ORAL PATHOLOGY

ONLINE

CONFERENCE Third year dental students

Supervised by Dr.Dalal ALQahtani

dalalq@ksu.edu.sa

College of Dentistry

King Saud University

SUMMARY

TOPIC NAME:

PEDIATRIC ORAL PATHOLOGY

DONE BY:

Riham AlBusayes

Reem AlRabiah

Mariam AlShamali,

Maha AlJarboua

Amani AlMohaimeed

DONE BY XMIND 2013

DEVELOPMENTAL

• ORO-FACIAL CLEFTS

• PALATAL CYST OF THE

NEWBORN

• CONGENITAL EPULIS

• NATAL/NEONATAL TEETH

• ANKYLOGLOSSIA

• CONGENITAL ABSENCE OF

TEETH

ORO-FACIAL CLEFTS

ORO-FACIAL

CLEFTS• Orofacial clefts are birth defects where

the lip, palate or both may be involved.

• A cleft is a separation in a body

structure, often resulting from the

failure of tissues to grow together

properly.

• Cleft lip and cleft palate are the single

most common congenital deformity

affecting the orofacial structures and

constitute about 13% of all reported

anomalies.

• Cleft lip and cleft palate can occur

unilateral or bilateral. Because the lip

and the palate develop separately, it is

possible to have a cleft lip without a cleft

palate, a cleft palate without a cleft lip, or

both together.

ETIOLOGY

it’s multi-factorial, many factors may be involved:

• Genetics.

• Environmental factors; alcohol consumption,

• Smoking, hypoxia during pregnancy, dietary

and vitamins deficiencies (like folic acid and

vitamin A deficiency)

• Drugs: corticosteroids (anti-inflammatory),

phenytoin (anti-convulsant).

• Infections during pregnancy.

• Maternal age.

• Problems with

feeding can occur

with orofacial clefts

which requires

treatment.

So, How can we treat orofacial

clefts?

TREATMENT

• Surgery

• Obturator

PALATAL CYST OF THE NEWBORN

(EPSTEIN’S PEARLS; BOHN’S

NODULES):• Occur in 65-85% of

newborns.

• Single or multiple, small (1-

3mm), white yellowish cysts

found in the palate of

newborn infants.

• If found at the median

palatal raphe, they’re called

Epstein’s pearls.

• If scattered on the hard

palate, they’re called Bohn’s

nodules.

PATHOGENESIS

• Researches have theorized that these

cysts may arise in one of two ways:

• First, epithelial entrapment at the midline

during the formation of secondary

palate. (Epistein’s pearls)

• Second, arise from epithelial remnants

derived from the development of the

minor salivary glands of the palate.

(Bohn’s nodules)

TREATMENT

• No treatment is required, as they’re

going to disappear several weeks after

birth.

CONGINITAL EPULIS

Clinical features:

• A soft tissue tumor

that occurs almost

exclusively on the

alveolar ridge of

newborns.

• Pink to red, smooth-

surfaced mass.

PATHOGENESIS

• Most of these tumors

are less than 2 cm, but

can reach up to 7.5 cm

• Two to three times more

common on the

maxillary ridge than

mandibular ridge.

• Most common in the

area of lateral incisor

and canine teeth.

• Shows a striking predilection for females

(90% of the cases), which suggest a

hormonal influence in its development.

HISTOPATHOLOGY:

• The overlying

epithelium shows

atrophy of rete

ridges

• Large-rounded

cells with granular

cytoplasm

TREATMENT:

• Surgical excision.

• Will not recur, even with incomplete

removal.

• In some patients, complete regression of

the tumor without treatment.

NATAL/NEONATAL

TEETH:• Natal teeth are teeth that are present at

birth.

• Neonatal teeth are teeth that emerge

through the gingiva during the first

month of life.

• Most common site:

mandibular central incisors area

TREATMENT

• They can be extracted if causing a

problem to the infant or the mother.

