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Oral Pathology > Developmental Disturbances of the Oral Region > Flashcards

Developmental Disturbances of the Oral Region Flashcards

1
Q

What is microdontia?

A

One or more teeth are smaller than normal.

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2
Q

True vs. Relative Microdontia

Give Examples

A

True is when the teeth are actually small. Relative is that teeth appear to be smaller as compared to other oral structures.

Pituitary dwarfism: True microdontia.
Jaw enlargement with normal size teeth: Relative microdontia.
Peg-shaped lateral incisors: True microdontia.

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3
Q

What is the most common form of microdontia?

A

Peg-shaped laterals.

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4
Q

Macrodontia

A

One or more teeth larger than normal. Can be true or relative, just like microdontia.

EX: Gigantism

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5
Q

Anodontia

A

Congenital absence of teeth. Can be total or partial. Total anodontia is rare, partial is common.

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6
Q

What is the most common form of partial anodontia?

A

Absence of a 3rd molar.

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7
Q

Supernumerary teeth

A

Excess number of teeth. Common in permanent dentition, uncommon in deciduous dentition.

Can be well formed or rudimentary. Can be symptomatic if residual mesenchymal tissues form cysts.

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8
Q

What is the most common supernumerary tooth?

A

Mesiodens. Between the central incisors.

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9
Q

Impacted teeth

A

Teeth forming in bone without erupting.

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10
Q

Dilaceration and problems that arise.

A

An acute bend or angulation of tooth root. Quite common and makes extraction difficult.

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11
Q

Taurodontism

A

Bull-like tooth with no CEJ. The tooth is like a post and straight with no delineation between the root and crown.

Can affect both permanent and deciduous dentitions.
Requires no treatment.

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12
Q

Taurodontism and associated systemic disorders

A

Amelogenesis imperfecta and down’s syndrome.

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13
Q

Dens Invaginatus

A

Dens in dente. Tooth within a tooth. Deep lingual invagination. More common in asians and native americans.

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14
Q

Dens in dente treatment and diagnosis

A

Most commonly there are no symptoms unless the invagination extends into the pulp. Radiographic features are diagnostic. Affected teeth are susceptible to caries and pulp inflammation so they are mostly extracted.

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15
Q

Gemination

A

Tooth twinning. Development of two crowns from a single tooth germ. Affects the anterior teeth. Counting teeth doesn’t work. There is no “normal” number of teeth.

Two crowns, 1 root.

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16
Q

Fusion

A

Union of 2 adjacent tooth germs through the roots by dentin bridges. One less tooth in the arch. May complicate restorative procedures, but the biggest problem is esthetics.

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17
Q

Concrescence

A

Union of adjacent roots through cementum, not dentin. (FUSION IS DENTIN). Only found on roots. Don’t usually have to do anything but periodontal problems are the main risk and can ankylose to the bone.

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18
Q

Enamel Hypoplasia

A

Enamel didn’t form properly. Generalized–> Flourosis. Turner’s tooth–>Single tooth

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19
Q

Turner’s Tooth

A

Enamel hypoplasia effecting only one tooth.

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20
Q

Enamel Flourosis

A

Resembles amelogenesis imperfecta. Generalized enamel hypoplasia.

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21
Q

Hutchinson’s Teeth and Mulberry Molars

A

Notched incisors and globular occlusal surfaces due to excess enamel. Associated with congenital syphilis.

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22
Q

Amelogenesis Imperfecta

A

Disorder of ameloblasts leading to a defect in mineralization of enamel matrix and generalized abnormalities of enamel.

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23
Q

What are the molecular causes of amelogenesis imperfecta?

A

ENAM gene mutations
FAM83H gene mutations
WDR72 gene mutations

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24
Q

What are the recognized types of amelogenesis imperfecta?

A

Hypoplastic, hypocalcified, hypomaturation.

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25
Q

Hypomaturational amelogenesis imperfecta

A

Normally shaped teeth with white opaque enamel. Looks like you have generalized enamel hypoplasia.

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26
Q

Hypocalcified amelogenesis imperfecta

A

Normally shaped teeth with soft and easily lost enamel. Can sometimes be plaque like.

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27
Q

Hypoplasatic amelogenesis imperfecta

A

Pitted enamel. Most important to be familiar with.

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28
Q

Dentinogenesis Imperfecta

A

A hereditary defect in dentin mineralization leading to constriced pulp chambers and opalecent dentin.

29
Q

Dentinogenesis Imperfecta genes, risk, etc.

