Achondroplasia 1

 Failure of cartilage proliferation at epiphyses and base of skull

 Short limbs
 Normal sized head and trunk
 Mandibule is protruded and middile 1/3 of face is retruded
 Concave facial profile
 Severe malocclusion
 Autosomal dominant
 Gene mutation is in FGFR3
 Normal intelligence
 Speech is unaffected
 Freuquent middle ear infections due to shortened eustachian tube
 Abnormal endochondral ossification
 Crowding
 No treatment is available

Cleidocranial dysplasia 1

 Autosomal dominant
 Supernumerary teeth
 Small , missing clavicles
 Delayed closure of cranial fontanells
 Depressed nasal bridge
 Retention of primary teeth
 Multiple impactions of permanent teeth
Sturge weber syndrome 1

 Uncommon , congenital syndrome of unknown etiology

 Facial lesions have port weine stain over distribution of trigeminal nerve course
 Patient has vascular problems in meninges and cerebral cortex
 They are at risk of developing seizure
Gorlin syndrome 1

 Autosomal dominant
 Multiple basal cell carcinoma ,
 Palmar pitting , palmar-plantar keratosis
 Multiple odontogenic keratocyst
 Mild mandibular prognathism
 Macrocephaly , mental retardation
 Cleft lip and palate
 Also known as nevoid basal cell carcinoma
 Caused by a mutation in PTCH ( tumor suppressor gene in chromosome 9 )
 Rib and vertebral anomalies
 Palm is very thick
 Blindness , eyes are set wide
 Hypogonadism

Gardner syndrome 1

 Autosomal dominant
 Multiple intestinal polyps
 Multiple jaw osteomas especially in angle of mandible
 Fibromas of skin
 Epidermal cysts
 Impacted teeth
 Supernumerary teeth
 Odontomas
 Most serious complication is multiple polyps in large intestine that lead to invasive colorectal
adenocarcinoma
 Pigmentation of retina of eye
 Females are at higher risk of thyroid carcinoma
 Also called familial colorectal polyposis
Eagle syndrome 1

 Calcification and elongation of stylohyoid ligament

 Pain in head and neck which is aggravated by swallowing , yawning , opening mouth
 Difficulty in swallowing
 Pain in turning head

Pierre robin syndrome 1

 Micrognathia
 Mand hypoplasia
 Glossoptosis ( posterior displacement of tongue )
 High arched or cleft palate
 Respiratory problems
Down Syndrome 1

 Trisomy 21
 Mental retardation
 Short skull
 Slanting eyes
 Macroglossia with fissures
 Mouth breathing habit
 Higher incidence of periodontal disease
 Higher incidence of congenitally missing teeth
 Malocclusion
 Mand prognathism
 Delay in eruption of teeth
 Decrease in caries

Albright syndrome 1

 Genetic disorder of bone

 Polystotic fibrous dyplasia
 Mostly in female
 Skin pigmentation of brownish macules called café au laits
 Premature sexual development due to endocrine abnormalities
 Hallmark of this syndrome is premature puberty in females
 Complications
1. Pathological fractures
2. Malignant transformation
Peutz- jeghres syndrome 1

 Caused by a mutation in gene LKB1 in chromosome number 19

 Intraoral pigmentations mostly seen in buccal mucosa and mucosal surface of lower lips , other
sites are gingiva , and hard palate
 Extraoral pigmentation seen in skin of face and extremitis
 Intestinal polyposis in small intestine ( jejunum )
 Patients are At high risk of GI adenocarcinoma and cancers of female reproductive system
 Blue , brown , black in color
 It resembles freckles on face

Treacher Collins Syndrome 1

 Autosomal dominant.
 Usually presents with cleft palate,
 shorten soft palate, malocclusion, anterior open bite,
 enamel hypoplasia
 some bones and tissues in the face aren't developed.
 Also called mandibular dysostosis
 Midface is underdeveloped
 Downslanting of eyes

CROUZAN SYNDROME: 1

 Autosomal dominant,
 mutation in fibroblast growth factor receptor II à fibrous joints between certain bones of the
skull (cranial sutures) close prematurely (craniosynostosis).
 Radiographically BEATEN METAL SKULL appearance
 Most notable characteristic of Crouzon syndrome is cranial synostosis, but it usually presents as
 brachycephaly, which results in the appearance of a short and broad head,
  exophthalmos
 proptosis (bulging eyes due to shallow eye sockets after early fusion of surrounding bones),
 hypertelorism (greater than normal distance between the eyes),
 hypoplastic maxillary
 mand prognathism