• They should be left in the mouth as long

as possible to decrease the likelihood of

removing permanent tooth buds with the

natal tooth.

Tongue-tie (Ankyloglossia)

Most of us think of tongue-tie as a situation we find ourselves in when

we are too excited to speak. Actually, tongue-tie is the non-medical

term for a

relatively common physical condition that limits the use of the tongue,

ankyloglossia.

THE

ETIOLOGY

Before we are born, a strong cord of tissue that guides development of

mouth structures is positioned in the center of the mouth. It is called a

frenulum.

After birth, the lingual frenulum continues to guide the position of

incoming teeth. As we grow, it recedes and thins. This frenulum is

visible and easily felt if you look in the mirror under your tongue. In

some children, the frenulum is especially tight or fails to recede and may

cause tongue mobility problems.

WHEN IS TONGUE-

TIE A PROBLEM

THAT NEEDS

TREATMENT?In Infants

Feeding ?

A new baby with a too tight frenulum can

have trouble sucking and may have poor

weight gain. Such feeding problems should

be discussed with your child's pediatrician

who may refer you to an otolaryngologist?

Head and neck surgeon (ear, nose, and

throat specialist) for additional treatment.

In Toddlers and

Older ChildrenSpeech ?

While the tongue is remarkably able to compensate and

many children have no speech impediments due to tongue-

tie, others may. Around the age of three, speech problems,

especially articulation of the sounds - l, r, t, d, n, th, sh, and z

may be noticeable. Evaluation may be needed if more than

half of a three year old child's speech is not understood

outside of the family circle.

Although, there is no obvious way to tell in infancy which

children with ankyloglossia will have speech difficulties later,

the following associated characteristics are common:

• V-shaped notch at the tip of the tongue

• Inability to stick out the tongue past the upper gums

• Inability to touch the roof of the mouth

• Difficulty moving the tongue from side to side

As a simple test,

caregivers or parents might ask themselves if the child can lick

an ice cream cone or lollipop without much difficulty. If the

answer is no, they cannot, then it may be time to consult a

physician.

Appearance ?For older children with tongue-tie, appearance can

be affected by persistent dental problems such as a gap between

the bottom two front teeth. Your child's physician can guide you

in the diagnosis and treatment of tongue-tie. If he/she

recommends surgery, an otolaryngologist Head and neck

surgeon (ear, nose, and throat specialist), can perform a surgical

procedure called a frenulectomy.

CONGENITAL ABSENCE OF

TEETHCongenital absence of teeth is a

heritably phenomenon probably

most often passed to each

generation by an autosomal

dominant pattern with incomplete

penetrance and variable

expressivity. Correlation of

hypodontia with systemic

disease leads to the hypothesis

that this frequent dental anomaly

may in some cases be a

microform of systemic

ectodermal dysplasia.

In dentistry, hypodontia is the condition at which the patient

has missing teeth as a result of the failure of those teeth to

develop (also called tooth agenesis).

Hypodontia describes a situation where the patient is

missing up to five permanent teeth, excluding the 3rd molars.

Missing third molars occur in 9-30% of studied populations. In

primary dentition the maxilla is more affected, with the

condition usually involving the maxillary lateral incisor.

The condition of missing over 5 (six or more) permanent

teeth, excluding 3rd molars or wisdom teeth, has been called

oligodontia. The condition for missing all teeth, either primary

and/or permanent), is called anodontia. A similar condition is

hyperdontia, in which there are more than the usual number

of teeth, more commonly called as supernumerary teeth.

Many other terms to describe a reduction in number of teeth

appear in the literature: aplasia of teeth, congenitally missing

teeth, absence of teeth, agenesis of teeth and lack of teeth

(a) Developmental absence of the primary upper lateral

incisors in a 3-year-old child.

(b) Panoramic radiograph showing the absence of the

upper lateral incisors as well as of one lower

ODONTOGENIC :

• Parulis

• Eruption cyst

PARULIS :

• Parulis is the end of a draining fistulous

tract of a necrotic primary tooth.

