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189 Cards in this Set
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what is the defect seen in cleft lip
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defective fusion of the medial nasal process with the maxillary process.
*** upper lip forms btw. 6th and 7th weeks |
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what is the defect seen in cleft palate
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failure of the palatal shelves to fuse.
1. primary palate: formed from the medial nasal process 2. secondary palate: formed from maxillary process *** palate forms between the 8th and 12th weeks |
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what is the most common manifestation of orofacial clefts
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45% cleft lip and cleft palate together
30% isolated cleft palate 25% isolated cleft lip |
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what orofacial cleft is seen more in males and what is more common in females
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males: cleft lip and cleft palate together
females: isolate cleft palate |
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cleft lip 70% are unilateral and 20% are bilateral. which side is most affected on a unilateral cleft lip
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unilateral CL occurs on the left side
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surgical repair is the treatment for a cleft lip or palate when can this surgery begin
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when child is 10 lbs.
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what syndrome is commonly associated with orofacial clefts
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pierre robin syndrome:
- cleft palate - mandibular micrognathia: sm. jaw - glossoptosis: tongue is small and posteriorly displaced into the airway |
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this developmental abnormality is more common in males. the uvula is commonly divided into 2 halves
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bifid uvula
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this abnormality is due to the failure of normal fusion of the embryonal maxillary and mandibular process forming a blind fisturlae or pit about 1-2mm in diameter and upto 4 mm in depth
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commissural lip pits
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T/F commissural lip pits and paramedian lip pits can both be seen unilaterally or bilaterally, can communicate with minor salivary ducts and are both are common
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false, true, and false paramedian lip pits are rare and usually located bilaterally to the midline of the lower lips
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what syndrome is double lips commonly seen in
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ascher's syndrome:
- double lip - blepharochalasis: edema of the upper eye lid: drooping of the upper eye - non-toxic thyroid enlargement |
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mucosal tissue that projects from the maxillary labial frenum
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frenal tag
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these are ectopic sebaceous glands that are seen in approx 80% of pop., they are located on buccal mucosa and upper lip
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fordyce granules: multifocal yellow spots
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what is fibromatosis gingivae
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progressive diffuse fibrous overgrowth of gingival tissue: dense, diffuse, smooth or nodular overgrowth of gingival tissue
*** gingiva is normal in color and not influenced by good oral hygiene this is how you differentiate it from hyperplasia caused by drugs - most cases begin before age 20 and may correlate with eruption of primary or permanent teeth |
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small jaw
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micrognathia
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what diseases commonly exhibit macrognathia
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- paget's disease of bone: overactive remodeling of bone resulting in net gain of osteoblast
- acromegaly: due to pituitary tumor that results from over prod of growth hormone - fibrous dysplasia |
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this rare condition features unilateral enlargement of the body or parts of the body. One side of the face grows faster than other, teeth may be enlarged, may have extra back hair, tongue commonly involved
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hemihyperplastia or hemifacial hypertrophy:
may be due to vascular or lymphatic abnormalities, neurogenic abnormalities, hormonal abnormalities, chromosomal abnormalities |
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uncommon degenerative cond. characterized by atrophic changes affecting one side of face, occuring first 2 decades of life, teeth smaller on one side of face and patient may have facial paresthesia, contralateral epilepsy, trigeminal neuralgia
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progressive hemifacial atrophy:
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what are the clinical features of segmental odontomaxillary dysplasia
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- painless, unilateral enlargement of the maxillary bone
- thickened bone trabeculae - often one or 2 bicuspids is/are missing - may be some defects in primary teeth |
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microglossia
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abnormally small tongue
aglossia: rare, missing tongue |
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macroglossia can be acquired or congenital/hereditary. what congenital or hereditary conds. feature macroglossia
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1. vascular malformation: hemangioma, lymphangioma when they occur in the head and neck area the tongue is where you will see them
2. hemihypertrophy: remember this is unilateral enlargement of body 3. down syndrome 4. neurofibromatosis |
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macroglossia can be acquired or congenital/hereditary. what acquired cond. prod macroglossia
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1. edentulous patients
2. myxedema 3. acromegaly 4. angioedema |
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this cond. commonly occurs in children, this enlarged growth may cause diff. eating or speaking, may cause open bine, may see a crenate lateral border of the tongue
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macroglossia
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fusion of tongue and floor of the mouth, may cause slight clefting of the tip of the tongue
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ankylglossia: tongue tie
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this condition often develops simultaneously with geographic tongue
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fissured tongue: tongue with furrows or grooves on dorsal surface of the tongue 2-6mm in depth
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epithelium has a granular layer and the nuclei are lost the keratin layer
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hyperorthokeratosis
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there is no granular cell layer and the epithelial nuclei are retained in the keratin layer
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hyperparakeratosis
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what is spongiosis
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intercellular edema of the spinous cell layer
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Thickened spinous cell layer. When you have this thickening you wont see as much of the pink color
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acanthosis
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epithelial dysplasia
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alteration in size, shape and organization of adult cells.
