REVIEWS AND CONTEMPORARY UPDATES

Ochsner Journal 18:339–344, 2018

© Academic Division of Ochsner Clinic Foundation
DOI: 10.31486/toj.18.0040

Oral Development and Pathology

Melinda B. Clark, MD, FAAP, David A. Clark, MD, FAAP

Department of Pediatrics, Albany Medical Center, Albany, NY

Background: The mouth is integral in the development of feeding, the initiation of digestion, and for speech and socialization.
Signs of systemic disease and nutritional deficiencies often manifest in the mouth, and poor oral health can exacerbate many
systemic conditions.
Methods: This review addresses the fetal development of the mouth, major anomalies, common minor physical findings, and
pathologic conditions and their management.
Results: Pediatric practitioners have historically been poorly trained in diagnosis and management of oral conditions, so this
article provides an overview of oral embryology and pathology, with a focus on hard and soft tissue disease identification,
triage, and management. For primary prevention to be effective, pediatric providers must be knowledgeable about the
process of dental caries, prevention of the disease, and available interventions, including fluoride.
Conclusion: The embryology and anatomy of the oral cavity are complex, and the mouth is crucial to many physiologic
processes. Pediatric primary care providers are uniquely positioned to prevent, identify, and triage dental caries, the most
common chronic disease of childhood.

Keywords: Abnormalities–mouth, dental caries, odontogenesis, pathology–oral

Address correspondence to David A. Clark, MD, FAAP, Department of Pediatrics, Albany Medical Center, 47 New Scotland Ave., Albany,
NY 12208. Tel: (518) 262-5333. Email: clarkd@amc.edu

INTRODUCTION ate the posterior hard palate as the soft palate and the uvula
The mouth reflects general health and well-being, such fuse during gestation weeks 10 to 12. Cleft lip and palate are
that you cannot “be healthy without a healthy mouth.”1 common congenital anomalies with a prevalence of 17 per
The mouth is where taste and chewing occur and is integral 10,000 live births.4 The etiology of clefts remains poorly un-
to digestion, respiration, speech, and socialization; it is also derstood, although genetic, syndromic, and environmental
a mirror reflecting systemic processes and health. Signs of factors have all been implicated. Cleft lip can be unilateral,
systemic disease and nutritional deficiencies often manifest bilateral (Figure 2), or median or of only the soft palate (mu-
in the mouth, and poor oral health can exacerbate many sys- cous cleft), although midline lip cleft is rare. Isolated cleft
temic conditions. Pediatric practitioners have historically palate is more common in females with no racial predilec-
been poorly trained in diagnosis and management of oral tion.4 Cleft lip with palate is twice as common as isolated
conditions, so this article provides an overview of oral em- cleft palate, with an incidence greater in males and those
bryology and pathology, with a focus on hard and soft tissue of Asian and Caucasian descent. Cleft palate without cleft
disease identification, triage, and management. lip is more likely to be associated with a syndrome.3
Teratogen exposures implicated in cleft development in-
OROFACIAL DEVELOPMENT clude organic solvents and agriculture chemicals, especially
The structures of the oral cavity derive from the first bran- pesticides,5 as well as viral infections, metabolic derange-
chial arch. By the end of the fourth week of development, the ment, and illicit drugs. Antiepileptic medications associated
frontonasal, 2 maxillary, and 2 mandibular processes are vis- with orofacial defects include diazepam, phenytoin, pheno-
ible. The face and palate complete midline fusion between 6 barbital, topiramate, and lamotrigine.5-7 Nutritional deficien-
and 12 weeks’ gestation, and the upper lip fuses by 6 cies in early pregnancy are also associated with increased
weeks’ gestation.2 cleft risk, the best known being folic acid, which is now rec-
Failure of midline fusion during embryogenesis results in ommended as a routine supplement in pregnancy.8 Supple-
the spectrum of cleft lip, cleft palate, cleft lip and palate, mentation is most beneficial early in the first trimester, with a
and mucous cleft palate (Figure 1). The medial nasal tissues reduction in midline defect rates by two-thirds in babies with-
fuse to form the lip during weeks 5 to 6 of embryonic devel- out a major chromosomal anomaly.9
opment; the anterior hard palate, alveolus, and philtrum Cleft lip and/or palate is associated with many genetic
form during weeks 6 to 10.3 The maxillary prominences cre- syndromes, including the spectrum of chromosome 22q11,

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Oral Development and Pathology

Figure 1. Mucous cleft palate.

