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Oral Pathology


Common soft tissue lesions of infants and toddlers and young school children will be described. Treatment choices, intervention or referral will be suggested. For further in-depth review of pediatric oral pathology, references are listed at the end of this section.

Shortly after birth and at the first examination, the physician or nursing staff may note round white nodules on or near the midline on the palate or on the alveolar ridges.




Figure III-7



These are Palatal and Dental Lamina Cysts (Epstein’s Pearl’s – palate; Dental Lamina Cysts – alveolar ridges; Bohn’s nodules – lateral hard & soft palate). They usually spontaneously exfoliate and require no treatment. (Figure III-7)


A localized, pedunculated or sessile smooth surface pink to red in color lesion may be present at birth usually in the upper anterior jaw and is called congenital epulis. The CONGENITAL EPULIS may cause feeding problems. This lesion may resolve on it’s own over a short period of time or may be excised depending on it’s size and interference with function. This lesion is most commonly located in the anterior maxillary and 90% occur in females.




Figure III-8



In infancy, the tongue, buccal mucosa and palate may be coated with a soft white plaque. If able to be removed with a gauze pad or tongue blade and a red raw undersurface is noted, the diagnosis most likely is PSEUDOMEMBRANOUS CANDIDIASIS (Thrush).  This is a fungal infection that should be treated with antifungal medication.  Nystatin suspension is the first choice for initial intervention and it can be applied to the oral mucosa by the parent with a gauze or swab.  (Figure III-9)




Figure III-9



At birth, or shortly after, there may be a tissue swelling in the midline of the lower jaw.  Upon palpation,  calcified tissue may be noted or there may be a tooth like object visible.  These are NATAL TEETH (at birth) or NEONATAL TEETH (after birth) and 90% of the time are one of the primary teeth and not a supernumerary (extra) tooth.  Usually poorly formed and quite mobile, they can interfere with feeding and consideration should be given to extract.  If the decision is made to keep the teeth, feeding (breast or bottle) can be performed on either side of the tooth (teeth).  This will avoid irritation to the mother’s breast and or irritation to the infant’s tongue.  To date, no report of tooth aspiration has been reported in the literature.




Figure III-10



A bluish, translucent, elevated, compressible lesion may appear on the alveolar ridge that is associated with an erupting tooth.  The ERUPTION CYST or ERUPTION HEMATOMA is blood or fluid filled and may cause discomfort.  This lesion may be compared to a blood blister.  If the lesion interferes with function, intervention should be considered. Before intervention, a HEMANGIOMA should be ruled out. Parents can be instructed to massage the alveolar ridge with a moist cloth several times a day or have the infant chew on a soft teething ring.  The parent should not be alarmed if the lesion pops and blood is mixed with the released fluid.  (Figure III-11)




Figure III-11



A mucosal ulcer secondary to trauma may be noted in infants and toddlers.TRAUMATIC ULCERATION on the ventral surface of the tongue in infancy has been referred to as RIGA FEDE’S DISEASE and is due to irritation from the erupting mandibular anterior teeth. Symptomatic treatment is usually recommended.  Riga Fede's Disease that is found in children with neurological disorders or oral desensitization should be followed closely.




Figure III-12



Other ulcers can be due to trauma, accidental or aggravated (child abuse), or herpes simples virus, (HERPETIC ULCERS), systemic deficiencies and/or probable immune defects (APTHOUS ULCERS).  Most often located on non-kerantinized movable tissues with a crater surrounded by an erythematous halo (except for ulcers secondary to a blunt object or a force as in child abuse).  Ulcers can be painful especially when eating and talking with symptomatic relief recommended and heal in usually 7-10 days.  (Figure III-13)





Figure III-13  




HERPETIC ULCERS are usually proceeded by prodromal tingling followed by vesicles that coalesce into a small ulcer without an erythematous halo.  They are usually located on the hard palate, the vermilian border of the lips and the attached ginigval tissue.  Healing occurs in 7-14 days and intervention is symptomatic.

A common tumor-like raised lesion is a FIBROMA, with usually a pedunculated firm surface and usually located on the mucosa, lips or tongue.  Another common tumor-like raised lesion is a PAPILLOMA, which has a soft, pedunculated, cauliflower-like surface, is pink to white in color, and is usually a solitary lesion that can be located almost anywhere in the mouth.  Surgical excision is the usual treatment of choice for these tumors with recurrence uncommon. (Figure III-14)





