Ch. 3 - Acquired and Developmental Disturbances of the Teeth and Associated Oral Structures Flashcards

1
Q

What is the single most common chronic childhood disease?

A

Dental caries

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2
Q

Define Incidence

A

refers to the occurrence of a new case of disease or injury in a population over a specified time period

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3
Q

Define Prevalence

A

the proportion of persons in a population who have a disease at a specified point in time or over a specified time period of time; includes all cases

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4
Q

How many children in the U.S. are born with cleft lip and palate?

A

Every 1 in 1000

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5
Q

What is cleft lip with or without palate caused by?

A

Failure of the maxillary first branchial arch to complete fusion with the frontonasal process in early gestation (4th to 12th week)

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6
Q

what is an alveolar abscess associated with?

A

pulpal necrosis

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7
Q

What percentage of pre-eruptive caries can you see on a BW and PAN?

A

BW - 2%, PAN - 0.5%

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8
Q

what’s another name for pre-eruptive caries?

A

Pre-eruptive coronal resorption or pre-eruptive intracoronal radiolucency

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9
Q

Impacted teeth or teeth delayed in eruption may be at higher risk for developing what kind of lesions?

A

pre-eruptive caries lesions

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10
Q

What are the charactersitics of taurodontism?

A

the body of the tooth enlarges at the expense of the roots; the pulp chamber is elongated and extends deeply into the region of the roots

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11
Q

What is seen as an isolated trait in individuals with syndromes such as tricho-dento-osseous syndrome, otodental dysplasia, and X-chromosome aneuploidies?

A

taurodontism

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12
Q

What stage is taurodontism an anomaly in?

A

morphodifferentiation

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13
Q

Dentinogenesis imperfecta is an anomaly in which stage?

A

histodifferentiation

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14
Q

What is the prevalence of the dentinogenesis imperfecta trait?

A

every 1:8000

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15
Q

The anomaly of DI may be seen in which condition?

A

osteogenesis imperfecta

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16
Q

Characteristics of (Shields) type I dentinogenesis imperfecta

A

with osteogenesis imperfecta

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17
Q

Characteristics of (Shields) type II dentinogenesis imperfecta

A

DI as an isolated incident

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18
Q

Characteristics of (Shields) type III dentinogenesis imperfecta

A

Shell like teeth, multiple pulp exposures; without OI; In this condition, normal dentin formation is confined to a thin layer next to the enamel and cementum, followed by a layer of disorderly dentin containing a few tubules. The roots of shell teeth are short, and the primary teeth may be exfoliated prematurely.

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19
Q

the clinical picture of dentinogenesis imperfecta

A

primary and permanent teeth are a characteristic reddish-brown to blue-gray opalescent color

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20
Q

What’s another name for Dentinogenesis Imperfecta?

A

Hereditary Opalescent Dentin

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21
Q

What do you see in DI soon after the primary dentition is complete?

A

Soon after the primary dentition is complete, enamel is worn and often breaks away from the incisal edges of anterior teeth and the occlusal surfaces of posterior teeth. The exposed soft dentin abrades rapidly, occasionally to the extent that the smooth, polished dentin surface is continuous with the gingival tissue

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22
Q

What is seen on radiographs of patients with DI? What happens to the pulp over time?

A

Radiographs show slender roots and bulbous crowns. The pulp chamber is large initially and undergoes obliteration. Periapical rarefaction in the primary dentition is observed only occasionally

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23
Q

characteristics of dentinogenesis imperfecta in permanent teeth

A

Slender roots with ribbon-like pulp canals and bulbous crowns are characteristic of dentinogenesis imperfecta. The primary molars show periapical rarefaction. Root fractures are common in older patients.

Teeth are reddish brown to blue gray
Enamel worn and breaks away from incisal and occlusal surfaces
Dentin may be continuous with gingiva
Slender root 
Bulbous crowns, obliterated pulp
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24
Q

Treatment plan for patients with DI?

A

The placement of stainless steel crowns on primary posterior teeth. Full-coverage restorations may be placed on the permanent teeth if the crowns need protection in late adolescence or young adulthood. Bonded veneer restorations on anterior teeth have also been used successfully for aesthetic improvement in patients with dentinogenesis imperfecta when full-coverage restorations are unnecessary. Unfortunately, the long-term prognosis of these teeth is poor, and, despite best efforts, they are usually lost in early adulthood. Teeth with periapical rarefaction and root fracture should be removed.

