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NBDE II > ORAL DIAGNOSIS Pathology and Diagnosis pt 2 > Flashcards

ORAL DIAGNOSIS Pathology and Diagnosis pt 2 Flashcards

1
Q

___ is a group of neoplasms of bone marrow. what are the precursors?

A
  • leukemias

- lymphocyte or myeloid precursors

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2
Q

in leukemias, malignant cells occupy and replace normal marrow cells, including ___. the malignant cells are also released into the ___

A
  • megakaryocytes (platelet forming cells)

- peripheral blood

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3
Q

what are the causes of leukemias?

A
  • genetic factors, such as chromosome translocations
  • environmental agents (benzene, radiation)
  • viruses (human T-lymphotropic virus 1)
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4
Q

classification of leukemia is based on ___ and ___

A

cell lineage and whether the disease is acute or chronic

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5
Q

what are the clinical features of leukemia?

A
  • bleeding (owing to reduced platelets), fatigue (owing to anemia), and infection (owing to agranulocytosis) are important clinical signs of leukemias
  • infiltration of gingival tissues by leukemic cells is common in chronic monocytic leukemia; gingiva is red, boggy, and hemorrhagic
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6
Q

what is the treatment for leukemias?

A

chemotherapy is quite successful for acute leukemias, but is less so for chronic leukemias

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7
Q

odontogenic cysts are derived from cells that are associated with ___

A

tooth formation

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8
Q

in odontogenic cysts, the stimulus for cystic change is unknown in all cysts except for ___ and ___

A

periapical cysts and some odontogenic keratocysts (keratocystic odontogenic tumors)

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9
Q

what is the most common odontogenic cyst? what is it always associated with?

A
  • periapical (radicular) cyst

- always associated with a nonvital tooth

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10
Q

how do periapical cysts form?

A
  • necrotic pulp causes periapical inflammation (can be acute or chronic)
  • rests of malassez within a dental granuloma epithelialize the lesion, resulting in the formation of a cyst
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11
Q

describe the difference in acute and chronic periapical cysts

A
  • if acute, a periapical abscess forms after periapical inflammation
  • if chronic, a dental granuloma (granulation tissue and chronic inflammatory cells) forms after periapical inflammation
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12
Q

how is a periapical cyst treated?

A

RCT, apicoectomy, or tooth extraction with apical curettage

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13
Q

how does a dentigerous cyst manifest radiographically?

A

a radiolucency around the crown of an impacted tooth

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14
Q

which teeth are most commonly affected by dentigerous cysts?

A

third molars and canines

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15
Q

an eruption cyst is a ___ cyst that occurs over a tooth that has erupted into the submucosa

A

dentigerous cyst

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16
Q

in dentigerous cysts, the epithelial lining from reduced enamel epithelium has the potential to transform into ___

A

ameloblastoma

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17
Q

a ___ is a unilocular or multilocular lucency in the lateral periodontal membrane of adults

A

lateral periodontal cyst

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18
Q

where are most lateral periodontal cysts located?

A

most are found in the mandibular premolar region and are associated with a vital tooth

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19
Q

___ is the soft tissue counterpart of a lateral periodontal cyst

A

gingival cyst of the adult

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20
Q

gingival cysts of a newborn present as ___ resulting from ___

A

multiple small gingival nodules resulting from cystification of rests of the dental lamina

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21
Q

gingival cysts of the newborn are also called ___. what are inclusion cysts in the palates of infants called?

A
  • bohn’s nodules

- epstein’s pearls

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22
Q

what is the treatment for gingival cysts of the newborn?

A

none

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23
Q

odontogenic keratocysts (keratocystic odontogenic tumors) are lesions that may be clinically aggressive, recurrent, or associated with which syndrome?

A

nevoid basal cell carcinoma (gorlin) syndrome

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24
Q

what characterizes nevoid basal cell carcinoma (gorlin) syndrome?

A
  • multiple odontogenic keratocysts
  • numerous cutaneous basal cell carcinomas
  • skeletal abnormalities
  • calcified falx
  • other stigmata
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25
Q

mutation of which gene is evident in syndrome-related odontogenic keratocysts and probably in many solitary cysts

A

PTCH tumor suppressor gene

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26
Q

why are odontogenic keratocysts now termed keratocystic odontogenic tumors?

