouth
Handbook: excess cellular cementum and fibrous acellular cementum
no good tx – antibiotics, caries prevention, minimize trauma
99
Oral s/s of Crohn’s Disease
Aphthous-like ulcers, tissue tags, cobblestone pattern, diffuse or nodular swelling (lips, gingiva), stomatitis; orofacial granulomatosis; Staph infection
Crohn’s – inflammatory dx of GI tract, starts in childhood, oral lesions precede GI lesions: 30%; cramping pain, diarrhea, nausea, weight loss, anemia, decreased growth
100
What am I?
Perioral freckling around the lips, nose, oral mucosa and hands; multiple melanotic macules;
small intestinal polyps
Peutz-Jeghers Syndrome
AD, first decade of life
Tx: none for oral lesions
Prog: high risk for multiple cancers including colon cancer
101
Neuroectodermal tumors of infancy are
1. Smooth surfaced, expansile lesions
2. More common in the mandible
3. Most likely to develop at 9-12 months
4. Vascular
5. Well circumscribed radiolucencies
Answer: 1. expansile
More common in the maxilla (anterior maxilla most common site), usually occurs in infants under 6 months, non-vascular, poorly circumscribed RL with floating teeth; txis excision
102
Most common site for minor salivary gland tumors
Hard palate
s/s: slowly growing nodule, nontender
prevalence: 5% of SG tumors occur in children, higher proportion are malignant about 50%
103
Most common benign salivary neoplasm
Pleomorphic adenoma
104
Most common malignant salivary gland neoplasm
Mucoepidermoid carcinoma
105
Most common developmental cyst
Dentigerous (follicular) cyst
painless expansion, tooth eruption failure
Tx: enucleate +/- tooth extraction; rarely occur
106
D/D for pericoronalradiolucency
hyperplastic dental follicle (\<5mm)
dentigerous cyst (\>5mm)
eruption cyst
unicystic ameloblastoma
ameloblastic fibroma
adenomatoid odontogenic tumor
calcifying odontogenic cyst
keratocystic odontogenic tumor
107
Which is false for unicysticameloblastoma?
A. 50% occur in 2nd decade
B. Represent 10-46% of ameloblastomas
C. 90% mandible, usu posterior
D. painful expansion
D.
Painless expansion, associated with unerupted tooth, usually 3rd molar
Classic feature: unilocular lucency with well-defined margins, may be scalloped
Tx: enucleation, recurrence rate 10-30%
\*\*ameloblastic fibroma similar to unicystic ameloblastoma – 70% posterior mandible, 75% associated with unerupted tooth, first 2 decades, M\>F, mixed odontogenic tumor, uni or multilocular, rare malignant transformation to ameloblasticfibrosarcoma
108
Keratocystic Odontogenic Tumor is associated with which syndrome?
Nevoid basal cell carcinoma syndrome
multiple BCC, KOT, epidermal cysts of skin, palmar/plantar pits, calcified falx cerebri, enlarged head, rib anomalies, ocular hypertelorism, spina bifida occulta
KOT:
Aggressive developmental cyst
Source: cell rests from the dental lamina
Wide age range, M\>F
Site: posterior mandible and ramus (60-80%)
s/s: pain, swelling, drainage, expansion
25-40% associated with unerupted tooth
uni or multilocular radiolucency
Tx: enucleate +/- ostectomy, 30% recur
109
T/F:
Central Giant Cell Granuloma generally occurs in the maxilla and does not cross midline.
False
70% mandible, often crosses midline
asymptomatic swelling
uni- or multi-locular radiolucency, +/- cortical perforation, root resorption; well delineated but not corticated margins
Tx: surgical curettage, recur 15-20%
60% \< 30 years, F\>M
110
What am I?
Bilateral painless expansion of posterior jaws, full face, upward displacement of eyes, wide alveolus
Cherubism
Autosomal dominant
4 quads involved
giant cell lesions
multilocular radiolucencies; displaced, unerupted teeth
111
D/D for a mixed radiopaque-radiolucent lesion in a pericoronal location:
Calcifying odontogenic cyst
Adenomatoid odontogenic tumor
Ameloblastic fibro-odontoma
Mixed lesion in a periapical or central location
Central ossifying fibroma,
Juvenile ossifying fibroma
112
Where do adenomatoid odontogenic tumors usually occur?