Figure III-14  



A localized, compressible, fluid-filled module with smooth surface, fluctuating in size and clear to bluish in color is called a MUCOCELE. Children who have a mucocele located in the lower labial mucosa, buccal mucosa or ventral tongue may continually play with and traumatize this lesion. Referral for evaluation and treatment is recommended. If found on the floor of the mouth it is called a RANULA and is associated with the sublingual salivary gland. Recurrence is common if not completely excised. Marsupalization is the treatment of choice for the ranula. Some of these lesions are associated with a history of trauma. (Figure III-15)




Figure III-15



A wide-spread oral and perioral infection associated with fever, discomfort, malaise, lymphadenopathy, intense red gingiva and multiple vesicles located throughout the mouth that rupture resulting in ulcers, drooling and halitosis is PRIMARY HERPETIC GINGIVOSTOMATITIS.  Occurrence is common during periods of seasonal changes (early spring/summer). It is a self-limiting disease secondary to the Herpes Simplex Virus (HSV) with dehydration and high temperatures a major concern. Supportive therapy, forced hydration, and antipyretics are indicated.  A recommended mouthwash for children who cannot expectorate is: Diphenhydramine Hydrochloride liquid 12.5 mg/5 ml and Maalox oral suspension; mixed in a 1:1 ratio Disp: 200ml Sig: rinse 1 to 2 teaspoons (5-10 ml) every 4 hours for 2 minutes; swish and spit or swish and swallow. Shake well before use and store at room temperature. It can be used for 60 days. For children who cannot expectorate, the suspension can be swabbed inside the mouth with a cotton tipped applicator. Viscous lidocaine is not recommended for children who cannot expectorate.


The current FDA recommendation is that systemic acyclovir is approved for children who are immunocompromised. For children who can expectorate the following can be recommended:  Rx: Peridex, PerioGard, or generic (chlorhexidine gluconate 0.12%) oral rinse. Disp: 480 ml (16 fl. oz) Sig: rinse with 15 ml for 30 seconds and expectorate.  Use twice daily after breakfast, and before bed for 7 days for gingivitis.

Chlorhexidine is very effective in the management of gingival inflammation that occurs secondary to herpetic infection. This rinse can irritate extensive ulcerations as most products contain 11.6% alcohol.  The anti-inflammatory effects can be beneficial to help improve oral hygiene, eating and oral comfort.


Parents should be informed that this condition can be easily given to other family members and should avoid sharing utensils, toothbrushes and foods.  It usually resolves in 7-10 days. (Figure III-16)




Figure III-16



Erythema Multiforme is an acute, sometimes recurrent, inflammatory disease of the skin and mucous membranes. Erythema Multiforme is described as a hypersensitivity reaction triggered by drugs, infections and exposure to toxic substances. Oral lesions occur in 25% of patients and consist of erythematous macules followed by vesicular bullae that rapidly form painful necrotic ulcers, often with a pseudomembranous membrane. These lesions can be found on the lips, tongue, palate, buccal mucosa and gingiva. Skin lesions begin as macules or wheals and evolve into papules or plaques. The center of the lesion may be vesicular, purpuric or necrotic. “Multiforme” refers to this changing pattern of a fixed lesion over several days.


Iris or target lesion are pathognomonic for erythema multiforme and have dusky centers that may develop concentric rings of variable color that may blister when the reaction is intense. Pruritus can be minimal or absent. There are two forms of this disease: Erythema Multiforme Minor, the most common type, may present as an immune-mediated response to Herpes Simplex Virus; Erythema Multiforme Major, or Stevens-Johnson Syndrome, is a serious systemic disorder involving at least two mucous membranes and the skin.


Treatment is local and symptomatic. Opthamologic evaluation is important because of possible visual impairment. Oral lesions can be managed with mouthwashes, glycerin swabs or chlorhexidine rinses. Topical anesthetics can be applied prior to eating. Skin lesions should be cleaned and antibiotic therapy may be appropriate to prevent secondary bacterial infection. Prophylactic acyclovir may be indicated in cases of herpes associated Erythema Multiforme. Treatment of Stevens-Johnson Syndrome requires an intensive care setting.

A lingual frenum is usually attached at the base of the tongue. When attached to the ventral tip of the tongue it may restrict tongue movements causing ANKYLOGLOSSIA (tongue tied).