- dysplasia usually begins in the basilar portions of teh epithelium. the more dysplastic the epithelium becomes, the more the atypical changes extend to involve all the epithelium |
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a type of papillary exophytic proliferation of squamous epithelium
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verrucous hyperplasia
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what areas of the mouth are keratinized
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hard palate, gingiva, alveolar mucosa, dorsal tongue
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what areas of the mouth are non-keratinized
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*** these non-keratinized areas are vulnerable to dev. premalignancy + malignancy
buccal mucosa and vestibule, labial mucosa and vestibule, floor of the mouth, lateral tongue, soft palate, gingival sulcus |
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what is the etiology that is seen in leukoedema
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- may be an anatomic variant more ocmmon in blacks
- seen more in smokers, and dec. with smoking cessation - alcolhol ingestion, bacterial infection |
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If leukoedema has no malignant potential why do you periodically have to observe it for changes
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needs to be observed to make sure there is no overlying leukoplakia is present, which is considered a premalignant white lesion that will not wipe off
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what is the most common papillary lesion of the oral mucosa
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squamous papilloma! seen in 1 in every 250 adults
- exophytic cauliflower like soft lesion, usually pedunculated but can be sessile, may be whit or pink and is slow growing |
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which benign tumor and tumor like lesions are associated/caused by HPV
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1. squamous papilloma: types 6 and 11
2. verrucous vulgaris: types 2, 4, 6, 40 3. condyloma acuminatum: mainly 2 and 6 high risk types 16,18, 31 = inc. risk for squamous cell carcinoma |
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what information of a condyloma acuminatum could differentiate it from a squamous papilloma
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condyloma acuminatum:
- is an STD that appears 1-3 months after sexual contact - proliferates rapidly in size - up to 2 cm in diameter: larger than a squamous papilloma squamous papilloma: - slow growing, - usually only a few mm in diameter up to 1.5 cm |
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a patient comes in with multiple nodular lesions that are flattened, they are all over on the lower lip and buccal mucosa, they are the same color as adjacent mucosa. This patient is native american and is a young child it is her first visit to the dentist
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focal epithelial hyperplasia (Heck's disease)
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When can a court allow a joint managing conservatorship?