Anterior region, Maxilla \> mandible
10-19 y.o., F \> M
mixed odontogenic tumor
s/s: painless expansion, 75% associated with crown of unerupted tooth, usually a canine
classic feature: unilocular lucency that extends along the root past the CEJ; may exhibit snowflake opacity
Tx: enucleate, recurrence rare
113
Where does ameloblastic fibro-odontoma usually occur?
Posterior mandible
usually children \< 10 y.o.
mixed odontogenic tumor
asymptomatic
frequently associated w/ unerupted tooth
pericoronal lucency with variable opacities
Tx: curettage; does not recur
114
This neoplastic lesion is often expansile, unilocular PA lucencywith variable calcification surrounded by a sclerotic border.
Central ossifying fibroma
Most common in posterior mandible
progresses RL – RO
slow growing, expansile lesion with bowing of the inferior cortex of mandible
displacement of teeth, root divergence and resorption
tx: excision
115
T/F:
Odontomas are more common in the maxilla.
True
Odontoma – common odontogenic neoplasm
occurs in children, mean age 14 y.o.
S/S: delayed tooth eruption, +/- expansion, radiolucent rim, may be cystic, max\>mand
Compound: tooth-like
Complex: calcified mass
Excise; do not recur
D/D: Calcifying odontogenic cyst, ameloblastic fibro-odontoma, eruption sequestrum, supernumerary tooth;
for complex odontomas – Pindborg tumor, Adenomatoid odontogenic tumor, central ossifying fibroma
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When does idiopathic osteosclerosis peak age-wise?
3rd decade; arise in late 1st or 2nd decade
Site: mandible, molar-premolar region
Xray: well-defined, oval density; usually uniformly opaque; periapical region
Tx: periodic evaluation, stabilizes
D/D: condensing osteitis, osteoma, focal cemento-osseous dysplasia, central ossifying fibroma
unknown cause
prevalence 5%
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T/F:
Treatment for cementoblastomais careful monitoring.
False
Tx: excision, extract tooth +/- root amputation, 22% recur
Age: children, young adults (75% \< 30 y.o.)
Posterior mandible; 50% first molar, rare for primary teeth
S/S: pain, bony expansion, displaced teeth
X-ray: opacity with radiolucent rim fused to roots
Uncommon odontogenic neoplasm
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Diffuse ground glass appearance of bone, facial asymmetry, painless unilateral enlargement of maxillary bone is seen in:
Craniofacial fibrous dysplasia
mandible may be involved
* *missing permanent premolars, hypoplastic 1o teeth**
micro: woven bone trabeculae in fibrous stroma
_Segmental odontomaxillary dysplasia very similar_ – painless unilat enlargement of maxillary bone with overlying **hyperplastic gingiva**, facial asym, missing premolars, hypoplastic primary teeth, large roots. Bone – thickened and coarse trabeculae. Also see hypertrichosis and hyperpigmentation of ipsilateral facial skin (Becker’s nevus), hypopigmentation of vermilion of lip
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What is the treatment for condensing osteitis?
Treat the tooth; resolves and stabilizes
aka focal sclerosing osteomyelitis
kids and young adults
site: mandible, molar-premolar region
associated with carious or nonvital tooth
X-ray: well-defined oval to irregular density, usu uniformly opaque, periapical region
D/D: idiopathic osteosclerosis, osteoma, focal cemento-osseous dysplasia, cementoblastoma
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Inflammatory lesion of the jaw that produces facial asymmetry, tenderness, affects mandible (premolar-molar region):
Osteomyelitis w/ proliferative periostitis
aka Garre’s osteomyelitis
Age: children, young adults
Xray: RO or RL, onion skin laminations of periosteum
Tx: treat the infx, bone remodels
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Burkitt’s Lymphoma is a malignancy of \_\_-lymphocytes
Rare, B-lymphocyte malignancy
Children, adolescents; M\>F; strong associated with EBV
Posterior mandible (and maxilla), single or multi quad
S/S: LAE, painful facial and gingival swelling, tenderness, tooth mobility (often 1st sign) and loss
X-ray: ill-defined RL “moth-eaten”; floating tooth appearance, +/- periosteal bone formation
Tx: multiagent chemotherapy, 85% 5-yr survival rate
D/D: leukemic infiltrate, Ewing’s sarcoma, primary malignancy (NH lymphoma), LCH, metastatic dx
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T/F:
Osteosarcomas of the jaws are common.