Infants and children with feeding or speech problems should be referred to a feeding or speech therapist to evaluate the etiology of the problem prior to surgical intervention. Most infants adapt early. Frenectomy may be indicated. (Figure III-17)




Figure III-17







HYPERDONTIA refers to an excess number of teeth. As a reminder, when eruption is complete there are 20 primary teeth and 32 permanent teeth. Occasionally you may note an extra primary tooth after counting teeth. Although most common with the permanent dentition they can be present in the primary dentition. An extra tooth is called a SUPERNUMERARY TOOTH. If localized in the midline of the upper jaw it is called a MESIODENS. More often they are not visible clinically and only are diagnosed when a radiograph is ordered secondary to the recommended guidelines for the ordering or radiographs or because of delayed exfoliation or eruption. (Figure III-18)




Figure III-18



HYPODONTIA (oligodontia) refers to congenitally missing teeth and is usually diagnosed when counting the teeth erupted and present. Hypodontia is most often correlated with a familial pattern. It is generally uncommon in the primary dentition unless a diagnosis of ECTODERMAL DYSPLASIA is also considered. (Figure III-19)




Figure III-19



FUSION and GEMINATION although rare (0.5%) can be noted upon examination and are more common in the primary dentition. Generally, radiographs are necessary to differentiate the two, fusion being two individual teeth being fused and geminiation a single tooth bud that develops into a bifid crown with only one root. (Figure III-20





Figure III-20  



Teeth may have extra cusps. The most common is a large cusp on the back (lingual) surface of the upper front teeth but can also be found on posterior teeth. When found on the anterior teeth it is called a TALON CUSP. (Figure III-21




Figure III-21





A disruption during the stages of tooth development may affect the enamel. Generally this is referred to as HYPOPLASIA (insuffucient quantity of enamel) or HYPOCALCIFICATION (enamel quantity normal but quality of enamel is poor) and can either be a hereditary defect or one induced by the environment. (Figure III-22)





Figure III-22  



A common hereditary defect is AMELOGENESIS IMPERFECTA (AI) with an incidence of one in fourteen thousand or as high as one in 4000. There are four types of AI with the hypoplastic (type I) and hypomaturation (type II) being the most common. There are 14 different sub-types of AI and the pattern of inheritance varies from one type to the next. The most common forms are generally inherited as an autosomal dominant or x-linked traits. Both dentitions are affected. Superimposed decay is common around the defects, because of the poor quality or absence of enamel. (Figure III-23)




Figure III-23




HYPOPLASIA can also be induced environmentally from systemic or local causes. Severe nutritional deficiencies, infection and rubella all can interfere with enamel development and lead to a defect in the enamel. Trauma in a localized area during formation can result in one or a few teeth being hypoplastic while all remaining teeth will have normal enamel.


A type of hypoplasia called FLUOROSIS is caused by excessively high amounts of ingested fluoride during tooth development. Fluorosis may range from mild, with lacy white mottling of teeth, to severe with pitting and brown staining.


A heritable defect of dentin (inner layer of the tooth) is DENTINOGENESIS IMPERFECTA (DI) that originates very early in tooth development and is a defect in the dentin matrix. Incidence is 1:8000 and is reported as one of three types: Shields Types I, II, or III. All types are inherited as an autosomal dominant trait. Shields Type I is associated with OSTEOGENESIS IMPERFECTA and the crowns have an amber translucent color. Shields Type II is known as HEREDITARY OPALESCENT DENTIN is very similar in appearance to Type I but does not occur with OI. Shields Type III is very rare and the teeth have a shell-like appearance and have frequent pulp exposures. (Figure III-24)




Figure III-24



Enamel color can also be affected either extrinsically or intrinsically. EXTRINSIC COLORATION is normally due to environmental stains and are more apt to occur when teeth are covered with biofilm and toothbrushing is irregular or not practiced. A very common extrinsic stain is a black stain on the crowns of teeth. History usually reveals that the child is anemic, on a liquid iron supplement and the teeth are not brushed by the caretaker. Infants and children can be referred to the dentist for removal of the stain and oral hygiene instruction. (Figure III-25)




Figure III-25



INTRINSIC STAINS are due to blood borne pigments (example congenital porphyeria, drug administration, tetracycline antibiotics from inter-uterine development to eight years of age). Excessive floride can also cause intrinsic stain (from diffuse white spots to brown mottling) with or without hypoplastic defects.





1. Acs G. Oral Manifistations of Systemic Diseases, Pediatric Basics, Winter 1998; 82:2-10.

2. Dummett CO. Anomalies of the Developing Dentition, in Pediatric Dentistry - Infancy Though Adolescence 3rd ed. Pinkham, J. ED, Philadelphia: W.B. Saunders Co, 1999;43-53.

3. Flaitz C. Oral Pathologic Conditions and soft tissue anomalies in Pediatric Dentistry - Infancy Though Adolescence 3rd ed. Pinkham, J. ED, Philadelphia: W.B. Saunders Co, 1999;12-42.

4. Laskaris G. Color Atlas of Oral Diseases in Children and Adolescents. New York: Thieme Stuttgart, 2000.




1. The Handbook -Pediatric Dentistry 2nd ed. Nowak AJ. 1999, Chicago, American Academy of Pediatric Dentistry, pp. 7-55.


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