oral-facial-digital syndrome, Treacher Collins syndrome, tri-

Figure 3. Trisomy 13 protruding cleft lip.
somy 13 (Figure 3), and Van der Woude syndrome.10 Cleft
palate can also result from embryonic tongue mechanical in-
terference with palatal fusion, usually stemming from micro- SOFT TISSUE ANOMALIES
gnathia with mandibular hypoplasia, known as Robin Congenital soft tissue lesions of the oral cavity are quite
sequence or Pierre Robin syndrome. common, and practitioners must be able to distinguish nor-
Care of the neonate with cleft lip and/or palate requires mal findings from those that require intervention. Epithelial
genetic and hearing assessment, as well as airway evalua- tissue remnants form oral inclusion cysts13 that are small
tion and aggressive feeding support.11 Surgical primary lip white or translucent papules or cysts seen in 75% of term
repair is often undertaken around 3 months of age and pri- newborns, although less commonly in premature infants.9
mary palatal repair around 9 months. Residual hypernasal Asymptomatic inclusion cysts require no further evaluation
speech and language delays are common following com- or management and typically resolve by 3 months of age. In-
pletion of all surgeries. Optimal management is attained clusion cysts are classified by their location. Epstein pearls,
through a multidisciplinary cleft and craniofacial team com- the most common of the 3 types, are found along the mid-
prised of experienced members of the medical, surgical, line raphe of the hard palate in 75%-80% of all neonates.14
dental, and allied health disciplines. Bohn nodules are heterotopic salivary gland remnants
Submucosal cleft palate is a mild or incomplete form of cleft seen on the buccal or lingual mucosal surface of the alveolar
palate. Examination may reveal a bifid uvula, muscular defect ridge (not the crest) or on the hard palate away from the
with overlying membrane, or a bluish mucosal line the length raphe (Figure 4). Dental lamina cysts are heterotopic sali-
of the soft palate.12 Submucosal cleft palate is clinically chal- vary gland remnants located on the crest of the alveolar
lenging to detect but is often functionally significant, as the le- ridge.
vator muscles must interdigitate across the palate to form the
normal levator sling. The levator muscle must elevate to re- ANKYLOGLOSSIA
tract the posterior soft palate and divide the nasal and oral Ankyloglossia (tongue-tie) is anchoring of the tongue an-
pharynxes to prevent velopharyngeal incompetence, which teriorly. The frenulum connects near the tip of the tongue,
adversely impacts both feeding and speech. limiting tongue extension to the lips or roof of the mouth,

Figure 2. Bilateral cleft lip and palate. Figure 4. Bohn nodules.