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T/F squamous papilloma, verrucous vulgaris, condyloma acuminatum, verruciform xanthoma are all painless, papillary sessile or pedunculated lesions that are all treated via excisional biopsy
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true
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this benign lesion usually grows to full size in 4-8 weeks, stay static for 4-8 weeks, and then undergoes spontaneous regression
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"self-healing" carcinoma, keratoacanthoma
many times confused with squamous cell carcinoma b/c: - usually on sun exposed skin, found in those that are 45+, crater form lesion with a central keratin plug, rarely occurs intraorally |
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keratocanthoma "self healing" carcinoma is many times confused with verrucous vulgaris how do you differentiate the 2
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-keratocanthoma is seen in those 45+ verrucous seen in children and young adults
- keratoacanthoma may be painful: verruca is painless and persistent - both may spontaneous regress |
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T/F you can contract white sponge nevus from person to person contact
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false: autosomal dominant transmitted condition due to defect of normal keratinization
will seen in childhood and may be present at birth or dev. early in childhood or adolescence rare, painless and persistent |
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name the 3 clinical types of leukoplakia
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1. fricitional keratosis: non- cancerous lesion, found due to irritation or consistent trauma
2. smoking related leukoplakia 3. idiopathic leukoplakia |
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what are the most common sites of leukoplakia
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buccal mucosa and mandibular alevolar mucosa
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what are the greatest risk of malignancy for leukoplakia
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lip, lateral border of tongue, floor of the mouth and soft palate
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true or false leukoplakia is a benign tumor/lesion
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false, considered a premalignant lesion: dysplasia is found in 5-25% of all biopsy And 1-17% undergo malignant transformation avg. inc. to 16% for smokers
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t/f snuff is less likely to cause alterations in oral tissue (mucosal dysplasia than chewing tobacco
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false snuff is more likely to cause an alteration in oral tiss.
SNUFF IS ENOUGH (to cause trouble that is) |
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this is a lesion that is painless and asymptomatic that may resemble leukoedema early on, and develops where tobacco is placed
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smokeless tobacco lesions
early on will be smooth and later will appear wrinkled or granular sometimes fissure and may alter taste in white patchy area |
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the pre-malignant condition causes:
- trismus - tongue that may become devoid of papillae - burning sensation - seen mainly in india and southeast asia - tissue is blotchy in areas of leukoplakia |
oral submucosal fibrosis: chronic, progressive scarring precancerous cond of oral mucosa due to the chronic placement of betel quid
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t/f nicotine stomatitis has no malignancy potential
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sorta true: no malignancy potential but does indicate that the patient is utilizing tobacco to a level that is toxic to mucosa
*** there is a high malignancy potential in those who reverse smoke #2 malignant potential for squamous cell carcinoma*** |
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what % of verruciform or granular types of dysplasias recur
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83%
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what is the most dangerous place for leukoplasia
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floor of the mouth 42% progress to malignancy
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what factors increase cancer risk in dysplasia
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1. persistence over several years
2. female patient 3. non-smoker 4. occurance on ventral tongue and floor of the mouth |
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what are the histological characteristics of keratosis with dysplasia
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1. hyperkeratosis
2. hyperchromatosis 3. inc. mitosis 4. keratin or epithelial pearls 5. tear drop rete ridges 6. DYSPLASIA |
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t/f keratosis with dysplasia may be reversible
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true
but it is assumed tht dysplasia progresses to carcinoma and the time for progression can vary from a few months to years |
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diffuse white and or papillary areas of oral mucosa with varying deg. of epithelial hyperplasia. It has the potential to dev. into verrucous carcinoma or well differentiated squamous cell carcinoma
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proliferative verrucous leukoplakia
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what are defining characteristics of PVL (proliferative verrucous leukoplakia)
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- 4:1 female to male ratio
- white papillary or warty - tends to spread buccal mucosa often common area - high rate of recurrence |
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red, velvety patch that has NO keratin. where is it most commonly found
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erythroplakia
found floor of mouth, tongue, soft palate |
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is erythroplakia seen more or less commonly than leukoplakia. and do they commonly show dysplasia
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seen less and majority show dysplasia = majority are rpe-malignant or malignant
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what would be your differential diagnosis for erythroplakia
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1. inflammation, denture irritation