False.
Osteosarcomas of jaws are uncommon.
Malignancy of bone that produces osteoid or immature bone
Age: kids to older adults, mean age 33
Site: mx = mand
S/S: swelling/pain common, mobile teeth, paresthesia, rapid or slow growth
X-ray: lucent, mixed or opaque, ill defined margins, spiking root resorption, widened PDL, 25% have sunburst or sunray pattern
Tx: surgery, chemo; poor prognosis
D/D: malignancies of bone (chondrosarcoma, Ewing’s sarcoma); intraosseous hemangioma, osteomyelitis w/ proliferative periosteitis, craniofacial fibrous dysplasia
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T/F:
Chewing tobacco is associated with candidiasis
False
Chewing tobacco IS associated with:
gingival recession
stained/sensitive teeth
root caries
halitosis
smokeless tobacco keratosis
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A differential diagnosis for a teething child should NOT include:
1. Febrile convulsions
2. Bronchitis
3. Eczema
4. H. flu meningitis
5. Primary herpetic gingivostomatitis
Answer: 5. Primary herpetic gingivostomatitis
Teething differential, need to R/O: febrile convulsions, URI, bronchitis, eczema, H. flu meningitis, fever \>101F not attributed to teething, dehydration,
Other problems during teething (but no cause-effect): otitis media, paroxysmal atrial tachycardia, GERD, diarrhea
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Conditions with macroglossia
Beckwith-Wiedemann syndrome
Down syndrome
MEN, 2B
Neurofibromatosis, type I
Mucopolysaccaridoses
Cretinism (hypothyroid), myxedema
Hemangioma, lymphangioma
Inflammatory: trauma, angioedema
Reactive, neoplastic lesions
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What drugs/herbal meds alter cytochrome p450?
Erythromycin, cimetidine, st johns wort, echinacea
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The antibiotic class that is bactericidal is:
1. Lincosamides
2. Macrolides
3. Penicillins
4. Sulfonamides
5. Tetracyclines
Answer: 3- Penicillins (inhibits cell wall synthesis= bactericidal)
Lincosamides (Clindamycin)- inhibit ribosomal protein synthesis;
Macrolides (erythromycin, azithromycin)- inhibit ribosomal protein synthesis; Sulfonamides- inhibit folic acid synthesis;
Tetracyclines- inhibit ribosomal protein synthesis
\*NB- Drugs that affect cell wall/cell membrane and DNA synthesis are usually bactericidal; drugs that inhibit protein/folic acid synthesis are usually bacteriostatic
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For questions 7 through 10 match the antimicrobial with the mode of action. Answers may be repeated or not used.
* Cephalosporins
* Clotrimazole
* Penicillins
* Tetracyclines
* alteration of cell membrane permeability
* inhibition of cell wall synthesis
* inhibition of nucleic acid synthesis
* inhibition of protein synthesis
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Augmentin =
Amoxicillin + clavulanic acid
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First evidence of development of the TMJ is seen at \_\_\_\_\_\_\_\_.
8 weeks
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TMJ development
1st decade – condyle becomes less vascularized and most of the major morphological changes are completed
2nd decade – continued but progressive slowing of growth
Undergoes significant changes in shape during growth (12-16 yrs)
From adolescence to adulthood condyle changes to a form that is greater in WIDTH than LENGTH
TMJ undergoes adaptive remodeling changes throughout life
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A rare condition where an elongated styloid process (more than 30 mm) is in conflict withthe adjacent anatomical structures:
Eagle syndrome
unilateral sore throat, dysphagia, tinnitus, unilateral facial and neck pain, otalgia
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What are the etiologic factors “suggested as contributing to the development of TMD”?
1. TRAUMA (impact injuries such as trauma to the chin)
- unilateral and bilateral intracapsular or subcondylar fractures are the most common mandibular fractures in children
2. Occlusal factors (low association)
- skeletal AOB, OJ \> 6-7 mm, CR to CO shift \> 4 mm, unilateral lingual crossbite, five or more missing posterior teeth, class III malocclusion
3. Parafunctional habits (bruxing, clenching, hyperextension, other repetitive behaviors)
- bruxism prevalence 38% under 17 y.o.
