OMPR pt 2

What are the 3 parts of the TMJ?
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Terms in this set (207)
What causes bifid condyle?trauma abnorma muscle attachment teratogens persistent fibrous septum within condylar cartilageWhat is the typical patient type for bifid condyle?adults - come in as *incidental radiographic finding*Where is the typical site for bifid condyle?unilateral mandibular condyleTrue or false, mediolateral bifid condylar heads more common than anterioposteriortrueWhat is the typical behavior of bifid condyle?innocuousWhat is condylar hyperplasia?enlarged condyle, long neck or lost ? mark shapeWhat is the typical patient of condylar hyperplasia?adolescent and young adult with *facial asymmetry* and posterior open bite on affected sideWhat is the typical site of condylar hyperplasia?unilateral mandibular condyle with enlarged head or neck of condyleWhat is the typical behavior of condylar hyperplasia?self limiting at skeletal maturity management depends on agree of esthetic concern or functionWhat is condylar hypoplasia?underdeveloped condyleWhat causes condylar hypoplasia?congenital (syndrome) acquired due to trauma, infection, radiotherapy, juvenile arthritisWhat is the typical patient of condylar hypoplasia?pediatric and adults with unilateral facial asymmetryWith unilateral condylar hypoplasia, where doe the mandible shift?affected side on openingIn bilateral condylar hypoplasia, how does the mandible shift?retrognathiaWhat is the typical site of condylar hypoplasia?mandibular condyle there will be premature contact on the AFFECTED side if there is a problem on BOTH sides you will see an anterior open bitewhat is the typical sequelae of condylar hypoplasia?degenerative joint diseaseWhat is coronoid hyperplasia?enlarged coronoid process *tip* of coronoid process extends *at least 1 cm above inferior rim* of zygomatic archWhat causes coronoid hyperplasia?hormonal influence hereditaryWhat is the typical patient of coronoid hyperplasia?adolescent males with *restricted mandibular opening*What is the typical site of coronoid hyperplasia?bilateral coronoidWhat i the typical behavior of coronoid hyperplasia?limited opening and may worsen during pubertyWhat cause degenerative joint disease?normal joint can no longer physiologically adapt to excessive mechanical loads and breaks down (*deterioration*) and attempts to adapt abnormally (*proliferation*)What is the the typical patient of degenerative joint disease?*adult females* asymptomatic signs and symptoms of TMJ disfunctionWhat is the typical site of degenerative joint disease?articular surface of TMJWhat is the typical behavior of TMJ degenerative joint disease*cyclic in nature* gradual onset followed by soponantous quiescent period only to recur and relapse againWhat causes rheumatoid arthritis?unknown trigger stimulates synovium to become hyper plastic and heavily infiltrated by inflammatory cellsthe synovial mass of tissue is in rheumatoid arthritis is called what?*pannus* and it creeps into doing surface to destroy themWhat is the typical pt type of rheumatoid arthritis?adult female 30-50 with *TMJ pain related to teeth clenching*What is the typical site of rheumatoid arthritis?*bilateral* TMJ involvementWhat is the typical behavior of rheumatoid arthritis?progressie chronic systemic inflammatory disease with exacerbation and remission periods *pencil in a cup*What is septic arthritis?destructive joint infectionWhat causes septic arthritis?direct spread of microorganisms to TMJ from ondontogenic infection/ cellulitisWhat is the typical patient with septic arthritis?pediatric and adult with *signs of acute inflammation* over TMJ trismus, lymphadenopathy *rare* vs degenerative & rheumatoid but still a *red flag*Where is the typical site of septic arthritis?unilateral TMJ with *joint effusion* from inflammatory process that *may increase radiographic joint space* and deviate mandible to unaffected sideWhat is the typical behavior of septic arthritis?inflammatory *destruction* of TMJ if no txWhat causes condylar fracture?physical blow to TMJWhat is the typical pt of condylar fracture?pediatric and adult with *anterior open bite and changes in occlusion* pain, swellling, limited range of motionWhat is the typical site of condylar fracture*unilateral condylar neck*What is the typical behavior of condylar fracture?prognosis depends on bone remodeling of the condyle mandibular hypolasia results if fracture occurs during growthCondyle neck fracture may be accompanied by what?