2. candidosis, TB 3. kaposi's sarcoma (most commonly seen in AIDS) |
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what age and what % of dysplasia will you see erythroplakia
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60-70 yr old
50-70% show dysplasia, carcinoma-in situ or squamous cell carcinoma |
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what has the highest risk of malignancy in speckeled erythroplaika and leukoplakia
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speckled leukoplakia has the highest risk> erythroplakia>leukoplakia
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what is your differential for speckled leukoplakia
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inflammatory lesion: these would regress after a couple of weeks if the irritation is removed
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of all oral cancers what % are squamous cell carcinoma
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94%
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what nutritional deficiency will put you at risk for squamous cell carcinoma
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Plummer vinson syndrome (5th malignant transformation potential)
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what disease puts you at highest risk from malignant transformation potential for squamous cell carcinoma
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Proliferative verrucous leukoplakia PVL
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what are the 2 most important histologic features of squamous cell carcinoma
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1. invasion: infiltration of neoplastic cells
2. degree of differentiation: well (good prognosis) , moderately and poorly differentiated |
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what is your 5 yr. survival rate for a T1 compared to squamous cell carcinoma that has metastasized, has nodal involvement
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85% compared to 10%
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what distant sites may an oral carcinoma metastasize to
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lung, vertebrae, liver and brain
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how do you distinguish fibromatosis gingivae from hyperplasia caused by drugs
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the gingiva is normal in color while in drugs it would be red, tissue is not usually inflamed and good oral hygiene does not necessarily appear to influence hyperplasia
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what congenital abnormalities also show micrognathia
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pierre robin syndrome remember that pierre robin has cleft palate, micrognathia of the mandible and glossoptosis and congenital heart dz
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how is micrognathia acquired
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often results fromTMJ disturbances
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benign migratory glossitis is seen in 1-3% of the population. who is it seen in
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- females 2:1
- those under psychosomatic (emotional stress) - those with a hypersensitivity to environmental factors |
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田
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field
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tian2
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accumulation of keratin on filiform papillae causing a brown or black pigment on dorsal tongue
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hairy tongue
pigment is due to staining by tobacco, certain food, medicines or chromogenic organisms |
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what is the cause of hairy tongue and is it symptomatic
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ASYMPTOMATIC
caused: -antibiotic therapy - poor oral hygiene - oxidizing mouthwases or antacids - overgrowth of microorganisms (fungal and bacterial) |
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what % of patients will have an enlarged or tortuous vein on the lingual surface of tongue. Are these veins related to CVD
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Common 2/3 of patients age 60+ b/c incidence increases with age. NOt related to cardiovascular dz
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failure of normal development migration of thyroid gland
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lingual thyroid nodule
remnants of thyroid tissue can be seen on dorsal posterior tongue |
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T/F when treating lingual thyroid nodules you want to do an excisional biopsy
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False: incisional biopsy ONLY you should also do a careful physical exam to demonstrate that there is a normal thyroid gland present
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what oral tonsils make up the waldeyer ring
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1. palatine tonsils
2. pharyngeal tonsils 3. lingual tonsils 4. may also include paliate papillae PPLPP |
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incomplete or defective formation of the organic enamel matrix of teeth that results in pits, grooves, or larger areas of missing enamel
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enamel hypoplasia
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what are some causes of enamel hypoplasia
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remember its incomplete or defective formation of organic enamel MATRIX!
causes: - exanthematous dz (measles, chicken pox, scarlet fever) in first 2 yrs. - antineoplastic therapy - nutritional def - congenital syphilis - HYPOcalcemia - ingestion of chemical (fluoride) |
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what is turner's tooth
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single tooth that has enamel hypoplasia (defective or incomplete formation of the organic enamel matrix of teeth)
usually caused by local infection or trauma |
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this tooth may have numerous parallel vertical wrinkles or grooves the surface of the crown may show shallow or deep depressions (pits). what abnormality is affecting this mouth and what teeth would be affected if it occured in the first 2 years of life or later around 4-5
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enamel hypoplasia
first 2 yrs: anteriors and first molars 4-5yrs: cuspids, bicuspids and second molars |
