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Summary (pediatric oral pathology)

Summary (Pediatric Oral Pathology)

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Summary (pediatric oral pathology)

  1. 1. ORAL PATHOLOGY ONLINE CONFERENCE Third year dental students Supervised by Dr.Dalal ALQahtani dalalq@ksu.edu.sa College of Dentistry King Saud University SUMMARY
  2. 2. TOPIC NAME: PEDIATRIC ORAL PATHOLOGY DONE BY: Riham AlBusayes Reem AlRabiah Mariam AlShamali, Maha AlJarboua Amani AlMohaimeed
  3. 3. DONE BY XMIND 2013
  6. 6. 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.
  7. 7. • 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.
  8. 8. 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.
  9. 9. • Problems with feeding can occur with orofacial clefts which requires treatment. So, How can we treat orofacial clefts?
  10. 10. TREATMENT • Surgery • Obturator
  11. 11. 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.
  12. 12. 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)
  13. 13. TREATMENT • No treatment is required, as they’re going to disappear several weeks after birth.
  14. 14. CONGINITAL EPULIS Clinical features: • A soft tissue tumor that occurs almost exclusively on the alveolar ridge of newborns. • Pink to red, smooth- surfaced mass.
  15. 15. 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.
  16. 16. • Shows a striking predilection for females (90% of the cases), which suggest a hormonal influence in its development.
  17. 17. HISTOPATHOLOGY: • The overlying epithelium shows atrophy of rete ridges • Large-rounded cells with granular cytoplasm
  18. 18. TREATMENT: • Surgical excision. • Will not recur, even with incomplete removal. • In some patients, complete regression of the tumor without treatment.
  19. 19. 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
  20. 20. 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.
  21. 21. 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.
  22. 22. 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.
  23. 23. 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.
  24. 24. In Toddlers and Older Children Speech ? 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
  25. 25. 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.
  26. 26. 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.
  27. 27. 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
  28. 28. (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
  29. 29. ODONTOGENIC : • Parulis • Eruption cyst
  30. 30. 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
  31. 31. PARULIS : • Treatment is to extract the abscessed tooth or preform root canal therapy
  32. 32. ERUPTION CYST : 1- Follicular enlargement appearing just before the eruption of tooth. 2- Blue-black in color (may contain blood).
  33. 33. TREATMENT : None unless infected, reassure the child and parent, follicle will rupture, but may need to surgically opened if infected.
  34. 34. REACTIVE • Mucocele • Chemical burn
  35. 35. MUCOCELE • Mucocele is a benign lesion characterized by an extravasation or retention of mucous in submucosal tissue from minor salivary glands.
  36. 36. 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.
  37. 37. 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.
  39. 39. 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.
  40. 40. CLINICAL FEATURES • Thin, homogenous white film. • Lateral pressure removes this white film expose painful ulceraltion.
  41. 41. INFECTIONS 1- HIV infection 2- candidiasis 4-Primary Herpetic Gingivostomatitis 5- Scarlet fever
  42. 42. 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
  43. 43. 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.
  44. 44. 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
  45. 45. CANDIDIASIS :
  46. 46. TREATMENT : Topical or systemic antifungal agent usually resolves the infection .
  47. 47. PRIMARY HERPETIC GINGIVOSTOMAT ITIS 1- 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.
  48. 48. PRIMARY HERPETIC GINGIVOSTOMAT ITIS 3- 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.
  49. 49. 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.
  50. 50. 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
  51. 51. TREATMENT : There is no vaccine, but the disease is effectively treated with antibiotics.
  52. 52. ULCERATIONS • Recurrent apthous ulcer
  53. 53. 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.
  54. 54. 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.
  56. 56. 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.
  57. 57. CLINICAL FEATURES: • Bluish- red or purple colour. • Homogeneous, sharp border, sessile prominence. • Spongy to palpation, blanching( +ve). • Asymptomatic.
  59. 59. 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.
  60. 60. 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.
  62. 62. 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.
  63. 63. HISTOPATHOLOGY: • Let’s watch this video to better understand the histopathology for lymphangioma: http://www.youtube.com/watch?v=x2-a2SyeI24
  64. 64. 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.
  65. 65. 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
  66. 66. 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.
  68. 68. HISTOPATHOLOGY: • Connective tissue mass with Pseudoepitheliumatous hyperplasia • Different giant cells; large stellate fibroblasts within the connective tissue
  71. 71. 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.
  73. 73. 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.
  75. 75. 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%
  76. 76. 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.
  77. 77. 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.
  79. 79. 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.
  81. 81. 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.
  82. 82. SYNDROMES  Down Syndrome.  Papillon-Lefevre Syndrome
  83. 83. 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.
  85. 85. 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
  86. 86. • PAPILLON-LEFEVRE SYNDROME :  also known as palmoplantar keratoderma with periodontitis, is an autosomal recessive genetic disorder caused by a deficiency in cathepsin C
  87. 87.  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)
  88. 88. MANAGMENT:  conventional therapy with oral hygiene instruction, professional cleanings, frequent recalls, and antibiotics have failed to prevent tooth loss.
  89. 89. TEETH ANOMALIES 1-Enamel hypoplasia 2-amelogensis imperfecta 3-dentinogenesis imperfecta 4-tetracyclin staining of teeth
  90. 90. 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.
  91. 91. It can be caused by any of the following: 1-Trauma 2-Bacterial infection 3-Slow enamel formation 4-Celiac disease CAUSES
  92. 92. 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
  93. 93. 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.
  94. 94. 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.
  95. 95. 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.
  96. 96. 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 :
  97. 97. 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 :
  98. 98. TETRACYCLIN STAINING OF TEETHTetracycline 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.
  99. 99. DRUGS THAT CAUSE STAINING OF TEETH Many 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.
  100. 100. 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.
  101. 101. TREATMENT OF TETRACYCLINE STAINED TEETH : It is very difficult to treat internal staining of teeth because it affects the dentin layer underneath the enamel.
  102. 102. CASE 1 • What is you diagnosis? • How are you going to manage it?
  103. 103. CASE 2
  104. 104. CASE 2 • Excisional biopsy was taken showing fibrous c.t • High power magnification showing which type of cells?
  105. 105. REFERENCES: https://pedclerk.sites.uchicago.edu/sites/pedclerk.uchicago.ed u/files/uploads/1-s2.0-S0031395505702601-main.pdf http://www.columbia.edu/itc/hs/dental/d7710/client_edit/Oral_P athology.pdf http://www.dentalcare.com/en-US/dental-education/continuing- education/ce4/ce4.aspx?ModuleName=coursecontent&PartID =2&SectionID=3 http://emedicine.medscape.com/article/909213-overview -http://www.entnet.org/content/tongue-tie-ankyloglossia 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
  106. 106. REFERENCES Pediatric 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/ http://www.hindawi.com/journals/crid/2014/723130/ http://www.sciencedirect.com/science/article/pii/S1741940905000907 http://sarcomahelp.org/rhabdomyosarcoma.html http://www.aapd.org/assets/1/25/Flaitz-22-04.pdf http://www.hindawi.com/journals/crid/2012/370242/fig1/ Oral and maxillofacial pathology, 3rd edition, Neville

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Summary (Pediatric Oral Pathology)


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