*parasyphyseal or contralateral mandibular body fracture* always check mandibular body for signs of fractureWhat is MPR in terms of CBCT?multi projectionWhat mulitprojections are seen in CBCT?linear oblique curved oblique serial transaxialOn a CBCT, what projection looks like a pan?ray sumWhat are 2 types of volumetric renderings on a CBCT/Indirection where you see maximum intensity projections like bone and direct where you see tissuesWhat are voxel sizes?kinda like a pixel for CBCTWhat voxel sizes are better for smaller and clearer fields of view?smaller voxelWhat size voxel are ideal for endo?smallWhat are limitations of CBCT? (3)poor soft tissue contrast image noise with large volume metal artifactsWhat are effective doses for dente alveolar and craniofacial CBCT?61 87What are 5 main indications for CBCT in dentistry?implant assessment location of impacted teeth Endodontics evaluation of pathology orthognathic sx evaluation of traumaIs CBCT recommended for initial exam of pt for implant placement?no use pan or intra oralIs CBCT recommended for post operative imaging of implant placement?only immediately after implant placementWhy is CBCT not recommenced long after implant placement to evaluate implant failure?metal artifacts - looks like there's bone loss when there isn't anyWhat are pathological soft tissue calcifications?heterotropic calcificationWhat is a nidus?focus of infectionWhat are 3 types of heterotrophic calcifications?dystrophic idiopathic metastaticWhat is a dystrophic calcification?calcification that form in degenerating diseased and dead tissue with normal serum calciumWhat is idiopathic calcification?calcification that results from deposition of Ca in normal tissue despite normal serum calcium and phosphate tissueWhat is metastatic calcification?minerals precipitate into normal tissue as a result of higher than normal serum calcium level due to a metabolic disorderCalcified lymph nodes, tonsillar calcifications and arterial calcifications are what type of calcifications?dystrophicSialoliths, phleboliths, laryngeal cartilage, rhinolith, antrolith are what type of calcifications?idiopathicStylohyoid ligament ossification, osteoma cutis, myositis ossificans are what type of calcifications?metastaticWhat is the etiology of dystrophic calcifications?trauma, inflammation, infectionWhat is a common location for dystrophic calcifications?longstanding chronically inflamed cystWhat is the most common location for a lymph node calcification?submandibular lymph node between posterior borer of ramus and cervical spineChaining may be seen in what type of calcification?lymphoidHow are lymphoid calcifications managed?no tx determine underlying causeWhere are tonsillar calcifications on a pan?oropharyngeal air space where the dorsal surface of the tongue crosses the mandibular ramusWhat is the periphery and shape of a tonsillar calcification?mostly a cluster of multiple small ill defined radipacities sometimes called rice grain appearancewhy should tonsillar calcifications be treated primarily in elderly?risk of aspiration pneumoniaWhat are 2 types of arterial calcifications?medial calcinosis calcified atheromaWhat is medial calcinosis?loss of elastic fibers of artery followed by Ca deposition within medial coat of vesselWhere is medial calcinosis commonly seen? (what 2 arteries)facial artery carotid arteriesWhat is the periphery and shape of medial calcinosis?thin radiopaque lines that follow course of an arteryWhat is calcified atheromatous plaque associated with?inflammation that results in fibroblastic proliferation and calcium salt depositionWhat is the most common location for calcified atheromatous plaque?bifurcation now carotid after above or below hyoid (C3/C4 level)What is the periphery and shape of calcified atheromatous plaque?single or multiple and irregular in shape heterogeneous radiopacity with radiolucent voidsWhen symptoms are present with calcified stylohyoid ligament, the condition is called what?Eagle syndromeWhat is osteoma cutis?rare tissue calcifications of the kin may be secondary to longstanding acneWhere are sialoliths most common?submandibular glandWhat are phleboliths?calcifications in veinsPhleboliths are commonly associated with what pathology?hemangiomasHow is a phlebolith differentiated from a atheromatous plaque on pan?shape is not uniformMultiple radiopacities with radiolucent center is the radiographic appearance of what soft tissue calcification?phlebolithWhat 4 GI diseases are associated with oral findings?Crohn's disease ulcerative coolitis pyostomatitis vegetans celiac diseaseWhat is Crohn's disease?A chronic inflammatory bowel disease that affects the lining of the digestive tractcWhat is the hallmark of the histopathology of Crohn's diseasetransmural granulomatous inflammation (sarcoid like and non caseating)What oral findings are common with Crohn's diseases? (4)recurrent aphthous lesions linear granulomatous ulcerations cobblestone mucosa enlarged lipsHow is Crohn's