Master Day 2

1. Identify “AOT” On radiographs, the adenomatoid odontogenic tumor presents as a radiolucency (dark area) around an unerupted tooth extending past the cementoenamel junction.

It should be differentially diagnosed from a dentigerous cyst and the main difference is that the radiolucency in case of AOT extends apically beyond the cementoenamel junction.

Radiographs will exhibit faint flecks of radiopacities surrounded by a radiolucent zone.

It is sometimes misdiagnosed as a cyst. And frequently in anterior maxilla! 2. Identify Dentigerous Cyst

3. Identify Eruption Cyst

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4. Identify

Doubtful Answer Molar appears to have DD and Premolar – DI

5. Identify ? :

How to identify? See the outer boundary n shape. Compare it with adjacent teeth moreover i see it like a prepared tooth for crown to diagnose.

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6. Identify Dentinogenesis imperfecta

7. Identify External Resorption

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8. Identify Genial tubercle

9. Identify Bilateral Tori

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10. Identify Mandibular Canal

11. Identify Ameloblastoma

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12. Identify Fusion

13. Identify Lateral Periodontal Cyst

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14. Identify Complex Odentoma

It's a complex odontome. Compound would show enamel dentin and cementum separately.

15. Identify Cementoblastoma

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16. Identify Underexposed / OverFixed

17. Identify Intermaxillary Suture

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18. Identify Zygomatic Process

19. Identify Coronoid Process

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20.

21.

May God be with us and help us nail NBDE PART 2 22. Identify

23. Identify

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24. Identify Stafne’s bone Cyst

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25. Identify Recurrent Caries :

26. Identify Age and Diagnosis ?

Over 7 Years Diagnosis would be retained deciduous lower incisors and coming to age is would be 7-8 here we have to consider the development of roots of 6 and roots of upper central incisors and lower lateral incisors. Coming to loss of D in 3rd arch, ref; Mc Donald pediatric book, if any primary teeth lost before 7 yr there

May God be with us and help us nail NBDE PART 2 would be delayed eruption of permanent teeth and if loss of primary teeth after 7 yrs would lead to premature eruption of permanent teeth. Here premolar is in eruption stage so it should be considered too. So age would be 7-8 yrs

27. Learn the fact

Complete craniofacial dysjunction by the Le Fort III osteotomy allows the surgeon to alter the orbital position and volume, zygomatic projection, position of the nasal root, frontonasal angle, and position of the maxilla and to lengthen the nose. The Le Fort II osteotomy allows the surgeon to alter the nasomaxillary projection without altering the orbital volume and zygomatic projection. The Le Fort I osteotomy allows for correction primarily at the occlusal level affecting the upper lip position, nasal tip and alar base region, and the columella labial angle without altering the orbitozygomatic region

28. The appearance of the curve of spee on the panoramic suggests that the patients chin was positioned too: A. Far forward B. Far back C. High D. Low

Answer is HIGH

May God be with us and help us nail NBDE PART 2 29. No answer available

May be lingual tori

30. Identify Underexposed/Overfixed +Lower border of mx.sinus

May God be with us and help us nail NBDE PART 2 31. Identify gemination, fusion has just two roots

32. Identify Answer is below the picture

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33. Identify flap Semilunar Flap

34. Identify Answer is below the Picture

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35. Identify Answer is below the picture

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36. Identify Answer is below the picture

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37. Identify

we have retained primary 1ts molar in lower right side Missing lower 3rd molar bilateral or extracted Chin is up means � frown Chin is down means � smile

In this Pano ... Chin down smiling Pt is 23 years’ old

38. Pt adult male. Present asymptomatic, necrotic, ulcerated area involving palatal mucosa. Histologically presents lobular necrosis of glandular parenchyma with squamous metaplasia and hyperplasia of ductal epithelium. Dx & Tx?

Necrotizing sialometaplasia. it is caused by ischemic necrosis of minor salivary glands. it will heal in 6-10 wks.