A

the new terminology reflects the concept that the lesion is a neoplasm with cystic architecture rather than a developmental cyst

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27
Q

the lining epithelium of odontogenic keratocysts is ___ and ___

A

thin and parakeratinized

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28
Q

how do orthokeratinized odontogenic cysts compare to odontogenic keratocysts?

A

orthokeratinized odontogenic cysts are less common and have much lower recurrence rate and is not syndrome-associated

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29
Q

calcifying odontogenic cysts are rare odontogenic cysts of unpredictable behavior. what is their recurrence?

A

has potential, especially for the solid variant

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30
Q

what characterizes calcifying odontogenic cysts microscopically?

A
  • ghost cell keratinization

- ghost cells may undergo calcification that may be detected radiographically (lucency with opaque foci)

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31
Q

what is the cutaneous counterpart of calcifying odontogenic cysts?

A

malherbe calcifying epithelioma or pilomatricoma

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32
Q

are glandular odontogenic cysts common? what is another name for them?

A
  • rare

- sialo-odontogenic cysts

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33
Q

are glandular odontogenic cysts (sialo-odontogenic cysts) aggressive?

A

may be locally aggressive and exhibit recurrence potential

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34
Q

the glandular odontogenic cyst (sialo-odontogenic cyst) name is derived from ___

A

glandlike spaces and mucous cells in epithelial lining

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35
Q

odontogenic tumors are bone tumors that are unique to the jaws, and the lesions are derived from ___ cells involved in the formation of teeth

A

epithelial or mesenchymal cells

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36
Q

are odontogenic tumors typically malignant?

A
  • no, they are almost always benign

- some may exhibit aggressive behavior and may have significant recurrence potential

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37
Q

ameloblastoma is a benign but aggressive odontogenic tumor with significant recurrence potential, especially if treated ___

A

conservatively

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38
Q

which variant of ameloblastoma is less aggressive and less likely to recur?

A

cystic variant (cystic ameloblastoma)

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39
Q

___ or ___ ameloblastomas exhibit banal behavior

A

peripheral or gingival

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40
Q

very rare malignant ameloblastomas are known as ___ and ___

A

malignant ameloblastoma and ameloblastic carcinoma

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41
Q

there are several microscopic subtypes of ameloblastomas, all of which mimic to some degree the ___

A
  • enamel organ

- no difference in behavior

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42
Q

what is the treatment for ameloblastoma?

A

ranges from wide excision to resection (want to avoid conservative treatment)

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43
Q

calcifying epithelial odontogenic tumor is also called ___

A

pindborg tumor

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44
Q

calcifying epithelial odontogenic tumors (pindborg tumors) are rare odontogenic tumors with unusual microscopy. describe their microscopy

A

sheets of large epithelioid cells with areas of amyloid, some of which may become calcified

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45
Q

how do calcifying epithelial odontogenic (pindborg) tumors compare to ameloblastomas?

A

similar age distribution and location but less aggressive than ameloblastomas

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46
Q

___ is an uncommon to rare odontogenic hamartoma that contains epithelial duct-like spaces and calcified enameloid material

A

adenomatoid odontogenic tumor

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47
Q

where do adenomatoid odontogenic tumors occur? do they recur?

A
  • 2/3 in the maxilla, 2/3 in females, 2/3 in the anterior jaws, and 2/3 over the crown of an impacted tooth
  • does not recur after conservative treatment
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48
Q

___ is an uncommon to rare tumor of myxomatous connective tissue (primitive-appearing connective tissue containing little collagen similar to dental pulp)

A

odontogenic myxoma (fibromyxoma)

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49
Q

which jaw do odontogenic myxomas (fibromyxomas) affect?

A

either jaw

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50
Q

how do odontogenic myxomas (fibromyxomas) present radiographically?

A

radiolucency often with small loculations (honeycomb pattern)

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51
Q

how are odontogenic myxomas (fibromyxomas) treated?

A
  • surgical excision

- moderate recurrence potential owing to lack of encapsulation and tumor consistency

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52
Q

central odontogenic fibroma is a rare tumor of dense ___ with strands of ___

A

dense collagen with strands of epithelium

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53
Q

how do central odontogenic fibromas present radiographically?

A

well-defined radiolucency in either jaw; often multilocular

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54
Q

how are central odontogenic fibromas treated?

