PEDIATRIC

PATHOLOGY
GLO ARBY ARGUELLES,
DMD
 ODONTOGENIC DEVELOPMENT

 Lobes = primary center of ossification of the tooth.

 Lobes are separated by developmental grooves in posterior teeth.
 Lobes are separated by developmental depressions in anterior teeth.
 All anterior teeth have four lobes (three labial and one cingulum).
 Premolars have three buccal lobes and one lingual lobe (Mn second PM = 3 buccal + 2 lingual).
 First molars have five lobes (one for each cusp).
 Second molars have four lobes (one for each cusp).
 Third molars have at least four lobes
TOOTH HISTOGENESIS (CHRONOLOGIC ORDER)

• Ectomesenchyme influences the downgrowth of oral epithelium → tooth germ.

• Elongation of inner enamel epithelial cells of enamel organ.
• Differentiation of odontoblasts.
• Deposition of the first layer of dentin.
• Deposition of the first layer of enamel.
• Deposition of root dentin and cementum
LIFE CYCLE OF A TOOTH (CHRONOLOGIC
ORDER)
• Initiation (bud stage): Interaction of oral epithelium ectomesenchyme → dental lamina.
• Proliferation (cap stage): Formation of the shape of the tooth and enamel organ.
• Differentiation (bell stage): Differentiation into specific tooth tissue types, histodifferentiation.
• Apposition: Cells from the bell stage begin depositing their corresponding tissues.
• Calcification: Primary teeth begin calcification during second trimester.
• Eruption: Emergence of tooth through gingiva.
 ODONTOGENIC PATHOLOGY

FUSION VS. GEMINATION VS. CONCRESENCE

FUSION GEMINATION CONCRESCENCE

Two tooth buds joined together One tooth bud splits A form of fusion
Evident of dentin contact Incomplete formation of two teeth Cementum contact
Appear as a Macrodont (large crown) Hard to differentiate vs. fusion Occurs after root formation completed

Usually with two root canals Two crowns on a single root Arise as a result of trauma

Usually seen in incisor areas Usually in incisor region

If the tooth count is reduced, it is fusion If tooth count is normal, it represents
gemination
 ODONTOGENIC PATHOLOGY
ATTRITION VS. ABRASION VS. EROSION
ATTRITION
Physiologic wearing away of tooth
structure.
Normal aging consequence.
Seen on incisal edges, occlusal surfaces, Result from abnormal mechanical habits Lingual surface of patients with chronic
and proximal surfaces of the teeth
Often present as flatten incisal edges
Example = bruxism
ABRASION EROSION
Pathologic wearing away of tooth Chemical loss. tooth structure due to
structure due to mechanical forces. tooth structure.
Toothbrush-abraded tooth presents with Labial surfaces of patients who ingest
a clinical V-shaped ditch on the affected large amounts of acidic beverages, or in
surface people who suck on citrus fruits
habits of vomiting (anorexia nervosa)
Eroded tooth usually displays a shallow
smooth scooped-out depression.
ODONTOGENIC PATHOLOGY
ENAMEL HYPOCALCIFICATION VS. ENAMEL HYPOPLASIA
ENAMEL HYPOCALCIFICATION
■ Normal quantity but bad quality
■ Defective maturation of ameloblast
■ Defect in mineralization matrix
■ Chalky teeth and yellow to brown
■ Affects both deciduous succedaneous
teeth
ENAMEL HYPOPLASIA
■ Normal quality but deficient quantity of
the enamel
■ Defective enamel matrix formation
■ No contact between teeth
■ Affects both deciduous and succedaneous
teeth
■ Hereditary and environmental form
■ Seen in children with hypoparathyroidism
 AMELOGENESIS IMPERFECTA

• Hereditary form of enamel hypoplasia.

• Involves the complete primary and permanent dentitions.
• Inherited dominant trait → soft and thin enamel.
• Teeth appear yellow to brown due to the thin enamel and dentin showing through.
• With a healthy enamel covering teeth are easily damage and susceptible to decay.
• Dentinal tissue and pulpal tissue are not affected.
• Teeth can be treated with full crowns since only the enamel is affected.
• Don’t get confused with dentinogenesis imperfecta.
• Radiographic you will see teeth similar to crown preparation
DENTINOGENESIS IMPERFECTA

• Inherited dominant trait

• Undermineralization of dentin
• Affect both deciduous and permanent teeth
• Gray to brown appearance: “opalescent hue”
• No pulp cavity.
• Bulbous crowns with short roots
• Type I associated with osteogenesis imperfecta (blue sclera, fragile bones, hearing loss)
• Type II most common
• Type III have multiple pulpal exposures in primary dentition
 EARLY CHILDHOOD CARIES (ECC)

• Formerly known as nursing bottle syndrome.