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39. Identify 8 is angle of Mandible and 9 is Hyoid Bone

40. Identify

Peutz-Jeghers Syndrome. Intraorally pigmentations may be located anywhere in the mucosa. Most frequently hard palate, Buccal mucosa and gingiva

May God be with us and help us nail NBDE PART 2 41. Identify

1- middle cranial fossa 5- styloid process 17- ear

42. Identify

Dens in Dente

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43. Identify 10- glenoid fossa 11- articular eminence 12-condyle 13-vertebra

May God be with us and help us nail NBDE PART 2 44. Identify : Compare with Dens in dente : 42nd Question

45. Identify 2-orbit 3- zygomatic arch 4- hard palate 6- max tuberosity

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46. Identify

Eagle’s Syndrome Elongated Styloid and calcification of stylohyoid ligaments.

47. Identify

odontogenic myxoma: non-encapsulated, no resorption of teeth, cortical expansion, honey-comb appearance

May God be with us and help us nail NBDE PART 2 48. Identify Punched out lesions without sclerotic border...multiple myeloma Punched out lesions with or without sclerotic border.... Langerhans cell histiocytosis

49. Identify

The arrow is pointing to alternating RLs at the level of border of mandible. This is also known as "onion skin" and it's seen in GARRE's Osteomyelitis.

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50. Identify Y is formed between nasal floor and maxillary sinus Y line of Ennis The straight line resembles the basal floor and the curved one for the maxillary sinus.

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51. Identify

Answer: Antral pseudocyst (mucous retention pseudocyst)

52. Identify

May God be with us and help us nail NBDE PART 2 53. Identify Internal Resorption

54. Turner's Hypoplasia***-Frequent pattern of enamel defects seen in permanent teeth secondary to periapical inflammatory disease of the overlying deciduous tooth. -The altered tooth is called Turner's tooth.

May God be with us and help us nail NBDE PART 2 55. Characteristics of enamel defects in Turner's Hypoplasia -Vary from focal areas of white, yellow or brown discoloration to extensive hypoplasia which can involve the entire crown. Most frequently noted in permanent bicuspids because of their relationship to the overlying deciduous molars.

56. In regards to traumatic injury, which teeth are most affected by Turner's Hypoplasia Maxillary central incisors

57. Identify problem, cause, treatment clinical features and treatment - Ingestion of fluoride results in enamel defects called dental fluorosis. -Permanent hypomutation of the enamel in which there is an increased surface and subsurface porosity of the enamel. -Altered tooth structure presents as areas of lusterless, white opaque enamel with zones of yellow to dark-brown discoloration. treatment: composites and full crown coverage

May God be with us and help us nail NBDE PART 2 58. Critical years for dental fluorosis During the 2nd and third years of life when anterior teeth are forming and fluoride levels are greater than 1 pt per million ingested.

59. definiton*** Loss of tooth structure caused by tooth to tooth contact during occlusion and mastication Destruction acclerated by: 1) poor quality or absent enamel 2) Premature contacts, edge to edge occlusion 3) intraoral abrasives, erosion or grinding habit

May God be with us and help us nail NBDE PART 2 60. Abrasion definition Loss of tooth structure secondary to the action of an external agent. Most common source is toothbrushing.

61. Erosion definition Loss of tooth structure caused by chemical reaction (other than bacteria) -usually to an acid external: lemon, vinegar, soft drinks internal: gastric secretions such as perimylolysis (people suffering from anorexia or buliema present this)

62. Attrition most often seen in these teeth and specific surfaces -Deciduous and permanent teeth -Occlusal and Incisor region of maxillary and mandibular teeth -Lingual of Maxillary anteriors -Labial of mandibular anteriors

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63. Abrasion

64. Internal Resorption

Destruction of teeth accomplished by cells located in the dental pulp.-Rare occurence, when injury to pupal tissue occurs such as physical trauma or pulpitis. -Process continues as long as vital pulp tissue is present. -Uniform well circumscribed symmetric radiolucent enlargement of the pulp chamber or canal. Pinktooth of Mummery. -When it affects the coronal pulp and expands it, the crown can display a pink discoloration:

May God be with us and help us nail NBDE PART 2 65. External Resorption*** -Destruction of teeth accomplished by cells in the periodontal ligament -Extremely common, all patients likely to have root resorption on one or more teeth. -impacted teeth can hit other teeth and cause damage. -Presents as a "moth-eaten loss of tooth structure in which radiolucency is well less- defined. -Most cases involve the apical or midportions of the tooth.