A

surgical excision with few recurrences

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55
Q

cementifying fibroma can be considered similar or identical to ___

A

ossifying fibroma

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56
Q

radiographically, how does a cementifying fibroma present?

A
  • well-circumscribed lucency

- some lesions are lucent with opaque foci

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57
Q

what population and location is cementifying fibroma common in?

A
  • adults and young adults

- typically in the body of the mandible

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58
Q

how is cementifying fibroma treated?

A

curettage or excision, rare recurrence

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59
Q

___ is a well-circumscribed radiopaque mass of cementum and cementoblasts replacing the root of a tooth

A

cementoblastoma

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60
Q

how are cementoblastomas treated?

A
  • lesion is excised and the associated tooth is removed with the lesion because of intimate association
  • no recurrence after excision
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61
Q

what are the clinical features of periapical cemento-osseous dysplasia?

A
  • cause unknown, no treatment requried
  • commonly seen at the apices of one or more mandibular anterior teeth
  • no symptoms; vital teeth
  • most frequently seen in middle aged women
  • starts as circumscribed lucency, which gradually becomes opaque
  • if entire jaw is involved, termed florid osseous dysplasia
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62
Q

what is the difference between an ameloblastic fibroma and an ameloblastic fibro-odontoma?

A
  • the latter lesion has an odontoma

- otherwise, they are the same lesion

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63
Q

which population is most affected by ameloblastic fibromas and ameloblastic fibro-odontomas? which location most common?

A
  • children and teens

- typically seen in mandibular molar regions

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64
Q

how do ameloblastic fibromas and ameloblastic fibro-odontomas present radiographically?

A
  • unilocular or multilocular radiolucency

- ameloblastic fibro-odontomas will present as a radiolucency with an opacity (odontoma)

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65
Q

what are the microscopic characteristics of ameloblastic fibromas and ameloblastic fibro-odontomas?

A

encapsulated myxomatous connective tissue lesion containing strands of epithelium

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66
Q

how are ameloblastic fibromas and ameloblastic fibro-odontomas treated?

A

enucleation or excision; rarely recurs

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67
Q

___ is an opaque lesion composed of dental hard tissues

A

odontoma

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68
Q

what are the two types of odontomas?

A
  • compound type contains miniature teeth

- complex type compose of a conglomerate mass

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69
Q

how are odontomas treated?

A

curettage, no recurrence

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70
Q

___ is a common fibro-osseous lesion that can be considered similar or identical to cementifying fibroma, although some may reach considerable size

A

ossifying fibroma

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71
Q

what are the clinical features of ossifying fibromas?

A
  • radiographically appears as either well-circumscribed lucency or a lucency with opaque foci
  • seen in adults and young adults, typically in the body of the mandible
  • a variant known as juvenile ossifying fibroma occurs in younger patients and may exhibit aggressive behavior
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72
Q

what are the microscopic characteristics of ossifying fibromas?

A

fibroblastic stroma in which new bony islands or trabeculae are formed

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73
Q

what is the treatment for ossifying fibromas?

A

curettage or excision, rare recurrence

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74
Q

fibrous dysplasia is an uncommon to rare unencapsulated fibro-osseous lesion assiciated with mutations of the ___ gene, affecting proliferation and function of ___ cells

A
  • GNAS1 gene

- fibroblasts and osteoblasts

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75
Q

what are the clinical features of fibrous dysplasia?

A
  • involves the entire half jaw, more common in maxilla
  • affects children and typically stops growing after puberty
  • radiographic pattern is diffuse opacity (ground glass)
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76
Q

describe the mccune albright syndrome associated with fibrous dysplasia

A
  • polyostotic (more than one bone) fibrous dysplasia
  • cutaneous cafe au lait macules
  • endocrine abnormalities (precocious puberty)
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77
Q

how is?fibrous dysplasia treated

A

surgical recontouring for cosmetic appearance

78
Q

___ is a circumscribed opaque mass of bone and osteoblasts that commonly affects young adults, with 50% of patients having associated pain

A

osteoblastoma

79
Q

how is osteoblastoma treated?

A

surgical excision with few recurrences

80
Q

microscopically, bone (nonodontogenic) lesions have ___ in common

A

multinucleated giant cells (important for diagnosis)

81
Q

___ is a reactive red to purple gingival mass believed to be caused by local factors

A

peripheral giant cell granuloma

82
Q

where are peripheral giant cell granulomas typically found?