Ectodermal dysplasia : 1

 X linked recessive
 Hair , nail ,teeth and sweat
 GI affected
 Anodontia
 Diminished sweat gland ( anhydrosis )
 Dystrophic nail
 Heat intolerance
 Hypothriochosis ( decrease in hair )
 Child appear more older than he or she is
 Male are more affected
 Tx by RPD but need to be changed periodically to accommodate jaw growth

Vander woudes syndrome : 1

 paramedian lip pit

 cleft lip
 cleft palate
Melkersson rosenthal syndrome 1

 Chelitis granulomatosis
 Facial paralysis
 Fissured tongue

Behjet syndrome
 Chronic inflamation of blood vessels
 Oral and genital ulcers.
 Conjunctivitis, uveitis, arthritis, headache.
 Tx by corticosteroids immune suppressive drugs to prevent blindness.

Plummer Vinson syndrome: 1

 Iron deficiency
 Kolionychia ( spoon nail )
 atrophic changes
 Dysphagia.
 It lead to scc of tongue and throat.
 Must be treated as soon as possible by giving
 Iron
 Vit. B complex.
 High protein diet.
 Occurs in middle aged women, rarely in males.

PA cemental dysplasia 3

 also called cementoma

 2. Mostly seen in middle aged black women .
 In mand incisor area
 Teeth are vital
  Composed of 3 stages
1. A.OSTEOLYTIC : radiolucent
2. B.cementoblastic :mixed
3. c.mature :radioaque surrounded by radiolucent line

Von Ricklinghausen disease 1

 Neurofibromatosis type 1
 Presence of 6 or more café au laits spots
 Presence of 2 or more neurofibroma
 Iris hamartoma ( lish nodules )
 Axillary freckling ( crowes sign )
 Optic gliomas
 Autosomal dominant , caused by mutation in tumor suppressor gene NF1
 Presence of supernumerary teeth

Cherubism 3

 Autosomal dominant
 initially there is progressive facial swelling bilaterally
 occur at 1- 4 years of age
 can affect maxi and mandi but mostly mand
  displacement of eye when maxilla is affected
 premature loss of deciduous teeth
 lack of eruption of many permanent teeth
radiographically
1. soap buble appearance
2. severe thining of cortical plate
 Histologically it resembles central giant cellgranuloma when there is abundance
fibroblast +multinucleated giant cell . pathognomic sign is eosinophilic perivascular , cuffing of
collagen

Oral manifestation of gigantism and acromegaly : 3

 Mandible prognathism
 Enlaged tongue
 Soacing btw teeth they are tipped to buccal or lingual side
 Roots are longer than normal

Pitutary dwarfism : 3

 Lack of growth hormone

 true microdontia
 delay in eruption and sheding of teeth
 crown and root of teeth appear smaller
 whole dental arch is small
 mandible is under developed

Oral manifestation of cerebral pulsy : 3

 Attrition of teeth
 Difficulty in swallowing and mastication
 Higher incidence of caries and periodontal disease

Glossopharyngeal Neuralgia : 3

 sharp electric shock like pain like TN but its less common
 Pain deep in throat and radiate to ear
 Unilateral
 Triggered by swallowing or chewing
  Involvement of tympanic branch of IX

Odontogenic kerato cyst : 3

 aggressive very high recurrence rate due to presence of daughter cyst

 Associated with gorlin syndrome ,
 mostly occur in site of third molar
 Radio : multilocular, unlocular
 Parasthezia of lip .
 keratin fluid

Dentigerous cyst 3

 Caused by fluid accumulation btw enamel surface and reduced enamel epi.
 Radio : unilocular or multilocular, sclerotic bony outline

Eruption cyst : contain tooth crown that has erupted through bone but not soft tissue

If bleeding occur it appear as blue deep called eruption hematoma

Nicotinic stomatitis 3

 It’s a hyperkeratotic lesion

 Characterized by generalized white alteration of palatal mucosa
 Caused by a heat generated during pipes smoking , not due to chemicals of tobacco therefore its
not premalignant