340 Ochsner Journal

 Clark, MB

with a notched or heart-shaped tongue on protrusion. Anky-

loglossia has a prevalence of 4%-10% but varies in severity
and clinical impact, resulting in considerable debate regard-
ing optimal management.15 Restricted tongue movement
can lead to a variety of problems in infants and children, in-
cluding challenges with breastfeeding latch, articulation
delay, and compromised oral health.16,17
Initial symptoms of ankyloglossia include maternal nipple
pain with breastfeeding, loss of suction, clicking sound while
feeding, poor latch, and suboptimal milk transfer.18 Signifi-
cant ankyloglossia can also contribute to articulation chal-
lenges but not a delay in absolute word production.19 Oral
hygiene may be compromised with ankyloglossia, increas-
ing the risk of dental caries and periodontal disease.
Management of ankyloglossia-related breastfeeding diffi-
culties should include lactation specialist consultation, but Figure 5. Natal tooth.
frenectomy has been shown to improve breastfeeding for
mother and newborn better than intensive lactation support
alone.20 Indications and timing of surgical division for anky- syndromes of chondroectodermal dysplasia (Ellis-van
loglossia have been investigated, and in one randomized, Creveld syndrome) and oculomandibulofacial syndrome
prospective, unblinded trial of neonates with ankyloglossia (Hallermann-Streiff syndrome).26
and feeding concerns, all infants who received immediate Humans develop 2 sets of teeth, classifying us as diphy-
division of the frenulum showed breastfeeding improve- odont. The primary dentition begins developing in utero at
ment, but only one neonate in the control group (intensive week 8 of gestation, and the first primary teeth emerge be-
lactation support) improved. Frenotomy was then offered tween 6 and 12 months of age. The primary dentition is a
to and performed for the infants in the control group, and complete set of 20 teeth by age 3 and consists of 8 incisors,
all but one baby improved and fed normally after the proce- 4 canines, and 8 molars. Primary teeth begin exfoliation at
dure.20 Frenotomy can be performed with blunt scissors, around 6 years of age, forced out by eruption of the perma-
cautery, or laser if a simple membrane is present, but frenu- nent teeth. The permanent dentition consists of 32 teeth: 8
loplasty is preferred for more complex anatomy.21 Ankylo- incisors, 4 canines, 8 premolars, and 12 total molars in 4
glossia is typically not indicative of underlying genetic sets of 3. The usual pattern of molar eruption is first molars
syndrome, but absence of the inferior labial frenum and lin- between 6 and 8 years of age, second molars between ages
gual frenulum is commonly noted in Ehlers-Danlos syn- 11 to 13 years, and third molars, or wisdom teeth, between
drome, and absence of the inferior labial frenum is ages 17 and 21 years.
strongly correlated with infantile hypertrophic pyloric steno- Human teeth contain 4 distinct types of tissue: pulp, den-
sis.22 tin, enamel, and cementum. The outermost layer of the tooth
Management of a constricted maxillary frenum is even is made of enamel, the hardest tissue in the body, that with-
more controversial. The maxillary frenum normally extends stands mechanical and thermal insults and protects against
over the alveolar ridge to form a raphe. Persistence of the infection. Under the thin layer of enamel is dentin, the yellow
raphe during dental eruption can lead to diastema, or widely substance forming the bulk of the tooth mass. The inner-
spaced central incisors. A prominent maxillary labial frenum most portion of the tooth is the pulp, containing nerves
may lead to esthetic concerns and to difficulty with plaque and blood vessels that enter the root through a small hole
control which potentiates dental caries risk. Maxillary frenec- in the tip. Teeth are held in place in the maxilla and mandible
tomy is clearly indicated in rare cases when the frenum at- bones by a layer of cementum that covers the root.
tachment exerts tension on the gingiva of a permanent
tooth or if cosmesis is unacceptable following orthodontic DENTAL CARIES
closure of the diastema.23 Additional research is needed to Dental caries, also known as tooth decay, is the most com-
better understand the appropriateness of performing pre- mon chronic disease of childhood,1 with 25% of children
ventive maxillary frenectomy on young children. ages 2-5 years27 and 59% of teenagers having at least 1
documented cavity.28 Most adults develop cavities and, of
DENTAL DEVELOPMENT AND DISEASE great public health concern, nearly 25% of adults 20-64
Humans are usually born edentulous, but tooth eruption years have untreated dental caries.29 Dental caries in the pri-
may occur before birth (natal teeth) or within the first mary teeth of children under 6 years of age is now termed
month of life (neonatal teeth) at a rate of 1:2,000 to early childhood caries (ECC), encompassing the previous
1:3,000 live births (Figure 5).24 Central mandibular incisors nomenclature of nursing caries and baby bottle tooth
are most likely to prematurely erupt; these are usually prima- decay. ECC is a multifactorial disease resulting from the inter-
ry dentition and not extra teeth,25 so they should not be ex- action of cariogenic microorganisms and fermentable carbo-
tracted without cause. Management is usually observation, hydrates but impacted by a wide range of social variables.30
although extraction may be considered if teeth are mobile At the most basic level, dental caries requires 4 compo-
and present an aspiration risk, interfere with breastfeeding, nents: teeth, bacteria, carbohydrate exposure, and time.
or cause Riga-Fede ulceration.25 Natal teeth are most com- Teeth become colonized with cariogenic bacteria once
monly an isolated finding but can be associated with genetic they emerge. The bacteria metabolize carbohydrates and

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Oral Development and Pathology