A

gingiva, typically anterior to permanent molar teeth

83
Q

peripheral giant cell granuloma is composed of which cells?

A

fibroblasts and multinucleated giant cells, similar to a central giant cell granuloma

84
Q

how is peripheral giant cell granuloma treated?

A
  • excision that extends to periosteum or periodontal ligament
  • occasional recurrences are seen
85
Q

___ is a nonodontogenic tumor that exhibits unpredictable clinical behavior; some are aggressive and have recurrence potential, whereas other have a bland course

A

central giant cell granuloma

86
Q

how do central giant cell granulomas present radiographically?

A
  • radiolucency

- sometimes loculated

87
Q

what age group are central giant cell granulomas common in? what is the common location?

A
  • teenagers

- anterior mandible

88
Q

central giant cell granulomas are composed of which cells?

A

fibroblasts and multinucleated giant cells, similar to peripheral giant cell granulomas

89
Q

what is the treatment for central giant cell granulomas?

A
  • excision, but occasional recurrence are encountered

- medical management (calcitonin or interferon) for large lesions is a possible option

90
Q

___ is a pseudocyst that is composed of blood-filled spaces lined by fibroblasts and multinucleated giant cells

A
  • aneurysmal bone cyst

- not a true cyst because, although there are cyst-like spaces, there is no epithelial lining

91
Q

how do aneurysmal bone cysts present radiographically? which age group?

A
  • multilocular lucency

- typically in teenagers

92
Q

what is the cause and treatment for aneurysmal bone cysts?

A
  • cause unknown

- excision and occasional recurrences

93
Q

hyperparathyroidism is also called ___, and is a result of ___

A
  • von recklinghausen’s disease of bone
  • multiple bone lesions results from effects of excessive levels of parathormone
  • may be caused by functioning parathyroid tumor or compensatory parathyroid hyperplasia secondary to renal failure, malabsorption, or vitamin D deficiency
94
Q

what are the clinical features of hyperparathyroidism (von recklinghausen’s disease of bone)?

A
  • multiple radiolucent foci of fibroblasts and multinucleated giant cells as well as loss of lamina dura around tooth roots
  • systemic signs include kidney stones, metastatic calcification, osteoporosis, neurologic problems, and arrhythmias (in addition to elevated parathormone and alkaline phosphatase)
95
Q

cherubism is an autosomal ___ condition of the jaws in children

A

dominant

96
Q

what are the clinical features of cherubism?

A
  • symmetrical bilateral swelling of one or both jaws
  • stabilizes after puberty and requires no treatment
  • loculated radiolucencies described as having soap bubble appearance
97
Q

how does cherubism present microscopically?

A
  • giant cells

- distinctive perivascular collagen condensation may also be seen

98
Q

what are two other names for langerhan’s cell disease?

A
  • idiopathic histiocytosis

- langerhan’s granulomatosis

99
Q

all forms of langerhan’s cell disease represent abnormal proliferation of ___

A

langerhan’s cells

100
Q

what are the radiographic features of langerhan’s cell disease?

A

punched out lesions or lucencies around tooth roots (floating teeth)

101
Q

what are the microscopic features of langerhan’s cell disease?

A
  • eosinophils are mixed with the tumor’s langerhan’s cells

- some langerhan’s cells are multinucleated

102
Q

what is the treatment and prognosis for langerhan’s cell disease?

A
  • treatment is variable, including excision, low-dose radiation, and chemotherapy
  • prognosis is very good when the disease is localized
  • acute disseminated form is usually fatal
103
Q

paget’s disease is a progressive metabolic disturbance of many bones, including which ones?

A

spine, femur, cranium, pelvis, and sternum

104
Q

what is the cause and treatment for paget’s disease?

A
  • cause is unknown

- treatment is generally symptomatic

105
Q

what age group does paget’s disease typically affect?

A

adults older than 50

106
Q

describe the jaw involvement in paget’s disease. other than the jaws, what are the signs/symptoms?

A
  • symmetrical enlargement
  • dentures become too tight
  • diastemas and hypercementosis may appear
  • other signs/symptoms include bone pain, headache, and altered vision and hearing (canal sclerosis)
107
Q

in paget’s disease, ___ may complicate surgery because ___

A

bleeding, because bone is highly vascular in early stages

108
Q

what are late complications of paget’s disease secondary to bone sclerosis?