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defective mineralization of the FORMED enamel matrix
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enamel hypocalcification: show and abnormal color: dec. translucence, inc. diffuse or demarcate white opacities
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T/F the stains that occur in enamel hypocalcification tend to dec. with age
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false they inc. with age
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in enamel hypocalcification the mineral content is low, but the organic content is high making the teeth especially caries susceptible
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true and false
organic > mineral but the teeth are NOT caries susceptible |
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what may cause mottling and hypoplasia which lead to inc. surface and subsurface porosity
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dental fluorosis: Ingestion of excess fluoride during tooth development
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what other factors would accelerate or exacerbate attrition
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end to end occlusion, bruxism, fluorosis, enamel hypoplasia (incomplete enamel matrix formation), dentinogenesis imperfecta
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you have a patient that has many flat or polished appearing wear facets. what do you suspect
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attrition
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Pathological wearing away of tooth structure by abnormal mechanical processes
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abrasion
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this tooth alteration is sharply defined and has a V-shape or notch
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abrasion
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this is a wedge shaped defect at the cervical area of the tooth due to bending . what usually causes this alteration
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Abfraction! usually due to bruxism that causes bending ofg the teeth at the cervical area of the tooth
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You have a patient come in and you notice that on the facial side of bicuspids and molars there are deep and narrow defects some of these defects are subgingival what does this person have
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Abfraction that is most likely cased by bruxism
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loss of tooth structure by a non-bacterial chemical action
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erosion: non-carious dental erosion
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Erosion of teeth prod. a smoothly rounded, scooped out depression. citrus fruits and stomach acids are common causes what surfaces do they commonly affect
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citrus fruits: labial surfaces of max. anterior teeth
stomach acid: erodes lingual surfaces of Maxillary teeth especially anteriors. Mandibular teeth are affected in severe cases |
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what are the 2 types of resporption
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internal and external
internal is assoc. with the dental pulp (may follow pulpal injury ie. caries, or physical trauma external resorption: assoc. w/ cells in the PDL |
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T/F internal resorption is far less common than external resorption
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true! external is extremely common 85% of all teeth
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what are some characteristics that a tooth undergoing internal resorption
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Pink tooth of mummery: remember associated with cells in dental pulp
presents with a uniform well circumscribed pulpal radiolucency in the pulp cahmber or canal until it reaches the PDL . the crown displays a pink discoloration |
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what would a tooth that is undergoing external resorption look like
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moth eaten area of tooth loss seen on:
cervical, midroot, apex, and in impacted teeth |
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what situations may cause external resorption
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1. tooth erruption
2. pathologic lesions: -inflammation/infection -tumors or cysts - systemic bone dz 3. reimplantation of teeth: b/c transplanted/reimplanted teeth have no PDL and are non vital they are eventally resorbend and replaced by bone. 4.tooth movement 5. impaction of teeth: when impacted teeth impinge or exert press on adj teeth may cause resorption of norm errupted teeth |
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pulpal inflammation can cause external and internal absorption what is diff. about these 2 processes
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pulpal infalmmation in internal resorption occurs as part of the activation of osteoclasts or dentinoclasts on internal surfaces of the root or crown while in inflammation in external resorption: is related to release of chem. mediators and inc. in vascularity and press.
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calcified tissue formed within pulp tiss
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pulp calcification and stones
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t/f the incidence of pulp calcification and stones increasees with age
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true! seen in:
66% of teeth in 10-20 yr. olds 90% of teeth in 50-70 yr olds |
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this type of pulp stone resembles dentinal tubules and looks more like secondary dentin than primary dentin.
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true denticles: more common in pulp chamber than in root area:
can be free (not attached to dentinal wall) or attached (extension of dentinal wall is the most common type) |
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what is dystrophic calcification
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the whole pulp multiplies
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localized masses of calcified tiss. with NO dentinal tubules. often shows a lamellar pattern.
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false denticles!