66. Environmental Discoloration of teeth: Extrinsic Staining examples 1) Bacterial Stains: cause surface staining of enamel, dentin and cementum. Seen initially on labial surfaces of the maxillary anterior teeth in the gingival 1/3. 2) Tobacco products, tea, coffee: brown discoloration of the surface enamel. On lingual surface of anterior teeth but usually widespread and less intense. 3) Medications: Fluoride and chlorhexidine or many other oral antiseptics like Listerine.

67. Environmental Discoloration of teeth: Intrinsic Staining Examples: 1) Congenital erythropoietic polyphyria (Gunther's disease) -Autosomal recessive disorder of porphyrin metabolism -results in increased synthesis and excretion of porphyrins and related precursors. -Diffuse discoloration of the dentition is noted as a result of the deposition of porphyrin in the teeth. -Stains teeth red -eyes are blood shot, show hirutism, sensitive to light, "wear-wolf disease"

May God be with us and help us nail NBDE PART 2 68. Intrinsic staining examples: 2) Hyperbilirubinemia -During this syndrome, developing teeth may also accumulate pigment and become intrinsically stained. -Gallbladder closes, causes bile to accumulate in blood and cause brown staining in system. -Deciduous teeth are affected as a result of this syndrome during the neonatal period. -teeth extremely dark brown Two most common causes: erythroblastosis fetalis biliary atresia

69. Primary impaction of deciduous teeth is rare but when it occurs it affects this tooth*** second molars.

May God be with us and help us nail NBDE PART 2 70. Ankylosis plays an important role in pathogenesis of impacted teeth. Permanent teeth most affected by impaction are*** third molars (mand then max) and then maxillary cuspids. Treatment for impacted teeth include: orthodontics, long-term watch, surgical removal, assisted eruption and transplantation.

Ankylosis definition, clinical features and treatment Cessation of eruption after emergence of teeth -occurs at any age but most obvious during first 2 decades of life: 9-18 yrs of age -occlusal plane of involved tooth is below that of adjacent teeth. -A sharp solid sound on percussion of the involved tooth noted if more than 20% of root is fused to the bone. Absence of periodontal ligament space may be noted. -fusion of root into jaw bone is smooth (resorption would show up ragged on radiograph) Treatment: Fused to adjacent bone, don’t respond to ortho, primary molars best treated with extractions and space maintainers.

71. lack of development of one or more teeth Uncommon in deciduous dentition. Very common in permanent dentition (pic example of hypodontia during ectodermal dysplasia)

72. and mesiodens also increased number of teeth and additional teeth are called supernumerary

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73. Clinical features of Hypodontia (teeth it most frequently occurs with) (most-> least) 1) third molars 2) second premolars 3) lateral incisors -More common in females than males

Hyperdontia clinical features -Single tooth hyperdontia occurs more frequently in the permanent dentition and 90% present in the maxilla anterior incisor region, followed by maxillary fourth molars and mandibular fourth molars.

74. Multiple supernumerary teeth (nonsyndromic) occur most frequently in the: mandibular premolar region. The differential diagnosis for multiple supernumerary teeth are 1) Gardner's syndrome (malignancies in large intestine) 2) Cleidocranial dysplasia

75. Natal teeth teeth present in newborns -should be extracted or will cause child severe pain

76. teeth present within the first 30 days of life (represent pre-maturely erupted deciduous teeth not supernumerary teeth) -should be extracted or will cause child severe pain

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77. Germination -A single enlarged tooth or jointed tooth in which the tooth count is normal when the anomalous tooth is counted as one. -1 crown, bifid pulp chamber, 1 root and 1 pulp canal. -Both primary and permanent dentitions -High frequency in the anterior maxillary region

78. Fusion -A single enlarged tooth or joined (double) tooth in which the tooth count reveals a missing tooth when the anomalous tooth is counted as one. -2 crowns, 2 separate pulp chambers, and 1 root. -Both primary and permanent dentitions -High frequency in the anterior maxillary region

79. -union of two adjacent teeth by cementum alone without the confluence of the underlying dentin. -Presents as two fully formed teeth, jointed along the root surfaces by cementum. -Frequently in the posterior maxillary region.

May God be with us and help us nail NBDE PART 2 80. Accessory Cusps: -Seen in oriental groups -Cusp-like elevation of enamel located in central groove or lingual ridge of the buccal cusp of permanent premolar or molar teeth. -Usually bilateral, marked by mandibular premolar predominance. -results in occlusal problems and prone to fracture frequently resulting in pupal exposure because the dens evaginatus contains pupal tissue.