Keratoacanthoma 3

 Benign neoplasm of epithelial tissue origin

 Filled with keratin
 Very closely resembles squamous cell carcinoma
  Seein in surfaces , exposed to sun

Condylar hyperplasia 3

 Unilateral enlargement of head and neck of condyle

 Crossbite malocclusion
 Mand prognathism
 Facial asymmetry
 Mand deviates toward unaffected side

Hereditary gingival fibromatosis 3

 Autosomal dominant
 Fibrous overgrowth affecting both gingival arches this overgrowth may be dense , diffuse ,
smooth , or nodular
 Srarts at time of eruption of permanent teeth
 Microscopically
1. Fibrous hyperplasia
2. Thickened epithelium
3. Elongated rete pigs
 Recurrence may occur

Malignant melanoma 3

 Represent 4% of skin cancers but it’s the most aggressive

 Most commonly in male , 50 years of age or older
 Most commonly seen in palate and maxillary alveolar ridge and gingiva
  ABCDE suammarized features of melanoma
1. Asymmetry
2. Border irregularity
3. Color variability
4. Diametergreater than 6mm
5. Evolution ( color changes get darker by time )
 Uncommon in oral mucosa

Osteosarcoma 3

 Most common malignant neoplasm of bone

 Mostly in male
 In maxilla occurs more inferiorly , while in mandible occurs more in posterior body and
horizontal ramus rather than ascending ramus
 Early symptoms is localized symmetrical widening of periodontal ligament space of 2 or more
teeth
 Other symptoms
1. Pain
2. swelling
3. displacement
4. loosening of teeth with paresthesia
 can be metastasize into lung and brain
 mandibular lesion has better prognosis than maxilla

multiple myeloma 3

 abnormality in plasma cells

 mostly seen in male , african americans , 60-70 yeas of age
  in 30 % it involves mandible , especially post- mand and cause pain , swelling , loosening of teeth
, paresthesia
 mostly involve skull , ribs , vertebrate , early symptom is pain in lumbar spine
 radiographically – multiple small punched out radiolucent lesions in bone , best seen by lateral
skull film
 in 15% of cases , amyloidosis occur
 has poor prognosis

basal cell carcinoma 3

 most common malignant neoplasm in humans and skin

 primary cause is excessive sun or x-ray exposure
 locally destructive and invasive to adjacent strectures but rarely metastasize
 clinically presented as a nodule with central ulceration , prominent surface telangiectasia
 40 years of age in male in nose mostly
 Treatment is by eradication
 Now days most efficient treatment modality of skin cancer is MOHS micrographic surgery ,
tumor is removed layer by layer , leaving surrounding tissues intact

Amelogenesis imperfecta 3

 Autosomal dominant
 Enamel chips easily
 Clinically hypoplastic pitting enamel
 Radiographically -enamel is thin
 Open contacts between teeth

Varices 3

 Dilated veins that appear blue

 Mostly seen in ventral of tongue
 Seen in elderly patients
 May be associated with hypertension
 May thrombose and calcify

Oral candidiasis 3

 Also known as thrush

 Caused by C. albicans
  Seen in buccal mucosa , tongue , palate
 Seen in pateints in which their immunity has problem , like in chemotherapy , HIV, or those
on immunosuppressive drugs
 Lesions are wiped off , leaving behind red, raw lesion
 Treatment by topical lozengens , or mouth rinses of nystatin
 Systemically by fluconazole or ketoconazole
Chronic lesion may be eryhtromatous
 Most common form of oral candidiasis is acute pseudomembraneous candidiasis

Lichen planus 3

 Presented as lacelike webbing , bilaterally in buccal mucosa

 Common in middle aged woman
 Its white striae called whickham striae
 May affect gingiva , presented as dequamtive gingivitis
 Asymptomatic form is reticular lichen planus
 Symptomatic form is erosive licken planus
 Patient may complain of burning sensation
 Microscopically –
1. hyper para or ortho keratosis
2. Degeneration of keratinocytes ( civatte bodies )
3. Degeneration in basal cells
4. Saw tooth shaped rete pigs
5. Infiltration of inflammatory cells
Leukoplakia 3