• It is a soft , solitary, reddish papule

located apical and facial to

the abscessed tooth.

• Purulent drainage may be observe

PARULIS :

• Treatment is to extract the abscessed

tooth or preform root canal therapy

ERUPTION CYST :

1- Follicular enlargement appearing just

before the eruption of tooth.

2- Blue-black in color (may contain blood).

TREATMENT :

None unless infected, reassure the child

and parent, follicle will rupture, but may

need to surgically opened if infected.

REACTIVE

• Mucocele

• Chemical burn

MUCOCELE

• Mucocele is a benign

lesion characterized by

an extravasation or

retention of mucous in

submucosal tissue from

minor salivary glands.

MUCOCELE

• Mucoceles are known

to occur most

commonly on the lower

lip, followed by the floor

of mouth (Ranula) and

buccal mucosa being

the next most frequent

sites.

MUCOCELE

• Trauma and lip biting habits are the main

causes for these types of lesions.

• Mucocele is a common oral mucosal

lesion but it is rarely observed in the

infant.

• Clinically they are characterized by

single or multiple, spherical, fluctuant

nodules, ranging from normal pink to

deep blue in color, and are generally

asymptomatic.

HISTOPATHOLOGY

CHEMICAL BURN

• Aspirin & tetracyclin burn

• Caused by ingestion of household

chemicals by children

• Or by ingestion of dentifrices or

mouthwashes.

• Or iatrogenic burns, caused by acid etch

to tooth surface reaching the soft tissue.

CLINICAL FEATURES

• Thin, homogenous white film.

• Lateral pressure removes this white film

expose painful ulceraltion.

INFECTIONS

1- HIV infection

2- candidiasis

4-Primary Herpetic Gingivostomatitis

5- Scarlet fever

HIV INFECTION :1- Children most commonly acquire HIV infection during

pregnancy or at birth from an infected mother.

2- Blood products, transfusion, and breast milk are other

sources of pediatric HIV infection.

3- The fungal disease most commonly seen in children

with HIV is oral candidiasis

4-HIV gingivitis is characterized by a linear erythema of

the facial and interproximal gingival margins and is

unresponsive to improved oral hygiene

HIV INFECTION :

5- HSV infection is the

most common viral infection

in children with HIV infection.

6- Of unknown cause,

parotid swelling is more common in

children than in adults with HIV.

CANDIDIASIS :

1- Acute pseudomembranous candidiasis,

or.thrush, is the opportunis- tic overgrowth of the

fungus Cundidu ulbicuns.

2- candidiasis may be a sequelae of oral broad-

spectrum antibiotics or may reflect other systemic

alterations, such as immunode- ficiency.

3-Clinically, oral lesions are characterized by

creamy or curdy white plaques that can be wiped

off, leaving a red, raw, and painful surface. Any

mucosal surface in the oral cavity can be affected

CANDIDIASIS :

TREATMENT :

Topical or systemic antifungal agent usually

resolves the infection .

PRIMARY HERPETIC GINGIVOSTOMAT

ITIS1- The initial infection with herpes simplex virus

(HSV) occurs in young children after contact with

an infected child or adult.

2- The manifestations of primary herpetic

infection may be flulike symptoms or subclinical.

In primary gingivostomatitis, after an incubation

period of approximately 1 week, the patient

complains of fever, malaise, and irritability.

PRIMARY HERPETIC GINGIVOSTOMAT

ITIS3- Marginal gingivae become fiery red,

edematous, and may bleed easily. Clusters of

small vesicles erupt throughout the mouth, then

burst to form yellow vesicles surrounded by a red

halo.

4- The vesicles coalesce to form large ulcers of

the oral and perioral tissues. The lesions are

accompanied by pain, fever, arthralgia,

headache, and cervical lymphadenopathy.

SCARLET FEVER :

1- Most commonly affects children

2- Scarlet fever is usually spread by inhalation.