A

jaw fracture and osteomyelitis

109
Q

how does paget’s disease present microscopically?

A
  • osteoblasts and multinucleated osteoclasts are found in abundance
  • as lesion advances, dense bone with numerous reversal or growth lines is seen, giving the tissue a mosaic pattern
110
Q

what is the treatment for paget’s disease?

A
  • directed at suppression of bone resorption and deposition

- bisphosphonates (and to a lesser extent, calcitonin) have shown efficacy

111
Q

what is the microscopic differential diagnosis for giant cell lesions of bone?

A
  • central giant cell granuloma
  • hyperparathyroidism
  • aneurysmal bone cyst
  • cherubism
112
Q

what are the classifications of langerhan’s cell disease?

A
  • eosinophilic granuloma (chronic localized form) - solitary or multiple bone lesions
  • hand-schuller-christian disease (chronic disseminated form) - bone lesions, exophthalmos, and diabetes insipidus
  • letterer-siew disease (acute disseminated form) - bone, skin, and internal organ lesions
113
Q

is inflammation of bone (and bone marrow) or osteomyelitis common in the jaws?

A
  • yes
  • most lesions are assocaited with extension of periodontal or periapical inflammation
  • others are associated with trauma to the jaws
114
Q

___ is a nonodontogenic lesion that is the result of acute inflammation fo bone and bone marrow of the jaws

A

acute osteomyelitis

115
Q

what are the causes of acute osteomyelitis?

A

extension of periapical or periodontal disease, fracture, surgery, and bacteremia

116
Q

what are the most common bacterial infectious agents responsible for acute osteomyelitis?

A

staphylococci and streptococci

117
Q

what are the signs/symptoms of acute osteomyelitis?

A

pain, paresthesia, and exudation are typically present

118
Q

when do radiographic changes present in acute osteomyelitis?

A

diffuse lucency appears only after inflammation has been present for an extended perio

119
Q

what is the treatment for acute osteomyelitis?

A

appropriate antibiotic and drainage of the lesion

120
Q

___ is a nonodontogenic lesionof bone that is the result of chronic inflammation of bone and bone marrow of the jaws

A

chronic osteomyelitis (chronic osteitis)

121
Q

what are the signs/symptoms of chronic osteomyelitis?

A

milder to moderate pain and possibly an exudate

122
Q

what is the radiographic presentation of chronic osteomyelitis?

A

lucent or mottled radiographic pattern

123
Q

how is chronic osteomyelitis treated?

A

antibiotics and sequestrectomy

124
Q

___ is form of chronic osteomyelitis that involves the periosteum

A

chronic osteomyelitis with proliferative periosteitis (garre’s osteomyelitis)

125
Q

chronic osteomyelitis with proliferative periosteitis (garre’s osteomyelitis) is usually associated with ___

A

carious molar in children

126
Q

what is the radiographic presentation of chronic osteomyelitis with proliferative periosteitis (garre’s osteomyelitis)?

A

lucent or mottled radiographic pattern plus concentric periosteal layering

127
Q

how is chronic osteomyelitis with proliferative periosteitis (garre’s osteomyelitis) treated?

A

tooth removal and antibiotics

128
Q

___ is a form of chronic osteomyelitis that involves bone sclerosis (opacity) resulting from low grade inflammation, usually secondary to chronic pulpitis

A

focal sclerosing osteomyelitis (condensing osteitis)

129
Q

how is focal sclerosing osteomyelitis (condensing osteitis) diagnosed?

A

asymptomatic and found on routine examination (radiographic)

130
Q

what is the treatment for focal sclerosing osteomyelitis (condensing osteitis)?

A

determine and address the cause, and possibly endodontics

131
Q

___ is a form of chronic osteomyelitis that involves bone sclerosis (opacity) resulting from low-grade inflammation, usually secondary to chronic pulpitis or periodontal disease

A

diffuse sclerosing osteomyelitis

132
Q

what are the signs/symptoms of diffuse sclerosing osteomyelitis?

A

low-grade pain, swelling, or drainage may be present

133
Q

what are late complications of diffuse sclerosing osteomyelitis secondary to densely sclerotic bone?

A

jaw fracture and osteomyelitis

134
Q

what is the treatment for diffuse sclerosing osteomyelitis?