25
Q

What is dentin dysplasia?

A

Dentin dysplasia is a rare disturbance of dentin formation

26
Q

what are the two types of dentin dysplasia?

A

radicular dentin dysplasia (type I) and coronal dentin dysplasia (type II)

27
Q

radicular dentin dysplasia (type I)

A
Primary and permanent dentition affected
Short, pointy roots
Root canals, pulp chambers absent
Chevron-shaped remnant in crown
Crowns opalescent blue or brown
28
Q

coronal dentin dysplasia (type II)

A

Primary teeth opalescent
Obliterated pulp chambers
Permanent teeth-normal color, thistle tube pulp configuration with pulp stones

29
Q

What stage is dentin dysplasia an anomaly in?

A

Dentin Dysplasia- Anomaly in apposition stage

30
Q

Dentin Dysplasia is inherited as what kind of trait?

A

DD is inherited as an autosomal-dominant trait

31
Q

amelogenesis imperfecta affects what dentition?

A

primary and permanent dentitions

32
Q

what is the prevalence of AI?

A

1-14,000 to 1-16,000

33
Q

what are the three types of AI?

A

3 types: Hypocalcified, hypomaturation, hypoplasatic

34
Q

what does hypoplastic AI look like?

A

Hypoplastic- thin enamel with spacing btwn adjacent teeth giving rise to pits;

Enamel matrix imperfectly formed
Hard enamel
Defective in amount
Roughened, pitted surface

35
Q

what does hypomineralized AI look like?

A

Hypomineralized- soft, poorly formed enamel with altered color and translucency

Matrix formation normal
Calcification deficient
Soft enamel

36
Q

what stage(s) can AI be an anomaly in?

A

Anomaly in apposition, mineralization, maturation, histodifferentiation stage

37
Q

treatment for AI?

A

Full coverage crowns

Veneers

38
Q

Odontogenesis Imperfecta, Enamel and Dentin Aplasia

A

Characteristics of both AI and DI
Primary teeth- no enamel, reddish-brown enamel, pulp exposure, pulpal degeneration, large pulp chambers
Permanent teeth-thin, gray enamel, brown dentin on facial of incisors and permanent first molars
SSCs

39
Q

Anodontia

A

Complete failure of the permanent teeth to develop
NOTE: Natal teeth are present at birth
Isolated or part of syndrome
Anomaly in initiation stage
Isolated primary teeth are not affected, part of syndrome, ectodermal dysplasia

40
Q

What stage is anodontia an anomaly in?

A

Anomaly in initiation stage

41
Q

Hypodontia

A

Hypodontia-Agenesis of fewer than 6 teeth, not counting thirds

42
Q

Oligodontia

A

Oligodontia-when more than 6 permanent teeth do not develop

43
Q

What stages of the life cycle are hypodontia and oligodontia and anomaly in?

A

Anomaly in initiation, proliferation stage

44
Q

what are circumvallate papillae? where can they be found? and what purpose do they serve?

A

From 10 to 15 large circumvallate papillae may be found on the posterior border of the dorsum. These papillae have a blood supply and are the site of numerous taste buds.

45
Q

Fungiform (mushroom-shaped) papillae

A

may be distributed over the entire dorsum of the tongue; however, they are present in greater numbers at the tip and toward the lateral margins of the tongue. Inflammatory and atrophic changes occurring on the dorsum of the tongue may involve the vascularized fungiform papillae

46
Q

filiform papillae

A

The most numerous papillae of the tongue are the filiform papillae, which are thin and hairlike, and evenly distributed over the dorsal surface. The filiform papillae are without a vascular core, and their continuous growth is slight.

47
Q

foliate papillae

A

represent a fourth type and are arranged in folds along the lateral margins of the tongue; the taste sensation is associated with these papillae.

48
Q

Gemination

A

it represents an attempted division of a single tooth germ by invagination occuring during the proliferation stage of the growth cycle of the tooth, in which case the geminated tooth appears clinically as a bifid crown on a single root. can be seen in both primary and permanent teeth but it appears more frequently in primary teeth

49
Q

Fusion

A

union of two independently developing primary or permanent teeth. the condition is usually limited to anterior teeth and may show familial tendency. fused teeth with have separate pulp chambers and pulp canals. a frequent finding in fusion of primary teeth is the developmental absence of one of the corresponding permanent teeth

50
Q

concresence

A

fusion of teeth involving only cementum

51
Q

what is cherubism also known as?

