This document provides information on odontogenic development, tooth histogenesis, the life cycle of a tooth, and various odontogenic pathologies including fusion, gemination, concresence, attrition, abrasion, erosion, enamel hypoplasia, dentinogenesis imperfecta, early childhood caries, acute necrotizing ulcerative gingivitis, craniofacial anomalies like cleft lip and palate, and systemic conditions that can affect oral and dental development such as achondroplasia, gigantism, gingivostomatitis, coxsackie virus, cretinism, and Down syndrome. Key details are presented on the characteristics, causes, and treatments for these

1. PEDIATRIC
PATHOLOGY
GLO ARBY ARGUELLES, DMD

2. 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

3. 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

4. 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.

5. ODONTOGENIC PATHOLOGY
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
FUSION VS. GEMINATION VS. CONCRESENCE

7. ODONTOGENIC PATHOLOGY
ATTRITION ABRASION EROSION
Physiologic wearing away of tooth
structure.
Pathologic wearing away of tooth
structure due to mechanical forces.
Chemical loss. tooth structure due to
tooth structure.
Normal aging consequence. Toothbrush-abraded tooth presents
with a clinical V-shaped ditch on the
affected surface
Labial surfaces of patients who
ingest large amounts of acidic
beverages, or in people who suck on
citrus fruits
Seen on incisal edges, occlusal
surfaces, and proximal surfaces of
the teeth
Result from abnormal mechanical
habits
Lingual surface of patients with
chronic habits of vomiting (anorexia
nervosa)
Often present as flatten incisal edges Eroded tooth usually displays a
shallow smooth scooped-out
depression.
Example = bruxism
ATTRITION VS. ABRASION VS. EROSION

8. ODONTOGENIC PATHOLOGY
ENAMEL HYPOCALCIFICATION ENAMEL HYPOPLASIA
■ Normal quantity but bad quality ■ Normal quality but deficient quantity
of the enamel
■ Defective maturation of ameloblast ■ Defective enamel matrix formation
■ Defect in mineralization matrix ■ No contact between teeth
■ Chalky teeth and yellow to brown ■ Affects both deciduous and
succedaneous teeth
■ Affects both deciduous succedaneous
teeth
■ Hereditary and environmental form
■ Seen in children with
hypoparathyroidism
ENAMEL HYPOCALCIFICATION VS. ENAMEL HYPOPLASIA

9. 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

10. 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

11. 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.

12. 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

13. SYSTEMIC PATHOLOGY
• 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
ACHONDROPLASIA

14. SYSTEMIC PATHOLOGY
• 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
GIGANTISM

15. SYSTEMIC PATHOLOGY
• 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.
GINGIVOSTOMATITIS

16. SYSTEMIC PATHOLOGY
• 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).
COXSACKIE VIRUS

17. SYSTEMIC PATHOLOGY
• 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.
CRETINISM

18. CRANIOFACIAL ANOMALIES
• 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.)
FACIAL CLEFTS

19. CRANIOFACIAL ANOMALIES
• 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
CLEFT PALATE (CP)

20. CRANIOFACIAL ANOMALIES
• 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
CLEFT LIP (CL)

21. CRANIOFACIAL ANOMALIES
• 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
CLEFT LIP (CL)
FOUR CLASSES OF CL

22. 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.
• CL revision at anytime but best after age 5
Rule of 10’s for timing of
CL repair Infant should
be: ≥10 weeks old, ≥10
g/dl hemoglobin, and
≥10 lbs.

23. • Collagen gene 2A1 mutation
• Hypermobility of joints
• Mitral valve prolapse
• Micrognathia leading to breathing and feeding difficulties
• Glossoptosis
• High arched CP
PIERRE ROBIN SYNDROME

24. • Also called mandibulofacial dysostosis
• Mutation of 5q32 gene
• Downslanting of eyes
• Notched lower eyelids
• Midface developmental deficiency
• Underdeveloped, malformed, and/or prominent ears
TREACHER COLLINS SYNDROME

25. • 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.)
DOWN SYNDROME

26. CONFUSING “OMAS”
HEMANGIOMA | LYMPHANGIOMA | NEUROFIBROMA
HEMANGIOMA LYMPHANGIOMA NEUROFIBROMA
Most common benign tumor of
infants
Well-circumscribed mass of
lymphatic vessels
Moderately firm and
encapsulated
Due to proliferation of blood
vessels
Most in neck and axilla Proliferation of Schwann cells
Growth is independent of the
growth of the child
Are red to blue translucent
masses that seem spongy
On tongue, buccal mucosa,
vestibule, and palate
Most appear within 1–2 weeks
after birth
Treated by excisional biopsy 5–15% may become malignant
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

27. CONFUSING “BUMPS”
MEASLES GERMAN MEASLES SMALL POX MUMPS
Called Rubeola. Called Rubella. Acute viral disease. Acute and contagious.
Paramyxovirus. Benign viral disease. Sx: high fever, nausea,
vomiting, chills, headache.
Unilateral/bilateral swelling of
salivary gland (parotid)
1–2-weeks incubation. Sx: red bump, swollen lymph
nodes, mild fever, and enamel
defects.
Ulcerated/vesicular lesions Replicates in the upper
respiratory tract.
Sx: fever, cough, a rash. Supportive treatment. Variola major is the severe
and most common form of
smallpox, more extensive
rash, and higher fever.
Spread by contact with
respiratory secretions, saliva ,
and fomites.
Koplik’s spots intraorally. Variola minor is a less
common presentation
smallpox, and a much less
severe disease.
Incubation time of 12–25
days.
Highly contagious viral
infection
Best to vaccinate Vaccinate with MMR
(measles, mumps. rubella)