3- Most of the clinical features are caused by

erythrogenic toxin, a substance produced by the

bacterium Streptococcus pyogenes when it is

infected by a certain bacteriophage.

SCARLET FEVER :

4- Scarlet fever is characterized by:

Sore throat,Fever, Bright red tongue with a

"strawberry" appearance , Forchheimer spots

(fleeting small, red spots on the soft palate)

,Paranoia and Hallucinations

TREATMENT :

There is no vaccine, but the disease is effectively

treated with antibiotics.

ULCERATIONS

• Recurrent apthous ulcer

RECURRENT APTHOUS

ULCER • The initial infection with herpes simplex

virus (HSV) occurs in young children after

contact with an infected child or adult.

• The manifestations of primary herpetic

infection may be flulike symptoms or

subclinical. In primary gingivostomatitis,

after an incubation period of approximately

1 week, the patient complains of fever,

malaise, and irritability.

BENIGNTUMORS

• Marginal gingivae become fiery red, edematous,

and may bleed easily. Clusters of small vesicles

erupt throughout the mouth, then burst to form

yellow vesicles surrounded by a red halo.

• The vesicles coalesce to form large ulcers of the

oral and perioral tissues. The lesions are

accompanied by pain, fever, arthralgia, headache,

and cervical lymphadenopathy.

BENIGNTUMORS

• HAEMANGIOMA

• LYMPHANGIOMA

• GIANT CELL FIBROMA

(RETROCUSPIC PAPILLA)

HAEMANGIOMA

• Infantile haemangiomas are benign

vascular neoplasms that have a

characteristic clinical course marked by

early proliferation and followed by

spontaneous involution.

• Haemangiomas are the most common

tumors of infancy and usually are

medically insignificant.

CLINICAL FEATURES:

• Bluish- red or purple colour.

• Homogeneous, sharp border, sessile

prominence.

• Spongy to palpation, blanching( +ve).

• Asymptomatic.

HAEMANGIOMA

MANAGEMENT

• Excisional biopsy, unless the lesion is

too large then injection of sclerosing

solutions or cryosurgery are preformed,

because biopsy to large hematomas

lead to haemorrhage.

LYMPHANGIOMA

• Lymphangiomas are uncommon congenital

hamartomas of the lymphatic system, usually

diagnosed in infancy and early childhood.

• Commonly located at head and neck, they are rarely

situated in the oral cavity.

• Preferred site of oral involvement is the tongue. In the

absence of proper therapy, lymphangiomas of the

tongue are extremely recurrent.

LYMPHANGIOMA

PATHOGENETIC

THEORIES:Three theories have been proposed to explain the origin

of this abnormality:

• The first suggests that a blockage or arrest of normal

growth of the primitive lymph channels occurs during

embryogenesis.

• The second that the primitive lymphatic sac does not

reach the venous system.

• While the third advances the hypothesis that, during

embryogenesis, lymphatic tissue lays in the wrong

area.

HISTOPATHOLOGY:

• Let’s watch this video to better understand the

histopathology for lymphangioma:

http://www.youtube.com/watch?v=x2-a2SyeI24

MANAGEMENT

• Surgical intervention represents the treatment of choice.

• Lesion extension and involvement of vital structures can

reduce, in some cases, the possibility of complete

resection.

• Sclerosing therapy should be considered for recurrences.

GIANT CELL FIBROMA

(RETROCUSPIC PAPILLA) • Asymptomatic sessile or pedunculated nodule

• Usually less than 1cm in size

• Occurs more in females than males.

• Occurs more in maxilla than mandible.

• Not associated with trauma (not reactive)

• 60% of lesion diagnosed during the first 3 decades of life.

• Occurs more in mandible than maxilla.

• 50% of cases occur in gingiva

• Can also occur on tongue and palate

GIANT CELL FIBROMA

(RETROCUSPIC PAPILLA) • Retrocuspid papilla is a giant cell fibroma that occurs on

the gingiva lingual to mandibular cuspids (canines).