create acid as a byproduct. The acid dissolves, or deminer- health assessments at routine visits through the age of 6
alizes, the enamel and eventually wears away the enamel years.41 Screening oral examinations are most easily con-
surface to create a hole in the tooth, termed a cavity. Once ducted in the knee-to-knee position with the child sitting fac-
a cavity has formed, the bacteria can proceed through the ing the caregiver and lying back on the lap of the examiner.
outer tooth and into the pulp, resulting in pulpitis or abscess. The oral examination should include visualization of all the
If the infection is not contained and the tooth definitively hard and soft tissues, with focus on the teeth for enamel de-
treated, the dental abscess can progress to osteomyelitis fects, presence of plaque, white spot lesions, overt decay,
of the jaw or spread to any contiguous soft tissue (face, and gingival health. For primary prevention to be effective,
neck, deep pharyngeal space, or brain) or the blood. pediatric providers must be knowledgeable about the pro-
Dental caries is a silent epidemic that disproportionately cess of dental caries, prevention of the disease, and avail-
affects those from the lower socioeconomic strata, those at able interventions, including fluoride.
the extremes of age, and minorities.31 Untreated tooth decay Fluoride is effective in cavity prevention with 3 main effects
leads to pain, interrupted sleep, inappropriate use of over- of enhancing enamel remineralization, inhibiting demineral-
the-counter medications, difficulty with chewing and eating, ization, and inhibiting bacterial metabolism, thereby limiting
and increased hospitalizations resulting from infectious acid production. The beneficial effect of fluoride is obtained
complications.31 Dental caries in the United States is re- by topical administration. Fluoride can be applied to tooth
sponsible for many school and work hours lost per year32 surfaces via fluoridated toothpaste, mouth rinses, fluoridated
and contributes to poor school performance.27 Good oral community water, dietary fluoride supplements, and fluoride
health is a necessary part of overall health, and studies varnish. The United States Preventive Services Task Force
have demonstrated the adverse effects of poor oral health (USPSTF) recommended in 2014 that primary care clinicians
on multiple other chronic conditions, including diabetes con- apply fluoride varnish to the primary teeth of all infants and
trol.33 Therefore, failure to prevent dental disease has health, children starting at the age of primary tooth eruption.42,43
educational, and financial consequences at the individual, The USPSTF made this recommendation a grade B recom-
family, and societal levels. mendation; thus, the service must be covered by the Afford-
Risk factors for ECC include having a mother/primary able Care Act and commercial payers without cost sharing.
caregiver with active cavities,34 frequent consumption of The 2014 American Academy of Pediatrics clinical report
sugary beverages and snacks, using a bottle at bedtime
“Fluoride Use in Caries Prevention in the Primary Care Set-
or through the night, prolonged frequent exposure to sugary
ting” provides a review of fluoride modalities, including rec-
liquids throughout the day,35 exposure to environmental to-
ommending fluoride varnish application in the medical home
bacco smoke,36 having special healthcare needs, xerosto-
2-4 times per year for all children ages 5 and under.44 Oral
mia, and insufficient fluoride exposure.37 Examination
health recommendations for screening, fluoride varnish,
findings that increase the risk for development of ECC in-
and fluoride supplements were added to the Bright Futures
clude visible plaque on the teeth and the presence of enam-
periodicity schedule in 2015.45
el hypoplasia. The most significant population-based risk
In June 2015, the Cochrane Oral Health group questioned
factors are low socioeconomic status and low education
the fluoridation of public water sources, especially in terms
and health literacy levels.38,39
of its effectiveness for adults. The group asserted that
Protective factors that aid in enamel remineralization in-
older studies were poorly controlled and that more research
clude exposing the teeth to fluoride, limiting the frequency
is necessary.46 In a letter to healthcare professionals dated
of carbohydrate consumption, choosing less cariogenic
foods, practicing good oral hygiene, receiving regular dental July 2, 2015,47 Katherine Weno, DDS, Director of the Division
care, and delaying bacterial colonization.37 If carious lesions of Oral Health, Centers for Disease Control and Prevention
are identified at the early white spot stage, the process can (CDC), responded forcefully in favor of water fluoridation,
be halted or even reversed by modifying the individual’s risk with her position supported by multiple studies.48-51 Five
and protective factors. days later, the American Dental Association reinforced the
Dental caries is preventable with proper oral hygiene, a position of the CDC.52
healthy diet, appropriate use of fluoride, and access to pre-
ventive dental services. All children should establish a dental CONCLUSION
home by or around their first birthday, a recommendation The embryology and anatomy of the oral cavity are com-
supported by the American Academy of Pediatrics, Ameri- plex, and the mouth is crucial to many physiologic process-
can Academy of Pediatric Dentistry, American Dental Asso- es. This review focused on common developmental and
ciation, and American Public Health Association.27,37,39 acquired defects: the spectrum of cleft lip and palate, soft
Despite these recommendations, the Medical Expenditure tissue anomalies, ankyloglossia, and the most common dis-
Panel Survey revealed that 89% of infants and 1-year-olds ease of the hard tissues, dental caries. Historically, pediatric
have office-based physician visits annually, compared with professionals have maintained ownership of soft tissue dis-
only 1.5% having dental visits.40 Because many children ease management, but this review highlights why and how
do not receive dental care at young ages, and risk factors pediatric primary care providers are uniquely positioned to
for dental caries are influenced by parenting practices, pedi- prevent, identify, and triage dental caries, which remains
atric primary care providers have a unique opportunity to the most common chronic disease of childhood.
participate in prevention of dental caries. The American
Academy of Pediatrics recommends that primary care pro- ACKNOWLEDGMENTS
viders perform oral health assessments on all children start- The authors have no financial or proprietary interest in the
ing at 6 months of age and recommends continued oral subject matter of this article.

342 Ochsner Journal

 Clark, MB

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This article meets the Accreditation Council for Graduate Medical Education and the American Board of Medical
Specialties Maintenance of Certification competencies for Patient Care, Medical Knowledge, and Practice-Based
Learning and Improvement.

344 Ochsner Journal