 Premalignant lesion , although shows no dyplasia

 Presented as white , thicknened , firmly attached patch , slightly raised , do not rub off
 Smoking , alcohol are precipitating factor
 Seen in older men
 Lesion that seen in floor of mouth , ventral of tongue , lateral of tongue are the most aggressive
 All leukoplakias should be biopsied
 Its clinical diagnosis , cannot be characterized as any specific disease

Addison disease 3

 Chronic adrenocortical insufficiency

 Bronzing of skin
 Diffuse , persistant intraoral pigmentation , seen in gingiva , hard palate , buccal mucosa
 Those patients cannot tolerate streses so indental procedure , stress should be avoided
 Weight loss
 Hypotension
 Decrease blood level of glucose and sodium but increase in potassium
 Clinical features don’t appear unless at least 90% of glandular tissue have been destroyed

Oral manifestation of erythroblastosis fetalis 3

 Teeth appear green , blue , brown , hue due to deposition of blood pigments
 Enamel hypoplasia in incisal edges of anterior teeth and in deciduous canine and 1 st molar
Pernicious anemia 3

 Lack of intrinsic factor so no absorption of vitamin B12 . which is essential for maturation of
RBC. So RBCs decrease in number
 Features
1. Glossitis
2. Angular cheilitis
3. Dysphagia
4. Odynophagia ( pain on swallowing )
5. Tingling and numbness of extremitis

From all leukemias, oral lesions are mostly observed in mylogenous leukemia as a 3

 Gingivitis
 Gingival haemorhage
 Petechia
 Purpura
 Ulcerations

Osteopetrosis 3

 Excessive density of bone

 Obliteration of bone marrow spaces
 Bone is dense but brittle
 Delay in eruption of teeth osteomyelitis following extraction
 Inactivity of osteoclasts
 Autosomal dominant or recessive
 No bone resorption
 Growth retardation , deafness, blindness
 Bone pain and fracture

Osteogenesis imperfecta 3

 Osteoblast fails to produce bone in adequate amount

 Synthesis of collagen I is defective
 Bones are very thin, fragile , and lack cortex
 Composed of immature woven bone
 Bone is susceptible to fracture
 Normal bone length
 Extreme fragility and porosity in bones
 Patient has blue sclera
  Dental manifestations same as dentinogenesis imperfecta
 Deciduous teeth are more severly affected than permanent teeth
 No treatment is available
 There is either less amount of collagen or poor quality of collagen

Oral manifestations of hypothyroidism: 3

 Mand. Is underdeveloped
 Maxilla is overdeveloped.
 Enlarged tongue.
 Delay eruption of teeth
 Delay in exfoliation of teeth.

Mucous membrane pemphigoid: 3

 Involves mucous membrane mostly , rarely skin

 Occurs 40-60 years of age in women
 Presented clinically as desquamative gingivitis
 Antibodies are directed against Laminin 5 and BP180
 Conjunctiva is involved , scarring adhesion called symblepharons cause blindness
 Histologically
1) No acantholysis
2) Vesicles are subepidermal

Angular Cheilitis 3

 Known as perleche
 Associated with decrease OVD ( occlusal vertical dimesntion )
 Mostly seen in elderly patients, and these who lick their lips and deposit small amount of saliva
in commissure of angle of mouth
 Clinically
1) Painfull ,red , cracked , dried lesions
2) Seen at corner of mouth
 Etiology
1) Caused by candida albicans
2) Staphylococci
3) Nutritional deficiency like vit B2, B3, B6, B12 , IRON
 Treated by nystatin

White Sponge Nevus 3

  Asymptomatic deeply folded grey or whitle lesion
 Thich and spongy in consistency ‘
 Bilaterally , symmetric , mostly in buccal mucosa
 Occurs early in life, before puberty
 No need for treatment
 Benign , no malignant transformation
 Autosomal dominant , mutation in keratin 4, 13
 Microscopically- perinuclear eiosiniophilic condensation of cytoplasm
 Usually occurs along occlusal plane

Eryhtema Multiform 3
 It’s a hypersensitivity reaction ,this reaction occurs superficial vessels of skin and
mucous membrane
 Affects children and young adult
 Precicpating factors
 Drugs ( penicillin , analgesia )
 Infections ( herpes, mycoplasma pneumonia )
 Pathognomic sign is iris or target lesions
 Erythema multiform minor characterized by
1) Haemorhaegic crusting of lips
2) 7-10 days before lesions appear there is fever and generlilized malaise