• Defined as rampant decay that results from sleeping with feeding bottle.

• Most common deciduous teeth = maxillary incisor.

• General involvement = maxillary anterior teeth.

• Also known as = baby bottle tooth decay (BBTD), bottle-mouth syndrome, early childhood caries, nursing caries, bottle caries, and
infant caries.

• Encourage infants to drink from a cup prior to first birthday.

• Supplement infant’s diets with nonliquid 4–6 months of age.

• Serve liquids with sugar from a cup.

• Initiate oral hygiene with the eruption of the first primary tooth.

• First dental visit within the first 6 months of eruption of first tooth.
 ACUTE NECROTIZING ULCERATIVE GINGIVITIS
(ANUG)

• Usually in people of 15–35 years old

• Also known as Vincent’s infection, Vincent’s angina, and trench mouth
• Symptoms = painful hyperemic gingival, punched out erosions covered by gray pseudomembrane, and fetid odor
• Risks = bad oral hygiene, poor nutrition, smoking, and stress
• Bacteria = Fusiform, Spirochetes, and Prevotella intermedia
• Rare in preschool children
• Treatment include: debridement, hydrogen peroxide rinses, and antibiotics
SYSTEMIC PATHOLOGY

ACHONDROPLASIA

• Form of short-limb dwarfism

• Equal frequency in male and females
• Large head with short arms and legs compared to trunk length
• Deficient cranial base growth
• Small maxilla
• Commonly will class III malocclusion
• Delayed eruption and exfoliation of teeth
• Underdeveloped mandible
SYSTEMIC PATHOLOGY

GIGANTISM

• Condition characterized by excessive height growth

• Rare condition of pituitary gigantism due to prepubertal growth hormone excess
• Oversecretion by a group of somatotrope cells of the anterior pituitary gland
• Enlarged tongue
• Mandibular prognathism
• Longer roots
SYSTEMIC PATHOLOGY

GINGIVOSTOMATITIS

• Herpes simplex virus-1 (HSV-1) infection → sores of mouth and gingival.

• Acute/primary form generally involves children under age of 3.
• Prodromal symptoms (fever, malaise, irritability, headache, dysphagia, vomiting,
lymphadenopathy) of 1–2 days before appearance of ulcers.
• Treatment: relief of symptoms and maintain nutritional and fluid intake.
• Sequelae: Recurrent herpes labialis, HSV-1 antibodies.
SYSTEMIC PATHOLOGY

COXSACKIE VIRUS

• Painful white/yellow ulcers with bright red surroundings.

• Cause aphthous ulcers.

• Trigger by stress, menstrual cycles, hormonal changes, allergies.
• Begin with tingling or burning sensation.

• Pain ↓ in 7–10 days with complete healing 1–3 weeks.

• Recurrent ulcers are primary on mucosa while herpetic lesions on tissue bound periosteum.
• Recurrent aphthous minor: less than 1 cm in diameter, last ≈2 weeks.

• Recurrent aphthous major: over 1 cm in diameter, last ≥2 weeks, and heal with scarring.

• Recurrent herpetiform: cluster of ulcers.

• Frequent recurrences of ulcers should be screened for diabetes mellitus or Behcet’s syndrome.
• Treatment include: topical steroids (Triamcinolone).
SYSTEMIC PATHOLOGY
CRETINISM

• Severe hypothyroidism
• Characterize by defective mental and physical development
• Dwarfed bodies with curved spines and pendulous abdomen
• Limbs are distorted
• Harsh and scanty hair
• Under developed mandible
• Over developed maxilla
• Enlarged tongue
• Delayed eruption of teeth
• Retained primary teeth
• Adult hypothyroidism = myxedema.
CRANIOFACIAL ANOMALIES

FACIAL CLEFTS

• Cleft lip (CL) and cleft palate (CP) account for half of the total number of defects.
• CL = separation of the two sides of the lip.
• CP = an opening in the roof of the mouth which the two sides of the palate did not join.
• Both CL and CP can be unilateral or bilateral.
• Unilateral CL and CP is an isolated nonsyndromic birth defect
• CL- and CP-associated syndromes include Stickler’s, Vander Woude’s, and DiGeorge syndrome.
• Chances of a family having more than one child with a cleft after having a child with unilateral CL and CP is
approximately 2–4%. (Keep in mind incidences do increase with additional family history and bilateral clefts.)
CRANIOFACIAL ANOMALIES

CLEFT PALATE (CP)

• Occur in approximately 1 in 700 live births (CL and CP).