• It’s usually bilateral, small pink papule.

• Retrocuspid papilla are quite common, they have been

reported in 25% - 99% of children and young adults.

GIANT CELL FIBROMA

(RETROCUSPIC PAPILLA)

HISTOPATHOLOGY:

• Connective tissue mass with Pseudoepitheliumatous

hyperplasia

• Different giant cells; large stellate fibroblasts within the

connective tissue

HISTOPATHOLOGY:

MALIGNANT

TUMORS:• EMBRYONIC

RHABDOMYOSARCOMA

• MUCOEPIDERMOID CARCINOMA

EMBRYONIC

RHABDOMYOSARCOMA• Rhabdomyosarcoma (RMS) is an aggressive malignant

neoplasm of skeletal muscle origin that represents 50% of

all soft tissue sarcomas in childhood, with most cases

occurring in the head and neck 40%.

• Within the microscopical patterns, the embryonal type is

the most frequent in the oral cavity.

EMBRYONIC

RHABDOMYOSARCOMA

HISTOPATHOLOGY

• Embryonal RMS is characterized by a mixture of

pleomorphic and skeletal immature muscle cells, the so-

called rhabdomyoblasts.

• These cells have a distinctive eosinphilic-rich cytoplasm

and proliferate in a myxoid loose stroma.

HISTOPATHOLOGY

MANAGEMENT

• Overall 5-year survival rates have improved to more than

80% with the combined use of surgery, radiation therapy,

and chemotherapy.

• However, in patients with metastatic disease, little

progress has been made in survival rates, with a 5-year,

event-free survival rate of less than 30%

MUCOEPIDERMOID CARCINOMA

• Salivary gland tumors are rare in children but when they

involve the minor salivary glands, there is an increased

risk that they will be malignant, and it is the palatal region

that is the most common site.

CLINICAL PRESENTATION:

• The presentation of this malignancy is a painless,

persistent enlargement. When the major salivary

glandsand tongue are involved, pain, paresthesia, and

difficulty with swallowing are noted more frequently.

• Intraoral lesions appear as a localized fluctuant nodule

with a bluish or reddish-purple, smooth, mucosal surface.

CLINICAL PRESENTATION:

HISTOPATHOLOGY

• These tumors are determined to be low, intermediate and

high grade based on defined microscopic criteria, which

are correlated with prognosis.

• Most pediatric cases of mucoepidermoid carcinoma are

diagnosed as low or intermediate grade tumors.

• Consisting of multicystic spaces and duct-like structures

in a fibrous connective tissue. The cysts and small islands

are composed of mucous, intermediate and epidermoid

cells with evidence of mucus pooling.

HISTOPATHOLOGY

MANAGEMENT:

• Management of a low grade mucoepidermoid of the minor

salivary glands involves wide local excision with adequate

tumor-free margins.

• High grade tumors require more aggressive surgery with

or without postoperative radiotherapy and chemotherapy.

• Individuals with low grade tumors have a good prognosis

with greater than a 90% cure rate. In contrast, high grade

tumors have a poor prognosis with only a 20 to 30%

survival rate.

SYNDROMES

Down Syndrome.

Papillon-Lefevre Syndrome

DOWN SYNDROME

also known as trisomy 21, is a

genatic disorder caused by the

presence of all or part of a third copy

of chromosome 21. It is typically

associated with physical growth

delays, characteristic facial features,

and mild to moderate intellectual

disability.

