Journal Reading 1

CUT BUNGA DARA PHONNA

2213501010027
GELOMBANG 51
 Should know the differentiation from
vascular malformation
INTRODUCTION Present at birth
Infatile Hemangioma
• Absent at birth, but may appear and
proliferate rapidly for months
INFALITE HEMANGIOMA • Appears during neonatal period
• Female 3 time more affected
Vascular tumor = benign neoplasms that are • Size: 0.5-5.0 cm
a result of proliferating endothelial cells. • rapid proliferation during the neonatal period
and continuing through infancy
Can be life threatening, • each its greatest dimension of growth by the
but can resolve on their child’s 5th month of life
own • most lesions slowly involute or shrink in size
THE MOST COMMON TUMOR OF INFANCY • Superficial or deep
• Superficial = brighter red, deep = blueish
hue
No realiable method for • Located: head and neck, but can affect trunk
determining which and extremites
lesion will
spontaneously resolve
REFERRAL
and which lesion need
intervention
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 INFALITE HEMANGIOMA
Local complication: bleeding, tissue destruction, and pain Identification of
genetic differences
Systemic sequelae: thrombocytopenia, congestive heart
may be useful in the
failure (CHF), and death
future
Increase incidence by: Twins, preterm infants, advanced
maternal age, and placental anomalies

GENETIC genetic variants associated with germline mutations in the VEGFR2, VEGFR3, and TEM8
FACTOR? genes. These genes regulate major angiogenesis-signaling pathways, suggesting
hyperactivation of VEGFR2 signaling in the pathogenesis of infantile hemangiomas

the expression of the GLUT 1 gene was present in infantile hemangiomas but
not in other vascular tumors.
still not enough
information to explain the
inheritance model
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 CASE PRESENTATION/
MATERIALS AND
METHODS

• Patient: infant, 5-month-old-female

• Parent’s chief: “she has a red thing that has been growing in
her mouth”

• Anamnesis:
 Patient was born at full term with no complication
 The lesion was not noted at birth
 patient was not displaying any abnormal signs or symptoms
for a child of that age
 Fed regularly and had normal sleep pattern
 Didn’t show excessive irritability
 No history of excessive vomiting, diarrhea, fever, or cough.
 The mother concerned about the location being in the mouth
and what the repercussions would be
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 5 month years old
Intra-oral examination:
• Size: 2.5 cm x 3.5 cm
• well-circumscribed red/crimson macule with a 1 mm white
dot in the center
• Located: on the posterior portion of the upper left alveolar
ridge spanning to the mid-palate
• no other abnormal soft tissue findings

No radiographs were taken

11 month years old

Intra-oral examination:
• Size: 3.5 cm x 3.5 cm
• well-circumscribed, non-contiguous, red/crimson macule
with a 1 mm white dot in the center
• Located: on the posterior portion of the upper left alveolar
ridge spanning to the mid-palate

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 DISCUSSION
HEAL WITH AND WITHOUT:
Scarring
Telangiectasia
INFATILE HEMANGIOMA Yellowish hypoelastic patches
Dermal atrophy

Appears: neonatal period (2w after delivery)

1st step (proliferative phase): growth rapidly, can last up to one year, mucosa/skin
becomes irregular, raised and crimson.

Final size during 5 month of the child’s life

Plateau phase: lesion slowly continuous to grow for 1-8 years

Involution phase (last): the color fades, and the mucosa is more pink
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 DIAGNOSIS:

Clinical Screening
Diascopy
exam question
Evaluate: size, borders, History, duration, CAUTION:
color, and location growth history and Avoid use glass or plastic
appearance breakage  induce
bleeding
Can range from
erythematous macule to a
deeper mass w/ red or blue
surface INFATILE HEMANGIOMA: CAN BE
Can affect:
LIFE-THREATING !!!
Trunk or
Oral
extremites High risk

Sequale IH  induce ulceration (common, 16%) and fissure formation

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 MANAGEMENT

INFATILE HEMANGIOMA

Oral and perioral Trunk or extremites

High risk Low risk

High propensity for bleeding or Consultation with dermatologist
ulceration with normal mastication

REFER TO: First line treatment for ulcerated

Specialist Medical Team:
Oral and maxillofacial pathology
Oral and maxillofacial surgery
Dermatologist
Pediatrician
or proliferating IH:
Oral propranolol (3 mg/Kg/day)
Evaluated at regular recall
intervals

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 CONCLUSIONS

Although the lesion of IH are generally benign in nature, there still need to be a proper diagnosis and
understanding of the prognosis, clinical course and treatment rationale.

Lesion <2 cm and not located on the face or in the oral cavity  less risk

Lesion that located in oral cavity  referred to a specific hemangioma team for evaluation

Role of the dentist or other health care provider  make an accurate diagnosis, provide guidance to
the family, provide proper referrals (OMP, ENT, or dermatologist)

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Journal Reading 2

CUT BUNGA DARA PHONNA

2213501010027
GELOMBANG 51
 consists of a group of diseases characterized
by non-caseating granulomatous lesions of
ORAL GRANULOMATOSIS hard and soft orofacial tissues
often associated with systemic involvement.

