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Exam 2: DHHD 5002 > Jones 2 > Flashcards

Jones 2 Flashcards

1
Q

What is PROGRESSIVE HEMIFACIAL ATROPHY (ROMBERG or PARRY-ROMBERG SYNDROME)?

A

Degenerative condition associated with atrophic changes on one side of the face

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2
Q

Cause of Progressive Hemifacial Atrophy

A

-Cause is unknown: malfunction of the cervical sympathetic nervous system, trauma, Lyme disease

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3
Q

Progressive Hemifacial Atrophy shares similar features to _______.

A

Scleroderma

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4
Q

When does Progressive Hemifacial Atrophy begin and who is it more prevalent in?

A
  • Begins during the 1st and 2nd decades

- Females > males

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5
Q

Features of Progressive Hemifacial Atrophy

A
  • Atrophy of the skin and subcutaneous structures
  • Hypoplasia of the underlying bone
  • Pigmented skin in affected area
  • “Coup de sabre” (strike of the sword); occurs on the midline of the forehead
  • Enophthalmos: due to loss of periorbital fat
  • Alopecia
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6
Q

Oral manifestations of Progressive Hemifacial Atrophy

A
  • Mouth and nose are deviated to the affected side
  • Unilateral atrophy of the tongue
  • Unilateral posterior open bite
  • Delayed eruption of teeth
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7
Q

Treatment of Progressive Hemifacial Atrophy

A
  • Atrophy progresses slowly for years and then becomes stable
  • Plastic surgery
  • Orthodontic therapy
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8
Q

Characterizations of CROUZON SYNDROME (CRANIOFACIAL DYSOSTOSIS)

A
  • Characterized by premature closure of the cranial sutures
  • Autosomal dominant trait
  • New mutations are due to an increase in paternal age
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9
Q

Cranial malformations of Crouzon Syndrome

A

Cranial malformations:

  • Brachycephaly (short head)
  • Scaphocephaly (long and narrow head)
  • Trigonocephaly (triangular shaped head)

Ocular proptosis, visual impairment, blindness, headaches, hearing deficits

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10
Q

Oral manifestations of Crouzon Syndrome

A
  • Midface hypoplasia due to an underdeveloped maxilla
  • Crowded maxillary teeth
  • Occlusal abnormalities
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11
Q

Treatment of Crouzon Syndrome

A
  • Early craniectomy to relieve increased intracranial pressure
  • Frontoorbital advancement
  • Midface advancement
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12
Q

Characterizations of MANDIBULOFACIAL DYSOSTOSIS(TREACHER-COLLINS SYNDROME)

A
  • Characterized by defects in structures derived from the 1st and 2nd branchial arches
  • Autosomal dominant trait
  • 60% of new mutations are due to increased paternal age
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13
Q

Features of Mandibulofacial Dysostosis

A

-Hypoplastic zygomas
-Narrow face
-Depressed cheeks
-Downward slanting palpebral fissures
-75% have a coloboma (notch in the outer portion of the lower eyelid)
-Missing lower lid lashes
Deformed or misplaced pinnae
-Absence of the external auditory canal: Leads to hearing loss

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14
Q

Oral manifestations of Mandibulofacial Dysostosis

A
  • Hypoplastic mandible
  • Retruded chin
  • Hypoplastic coronoid and condylar processes
  • Cleft palate (1/3 of cases)
  • Hypoplastic or missing parotid glands
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15
Q

Treatment of Mandibulofacial Dysostosis

A

-Mild cases: no treatment
-Severe cases:
Cosmetic surgery, Orthodontic therapy, Orthognathic surgery

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16
Q

Characteristics of CLEIDOCRANIAL DYSPLASIA

A
  • Characterized by defects that primarily involve the skull and clavicles
  • May affect other bones
  • Autosomal dominant trait
  • 40% of cases are spontaneous mutations
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17
Q

Features of Cleidocranial Dysplasia

A
  • Short stature, enlarged skull, frontal and parietal bossing
  • Ocular hypertelorism, broad nose base
  • Midface hypoplasia leading to a relative prognathism
  • Long neck, narrow shoulders with marked drooping
  • Mobile shoulders due the absence or hypoplasia of the clavicles
  • Clavicles are absent in 10% of the cases
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18
Q

Oral manifestations of Cleidocranial Dysplasia

A
  • Narrow high-arched palate, cleft palate
  • Retained primary teeth
  • Unerupted secondary teeth
  • Supernumerary teeth
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19
Q

Treatment of Cleidocranial Dysplasia

A
  • Extraction of primary and supernumerary teeth
  • Exposure and orthodontic extrusion of permanent teeth
  • Orthognathic surgery
20
Q

Characteristics of Double Lip

A
  • Redundant mucosal fold
  • Incidence: rare
  • Congenital or acquired: trauma, parafunctional habits
  • Site: upper lip
  • Visible with smiling or tensing of lip
21
Q

Treatment of Double Lip

A
  • Treatment: cosmetic surgical reduction

- Prognosis: excellent

22
Q

Association of Double Lip with ________.