A

determine and address the cause and possibly antibiotics

135
Q

___ is a form of chronic osteomyelitis characterized by exposed bone in maxillofacial region for longer than 8 weeks in a patient who has received a bisphosphonate medication

A

bisphosphonate related osteonecrosis of the jaws

136
Q

what is the usual presenting symtpom of BRONJ?

A

jaw pain

137
Q

what are the projecting outcomes of BRONJ?

A

tooth mobility, infection, sequestration, and pathologic fracture

138
Q

in BRONJ cases, risk of development is much greater with IV bisphosphonates as opposed to oral drugs, and osteonecrosis is more likely to develop in areas of ___

A

oral trauma

139
Q

what is the treatment for BRONJ?

A

conservative local measures such as chlorhexidine rinses, antibiotic therapy, and conservative surgery

140
Q

malignancies manifesting bone include ___

A

sarcomas, lymphomas or leukemias, and metastatic carcinomas

141
Q

what is a frequent presenting symptom of malignancies manifesting in bone?

A

numb lip, which represents neoplastic invasion of nerves

142
Q

___ is a sarcoma in which new bone (osteoid) is formed

A

osteosarcoma

143
Q

what is the cause of osteosarcoma?

A

unknown, although an association with several specific genetic alterations has been detected

144
Q

what are the signs and symptoms of osteosarcoma?

A
  • pain, swelling, and paresthesia are typically present

- PDL invasion results in uniform widening

145
Q

what is the mean age of patients affected by osteosarcoma?

A
  • 35 years old

- ranges from 10-85 years

146
Q

which jaw is more commonly affected with osteosarcoma?

A

mandible

147
Q

most malignant jaw tumors are microscopically ___ lesions

A

low grade

148
Q

describe the treatment and prognosis of osteosarcoma

A
  • treated with resection and usually neoadjuvant chemotherapy (preoperative ) or adjuvant chemotherapy (postoperative)
  • 5 year survival rate 25-40%
  • prognosis is better for mandibular tumors than for maxillary tumors
  • initial radical surgery results in survival rate of 80%
149
Q

___ is a rare sarcoma of the jaws in which cartilage is produced by tumor cells

A
  • chondrosarcoma

- clinical features and treatment are similar to osteosarcoma

150
Q

___ is a rare “round cell” malignant radiolucency of children

A

ewings sarcoma

151
Q

how is ewings sarcoma treated?

A

aggressive multimodality therapy with a fair prognosis

152
Q

what are the malignancies most commonly metastatic to the jaws?

A
  • adenocarcinoma of the breast
  • carcinoma of the lung
  • adenocarcinoma of the prostate
  • adenocarcinoma of the colon
  • carcinoma of the kidney (renal cell)
153
Q

metastatic carcinoma that metastasizes to the jaw presents with which signs/symptoms? how is it noted radiographically?

A
  • pain, swelling, and especially paresthesia

- ill-defined lucent to opaque radiographic changes are noted

154
Q

white sponge nevus is an autosomal ___ condition secondary to mutations of ___ or ___

A
  • dominant

- keratin 4 or 13

155
Q

how does white sponge nevus present clinically?

A

asymptomatic white, spongy-appearing buccal mucosa bilaterally

156
Q

how is white sponge nevus diagnosed? what is the treatment?

A
  • biopsy for diagnosis

- no treatment necessary

157
Q

the term epidermolysis bullosa encompasses several ___ and one ___

A
  • genetic conditions

- acquired disease

158
Q

hereditary patterns associated with epidermolysis bullosa range from ___ to ___

A

autosomal dominant to autosomal recessive

159
Q

what is clinically common to all forms of epidermolysis bullosa?

A

the appearance of bullae from minor trauma, especially over elbows and knees

160
Q

what are the characteristic oral lesions associated with epidermolysis bullosa?

A
  • blisters, scarring, and hypoplastic teeth

- seen in the severe recessive form

161
Q

hereditary hemorrhagic telangiectasia is a rare autosomal ___ condition in which telangiectatic vesssels are seen in ___, ___, and occasionally ___

A
  • dominant

- mucosa, skin, and occasionally viscera

162
Q

in hereditary hemorrhagic telangiectasia, ___ or ___ are an occasional source of bleeding

A

red macules or papules (telangiectasias)

163
Q

what is a frequent presenting sign of hereditary hemorrhagic telantiectasia?