disease treated?immunosuppressant (cyclosporin) corticosteroids, chemotherapeutics iron folate surgical removalWhat is ulcerative colitis?Ulcerative inflammatory bowel disease, just in the LARGE intestineGranulomas are common in which IBD?Crohn's (not ulcerative colitis)What are oral manifestations of ulcerative colitis? (3)recurrent oral ulcerations papillary mucosal projections with deep linear ulcers intraepithelial pustules of mucosaWhat is pyostomatitis vegetans?intraepithelial pustules of the mucosa seen in IBDHow is ulcerative colitis managed?anti inflammatory meds like sulfasalazine or prednisoneWhat is found in the histology of pyostomatitis vegetates?inflammatory cells, typically eosinophils (not typical for GI)How is pyostomatitis vegetans treated?tacrolimus sulfasalazine or prednisoneWhat is celiac disease?gluten intoleranceWhat are oral symptoms of celiac disease? (2)aphthous like ulceratons enamel defects and pittingWhat is amyloidosis?Deposition of a misfolded protein that can be localized or systemic; if systemic, can be primary (AL deposited due to plasma cell issue) or secondary (AA deposited due to chronic inflammation and overproduction of SAA which becomes AA)What is primary amyloidosis associated with?Multiple myelomaWhat can lead to secondary amyloidosis?reactive systemic amyloidosis hemodialysis heredity form renal failure CHF localized dermal amyloidosiamyloid deposit can lead to what? (4)macroglossia carpel tunnel syndrome hepatomegaly dry mouthWhat is the molecular configuration of amyloid deposits?beta pleated sheetsWhat are oral feature of amyloidosis? (4)macroglossia * gingiva blue and large xerostomaia mucosal petachiaeWhat stains are used for amyloidosis diagnosis?congo red apple green birefrignence under polarized lightHow is amyloidosis treated?Primary: treat MM (chemo) Secondary: treat the underlying inflammatory condition (ex = renal transplant)What oral findings are more commonly assoicated with type 1 diabetes?periodontal disease delayed healing infection riskWhat oral finding is seen equally in type 1 and 2 diabetes?sialadenosisWhat are the T4 and TSH levels seen in hyperthyroidism?T4 (thyroxine) elevated TSH decreasedWhat i the most common form of hyperthyroidism?Graves diseaseWhat oral finding is common in hyperthyroidism?early eruption of teethWhat is a precipitating factor of thyrotoxicosis?stress (seeing a dentist)What are 2 forms of hypothyroidism?cretinism (children) myxedema (adults)What are lab levels (T4 and TSH) in hypothyroidism?low T4 and high TSHWHat are oral findings seen in hypothyroidism?thickened lips and macroglosia bc of GAG accumulation in children, failure of tooth eruption even though they develop normallyIf chidlren with hypothyroidism are not treated in time, what can develop?permanent CNS damage and mental retardationWhat systemic condition may mimic central giant cell granuloma in bonehyperparathyroidismbrown tumor and giant cell lesions are seen in what disorder?hyperparathyroidismWhat are symptoms of hyperparathyroidism?renal calculi duodenal ulcer change in mental status bones, moans & groansWhat lab findings are seen in hypoparathyroidism? (PTH, Ca, PO4)low PTH low Ca high phosphate normal renal functionWhat 2 syndromes present with hypoparathyroidsm?DiGeroge enodcrne candidiasisWhat is chvostek's sign?Tap on facial nerve and get a twitch with low Ca due to hypoparathyroidismPersistent _____________________________ may be seen in hypoparathyroidism in young childrenoral candidiasis *ALSO if develops in young children tooth development an be affected (pitting enamel hypoplasia and failure of eruption)*What are the lab value of pseudohypoparathyroidism (activation of target cells dysfuncitonal)high PTH low Ca low PO4-What are oral findings of pseudohypoparathyriodism? (5)general enamel hypoplasia widened pulp chambers oligodontia delayed eruption blunting of tooth apicesWhat is hereditary hypophasphatemia?vitamin D resistant rickets *x-linked inheritance*What are oral findings of hereditary hypophasphatemia?teeth with enlarged pulp chambers and long pulp horns (small exposure leads to PA radiolucency); it appears that otherwise normal teeth have periapical pathology)What lab finding is noted in hereditary hyophashatemia?low serum phosphateWhat is hypophosphatasia/bone abnormality that resembesl rickets *autosomal recessive*What is the oral finding seen in hypophosphatasia?premature loss of primary teeth (lack of cementum) *not from periodontal disease, thought that marked reduction, or lack of cementum allows exfoliation*What are lab findngs assoicated with hypophosphatasia?low alkaline phosphatase high blood phosphoethanolamineWhat oral findings are seen in acromegaly? (3)mandibular prognathism macroglossia diastema