• DENTAL MANIFESTATIONS IN DOWN SYNDROME:

. DELAYED ERUPTION OF BOTH PRIMARY AND PERMANENT DENTITIONS MICRODONTIAENAMEL HYPOCALCIFICIATION AND HYPOPLASIA COMMON 1/3 MORE CARIES RESISTANT THAN THEIR NON-DS SIBLINGS GINGIVITIS DEVELOPS EARLIER AND MORE RAPIDLY V-SHAPED PALATE, INCOMPLETE DEVELOPMENT OF THE MIDFACE COMPLEX, SOFT PALATE INSUFFICIENCYABSENT INCISORS MAKE ARTICULATION DIFFICULT SCALLOPED, FISSURED TONGUE WITH BIFID UVULA, CLEFT LIP/PALATE, ENLARGED TONSILS/ADENOIDSREDUCED SALIVARY FLOW HIGHER INCIDENCE OF BRUXISM, PARTICULARLY IN AGES 0-6 YEARS. BRUXISM TENDS TO DECREASE AFTER AGE SIX

DENTAL MANAGMENT

An aggressive preventive dental program is recommended for

patients with Down syndrome. The program should include:

Three to four month recalls: Consistent preventive care can help

reduce periodontal disease

Dietary counseling and encouragement of good oral hygiene:

Practical advice to minimize consumption of cariogenic foods

and the effects of such foods on tooth structure

Topical fluoride application: For caries prevention and/or

reduction of dentinal hypersensitivity

Chlorexidine gluconate 0.12% rinse: For reduction of bacteria that

cause periodontal disease

• PAPILLON-LEFEVRE SYNDROME :

also known as

palmoplantar keratoderma

with periodontitis, is an

autosomal recessive genetic

disorder caused by a

deficiency in cathepsin C

charecter of the syndrome:

1- hyperkeratosis of the palms and soles

2- premature loss of the primary and permanent dentitions

3- Hyperkeratotic lesions of the elbows and knees also may be found

4- Periodontal inflammation begins soon after the primary teeth erupt

5- Bone loss is severe, so that primary teeth are lost by 5 years of age (, permanent teeth also were lost within a few years of eruption)

MANAGMENT:

conventional therapy with oral hygiene instruction, professional

cleanings, frequent recalls, and antibiotics have failed to prevent

tooth loss.

TEETH ANOMALIES

1-Enamel hypoplasia

2-amelogensis imperfecta

3-dentinogenesis imperfecta

4-tetracyclin staining of teeth

ENAMEL HYPOPLASIA

Enamel hypoplasia is a defect of the teeth in

which the enamel is hard but thin and deficient

in amount,caused by defective enamel matrix

formation with a deficiency in the

cementing substance. Usually the condition

involves

part of the tooth having a pit in it. In some

cases, the natural enamel crown has a hole in

it, and in extreme cases, the tooth has no

enamel, which doesn't mean the tooth doesn't

exist

because dentin is also a component of teeth.

It can be caused by any of the following:

1-Trauma

2-Bacterial infection

3-Slow enamel formation

4-Celiac disease

CAUSES

Amelogenesis imperfecta (AI) presents with a rare abnormal

formation of the enamel or external layer of the crown of teeth.

Enamel is composed mostly of mineral, that is formed and regulated by

the proteins in it.

Amelogenesis imperfecta is due to the malfunction of the proteins in the

enamel: ameloblastin,

enamelin, tuftelin and amelogenin.

People afflicted with amelogenesis imperfecta have teeth with abnormal

color:

yellow, brown or grey; this disorder can afflict any number of teeth of both

dentitions.

The teeth have a higher risk for dental cavities and are hypersensitive to

temperature changes

as well as rapid attrition, excessive calculus deposition, and gingival

hyperplasia.

AMELOGENESIS IMPERFECTA

GENETICS

Mutations in the AMELX, ENAM,MMP20, KLK-4,FAM83H,

WDR72,

C4orf26, SLC24A4 LAMB3 and ITGB6 genes have been

found to

cause amelogenesis imperfecta (non-syndromic form).

About 5% of amelogenesis imperfecta cases are caused by

mutations in the AMELX gene and

are inherited in an X-linked pattern.

A condition is considered X-linked

if the mutated gene that causes the disorder is located on

the X chromosome, one of the two

sex chromosomes. In most cases, males

with an X-linked form

of this condition experience more severe

dental abnormalities than affected females.