81. **** -Deep surface invagination of the crown or root that is lined by enamel. -Due to defect in enamel -Two forms: coronal or radicular -Coronal is seen more frequently -Teeth affected mostly: permanent maxillary lateral incisors and maxillary central incisors -Invagination maybe large and resemble a tooth within a tooth "dens in dente" -If opening of invagination becomes carious, pupal necrosis may result. Treatment: small restoration

82. Ectopic Enamel presence of enamel in unusual locations, mainly the tooth root. (if u have enamel bud at junction of CEJ...periodontal defect will result) ex) enamel pearls -hemispherical structures of enamel -most frequent: roots of max. molars, mand molars: second most frequent. -majority at furcation area or near CEJ. -precludes normal periodontal attachment. -less resistant to breakdown, rapid loss of attachment likely.

May God be with us and help us nail NBDE PART 2 83. *** Enlargement of the body and pulp chamber of multi-rooted tooth with apical displacement of pulp chamber and bifurcation. -affected teeth are rectangular in shape -pulp chambers have increased apico-occlusal height and bifurcation (if present) close to apex. -Unilateral or bilateral -Permanent teeth affected more -Isolated trait or w/ 1) Down's 2) Klinefelter's 3) Ectodermal dysplasia 4) Amelogenesis imperfecta

84. *** Abnormal angulation or bend in the root, or less frequently the crown of a tooth. -arise following an injury that displaces that calcified portion of the tooth germ with the remainder of the tooth being formed at an abnormal angle. -Permanent maxillary incisors most frequently affected.

85. Supernumerary roots*** increased number of roots on a tooth. -occurs more frequently on third molar teeth.

86. Hypoplastic Type Generalized: pinpoint pits Localized: horizontal row of pits in the middle 3rd of facial surface Incisal edge or occlusal surface= not affected Crown prep: like teeth on x-ray! <- amelogenesis differentiation

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87. Hypocalcified -Matrix laid down normally, abnormal calcification/mineralization takes place -SOFT ENAMEL EASILY LOST -YELLOW-BROWN OR ORANGE ENAMEL -EASILY STAINED, RAPID CALCULUS FORMATION X:ray: density of enamel similar to dentin

88. Hypomaturation type Matrix lad down, mineralizes normally, but crystal DO NOT form -teeth normal in shape, OPAQUE, WHITE-BROWN-YELLOW DISCOLORATION -Enamel is SOFT AND CHIPS OFF, pierced with explorer x-ray: enamel looks like dentin (enamel has fallen off DEJ)

89. Ameleogenesis imperfecta picture no enamel on teeth

May God be with us and help us nail NBDE PART 2 90. Dentinogenesis Imperfecta** -Hereditary disturbance in formation of dentin -aka "hereditary opalescent dentin" -May be seen w/ association to osteogenesis imperfecta -most cases in US traced from whites from English Channel

pic: large bulbous crowns and thinning roots

91. Detinogenesis Imperfecta clinical description** -Autosomal dominant -Severity depends on age *DECIDUOUS most severely affected -Followed by perm. incisors and 1st molars (order of eruption) -2nd and 3rd molars LEAST AFFECTED -Exhibit a blue/brown discoloration with translucence -Enamel strips off easily from underlying dentin (like amelogenesis!) **Differentiation: Bulbous crowns (like tulips!), cervical constriction towards roots, thin roots, obliteration of root canals and pulp chambers. "shell teeth"= LARGE PULP CHAMBERS, THIN DENTIN

92. Dentinogenesis Imperfecta broad crowns, thin roots, cervical constriction, pulp chamber disappear/non-existant, enamel present but easily taken off (DEJ doesn't hold enamel well)

93. ** (Type 1) Type 1 or radicular dentin dysplasia (rootless teeth) -short roots: malformation of root dentin -Autosomal dominant pattern -Enamel and Coronal dentin =NORMAL *x-ray: deci teeth SERVERLY affected with little or no pulp and very short roots. *perm teeth: little to no pulp present to CRESCENT SHAPED PULP CHAMBERS.