may be large enough to fill pulp chamber (called dystrophic calcification |
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small foci of calcified tiss in PDL
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cementicle
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what is a stain formed on the outside of the tooth called
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extrinsic stain
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where will you see a tobacco stain
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ususally light brown to black from tar seen on the lingual, cervical 1/3 of tooth also in the pits and fissures
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what may cause a yellow stain
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yellow stain is due to discoloration of dental biofilm that is common to all ages usually due to food pigments but.... tetracycline can also cause a yellow (to yellow brown) stain but it is intrinsic
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this stain occurs at all ages but is more common in females and is often found in a CLEAN mouth and will reoccur
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black stain: forms along the gingival third near the gingival margin and follows the contour of gingival crest 1mm above crest
seen on both facial and lingual |
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t/f a black stain in a clean mouth is commonly see on the surfaces of maxillary anterior teeth
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false see on both facial and lingual but rarely on max anterior teeth
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what bacteria cause a black stain
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usually gram + rods
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what is the etiology that causes an extrinsic green stain
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- pigmentation of Nasmyth's membrane
- pigment may be prod. of chromogenic bacteria or fungus - may be due to action of bacteial enzymes or blood pigments of inflamm. gingival exudates |
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a thick furry deposit that affects the cervical third of facial surface of max incisors is called what and who does it affect and what is it associated with
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extrinsic green stain!
Boys are affected 2:1 stain is associated with poor oral hygiene and may be decalcification underlying enamel |
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which stain is thick and hard and may have a roght surface that is dark mahognay brown almost black
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betel leaf stain
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t/f extrinsic orange stain is infrequently seen
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true: light, thin deposit varying from orange to brick red: involves both facial and lingual surfaces of incisors may be caused by chromogenic bacteria
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t/f metallic stains can always be polished off
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false: while enamel stains polish off but stained cementum or dentin may require bleaching
silver and iron = black copper and brass = green |
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stain caused by pigment deposition inside tooth during development
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intrinsic stain
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what color are non-vital teeth stained and why
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teeth turn grey or grey brown: due to breakdown of blood pigments and can be removed by bleaching
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what color changes will aging have
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enamel becomes thinner and teeth appear more yellow b/c dentin shows through better.
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t/f older teeth are more subject to extrinsic staining
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true
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this stain is cuased by a hemolytic anemia and will appear gren, brown, or bluish
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erythroblastosis fetalis: Rh incompatibility btw. mother and fetus. the hemolysis may be severe enough that blood pigments are deposited in the dev. teeth.
ONLY TEETH or portions DEVELOPING DURING PRENATAL AND PERINATAL STAGES AFFECTED |
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what affect does destruction of bile ducts in neonatal period have on color of teeth
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destruction of bile ducts cuases cholestasis and jaundice; excess serum bile pigments can be depostied in dev. organic matrix of teeth giving them a green color
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T/f biliary atresia will also affect permanent teeth
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false if jaundice is corrected permanent teeth will be normal
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you have a patient that has an inborn error of metabolism. He tells you that he has a photsensitivity to sun, he has skin vesicles/bullae, and red urine. what inborn error does he have and how does it affect his teeth
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congenital prophyria: inability to metabolize parphyrin = over prod. of uroporphyrin
teeth: red to brown discoloration of primary or permanent teeth and the stained teeth will fluoresce red |
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why is tetracycline contraindicated for children less than 7/8 years and pregnant women
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this antibiotic acts as a vital dye and is incoproated into bone and teeth b/c it binds with calcium.
the drug is deposited only during dentinogenesis and becomes highly conc. in dentin * tetracycline can also cross the placenta teeth become yellow to yellow-brown and fluoresce yellow may affect the entire crown or occur in a band like fashion |
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T/F: Hypodontia (partial) is common especially in deciduous teeth
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false: partial hypodontia is common with some familal tendency EXCEPT in deciduous teeth
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Retroviruses
env? structure? capsid symmetry? |
envelope
ss + linear icosahedral |
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accessory teeth
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hyperdontia 1-3 % of pop.
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where do supernumerary teeth most commonly occur
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90% Occur in the max
86% are single tooth hyperdontia |
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what is a mesiodens
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supernumerary tooth betwen the centrals
It is the most common place to se a supernumerary tooth |
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what is the second most common tooth to see hyperdontia
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max. 4th molar = distomolar or distodens
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what syndroms may you see hyperdontia
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cleidocranial dysostosis and gardner's syndrome
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what disorders commonly feature microdontia
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dwarfism (pituitary) and down's syndrome
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what teeth are commonly affected by microdontia of single tooth
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lateral and third molar
lateral often familial "peg lateral" |
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macrodontia like microdontia of a single tooth is common
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false it is uncommon and could be confused with fusion
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what dz features generalized macrodontia
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giantism (pituitary)
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in this developmental alteration in shape of teeth there is a single enlarged tooth with a single root and root canal which the tooth count is normal
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gemination
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what is fusion
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union of two separate tooth germs may be union to form large tooth or be union by roots only.