Pemphigus 3
  Common in Jewish people , 30-50 years of age
 Antibodies are directed against desmosomal adhesion molecuoles Dsg3
 Mucosal inflammation of skin , oral cavity , nasal , eyes , genital.
 Large areas of ulcerations and erosions in oral mucosa
 Treated by high concentration of corticosteroids and methotrexate
 Histologically
1) Acantholysis
2) Vesicles and bullae are intraepithelially
3) Tzanc cells
 Clinically there is nikolskys sign

Dentin Dysplasia 3

 Autosomal dominant
 Normal enamel , atypical dentin , with abnormal pulpal morphology
 Type 1 ( radicular type ) :
1) complete obliteration of pulp
2) Very short and conical root
3) Periapical lesions

 Type 2 ( coronal type ): pulp ascends and flares into dentin into flame shaped and
multiple pulp stones occur
  Note in this type primary tooth will appear like dentinogenesis imperfect amber like
while permanent tooth will appear normal.

Deintinogenesis imperfecta 3

 Autosomal dominant
 Both dentitions are affected
 Type 1 is associated with osteogensis imperfect so patients has history of blue sclera
and pathological fractures
 Type 2 is not associated with osteogenesis imperfecta
1) Teeth appear yellow , brown , grey
2) Broad crowns
3) Constricted cervical area ( bell shaped )
4) Radiographically, no pulp chamber or root canals
5) Dentin is easily exposed

 Type 3 charactrized by
1) little dentin , very large pulp , rarely occur , amber like teeth , brandywine tooth
2) Multiple pulp exposure
3) Periapical radiolucencies

Leukoedema
  Normal variant of normal mucosa.
 Appears as filmy opalescence- greyish white coating.
 Bilaterally, in buccal mucus a, along occlusal plane of premolar and molar teeth.
 Diagnostic tool when tissue is stretched white disappears unlike leukoplakia (which doesn’t
disappear).
 No need for TX.
 Nome lignin trans for motion.

OTHER NOTES
Mucosal burn , Caused due to

 Chemical burn
 1. Topical aspirin
2. Application of phosphoric acid by dentist
3. Excessive use of alcohol based mouthrinses

 Thermal burn
1. Hot food affecting hard palate
2. Hot liquids affecting soft palate

Erythroplakia

Leukoplakia premalignant lesions

Actinic chelitis

No filiform papillae median rhomboid glossitis

Desquamated filiform papillae geographic tongue

Hypertrophy of filiform papillae hairy tongue

Factors that accelerate wound healing

1. Hyperthermia
2. Younger age
3. Higher vascularity
4. High protein and vitamin C diet

Excisional biopsy is indicated for 1 cm exophytic mass ( which is a lesion that grows outward
from epithelial surface ) on the cheeks

For children – toxic dose of fluoride is 5mg/kg while lethal dose is 15mg/kg
For adult – lethal dose is 2 g

Acute fluoride poisoning

1. Nausea
2. Vomiting
3. Diarrhea
4. Abdominal pain
5. Hypotension

Chronic fluoride poisoning

1. Osteosclerosis in bones
2. Dental fluorosis if it occurs at calcification stage of tooth
 As person ages fluoride accumulates slowly in bones
When Ca intake is increased , dietary absorption of fluoride will be decreased

 Carcinoma in situ is the most severe form of epithelial dysplasia , that shows maximum
cytological and architectural changes

 the most common location of Squamous cell carcinoma is lower lip due to increase of
exposure to sun , most common intraoral location is posterior lateral aspect of tongue ,
and 2nd location is in floor of mouth

 SCC has a good prognosis in lower lip , buccal mucosa and gingiva but best is in lower

 Dysplastic nevus is larger than normal nevi , has irregular border , also has high
tendency for malignant transformation

 Large congenital nevi has a high tendency for melanoma

Starry sky appearance microscopically burkitts lymphoma

Onion skin appearance radiographically ewing sarcoma and onion skin appearance
Sun ray appearance radiographically osteosarcoma

Hepititis virus is very heat resistant , more than HIV , but it can be destroyed by autoclave

Age and some conditions

Ameloblastoma 30-70

Malignant ameloblastoma 30

Odontogoneic myxoma 30

AOT teens

Pindborg over 40

Ameloblastic fibroma / odontoma children , yound adult

 Host response to malignancy is best reflected by lymphocytic infiltration at edge of tumor