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94. Dentin Dysplasia (Type 2)** CORONAL Dentin Dysplasia -Similar to DI!!!!! -Autosomal dominant -Blue/brown translucency of teeth X-ray: bulbous crown, cervical constriction, thin roots, early obliteration of pulp chamber Perm Teeth: classic thristle-tube or flame shape CANT TELL DIFFERENCE BETWEEN DD TYPE 2 AND DI!

95. "ghost teeth" -uncommon condition found in both dentitions -localized non-hereditary developmental abnormality involving enamel, dentin and pulp. (ALL LAYERS AFFECTED) -idiopathic -no racial or sexual predilection bi-modal peak: eruption of prim teeth 2-4 years perm dentition: 7-11 yrs

96. Regional Odontodysplasia Clinical Characteristics -Several contiguous teeth affected usually in maxillary anterior -Involvement of primary teeth is followed by perm teeth being affected -failure of eruption -teeth that erupt have small irregular, brown - yellow rough surfaced crowns x-ray: -thin enamel and thin dentin surrounding enlarged pulp -pale wispy image of teeth "ghost teeth" -densities of enamel and dentin appear fuzzy -teeth have no shape -localized

May God be with us and help us nail NBDE PART 2 97. Congenital leukokeratosis () It is a rare disorder which is inherited in an autosomal dominant trait.

Symptoms and signs: present as white, whitish- greyish, peeling, it is a painless and complication-free disorder on the buccal mucosa and the mucosal layers of the nose, oesophagus and the ano-genital region. These lesions appear first at the time of birth or during childhood. This disorder occurs mostly on the loose mucous membrane of the mouth (buccal mucosa, soft palate, the ventral surface of the tongue, the mucosal surface of the lips, floor of the mouth, etc.). The gingival and the dorsal surfaces of the tongue are usually unaffected.

Differential diagnosis: leukoplakia, , lichen oris, fungal infections.

98. Mechanical injuries

The main cause of traumatic ulcers is usually a single physical damage (for example, fights, sports, epilepsy, bone, sharp, broken tooth and prosthesis, etc.), which causes yellowish, painful, soft changes various in diameter on the affected mucosal tissue. These ulcers are surrounded by a thin, erythematous halo. They heal spontaneously in 6–10 days but leave scarring behind.

Differential diagnosis: specific ulcers (tuberculosis, lues), aphtha or carcinoma.

May God be with us and help us nail NBDE PART 2 99. fissuratum (denture granuloma)

There are two major factors in the development of a denture granuloma: the pathologically mobile denture and the pressure of its edge on the surrounding mucosal tissue. An may most commonly occur in the middle third of the mandibular bones and is more common on the buccal surface than on the lingual surface. The epidermal layer of the mucosa may develop increased keratinisation. These lesions may become pale, hard and more flexible to the touch where the accumulation of connective tissue fibres is more extensive.

Differential diagnosis: gingival cancer, Hydantoin hyperplasia, epulis.

100. Morsicatio buccarum et labiorum The cause is that nervous, anxious children and young adults may repeatedly chew or bite their facial mucosa, lips or sometimes even their tongue as a bad habit. This constant mechanical trauma causes white desquamation of the effected epithelium, with erosions or even ulcers to develop mainly in the line of dental occlusion and buccal mucosa. This bad habit is commonly accompanied by bruxism.

Differential diagnosis: leukoplakia, candidiasis, ulcers caused by inflammations and cancer.

May God be with us and help us nail NBDE PART 2 101. Recurrent infection (herpes labialis, cold sore) Pathogen: Herpes simplex virus After the primary infection, the virus becomes latent in the epithelium and in the ganglia of the trigeminal nerve.

Symptoms: it usually affects the lips or the boundary between the lips and the skin. Predisposing factors include exposure to sun, fever (fever blisters), upper respiratory tract infections, pneumonia, malaria, meningitis, physical or emotional stress, menstruation, dental treatment, stress, gastroenteritis, AIDS, pregnancy, trauma, local irritation, etc.. Before the development of blisters, fever and enlargement of lymph glands may develop. At the onset of the disease an itchy, burning sensation (prodrome) and redness are present. A few hours later clusters of vesicles are formed, which are 1-3 millimetres in diameter. Vesicles become coalesced, and after two or three days they rupture and become ulcerated with yellowish crusts. The surrounding skin is erythematous. Skin lesions usually heal in 8-10 days without scarring. Sites and frequency of recurrences vary from patient to patient.

Differential diagnosis: Herpes zoster, .