TREATMENT

Preventive and restorative dental care is very important as

well as considerations

for esthetic issues since the crown are yellow from

exposure of dentin due to enamel loss.

Full-coverage crowns are sometimes being used to

compensate for the abraded enamel. Usually

stainless steel crowns are used in children which may be

replaced by porcelain once they

reach adulthood. In the worst-case scenario, the teeth may

have to be extracted and implants or

dentures are required.

DENTENOGENESIS IMPERFECTA

Dentinogenesis imperfecta is a disorder of tooth

development. This condition causes the teeth to be

discolored (most often a blue-gray or yellow-brown color)

and translucent. Teeth are also weaker than normal, making

them prone to rapid wear, breakage, and loss. These

problems can affect both primary (baby) teeth and

permanent teeth.

Type I: Type of dentinogenesis imperfecta with similar

dental abnormalities usually an autosomal dominant trait

with variable expressivity but can be recessive if the

associated osteogenesis imperfecta is of recessive type.]

Type II : Occurs in people without other inherited disorders

(i.e. Osteogenesis imperfecta). It is an autosomal dominant

trait. .

Type III: Type is rare; its predominant characteristic is bell-

shaped crowns, especially in the permanent dentition.

Unlike Types I and II, it involves teeth with shell-like

appearance and multiple pulp exposures

TYPE OF DI :

The objectives of early treatment of DI in the primary

dentition are as follows: 1. Maintain dental health and

preserve vitality, form, and size of the dentition. 2. Provide

the patient with an esthetic appearance at an early age, in

order to prevent psychological problems. 3. Provide the

patient with a functional dentition. 4. Prevent loss of

vertical dimension. 5. Maintain arch length. 6. Avoid

interfering with the eruption of the remaining permanent

teeth. 7. Allow normal growth of the facial bones and

temporomandibular joint (TMJ). 8. Establish a rapport with

the patient and the patient’s family early in the treatment.

TREATMENT :

TETRACYCLIN STAINING OF

TEETH Tetracycline can stain the teeth anywhere from a bright

yellow shade to dark brown. Usually the staining starts

out as a yellow color. Over time, as the tooth is exposed

to light, a chemical reaction occurs and the yellow turns to

a dark brown color.

DRUGS THAT CAUSE STAINING OF

TEETHMany of tetracycline’s homologues (similar drugs) are all

associated with discoloration. Chlortetracycline,

demethylchlortetracycline and oxytetracycline can all

cause brown/gray/yellow staining of the teeth.

Ciprofloxacin is an antibiotic that can be given

intravenously to infants for treatment of a Klebsiella

infection. It can stain the teeth a green color, but the

staining is usually more mild than tetracycline staining.

Minocycline hydrochloride is an antibiotic used to treat

acne and rheumatoid arthritis.

PREVENTION :

Tetracycline can cross the placental barrier and

incorporate into the developing tooth. It should be

avoided (if possible) by mothers who are pregnant and

also in kids until they are at least seven or eight years of

age.

TREATMENT OF TETRACYCLINE STAINED

TEETH :It is very difficult to treat internal staining of teeth because

it affects the dentin layer underneath the enamel.

CASE 1

• What is you diagnosis?

• How are you going to manage it?

CASE 2

CASE 2

• Excisional biopsy was

taken showing fibrous

c.t

• High power

magnification showing

which type of cells?

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http://emedicine.medscape.com/article/909213-overview

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http://jada.ada.org/content/96/2/266.long

http://ejo.oxfordjournals.org/content/27/5/443

http://en.wikipedia.org/wiki/Amelogenesis_imperfecta

http://en.wikipedia.org/wiki/Enamel_hypoplasia

REFERENCESPediatric Gastroenterology: A Color Handbook

http://emedicine.medscape.com/article/1083849-overview

http://www.rjme.ro/RJME/resources/files/470406373377.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2640069/

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Oral and maxillofacial pathology, 3rd edition, Neville