Inflammatory
Sarcoidosis Tubeculosis Leprosy
bowel disease

Merkelson
Granulomatosis Meishners
Rosenthal
with polyangiitis chelitis
disease

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 Often on Early adult-hood
Etiology: UNKNOW Rare on children
Can caused by:
Sarcoidosis genetic, exposure to certain environmental agents and infectious
organisms (viruses, mycobacterium, propionibacterium acnes, borrelia
burgdorferi) and allergens

Diagnosis:
Characterized by:
clinical presentation, system involved, clinical and radiographic assessment,
non-caseating
and laboratory tests
granuloma formation

Clinical features:

Multi organ Occur in acute and May be progressive Oral involvement

involvement chronic form or regress (uncommon):
spontaneously Gingival
enlargement

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 11 years old female patient of Asian
origin and Dravidian descent

CASE REPORT Chief complaint: swollen gums since one

year, which had gradually covered her
teeth

Anamnesis:
• Pain and Bleeding (while brushing
teeth)
• Difficulty in chewing food
• Notice when she was 10 y.o
• Puberty at 10y 6m
• No history: spontaneous gingival
bleeding or drug intake
• No family history with similar complaint

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 Extraoral examination:
• Competent lips and a straight facial
profile
CASE REPORT • Lips: swollen and nontender with
perioral skin discoloration

Intraoral examination
• Mild crowding dentition
• Enlargment of the gingiva involving both facial
and palatal/lingual aspect of all teeth
• Gingival enlargement: red, smooth (bsc loss
stippling), shiny, obliteration of gingival
contour
• Interdental papilla: swollen and lobulated
• BOP (+)
• Poor OH

Panoramic radiograph: minimal interdental bone loss

Routine hematologic examination: all values  normal
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 Can caused by: Poor OH, Hormonal changes, systemic illness,
Gingival Enlargement metabolic disease, hematologic disorder,
nutritional deficiency, or it may be hereditary,
drug induced or idiophatic

IN THIS CASE:
the quantity of plaque deposits did not commensurate with the
Poor OH
quantum of gingival enlargement.

Crowding dentition aggravated the inflammation

Pubertal gingivitis? patient had attained puberty a year ago

hereditary gingival the parent gave a negative family history for similar
enlargement? condition

Drug induced
EXCLUDED
No intake of any systemic medication
hyperplasia?

Melkersson-Rosenthal Not associated with any facial paralysis and

15 Syndrome? fissured tongue
 PROVISIONAL DIAGNOSIS: IDIOPATHIC GINGIVAL ENLARGEMENT

Trearment planning:
• CHX 0.2% = rinse twice daily, 10 mL, for 2 weeks
• Gingival tissue showed no improvement  surgical excision (under local anesthesia,
using external bevel gingivectomy technique, and send the excised tissue for
histopathologic examination)

Histopathologic examination
• There is non-caseating granulomatous of epitheloid histiocyte with numerous
multinucleated Langerhans giant cells

Suspect: Tuberculosis, Crohn’s disease and Sarcoidosis

EXCLUDED EXCLUDED REFER TO PEDIATRICIAN

Mantoux test and sputum test: negative The patient didn’t give any history of No pulmonary involvement
Chest radiograph: absence of hilar gastrointestinal disturbances, or No other systemic features of
lymphadenopathy changes in bowel habit sarcoidosis

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 • Differential count of white blood cells revealed mild eosinophilia (5%).
• Biochemical analysis showed elevated levels (1048.35 nkat/L) of serum Angiotensin Converting
Enzyme (sACE).
• Serum and urinary calcium level = normal

The clinicopathologic picture and biochemical laboratory investigations strongly indicated a diagnosis of
OROFACIAL SARCOIDOSIS

Treatment:
• Gingival excision was complete previously
• Observation for 6 months and no systemic medication
• Follow-up 1 week, later at 1, 6, 12 and 18 months

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 There are no pathognomic clinical
DISCUSSION features of oral sarcoidosis

ORAL SARCOIDOSIS SYSTEMIC SARCOIDOSIS

• On 20-60 decade of life (often female) Involve tissues in maxillofacial region
• Affect any site of the mouth (salivary gland, mandibular lymph
• Most often: asymptomatic nodes and ocular area
• Clinical appearance: redness, swelling,
papule, or submucosal nodule
with/without ulceration or presence of
perforation
Diagnosis:
• Clinical feature
• Histopathological evidence (non-
caseating epithelioid granuloma)
• Elevated serum Angiostensin Converting
Enzyme (sACE) levels
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 IN THIS CASE: AFTER 18 MONTHS

Asymptomatic and had no history
of abdominal pain or
gastrointestinal disturbances
no recurrence of gingival
enlargement and no new
Follow-up
complains related to general
health and well-being of the child

Thus, based on the clinical, biochemical and histological evidence the present case is of

orofacial granulomatosis— sarcoid type/sarcoidosis

should be considered as one of the differential diagnosis for gingival

enlargements in young individuals when the other causes are ruled
out and the patient appears apparently healthy

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 CONCLUSION

• Orofacial sarcoidosis in children is a rare condition

manifesting as generalized gingival enlargement and non-
tender lip swelling.
• Pediatric dentist and oral health physicians should be
aware of this condition and its management.

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 THANK YOU

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