A

English or french ancestry. 1:8000 in the US.
Several different forms.
Often associated with osteogenesis imperfecta (COL1A1 and COL1A2 gene mutations) and a type 1 collagen defect.

30
Q

Dentin Dysplasia

A

Hereditary defect of dentin. Two types: 1 and 2

Coronal dentin appears normal

31
Q

Type 1 Dentin Dysplasia

A

Normal coronal dentin and root dentin is gnarled with shortened roots. Can get periapical disease and cysts.

32
Q

Type 2 Dentin Dysplasia

A

Affected teeth may show delayed eruption. Considered to be a form of dentinogenesis imperfecta. Debated.

33
Q

Regional Odontodysplasia

A

Ghost tooth Syndrome.
Developmental disorder that affects both dentitions, but more often the permanent teeth.
Enamel and dentin are very thin and undermineralized.
Large pulp.
Very obvious radiographic appearance.

34
Q

Regional Odontodysplasia peak incidence. (age)

A

Ages 2-21.

Pediatric associated disease. Never seen past the age of 21.

35
Q

Regional Odontodysplasia vs Dentin Invaginatas

A

DI only affects one tooth while RO affects a quadrant. Age is also a big factor. RO is only found in kids.

36
Q

Surrounding soft tissue effects in Regional Odontodysplasia

A

Hyperplastic, may contain coalcifications, may contain epithelial rests left behind from developing tooth germs that form cysts.

37
Q

Location of Regional Odontodysplasia

A

Maxilla involved more than mandible. Affects several teeth in a quadrant and multiple quadrant involvement is rare.

38
Q

Congenital pits

A

Autosomal dominant inheritance often associated with cleft lip/palate (Vander Woude Syndrome).
Occur along labial commissure.
Blind tracts or minor salivary gland orifices. 1-4 mm and may contain fluid.

39
Q

Double lip

A

Horizontal redundant fold of the mucous membrane usually found on the inner aspect of the upper lip and sometimes on the lower lip.
Normally only seen when the patient “tenses” the lip.

40
Q

What syndrome is double lip associated with?

A

Asher syndrome: non-toxic thyroid goiter, drooping eyelids and double lip.

41
Q

Ankyloglossia

A

Fibrous union of the tongue to the mouth floor. Occurs in 1 to 10% of neonates. Loss of tongue mobility. Easily corrected through surgical repositioning of the lingual frenum. Only problem is speech impediment

42
Q

Macroglossia

A

Large tongue. Can be congenital or acquired. Problems with chewing, biting, eating and speech. Relative.

43
Q

What other conditions does macroglossia occur with?

A

Hemangioma and lymphangioma.

Nerofibromatosis and amyloidosis.

44
Q

Fordyce’s Granules

A

Clusters of sebaceous glands in the oral cavity involving the oral mucosa. No different than sebaceous glands elsewhere and occur as yellow or white maculopapular lesions. Very common and occur in some studies in as high as 60% of patients.

Ectopic sebaceous gland. Sebaceous carcinoma can arise.

45
Q

Leukoedema

A

White translucent-streak like appearance of buccal mucosa. More common in african americans. Epithelial cells contain more fluid than normal cells and the fluid appears as clear ballooning cells microscopically. No treatment is necessary.

46
Q

What is the distinguishing factors of leukoedema?

A

At least 7 other diseases look exactly like it.

When you stretch the tissues, the lesion will disappear.
Almost always bilateral.

47
Q

White Sponge Nevus general features

A

Autosomal dominant hereditary disorder. Also known as “white folded dysplasia”. Mucous membrane is white, elevated, folded and thickened. May not appear until adolescence. Asymptomatic. Can involve skin and is classified with dermatologic disorders. Keratin 4 and 13 are over expressed.

48
Q

White Sponge Nevus clinical features

A

White and plaque like. Does not disappear when you stretch the tissue. Multifocal, can show up on tongue, floor of mouth, and buccal mucosa. Leukoplakia, but is associated with a specific disease process. Can ulcerate and be painful, but doesn’t turn into cancer.

49
Q

White Sponge Nevus Histopathology

A

Thickened stratum corneum. Ancanthosis of stratum spinosum. Shrunken, pyknotic nuclei.
Lot’s of keratin.

50
Q

White Sponge Nevus Diagnosis

A

Need clinical features, histopathology and family history. May resemble leukoedema, hyperkeratosis and lichen planus.

51
Q

Lingual Thyroid Nodule

A

Ectopic Thyroid tissue in the tongue. May occur in 10% of the population. More common in females. Becomes apparent at puberty. Histology resembles normal thyroid gland. Typically asymptomatic. Hypothyroidism associated in 33% of patients. Don’t cut it out! Almost never turns into cancer.