- Literature on the association between parafuntion and TMD in kids is contradictory
4. Posture
5. Changes in freeway dimension of rest position (normal is 2-4 mm)
6. Orthodontic treatment – current literature does NOT support that development of TMD is caused by ortho tx regardless of whether premolars were extracted
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TMD prevalence in primary dentition
25-34%
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Clicking seen more frequently in (F/M)?
Females
in general the s/s of TMD increase with age
somewhere around 20% for kids (multiple studies in reference manual, p. 271)
clicking 2.7% primary, 10.1% late mixed, 16.6% perm dentition
s/s TMD lower in children compared to adults, higher prevalence in girls (onset correlated with puberty)
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Recommended radiographs/imaging to examine for TMD
Panoramic, full mouth periapicals,ceph, TMJ tomography, MRI imaging
TMJ arthography is not recommended as a routine diagnostic procedure
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TMDs can be grouped into three classes:
1. Disorders of the **muscles of mastication**
(e. g. muscle spasm, muscle inflammation, etc.)
2. Disorders of the **TMJ** itself
(e. g. internal disk derangement, disk displacement with reduction – clicking, anterior disk displacement w/o reduction – mechanical restriction or closed lock)
3. Disorders in other related areas that may **mimic** TMD
(e. g. chronic mandibular hypomobility, inflammatory joint disorders such as juvenile RA, degenerative joint disease, extrinsic trauma such as fracture)
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Treatment of TMD
Few studies on TMD tx modalities for kids on a long term basis, but they suggest that **simple, conservative, and reversible** therapies are the most effective
Most common – information combined with occlusal appliance therapy. Has been shown that combined approaches are more successful in tx of TMD than single tx modalities
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Reversible types of TMD treatment
- Patient education (e.g. relaxation training, developing behavior coping strategies, pt awareness of clenching and bruxing)
- Physical therapy (e.g. jaw exercises or transcutaneous electric nerve stimulation [TENS], ultrasound, iontophoresis, massage, thermotherapy, coolant therapy)
- Behavioral therapy (e.g. avoiding excessive chewing of hard foods or gum, voluntary avoidance of stressors, habit reversal, decreasing anxiety, stress and/or depression)
- Prescription medication (e.g. NSAIDs, anxiolytic agents, muscle relaxers). Antidepressants have proven beneficial but should be prescribed by PMD
- Occlusal splints to provide orthopedic stability to the TMJ – may be used to decrease parafunctional activity
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Irreversible types of TMD treatment
- Occlusal adjustment (i.e. permanent alteration of the occlusion or mandibular position by selective grinding or full mouth restorative dentistry)
- Mandibular repositioning (designed to alter the growth of permanently reposition the mandible – headgears, functional appliances)
- Orthodontics
\*\*irreversible therapies should be avoided in children due to inadequate data supporting their usefulness in txof TMD
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Crepitus may indicate what type of joint changes?
Degenerative joint change that is not yet painful
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What Syndromes are Associated with Lymphangiomas?
1) Turner Syndrome (45,x – when female is partially or completely missing X chromosome)
2) Noonan Syndrome – AD, male version of Turner’s Syndrome \*heart defect (pulmonary stenosis, asd), short stature, learning problems, impaired blood clotting, etc)
3) Fetal Alcohol
4) Trisomies
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What amount of flow is needed for emergency oxygen delivery from a self inflating bag valve mask
15L/min
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What amount of oxygen do you need in an emergency?
Positive pressure oxygen delivery system capable of administering greater than 90% oxygen at 10 L per minute flow for at least 60 minutes 650 L "E" cylinder
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Compression rate of CPR for adults, children, and infants
At least 100 bpm
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Dosage of diphenhydramine indicated for an allergic reaction (mild or delayed)
1 mg/kg
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Drug of choice indicated for an acute asthmatic attack unresponsive to a bronchodilator (include concentration 1:xxxxxxx)
Epinephrine 1:1000
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Early signs of syncope
Feeling of **warmth, loss of color** – ashen-gray skin tone, perspiration, reports feeling faint or feeling nauseous, exhibits slightly lower BP and tachycardia
**Late stage:**
pupils dilate, yawning, hyperpnea, cold extremities, hypotension, bradycardia, visual disturbances, dizziness, LOC
**Management:**
stop tx, assess and recognize
position pt to increase cerebral blood flow
BLS with supplemental oxygen
determine cause (e.g. hypoglycemia?)
vital signs
if not self-limiting, active EMS
physician referral
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