a single enlarged tooth or joind tooth in which the tooth count reveals a missing tooth |
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teeth united by cementum only. thought to arise as a result of traumatic injury or results of crowding
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concrescence: fusion occurs AFTER root formation
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what problems are associated with a talon cusp
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problems with esthetics: usually contains horn of pulp so you cannot grind away these teeth and caries control
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what teeth and what arch usually have additional cusps
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aka cusp of carabelli are common on lingual of maxillary molars and buccal accessory cusps are occasionally encountered on molars and bicuspids
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what is dens evaginatus and who will you most likely see them in
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cusp like elevation of enamel located in central groove on lingual ridge of the buccal cusp of permanent bicuspids and molars
seen in asians, inuits, and native americans |
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this accessory cusp is most common in the max lateral and arise as a result of an inbagination in the surface of a tooth crown before calcification. Like a canal that is open to the outside that is lined by enamel
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dens in dente (dens invaginatus)
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tiny glowbule of enamel found near bifucation on root surface near CEJ
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enamel pearl usually found in max molars
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usually seen in molars and the body of the tooth is enlarged at the expense of the roots
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taurodontism
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excess secondary cementum or root surfaces. lamina dura and PDL space should form aclearly visible outline on the outside of teh region of hypercementosis
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hypercemntosis
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how will hypercementosis in paget's dz differ from other hypercemntosis
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in page's the lamina dura will disappear while normally the lamina dura and PDL space sould form a clearly visible outline
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t/F extraction in hypercemntosis is contraindicated
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true! if extraction is required hypercemtosis may cause a complication due to it could form a concrescence of the root (fused root)
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angulation, bend, or curvature in the root or crown
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dilaceration: may be caused by trauma or alteration in angulation at tooth germ during formation
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what teeth are dilacerations most commonly seen in
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permanent max. incisors
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amelogenesis imperfecta is an inherited dz that affects the enamel what are the 3 classifications
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1. hypoplastic: enamel has not formed full thickness
2. hypocalcified: enamel is soft and can be removed easily, poorly mineralized and chips easy 3. hypomaturation: norm. thickness but enamel can be pierced by explorer |
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In this disorder teeth are:
-amber color - short roots - enamel chips off easily - roots fracture - teeth are bell shaped |
DI: dentinogenesis imperfecta
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in this dev. alteration the enamel is normal and teeth have a normal clincal appearance except for the extremely short roots . But the dentin is extremely thin and pulp chambers are very large
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shell teeth = dentinogenesis imperfecta type III
affects decidous teeth most often |
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what developmental abnormalities have teeth that appear clinically normal
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1.DI = dentinogenesis imperfecta
enamel normal but dentin extremely tin and pulp chamber very large, extremely short roots. most freq. deciduous teeth 2. DD= dentinal dysplasia clinically norm. in morphology and color, normal eruption normal enamel but dentin and pulp defective; coronal dentin and tooth color is norm. but root dentin is abnormal with shortened and tapered roots |
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this developmental disturbance of several adj. teeth in which the enamel and dentin are thin and irregular and fail to adequately mineralize (enamel layer often not evident) with a large pulp. teeth assume a "ghost like" appearance
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regional odontodysplasia
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in this developmental disturbance both enamel and dentin are involved, the enamel layer often not evident, there is delayed or total failure in eruption and the shape of teeth is altered
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regional odontodysplasia
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what form of irreversible pulpitis may feature a fistulous tract
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chronic pulpitis: rememer pain is not a prominent feature while in acute pulpitis pain will persist for 20-30 sec. after stimuli is removed
- this reduction in pain may be possible due to the fistulous tract allowing for press to release |
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this pulp diagnosis will have no reaction to pulp test
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necrotic pulp
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HBsAb
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provides immunity to hep B
surface antibody |
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which developmental alternations feature enlarged pulps
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shell teeth ( dentinogenesis imperfecta type III) and regional odontodysplasia