52
Q

Oral (Lingual) Tonsil

A

Reactive lymphoid tissue within tongue. Also known as foliate papillitis. Appear as elevated nodules or red plaques on tongue or floor of mouth. Histologically appears as normal lymphoid tissue with germinal centers and crypts.

Common. Usually bilateral.

53
Q

Hemifacial Hypertrophy

A

Some facial asymmetry is normal, but this abormal asymmetry. One or both sides of the face. May be present at birth and increases with age, but you don’t really see or notice it until 6 months or a year of age. Can be caused by trauma, infection, heredity, nerve dysfunction.

54
Q

Hemifacial Hypertrophy associated disorders

A

Neurofibromatosis
Fibrous Dysplasia
Arteriovenous malformation

55
Q

Hemifacial Hypertrophy clinical signs

A

Unaffected side may appear large. Affected side my be pigmented. Left side is more commonly affected. Delayed tooth development and or eruption. No treatment other than cosmetic surgery.

56
Q

Cleft lip/palate etiology

A

Heredity and environmental factors implicated. 40% of cleft lip with/without cleft palate is inherited. 20% of isolated cleft palate inherited. Nutritional deficits, trauma, stress, alcohol, drugs, infections are environmental factors implicated in cleft development.

57
Q

Cleft lip/palate incidence

A

1-700 to 1-1000 births. Isolated cleft lip or cleft palate account for 25% of cases. Isolated cleft palate 1-500 to 1-3000 births. 80% of cleft lips will be unilateral. Bilateral cleft lip increases the chance of a cleft palate. The highest to lowest frequency goes: Indians, Asians, White, blacks.

58
Q

Cleft lip/palate treatment

A

Palate surgery usually delayed until 12-18 months. Lip surgery usually performed during first few months. Genetic counseling is important.

59
Q

Facial Osteoporotic Bone Marrow Defect

A

An area of hematopoietic bone marrow within bone that is large enough to produce a radiolucency in edentulous space. Asymptomatic. No cortical expansion. Contains normal hemopoietic bone marrow. Biopsy may be necessary to differentiate.

60
Q

What are the things that differentiates a facial osteoporotic bone marrow defect and what other diseases do they resemble?

A

Almost always in the mandible and almost always women. No expansion of the bone.

Resembles central giant cell granuloma, metastatic disease, odontogenic tumor.

61
Q

Cleidocranial Dysplasia

A

Abnormalities of facial bones and clavicles. Associated with delayed eruption and supernumerary teeth. Big frontal bone (frontal bossing), occipital bones and underdevelopment of the mid face and maxilla. Broad, flat, wide nose.

62
Q

Treatment of Ceidocranial Dysplasia

A

Can extract teeth. Orothodontics may help some patients. Treatment is generally ineffective.

63
Q

What are other names for the Lingual Mandibular Salivary Gland Depression?

A

Stafne bone cyst, static bone cyst, lateral bone cyst

64
Q

General features of the Lingual Salivary Gland Depression

A

Developmental disorder. Caused by a focal concavity of the cortical bone on the lingual surface of the mandible that contains salivary gland tissue. No cortex on the lingual side of the mandible so there is a radiolucent defect.

65
Q

Lingual Salivary Gland Depression X-Ray and Diagnosis

A

Appears as radiolucency below the inferior alveolar canal. Depression contains normal salivary gland tissue. Biopsy or sialography may be needed to establish diagnosis. Can look like cancer, cysts, etc.

66
Q

Median Rhomboid Glossitis General Features

A

Once believed to be a congenital anomaly of tongue development. Most cases are discovered in adults. Now thought to be related to chronic Candida infection causing central papillary atrophy of the tongue. Uncommon.

67
Q

Median Rhomboid Glossitis Clinical Features

A

Appears as a bald spot in the posterior midline of the tongue midline. Filiform papilla are gone. Antifungal therapy may help, but it is recurrent. It will burn and hurt.

68
Q

Benign Migratory Glossitis Clinical Features

A

Geographic Tongue. Multiple, irregular bald areas on the tongue. Localized desquamination of filiform Papillae. Multifocal. Found in many areas, such as buccal mucosa or floor of the mouth. Doesn’t always have symptoms.

69
Q

Geographic Tongue Etiology and treatment.

A

Occurs in 1 to 3% of the population. Females are affected more often than males. Etiology unknown. May be associated with Candida infestation, oral contraceptive use, allergies, diabetes mellitus, psychological conditions.

Antifungal therapy may help.

Oral Pathology (3 decks)

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