  Most charactricstic feature of malignancy as opposed to inflammatory lesion , is that
malignant will grow after removal of causative agent while inflammatory lesion will not
grown after removal of causative agent

 Feature that distinguish between malignant and benign neoplasm is ability to metastasize

Location of some lesions

Pyogenic granuloma – gingiva in facial aspect of maxillary gingiva

Nevi – hard palate

Eryhtroplakia – floor of mouth , soft palate , ventral of tongue

Peripheral giant cell granuloma – gingiva

Tori- superior to mylohyoid ridge

Peripheral ossifying fibroma, which is a hyperplastic reaction contains mineralized products.

While
Peripheral odontogenic fibroma contains island of odontogenic epithelium.

 Histology of mucoepidermoid carcinoma is squamous calls, mucous secreting and intermediate

calls.

 Hisology of pleomorphic a adenoma - cells that arrange into duct like strecture, chondroid areas

 Warhin tumor multiple cystic spaces filled with eosinophilic coaglum. And papillary projections
within coagulum, and papillary projection within those coagulum, ply belayed wipe, luminal
layer composes of columinar while basal layer composed of cuboidal cells

 HSV-2 transmitted by sexual contact.

HSV- Remains latent in trigeminal ganglion.
VZV remains laten in Sacral ganglion.
Primary hepatic gingivostomatitis

 caused by HSV-1.
 Occurs in children below 3 yrs. of age and young adult.
 Prodromal symptoms like fever, lymphadenopathy, malaise, odynophagia occur 1-2 days before
lesions.
 Lesions occur on keratinized, movable and attached mucosa.
 Vesicles rupture easily and forms ulcer with eythromatous halo.
 It takes 7- days to heal without scarring.
 TX by debridment, fluid intake, and good oral hygine

 Herpangina this lesion is caused by coxsackie virus differs form the other lesions by its
location, it occurs in post of palate, occurs in post of soft palate, nasopharynx in anterior
-faced of tonsils,
Usually occurs in summer, has fever, sore throat , difficulty in swallowing. Course doesn’t
take more than a weak.

 Scarlet fever
 System infection caused by strep. Pyogenic.
 Strawberry Tongue
 skin rash
 Pyrogenic exotoxin causes this Rash.

 Actinomycosis
1. Bacteria infection caused by Actinomyces israelli
2. Not contagious
Purple abscess in jaw with sinus tract that contains sulfur granule. (TX by long term penicillin).
Histoplasmosis mostly occur in Ohio River Valley.

Coccidiodomycosis African American (lung infect).

 Stafne bone defect or cavity m it’s a developmental anomaly and it’s anatomical depression
in lingual aspect of body of mand. Inferior. To mand canal It contains submand .gland tissue,
therefore no
Tx is needed. Also called submand salivary gl- depression or static bone cyst (its not a true
cyst).
 Location of salivary gl. Pathosis :-
 canalicaular adenoma
 Basal cell adenoma
 Warthin tumor
 Ranula
 Mucocele
Most common of minor salivary gland tumor is
Most common of major salivary gland tumor
Pleomorphic adenoma
mucoepidermoid carcinoma
ACC palate
PLGA palate
 Acute lymphocytic leukemia
 Chronic lymphocytic leukemia
 Acute myelogenious leukemia
 Chronic myelogenious leuke
Location of cysts:
 Dentigerous cyst
 OKCs
 Lat.perio. cyst
 Epstein Pearls
 Bohns nodules
 Gingival cyst of adult
 Simple bone cyst
 Glandular O. cyst
 Median Palatal cyst
locations of odontogenic tumors
 ameloblastoma
 AOT
 Pindborg tumor
 Ameloblastic fibroma
 Compound odontoma
 Complex odontoma
 Cementoblastoma
 Focal cementoosseous dysplasia
upper lip, white.
parotid, Caucasians.
parotid
floor of mouth
lower lip
palate
parotid.
palate.
parotid, 2 nd loc. Palate.
{Most common in children}
{ Most common type, least malignant}.
{ Most common type in adult, most malignant}.
{ Associated with philadilphia chromosome
(exchange of material btw chr.9 and 22)}.
Impacted teeth
In mand. In post body and add ending ramus.
mand. Lt, c, premolar area.
along mid palatal raphe.
scattered into hard palate.
canine- premolar area.
mand btw canine and ramus.
ant. Mand.
along median palatal raphe.
mandibular posterior molar area and ramus
anterior maxilla in canine region rarely seen in mandible
posterior of body of mandible
molar area of mandible
anterior maxilla
posterior jaw
mand first molar
posterior mand
  Periapical COD mandibular incisor