remember that dentinogenesis imperfecta types I and II have no pulps b/c of cont. deposition of abnormal dentin |
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In what developmental alterations do the teeth appear clinically normal to the eye
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dentinal dysplasia and shell teeth (dentinogenesis imperfecta type III)
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why doing a pulp diagnosis what information can you gather from transillumination
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may show if there is pulpal death
may show discoloration fo the crown = breakdown of blood vessels within a tooth It is also a very good way to detect carious lesions in anterior teeth |
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this periapical diagnosis has frequent spontaneous pain that can be excruciating and often throbbing, it is extremely painful to touch and is in supra occlusion, you will see NO overt swelling
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acute apical periodontitis
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accumulation of acute inflammatory cells at the apex of the tooth with pain and SWELLING
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periapical abscess
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this pulpal diagnosis is usually apinful with rapid onset, it is painful to percussion, the pain is NOT very localized (PA) adjacent teeth are painful, patient usually has swelling
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periapical abscess
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If you have a periapical abscess will the tooth pulp be vital
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NO an apicial abscess will result in a non-vital pulp
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I am an infection that travel facial planes ( path of least resistance
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cellulitis
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I am an infection of bone (along medullary spaces)
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osteomyelitis
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what is a parulis
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gum boil
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what is ludwig's angina
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the floor of the mouth and neck elevates the tongue = blocks airway
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what is a carvernous sinus thrombosis
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infection from maxillary anterior premolar and molar teeth with extension into maxillary sinus, orbit and cranial vault - very serious
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which sequella of an untreated abscess have serious complications
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ludwig's angina and carvernous sinus thrombosis
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you have taken a radiograph of a patient's tooth you see a radiolucency around the apical region of the root, the patient does not complain of any pain what would your differential diagnosis be
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chronic apical periodontitis (periapical granuloma) and apical periodontal cyst
these 2 appear identical on a radiograph. |
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how does chronic apical periodontitis differ from apical periodontal cyst
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an apical periodontal cyst must have an epithelial lining the source
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what syndromes are associated with hypodontia
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hereditary ectodermal dysplasia: HED missing hair on head, sebacous glands, and no eye brows
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you are looking at an x-ray you see a circumscribed area of radiopaque sclerotic bone, the entire root outline is visible. The x ray belongs to a young girl and the lesion is seen in the mand. first molar area what is your pulpal diagnosis
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chronic focal sclerosing ostomyelitis: bone sclerosis associate with apices of tooth with pulpitis
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a metastatic carcinoma to the submandibular (cervical) lymph nodes came from where
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upper respiratory tract and nasopharyngeal area
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cancers of the lung, breast, colon, prostate, kidney, thyroid, stomach and skin if metastasize to the oral cavity and neck go where
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the jaw bones but most commonly the mandible
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where is the most common site for soft tiss. metastasis
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the gingiva 50% often looks like a pyogenic granuloma. the teeth may become loose
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what are the symptoms commonly seen in metastatic carcinoma
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swelling or expansion of the jaws (mostly in the molar region) most have pain or discomfort and teeth may become loose
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most common type of carcinoma
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basal cell carcinoma
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t/f both basal cell carcinoma and verrucous carcinoma tend not to metastasize and are not invasive
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true and false: basal cell carcinoma does not metastasize but is invasive, while verrucous carcinoma is not usually infiltrative and does not metastasize
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this carcinoma does not metastasize and is not usually highly infiltrative, slow growing and exophytic, it may develop from PVL, is a low grade variant of oral squamous cell carcinoma
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verrcous carcinoma
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what places are the worst and best to get squamous cell carcinoma
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best:
Lower lip: 90% buccal mucosa: 50% floor of the mouth: 40-50% worst: oropharyngeal: 80% have metastasis on discovery max sinus: 5 yr. 10% tongue 20-30% 5 yr. survival |
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