102. Verruca vulgaris (common wart)

Pathogen: human papillomavirus (HPV) – a member of the papovavirus family. The wart occurs less frequently in the oral cavity than on the skin, but more commonly than previously believed.

Symptoms: they usually appear on the lips, tongue and palate, but any other location in the oral cavity may occur. They appear abruptly and grow rapidly (viral origin), they are broad based and have a whitish-grey, papillary surface (usually feel hard on the skin). Verrucae may appear as multiple and confluent lesions.

Differential diagnosis: Papilloma, verrucous leukoplakia

May God be with us and help us nail NBDE PART 2 103. Acute pseudomembranous candidosis (thrush) The commonest Candida albicans-caused oral disease.

Predisposing factors: inappropriate oral hygiene, heavy smoking, xerostomia, radiotherapy, the administration of antibiotics, corticosteroids or cytostatic drugs, diabetes mellitus, chronic systemic diseases, autoimmune diseases, leukaemia, AIDS, immunosuppression. It mostly presents in newborns and children suffering from chronic illnesses.

Symptoms: the appearance of cream-coloured or pearl-white, bluish-white plaques which leave a slightly burning, erythematous surface if wiped off is characteristic of this type of candidiasis. Predilection sites include the bucca, the palate and the tongue. It is common in newborns and infants. In case of acute pseudomembranous candidiasis in adults, an underlying systemic disease has to be considered.

Differential diagnosis: Lichen, leukoplakia (cannot be wiped off), morsicatio buccarum, allergic .

104. Chronic atrophic candidosis (denture stomatitis) It is a common chronic disease of the mucous membrane especially in patients wearing upper dentures. Tight fitting dentures provide favourable circumstances: they practically function as a substrate for the growth of Candida.

Symptoms: well-circumscribed, red, oedematous, sometimes eroded mucous membrane corresponding with the plate of the upper denture is characteristic of the disease. Chronic atrophic candidiasis is symptom-free. Differential diagnosis: contact allergy of the palate.

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105. Recurrent aphthous ulcer (Mikulicz’s aphtha; minor aphtha)

The etiology is not yet explained. It might be an autoimmune, viral, bacterial (Streptococci), genetic (familial) or allergic disease or could be influenced by mechanical injuries, gastrointestinal diseases (Crohn’s disease), psychic stress, menstrual cycle (hormonal factor), walnut or chocolate consumption, etc., or by hypovitaminosis (B12, folic acid).

It is the most frequent disease of the oral mucous membrane. Recurrent aphthae are more frequent in adulthood and in women. It is rare among smokers (mucosal hyperkeratinisation).

Symptoms: initially erythema and oedema develops on the corresponding area, accompanied by a nipping, burning sensation or by paraesthesia. It can be either solitary or multiple. The development of ulcers is not preceded by vesicle formation. Well-demarcated lenticular (3–10 mm) painful ulcers on erythematous bases, covered with yellowish fibrous pseudomembranes are present. After 1 or 3 weeks, they heal without leaving scars. They might persist for years, but their frequency varies from person to person. They might be accompanied by lymphadenomegaly, too. Predisposed areas are the vestibular surface of the lips, the floor of the mouth, the ventral surface of the tongue and the cheek (non-keratinized mucosal epithelium). It is rare on the hard palate, the gingiva and the back of the tongue; these areas are usually affected by gingivostomatitis herpetica.

Differential diagnosis: herpetic stomatitis, allergic stomatitis.

May God be with us and help us nail NBDE PART 2 106. Major aphtha (Sutton’s aphtha) Recently major aphthae have been considered to be the rare severe form of aphthous ulcer.

Symptoms: 1–4 cm in diameter, usually solitary, but might have multiple forms, too (giant aphtha). Very painful crater-like ulcers of variable depth, covered with yellowish-grey fibrous pseudomembranes. The lesion usually heals with deforming mucosal scarring after epithelisation. Women are usually more affected. Predilection areas are the oropharyngeal region, the soft palate, the cheeks and the tongue. It causes severe pain, fever, , lymphadenitis and difficulties in swallowing or eating. It may persist for several months or even for one or two years and tends to recur. Biopsy is mandatory.

Differential diagnosis: tumorous ulcer, decubital ulcer, specific ulcer: TB, lues.