A
  • epistaxis (nosebleed)

- oral bleeding may also occur

164
Q

cleidocranial is an autosomal ___ condition manifested by many alterations, especially of teeth and bones

A

dominant

165
Q

what are the most distinctive features of cleidocranial dysplasia?

A
  • delayed tooth eruption and supernumerary teeth
  • hypoplastic or aplastic clavicles
  • cranial bossing
  • hypertelorism
166
Q

___ is an X-linked recessive condition that results in partial or complete anodontia

A

hereditary ectodermal dysplasia

167
Q

in addition to partial or complete anodontia, patients with hereditary ectodermal dysplasia may also have hypoplasia of ___

A

other ectodermal structures, including hair, sweat glands, and nails

168
Q

gardners syndrome is an autosomal ___ disorder

A

dominant

169
Q

what are the clinical characteristics of gardners syndrome?

A
  • intestinal polyps
  • osteomas
  • skin lesions
  • impacted permanent and supernumerary teeth
  • odontomas
170
Q

which syndrome involves intestinal polyps that have a very high rate of malignant conversion to colorectal carcinoma?

A

gardners syndrome

171
Q

what are two other names for osteoporosis?

A

albers-schonberg disease and marble bone

172
Q

___ is a generalized bone condition that may be inherited as an autosomal dominant (less serious) or recessive (more serious) trait

A

osteoporosis (albers-schonberg disease, marble bone)

173
Q

in osteoporisis, lack of bone remodeling and resorption leads to ___

A

bone sclerosis

174
Q

what are the complications associated with osteoporosis?

A

bone pain, blindness and deafness from sclerosis of ostia, anemia from sclerosis of marrow, and osteomyelitis secondary to diminished vascularity

175
Q

___ is a rare group of hereditary conditions that affect enamel tissue intrinsically

A

amelogenesis imperfecta

176
Q

T or F:

in amelogenesis imperfecta, anterior teeth in the primary dentition only are affected

A
  • false

- all teeth of both dentitions are affected

177
Q

what are the dental characteristics of amelogenesis imperfecta?

A
  • enamel is typically yellow in color, reduced in volume, and pitted
  • dentin and pulps are normal
  • although teeth are soft, there is no increase in caries rate
178
Q

T or F:

due to softening of enamel in amelogenesis imperfecta, there is a significant increase in caries rate

A

false - no increase in caries rate

179
Q

what is the dental treatment for amelogenesis imperfecta?

A

represents a cosmetic problem that is treated with full crown coverage

180
Q

dentinogenesis imperfecta is an autosomal ___ condition in which there is intrinsic alteration of ___

A
  • dominant

- dentin

181
Q

which teeth are affected in cases of dentinogenesis imperfecta?

A

all teeth of both dentitions

182
Q

describe how teeth are affected in cases of dentinogenesis imperfecta

A
  • teeth have yellow or opalescent color
  • extreme occlusal wear secondary to enamel fracture (poor dentin support)
  • short roots, bell shaped crowns, and obliterated pulps
183
Q

dentinogenesis imperfecta may be seen with what other hereditary condition?

A

osteogenesis imperfecta

184
Q

what is the dental treatment for dentinogenesis imperfecta?

A

represents a cosmetic problem that is treated with full crown coverage

185
Q

dentin dysplasia is an autosomal ___ condition in which there is intrinsic alteration of ___

A
  • dominant

- dentin

186
Q

which teeth are affected in cases of dentin dysplasia?

A

all teeth of both dentitions

187
Q

describe how teeth are affected in cases of dentin dysplasia

A
  • teeth have normal color
  • pulps are bliterated but may have residual spaces (chevrons)
  • roots are short and are surrounded by dental granulomas or cysts that may contribute to tooth loss
188
Q

what is the dental treatment for dentin dysplasia?

A

teeth are not good candidates for restoration

189
Q

regional odontodysplasia is a dental abnormality of unknown cause. what are some possible causes that have been suggested?

A
  • genetics
  • trauma
  • nutrition
  • infection
190
Q

describe the clinical and radiographic presentation of regional odontodysplasia

A
  • a quadrant of teeth exhibit short roots, open apices, and enlarged pulp chambers
  • the radiographic appearance of these teeth has suggested the term “ghost teeth”
191
Q

what is the dental treatment for regional odontodysplasia?

A

teeth are usually extracted because of the poor quality of enamel and dentin

NBDE II (35 decks)

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