Causes of following lesions

 germination idiopathic

 fusion external pressure or crowding

 concrescence trauma or crowding resulting in close approximation

of adjacent root

 dilacerations trauma to tooth germ during root development

 enamel pearl abnormal displacement of ameloblast during tooth formation

 taurodontism failure of hertwig epithelial root sheath to invaginate
at proper level

 dens in dente invagination of enamel organ into crown of tooth

before mineralization , mostly seen in maxillary lateral

incisor

 turners hypoplasia portion of enamel is missing or diminished in

permanent tooth usually affect one tooth in mouth
called turner tooth.

 Defect in quantity of enamel result in hypoplasia

 Defect in quality of enamel result in hypocalcification
 Defect in crystal strecture of enamel lead to hypomaturation

Risk factors of alveolar osteitis

 Smoking
 Osteopetrosis, paget disease.
 Radiotherapy—endarteritis—ischemia of bone.
 Limited vascular supply

Histological features of malignant neoplasm

 Anaplasia ( hallmark of malignant transformation )

 Mitosis ( abnormal division )
 Pleomorphism (abnormal multiple shapes)
 Hyperchromatism ( chromatin becomes denskly deep in color )
  Increase in nuclear cytoplasm ration 1:1 instead of 1:4( normal )

most common cause of xerostomia is medication

most common disease that cause xerostomia is sjogren syndrome which occurs in postmenopausal
women, other diseases that cause xerostomia

 amyloidosis
 sarcoidosis
 rheumatoid arthritis
 systemic lupus erythromatousus

 Most common malignant neoplasm in major and minor salaivary glands is mucoepidermoid
carcinoma

 2nd most common malignancy in parotid and children salivary glands is acinic cell carcinoma
(which has the best prognosis)

 2nd most common malignancy in minor salivary glands is PLGA (Polyamourphous

Adenocarcinoma )

 most common benign neoplasm is pleomorphic adenoma

 2nd most common benign neoplasm in parotid is warthin tumor ( papillary cystadenoma)

Traid of congenital syphilis

 Hutchinson incisor were upper central incisors appear smaller than normal with notch in
incisal area , this notch is caused due to absence of central tubercle or calcification
centers in congenital syphilis ,also presence of mulberry molars
 Interstitial keratosis
 8th nerve deafness
 The only way to distinguish between granuloma and cyst is biopsy

 Koplic spot in oral cavity is seen opposite to molars and cannot be wiped off , seen in
measles ( rubeola)

 Very serious complication of Ludwig angoina is edema of glottis

 5 years survival rate of melanoma in oral cavity is less than 20 % , in skin more than 65%

 5 years survival rate of SCC ( SQUAMOUS CELL CARCINOMA ) is 45-50%

  but with neck metastasis its 25%

 Treatment of dentinogenesis imperfect is crown

 Trearment of amelogenesis imperfect is esthtical problem so no therapeutical treatment

is needed

 Treatment of regional odontodysplasia is extraction

 Internal root resorption is caused by multinucleated giant cells in pulp granulation tissue. In
order for this resorption to occur , granulation tissue must be present.
 With loss or alteration of odontoblast layer or predentin resulting in oval shaped enlargement of
root canal space

 Internal root resorption is asymptomatic , no pain , no swelling , most apical part of pulp is vital

 Treated by ROOT CANAL THERAPY , it has very good prognosis

 Petechia – 1-2 mm
 Purpura – 3mm – 1 cm
 Ecchymosis – more than 1 cm

 In TTP and ITP , tooth extractions are contraindicated due to excessive bleeding.

 Oral manifestation of ITP

1) Gingival hemorrhage
2) Petechial on the palate

 Cyclic neutropenia is characterized by deficiency of neutrophils followed by normal cell count so

features will be :
1) Severe gingivitis
2) Recurrent fever
3) Oral ulcerations