107. Pemphigus vulgaris Pemphigus vulgaris is a chronic, life-threatening autoimmune skin, mouth and other mucous membrane disorder characterised by blistering of the skin and . Sometimes pemphigus appears in reaction to a viral infection, certain drugs (D- penicillamine, antihypertensive Captopril), thymoma or myasthenia gravis. Symptoms: it usually affects elderly women. Blistering starts intraepithelially, the surrounding mucosa is not erythematous. The thin-walled intraoral bullae easily burst leaving painful erosions covered with whitish-grey fibrinous diphtheroid coating. The erosions may also bleed. Painful erosions may cause difficulty swallowing and eating and increased salivation. Erosions heal without scarring. Sites of greatest involvement include the buccal mucosa, tongue, palates and the gingiva. Nikolsky’s sign is positive (when the surface of the unaffected skin and oral mucosa is rubbed, and the skin and mucosa separate easily). The diagnosis is established on the basis of skin symptoms and the histopathological examination. In order to adjust the drug therapy, hospitalisation is necessary. Differential diagnosis: herpetic gingivostomatitis, erosive lichen oris, .

May God be with us and help us nail NBDE PART 2 108. Varicosity of the tongue It is a diffuse dilation of the veins occurring in an elderly age (varix). The dark blue varicosity on the ventral surface of the tongue or sometimes on the floor of the mouth is often called caviar lesion. The varicosity of the tongue is most common among patients suffering from cardiopulmonary diseases. Due to its tumour-like surface, it may cause cancerophobia.

Differential diagnosis: haemangioma, Kaposi’s sarcoma, malignant melanoma.

109. Angular (perlèche) In children and young adults Staphylococcus or Streptococcus infection results in pyoderma of the labial commissure.

110. Median rhomboid The disease used to be classified as a developmental disorder (the persistence of tuberculum impar), but today the role of chronic Candida infection and decreased vascularity is emphasized. It is common among smoking men and among diabetic patients. The lesion occurs more frequently in denture-wearing patients.

May God be with us and help us nail NBDE PART 2 111. The cause of the disease is not clarified; familial predisposition, psychological factors, vitamin deficiency, malnutrition, exudative diatheses and endocrine disorders may play a role in the development of the lesion. It can be an accompanying symptom of psoriasis, reactive arthritis and diabetes mellitus.

112. Lingua villosa (hairy tongue) The condition is considered to be a multi- aetiological disease, which presents more frequently in elderly denture-wearing patients. Hairy tongue is often idiopathic, but it can also be triggered by antibiotics, corticosteroids, vitamin A or B deficiency, radiotherapy, chemotherapy, inappropriate oral hygiene, emotional stress, Candida albicans, heavy smoking, gastrointestinal disorders or hydrogen peroxide.

Symptoms: the hairy surface is caused by the elongation, thickening (hypertrophy) and keratosis of the filiform papillae. The yellowish-greenish, brownish-black colour can be explained by the presence of pigment- producing bacteria and Aspergillus species (not Candida albicans), foods, medications, consumer goods and smoking.

Differential diagnosis: Coated tongue.

May God be with us and help us nail NBDE PART 2 113. Xerostomia

Xerostomia is not a disease but a symptom. Xerostomia may be caused by a wide range of conditions, the main cause being temporary or permanent cessation of salivary secretion.

114. Patient with due to mouth breathing

115. Pregnancy epulis (If given pt is pregnant otherwise Epulis

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116. Ulcers due to agranulocytosis

117. due to calcium- channel blocker medication

118. Periapical abscess - fistula with opening

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119. A lateral periodontal cyst can also show the signs of a periodontal abscess. In case of infection, there is shiny, reddish swelling besides the root, and a fistula may often develop. This disease has its typical radiographic appearance: sharp edged, radiolucent picture, wide periodontal space around the root.

120. Aggressive periodontitis is a term including Local Juvenile Periodontitis and General Juvenile Periodontitis, also known as Early Onset Periodontitis (EOP).

Typical features are fast progression and vertical bone resorption starting proximally, resulting in intra-osseal periodontal pockets. Due to the fast progression and destructive manner, secondary symptoms (hypermobility, pocket formation, abscess formation, changes in position and angulation, hypereruption) develop quickly. After thorough questioning, the presence of the disease in the family is often revealed.