• CP alone is seen in approximately 1 in 2000 live births.
• Occurs during sixth to eighth week in utero.
• Isolated clefts are more common in females.
• Fissure in the midline of the palate due to failure of fusion of the two sides of the palate.
• Impaired speech and swallowing.
• Inability for soft palate to close the air flow into the nasopharynx
CRANIOFACIAL ANOMALIES

CLEFT LIP (CL)

• Occurs during fifth to sixth week in utero

• Failure of maxilla and frontonasal processes to merge
• More common in males
• More frequent on the left side than the right
CRANIOFACIAL ANOMALIES

CLEFT LIP (CL)

FOUR CLASSES OF CL

• Class I: Unilateral notching of vermillion not extending to lip

• Class II: Same as class I but extending into lip but not to floor of the nose
• Class III: Class II + extending into floor of the nose
• Class IV: Any bilateral cleft of the lip
TIMING OF TREATMENT FOR CL AND CP

• CL repair should occur 10 weeks after birth.

• CP repair should occur 9–18 months after birth.
• Pharyngeal flap or pharyngoplasty 3–5 years or later depending on speech development.
• Alveolar reconstruction 6–9 years based on dental development.
• Cleft orthognathic surgery 14–16 years in girls and 16–18 years in boys.
• Cleft rhinoplasty surgery depends on skeletal maturity. Rule of 10’s for timing of
CL repair Infant should be:
• CL revision at anytime but best after age 5 ≥10 weeks old, ≥10 g/dl
hemoglobin, and ≥10 lbs.
PIERRE ROBIN SYNDROME

• Collagen gene 2A1 mutation

• Hypermobility of joints
• Mitral valve prolapse
• Micrognathia leading to breathing and feeding difficulties
• Glossoptosis
• High arched CP
TREACHER COLLINS SYNDROME

• Also called mandibulofacial dysostosis

• Mutation of 5q32 gene
• Downslanting of eyes
• Notched lower eyelids
• Midface developmental deficiency
• Underdeveloped, malformed, and/or prominent ears
DOWN SYNDROME

• Low caries susceptibility.

• Trisomy 21.
• Delayed physical and mental development.
• Delayed eruption of teeth.
• Short and stocky stature.
• Face is broad and flat, with slanting eyes, and a short nose.
• Ears are small and low set.
• Heart defects are common! (Check for prophylactic requirement.)
CONFUSING “OMAS”
HEMANGIOMA | LYMPHANGIOMA | NEUROFIBROMA
HEMANGIOMA LYMPHANGIOMA NEUROFIBROMA
Most common benign tumor of Well-circumscribed mass of Moderately firm and encapsulated
infants lymphatic vessels
Due to proliferation of blood Most in neck and axilla Proliferation of Schwann cells
vessels
Growth is independent of the Are red to blue translucent masses On tongue, buccal mucosa,
growth of the child that seem spongy vestibule, and palate
Most appear within 1–2 weeks Treated by excisional biopsy 5–15% may become malignant
after birth
5 times more in girls Multiple lesions need to consider
fibromatosis (Von ■ Reckling-
Hausen’s)
Frequent on lips, tongue and
buccal mucosa
Often self-involute or can be
surgically removed
CONFUSING “BUMPS”
MEASLES
Called Rubeola.
Paramyxovirus.
1–2-weeks incubation.
Sx: fever, cough, a rash.
Koplik’s spots intraorally.
Highly contagious viral infection
GERMAN MEASLES SMALL POX
Called Rubella. Acute viral disease.
Benign viral disease. Sx: high fever, nausea, vomiting,
chills, headache.
Sx: red bump, swollen lymph Ulcerated/vesicular lesions
nodes, mild fever, and enamel
defects.
Supportive treatment. Variola major is the severe and
most common form of smallpox,
more extensive rash, and higher
fever.
Variola minor is a less common
presentation smallpox, and a
much less severe disease.
Best to vaccinate
MUMPS
Acute and contagious.
Unilateral/bilateral swelling of
salivary gland (parotid)
Replicates in the upper
respiratory tract.
Spread by contact with
respiratory secretions, saliva ,
and fomites.
Incubation time of 12–25 days.
Vaccinate with MMR (measles,
mumps. rubella)