A

Association with Ascher syndrome:

  • Double lip
  • Blepharochalasis
  • Non-toxic thyroid enlargement
  • Autosomal dominant inheritance
23
Q

Characteristics of Fordyce Granules

A
  • Ectopic sebaceous glands
  • Incidence: common (80% of population)
  • Multiple yellow, white papular lesions
  • Site: buccal mucosa, upper vermilion
  • Age: adults
  • Asymptomatic
24
Q

Histology and Treatment of Fordyce Granules

A
  • Histology: Submucosal sebaceous lobules
  • Treatment: none
  • Prognosis: excellent
25
Q

Characteristics of Leukoedema

A
  • Incidence: common
  • Etiology: unknown - edematous mucosa
  • Normal anatomic variation
  • Race: Blacks (90% - adults, 50% - children)
  • Site: buccal mucosa
  • Milky opalescent gray white folded mucosa
  • Diminishes on stretching, does not rub off
  • Smokers - more common/severe
26
Q

Histology and Treatment of Leukoedema

A 
-Histology: 
Acanthosis
Intracellular edema 
Hyperparakeratosis
-Treatment: none required
-Prognosis: excellent
27
Q

Characteristics of Linea Alba

A
  • Common alteration of the buccal mucosa
  • Associated with pressure, frictional irritation, or sucking trauma
  • Bilateral white lines at the level of the occlusal plane of the adjacent teeth
28
Q

Histology and Treatment of Linea Alba

A

Histopathologic features:

  • Hyperorthokeratosis
  • Intracellular edema

Treatment and prognosis:

  • None
  • Spontaneous regression may occur
29
Q

Characteristics of Macroglossia

A
  • Enlarged tongue
  • Incidence: common
  • Wide variety of causes: Hereditary/congenital, acquired
  • Common in children
  • Crenated lateral border
30
Q

Complications of Macroglossia

A
  • Open bite and malocclusion
  • Airway obstruction
  • Speech difficulties
  • Drooling
  • Feeding problems
  • Ulceration and infection
31
Q

Heredity/congenital associations of Macroglossia

A
  • Vascular malformations
  • Down syndrome
  • Neurofibromatosis
  • Multiple endocrine neoplasia syndrome
  • Cretinism
  • Mucopolysaccharidoses
  • Beckwith-Wiedemann syndrome**
  • Facial hemihypertrophy
32
Q

Features of Beckwith-Wiedemann Syndrom (associated with Macroglossia)

A
  • Omphalocele
  • Visceromegaly
  • Gigantism
  • Neonatal hypoglycemia
  • Visceral malignancies
  • Nevus flammeus
  • Maxillary hypoplasia
33
Q

Acquired associations of Macroglossia

A
  • Edentulous
  • Amyloidosis
  • Myxedema
  • Acromegaly
  • Angioedema
  • Neoplasms: carcinoma
34
Q

Histopathology and Treatment of Macroglossia

A 
Histopathology:
- Related to specific cause
Treatment: 
- Reduction glossectomy 
Prognosis: 
- Good
- Related to specific cause
35
Q

Characteristics of Ankyloglossia

A
  • Short thick lingual frenum
  • Limitation of tongue movement
  • Incidence: common
  • Range of severity
  • Complications: open bite, speech and swallowing problems
36
Q

Treatment of Ankyloglossia

A
  • Treatment: frenectomy (defer until after age 4-5)

- Prognosis: good

37
Q

Characteristics of Lingual Thyroid

A
  • Ectopic thyroid tissue
  • Incidence: uncommon
  • Failure of thyroid migration
  • Tongue base mass
  • Gender: female > male (4:1)
  • Becomes evident at puberty or during pregnancy and menopause
  • 70% - represents only thyroid tissue
38
Q

Symptoms and Diagnosis of Lingual Thyroid

A

Symptoms: - Mass sensation - Dysphagia, dysphonia, and dyspnea
Hypothyroidism (15-33%)
Diagnosis: - Thyroid scan (iodine isotopes, technetium) - Biopsy with caution (highly vascular)

39
Q

Treatment of Lingual Thyroid

A

Treatment: - Suppression (thyroid hormone therapy) - Ablation (radioactive iodine) - Surgical resection
Prognosis: good
Malignancy - Rare (1% incidence)

40
Q

Characterizations of Fissured Tongue

A
  • Grooves or fissures on dorsal tongue
  • Incidence: common; 2-5% of population
  • Local factors, aging
  • Gender: male > female
  • Increasing prevalence and severity with age
  • Asymptomatic; mild burning or soreness
41
Q

Treatment of Fissured Tongue

A

Treatment:
- No specific therapy
- Hygiene measures: brushing
Prognosis: good - benign condition

42
Q

Associations of Fissured Tongue

A 
Geographic tongue
Melkersson-Rosenthal syndrome
- Orofacial granulomatosis 
- Facial paralysis
- Fissured tongue
Down syndrome
43
Q

Characterizations of Hairy Tongue

A 
Dorsal tongue surface
Incidence: 0.5% of adult population
Associated conditions: 
- Smoking
- Antibiotic therapy
- Debilitation, poor oral hygiene
- Oxidizing mouthrinses
- Antacids
44
Q

Features and Symptoms of Hairy Tongue

A

-Elongated filiform papillae and/or hyperparakeratosis
-Microbial colonization
-Pigmentation/staining (microbial/exogenous)
-Symptoms:
Gagging
Dysgeusia
Halitosis
Esthetic concerns

45
Q

Treatment of Hairy Tongue

A

Treatment:

  • Eliminate predisposing factors
  • Oral hygiene measures: Brushing/scraping tongue

Prognosis: good, benign condition

46
Q

Characterizations of Varicosities

A
  • Dilated tortuous veins
  • Etiology: aging
  • No association with hypertension or cardiovascular disease
  • Asymptomatic
  • Sublingual: 2/3 adults > 60 years of age
  • Solitary: lips, buccal mucosa
47
Q

Histology and Treatment of Varicosities

A
  • Histology: dilated thin walled vein
  • Thrombosis: leads to phlebolith
  • Treatment: None required or Surgical removal
  • Prognosis: good, benign condition

Exam 2: DHHD 5002 (10 decks)

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