Secondary signs of AgP: tipping, movement, diastema forming between central incisors, deep bite

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121. Peri-implant mucositis: reversible soft tissue lesion around implants

Peri-implantitis: inflammation affecting osseointegrated implants in function, resulting in supporting bone loss

122. Papilloma

Papilloma is a benign epithelial tumour, which frequently appears on the oral mucosa. Local irritation and infection, especially viral infection (human papilloma virus) may play a role in its development.

Symptoms: a pedunculated or sessile, white, or whitish-grey, papillary surfaced tissue growth, which does not cause any symtoms. A slowly proliferating, smaller or larger epithelial tumour may also develop. It occurs mostly in the palates, tongue, gingiva and lips.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and .

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123. Fibroma Fibromas are benign, slow-growing tumours of the oral cavity composed of connective tissue. Fibroma is the most common tumour of the oral mucosa, which particularly occurs on the buccal mucosa and on the tongue. In the oral cavity, fibromas are reactive proliferative lesions, which develop secondarily to irritation (by sharp tooth edges, artificial teeth or calculus) or low grade infection. The lesion feels solid or soft on palpation. It is sessile or pedunculated, smooth-surfaced, reddish or pale and covered with intact mucosa, but as a result of mechanical irritation it may become whitish leukoplakia due to keratinization or may become ulcerated. No other clinical sign or pain can be observed.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma. epulis, , granuloma fissuratum and neurinoma.

May God be with us and help us nail NBDE PART 2 124. Cavernous haemangioma This type of haemangioma is a hamartoma (not a neoplasm), which histopathologically does not have a capsule. It mostly involves the tongue, lips and the buccal mucosa, and reaches an extreme size (macrocheilia, macroglossia), thus hindering speech and swallowing. It occurs as a flat or exophytic, painless growth with a raspberry-like appearance. Its colour ranges from red to dark blue 125. Pyogenic granuloma The tumour-like reactive tissue proliferation may develop in response to trauma or infection, but it may also occur as a result of hormonal changes (pregnancy, menopause, or puberty), the administration of oral contraceptives, steroid drugs and anti- diabetics. Most frequently it develops on the gingiva, bucca, lips and tongue. It is a raised, pedunculated, flat or wart-like lesion with a dark red or pink colour depending on the vascularisation of the affected area. In case of ulceration, it is covered with yellowish fibrin. Its diameter ranges from a few millimetres to a centimetre. It is a painless tumour, which easily bleeds.

126. Postextraction granuloma This reactive, inflammatory tumour-like lesion develops after tooth extraction as a result of retained root, broken pieces of bones, amalgam or other foreign body.

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127. Epulis granulomatosa It is not a real neoplasm, but a reparative tissue proliferation arising from the mucoperiosteum of the tooth socket or from the periodontal membrane. The diagnosis of ”epulis” may be applied only clinically. The growth is a painless, red lesion, which is prone to bleeding and occurs mostly on the vestibular surface of the front and premolar teeth. It is mostly brought about by chronic inflammation (tartar, excess filling, or crown).

128. Pigmented nevus (intradermalis)

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129. Torus Mandibularis

130. Leukoplakia Simplex (Homogenous)

May God be with us and help us nail NBDE PART 2 131. Non-homogenous leukoplakia Verrucous leukoplakia

132.

133. (Reticular Lichen)

May God be with us and help us nail NBDE PART 2 134. Cancer of lower lip

135. Cancer of floor of mouth

May God be with us and help us nail NBDE PART 2 136. Gingival cancer The disease develops mostly on toothless alveolar ridges, where it spreads from the gingiva to the alveolar mucosa and to the surrounding oral structures. Gingival cancer accounts for 8–12% of oral cavity tumours.

Beside smoking and alcohol, mainly chronic irritating factors (odontolith, prosthesis, etc.) may play a role in triggering gingival cancer. The disease destroys the periosteum and the bone if it reaches them, and loosens the teeth. Gingival cancer is more frequent on the mandibular gingiva than on the maxillary, and mandibular gingival cancer metastasises regionally more frequently. Metastases occur mainly in the submandibular region. Similarly to oral cavity cancers located elsewhere, it is mainly the disease of the elderly (50–70-year-old) men, and histologically most of the cases are squamous epithelial cancers. Incisional biopsy is necessary.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma. epulis, pyogenic granulomas.

To be continued………..

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