formation - Acromegaly: excess production of growth hormone *after* closure of epiphyseal plates - Gigantism: excess production of growth hormone *before* closure of epiphyseal platesWhat are oral manifestaitons of addison's disease?diffuse or patchy macular pigmentationsWhat are lab values of primary addisons?high ACTHWhat is addison's disease?Under secretion of the adrenal cortex.Dermatits, dementia and diarrhea is seen in what vitamin deficiency?Pellagra (B3)What are oral symptoms of iron deficiency anemia? (4)angular cheilits dysphagia atrophic glossitis glossodyniaWhat syndrome is associated with iron deficiency anemia?plummer vinson syndrome which also has esophageal strictures which are premalignant -*Iron deficiency typically HYPOCHROMIC, MICROCYTIC*What are oral manifestaitions of pernicious anemia?burning sensation of tongue, lips buccal mucosa *MEGALOBLASTIC*What must you rule out in ps with burning mouth syndrome?pernicous anemiaWhat is uremic stomatitis?uncommon complication of acute renal failureWhat are clinical symptoms uremic stomatitis?abrupt onset of white plaques or crusts bad taste and burning odor of ammonia or urine on pts breathHow is uremic stomatitis treated?clear when renal dialysis begins acidic mouth rinsesWhat is reiter's syndrome?abnomrmal immune response to infection that leads to: polyarthritis conjucntivitis urethritisWhat are oral manifestions of reiter's syndrome?oral lesions, *painless* oral ulcerations erosions on tongue that *mimic geographic tongue*Extrinsic Staining Nathoo TypesN1 - colored material (chromogen) binds to tooth surface (tea, coffee, wine) N2 - Colored materials changes color after binding to the tooth. Are N1 stains that darken over time (still remove with OHI) N3 - Colorless materials (pre-chromogens) binds to the tooth and causes a stain after a chemical reaction. Carbohydrate rich foods, stannous fluoride and chlorhexidineT/F only humans are susceptible to chromogenic bacterial stainingfalse! she gives the example of sea lionsChromogenic bacteria is an Extrinsic Staining Nathoo Type?N3! (colorless material that stains after chemical reaction)Please list some extrinsic staining- chromogenic bacteria - tobacco, betel quid - tea, wine, coffee, - gingival hemorrhage - restorative material (amalgam) - medications, antimicrobials - iron - stannous fluoride, chlorhexidineChromogenic bacteria can produce various colorations: green, black, brown and orange. They are typically located at _gingival marginsChromogenic bacteria can produce various colorations: black, black, grown and orange.. __ species produce black stains.ActinomycesChromogenic bacteria can produce various colorations: black, black, grown and orange. Black brown stains aresecondary to interaction of bacterial hydrogen sulfide and iron in the saliva, forming ferric sulfideChromogenic bacteria can produce various colorations: black, black, grown and orange. Green stain?penicillium and aspergillus speciesCoffee and Tea are able to stain teeth. Due to the deposition of _ tea and other beverages on the _ and _ sidesTannins buccal and lingual surfacesExtrinsic staining: __ in the salivary pellicle bind to some dietary pigments (grapes and black tea)Proline rich proteinsDegree of staining from dietary pigments (N1) has been shown to be influenced in part by (low/high) pHlowStannous fluoride staining; type __ and explain(N3) secondary to stannous ion reacting with bacterial sulfides black stain affecting labial surfaces of anterior teeth and occlusal surfaces of posterior teethChlorhexidine staining, Cetylpyridinium chloride (cepacol, scope), Iron solutions and stannous fluoride are all _ types of staining and are (localized/regional/generalized) and (intrinsic/extrinsic)N3 Generalized extrinsicChlorhexidine Extrinsic Staining Nathoo Type and color/location?N3 type staining yellow-brown staining affecting interproximal surfacesChlorhexidine has been shown to bind to __ in vitrodietary chromogensChlorhexidine stains _ color and primarily affects _ surfaces. An increased frequency of staining is associated withyellow/brown on inter proximal surfaces increased staining with tannin containing beveragesIntrinsic staining - Localized color changes: white? (4 possibilities)- mild trauma to teeth during enamel formation - periodical infection of primary tooth - traumatic injury to primary tooth - incipient cariesIntrinsic staining - Localized color changes: yellow? (5 possible reasons)- moderate trauma to teeth during enamel formation - periodical infection of primary tooth - turner tooth - composite restoration - cariesLocalized Intrinsic staining - Localized color changes: brown (7 possible reasons)- severe trauma to teeth durin enamel formation - periodical infection of primary tooth - turner tooth - traumatic injury to primary teeth - restoration - caries - pulpal traumaLocalized Intrinsic staining - Localized color changes: Gray/Blue/black (3 possible reasons)- amalgam - metal crown margin - pulpal traumaRegional Intrinsic staining: whiteRegional: infection/trauma during enamel formation, mild fluorosis, nutritional deficiency recall local white: - mild trauma to teeth during enamel formation, periodical infection of primary tooth, traumatic injury to primary tooth, incipient cariesRegional Intrinsic staining: yellowinfection, trauma during enamel formation, moderate fluorosis, nutritional deficiency, epidermolysis bulls, regional tooth abrasion/erosion, hyperbilirubinemia recall: localized yellow: - moderate trauma to teeth during enamel formation - periodical infection of primary tooth - turner tooth - composite restoration - cariesRegional Intrinsic staining: brownsevere fluorisis recall: localized brown includes - severe trauma to teeth durin enamel formation - periodical infection of primary tooth - turner tooth - traumatic injury to primary teeth - restoration - caries - pulpal traumaRegional Intrinsic staining: blue/grey/blacktetracycline therapy recall: local = - amalgam - metal crown margin - pulpal traumaRegional Intrinsic staining: greenhyperbilirubinemia (secondary to hemolytic disease of newborn, biliary atreziaGENERALIZED Intrinsic Staining: Whitemild fluorosis Amelogenesis ImperfectaGENERALIZED Intrinsic Staining: YellowModerate fluoriosis Amelogenesis Imperfecta Dentinogenesis imperfecta Dentinal Dysplasia Epidermolysis Bullosa Hyperbiliruninemia Generalized tooth attrition/erosionGENERALIZED Intrinsic Staining: Brownporphyria Tetracycline therappyGENERALIZED Intrinsic Staining: blue/grey/blacktetracycline or minocycline therapy (during developmental stages)GENERALIZED Intrinsic Staining: green:hyperbilirunbinemia (Secondary to hemolytic disease of newborn, or biliary atresia)T/F Tetracycline is an intrinsic stain T/F Minocyclne can be intrinsic and extrinsicTRUE! Tetracycline is only during development. Minocycline is during and after tooth formationTetracycline is an intrinsic stain. It gets incorporated into the _calcification process of developing teeth by chelating calcium ionsT/F Tetracycline causes discoloration after completion of tooth formationfalse! only during development of teeth by chelating calcium ions. recall: minocycline staining occurs during tooth formation and after eruptionErosion predominates in areasthat are not protected by salivary secretionsErosion common presentationcupped lesions with central depression of dentin surrounded by elevated enamelPrimary or secondary Erosion if seen only on the incisal part of anterior teethsecondary to external sourceIf erosion is limited to palatal surfaces of max anterior teeth an occlusal surfaces of posterior teethsuspect regurgitation_ is a focal area of enamel hypoplasia/discoloration due to trauma to an unerupted tooth or periodical inflammatory disease of an overlying deciduous toothturner toothSevere fluorosis: _ and _ in developing teeth is correlated with extent of fluorosisdose and duration of fluoride exposureIngesting excess fluoride during early maturation stage of enamel formation leads tohypo mineralized enamelWhat can someone argue is a benefit of fluorosisstaining BUT resistant to cariesT/F Sometimes viruses or fevers can cause intrinsic stains especially if it occurs during developmental stagestrueCalcification and eruption of upper central incisors?calcification = 3-4mo eruption is 7-8yearsCalcification and eruption of first molars and eruptioncalcification at birth eruption is 5-7 years (lowers first)Hyperbilirubinemia stainingrecall: bilirubin is breakdown of RBC , so we will get more pigment of hemolytic diseasescongenital erythropoietic porphyria (CEP)autosomal recessive of porphyria metabolism, which hold iron in blood and gives its red color fun fact: king george III had thisamelogenesis imperfecta type 1 akahypoplasticdentinogenesis imperfecta is auto (dominant/recessive) and can affect (primary/permanent) teethautosomal dominant BOTH primary and permanent blue-brown discoloration of teeth opalescent teeth bulbous crowns obliteration of root canals and pulp chambers "expansive pulp shell teeth" Type 1 = osteogenesis imperfectaType one of dentinogenesis imperfectaOsteogenesis imperfectablue sclera is often seen inosteogenesis imperfecta - association with dentinogenesis imperfectaDentin dysplasia in primary vs permanent teethprimary = blue/amber/brown translucence, similar to DI Permanent = normal color and enlarged pulp chambersmanagement of tooth discolorationdental care diet habits oral hygiene enamel microabrasion bleaching dental restorations consultations