A

Cherubism (Familial Fibrous Dysplasia)

52
Q

what is cherubism?

A

Cherubism is a rare childhood disease affecting jaw development. The children have “chubby” facies and upturned eyes, giving the condition its name. Cherubism is usually inherited as an autosomal-dominant trait, with somewhat reduced penetrance in females.

53
Q

Ramon syndrome

A

(cherubism, eye anomalies, epilepsy, mental deficiency, hypertrichosis, lack of growth, juvenile rheumatoid arthritis, and gingival fibromastosis).

54
Q

what are radiographic characteristics of cherubism and outcomes of the disease?

A

Characteristically there is a symmetric enlargement of the jaws that may be noted at an early age. Radiographically the condition presents multilocular areas of bone destruction (soap-bubble lesions) and thinning of the cortical plate ( Fig. 3-10 ). Teeth in the involved area may exfoliate prematurely because of the loss of support or root resorption or, in permanent teeth, because of interference in the development of roots. Spontaneous loss of teeth may occur, or the child may pull the teeth from the soft tissue. Developing permanent teeth are usually ectopic, being displaced by the growing lesion.

55
Q

what is acrodynia and what are its effects?

A

Acrodynia or pink disease results from the exposure of young children to minute amounts of mercury; ointments and medications are the usual sources of the mercury.
The clinical features of the disease include fever, anorexia, desquamation of the soles and palms (causing them to be pink), sweating, tachycardia, gastrointestinal disturbance, and hypotonia. The oral findings include inflammation and ulceration of the mucous membrane, excessive salivation, loss of alveolar bone, and premature exfoliation of teeth

56
Q

Hypophosphatemia (Familial or X-Linked Hypophosphatemic Rickets or Vitamin D–Resistant Rickets)

A

hypophosphatemia is the most common inherited abnormality of renal tubular transport. 19 Clinical features become evident in the second year of life and include short stature and bowing of the lower extremities in affected boys. Premature tooth exfoliation is sometimes also a feature. The inheritance pattern of the disease is usually X-linked dominant, and the disorder is twice as common in females as in males.

57
Q

Cyclic Neutropenia (Cyclic Hematopoiesis)

A

Cyclic neutropenia is an autosomal-dominant condition in which affected individuals are at risk for opportunistic infection during intervals of neutropenia that occur in a 21-day cycle concomitant with oscillation in bone marrow blood cell production. The condition may appear at any age, and numerous cases in children have been reported. The patients have fever, malaise, sore throat, stomatitis, and regional lymphadenopathy as well as headache, cutaneous infection, and conjunctivitis accompanying the neutropenia. Children exhibit severe gingivitis with ulceration. When the neutrophil count returns to normal, the gingiva may return to a nearly normal clinical appearance. Children experiencing repeated insults from the condition have a considerable loss of supporting bone around the teeth.

58
Q

conditions that may cause premature exfoliation of teeth

A

Premature exfoliation due to periodontal disease may be caused by quantitative neutrophil disorders or qualitative disorders, including acatalasia, Chédiak-Higashi syndrome, or leukocyte adhesion defect (LAD). Early loss of primary teeth is seen in other systemic conditions, such as Coffin-Lowry syndrome, Down syndrome, Ehlers-Danlos syndrome types IV and VIII, Hajdu-Cheney syndrome, hyperpituitarism, hyperthyroidism, juvenile diabetes, Papillon-Lefèvre syndrome, progeria, Singleton-Merten syndrome, Langerhans’ cell histiocytosis (see Chapter 28 ), and the leukemias

59
Q

Amelogenesis occurs in how many stages… and what happens?

A

Amelogenesis occurs in three stages. In the first stage, the enamel matrix is secreted by ameloblasts and in the second stage, it undergoes calcification; a final stage of enamel maturation, with crystal growth and removal of water and protein, continues until eruption. Local or systemic factors that interfere with normal matrix formation cause disorders of tooth quantity with enamel surface defects and irregularities termed enamel hypoplasia . Factors that interfere with calcification and maturation of the enamel and are disorders of quality are termed enamel hypocalcification .