JVD 2010 deck Flashcards
According to “Building a telescoping inclined plane” by Legendre, what does is added to the traditional acrylic IP?
An 18g and 21g needle with the hubs cut off as a cross bar across the palate covered in acrylic/protemp, then an orthodontic wire around the maxillary canine and third incisor for a base of the IP
According to “Surgical extractions for PD in a western lowland gorilla” by Huff, what teeth were extracted from the 30y male gorilla? what may have been a contributing factor to his PD?
28, 29, 30, 31, 32 all PD 4 with buccoversion of 30; low pH from chronic regurge.
According to “Modified distal wedge excision for access and Tx of an infra bony pocket in a dog” by Klima, Goldstein, how was the infra bony pocket of 309 treated in a 6y Dachshund?
Staged procedure to extract 310 with PD3-4 then return for perio surgery of 309 in 6 weeks; surgery entailed a modified wedge resection along the alveolar crest, exposure to the site, and placement of a bone graft with osteoconductive, synthetic bioactive ceramic, then sutured closed and recheck radiographs in 6mo
According to “Modified distal wedge excision for access and Tx of an infra bony pocket in a dog” by Klima, Goldstein, why was this called bone augmentation not GTR? what # of walled defect was this? what time of bone graft was used? what suture? could things have been done better per the author?
no membrane was placed; 3 walled; osteoconductive biogloss (alloplast); 4-0 chromic gut; could have used membrane for GTR, autograft is best, and could have used 4/5-0 monocryl as chromic gut only lasts 14d and is extremely inflammatory/irritating as it is absorbed by phagocytosis not hydrolysis
According to “Modified distal wedge excision for access and Tx of an infra bony pocket in a dog” by Klima, Goldstein, what did the wedge resection look like?
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According to “Modified distal wedge excision for access and Tx of an infra bony pocket in a dog” by Klima, Goldstein, what was the outcome? what is circumferential bone loss around a tooth called? what is the “col”?
complete resolution of clinical signs… no histo so unsure if regeneration or repair but on rads normalizing PDL space; cupping defect, osseous crater; co is the interdental valley of non-keratinized tissue between two closely positioned teeth (site of inflammation and bacterial accumulation)
According to “Modified distal wedge excision for access and Tx of an infra bony pocket in a dog” by Klima, Goldstein, define allograft and alloplast. what is the purpose of a membrane?
allograft from same species, mineralized freeze-dried bone allograft (FDBA) and decalcified freeze-dried bone graft (DFBDA), osteoconductive, osteoinductive; alloplast osteoconductive only (no inductive or genic properties), synthetic material including plaster of Paris, calcium carbonates tricalcium phosphate, hydroxyapatite, and bioglass (used here), promotes repair, not necessarily regeneration; prevent downgrowht of epithelium and healing w long junctional epithelium and CT, goal to get regeneration not repair
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, a 10y MN Dachshund presents for a COHAT. Define this term. What did they find on oral exam? What was the tx recommendation?
comprehensive oral health assessment and treatment; Stage 3 PD palatal 104, Stage 2 304, 404, TR 205; recommended X 205, RPO and placement of bone graft (alloplast) palatal 104, RPC and doxirobe of 304, 404, followed by daily tooth brushing and COHAT q6mo w rads to monitor
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, what # walled defect was palatal 104? what are most common sites for this type of defect in the dog? what percentage of doxycycline gel was used? what was the tx outcome in 6mo?
3 walled; btwn mandibular first and second molars and palatal maxillary canine; standard 8.5%; complete healing of 104 pocket (3mm) and 304/404 (2mm)
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, what are some of the mechanisms in which periodontal bacteria evade host defenses and cause tissue destruction? what are some mediators produced that are part of the host response to tissue destruction? what mediator is partly responsible for bone loss? bone loss in PD is not necrosis, explain this.
IgA and IgG degrading proteases degrade specific antibodies, leukotoxins that inhibit PMNS, heat sensitive surface proteins that lead to apoptosis of PMNs and inhibit IL-8 production of epithelial cells causing impairment of PMN response to bacteria; proteinases (MMPs, elastase, cathepsin G, neutrophil serine proteinase), cytokines (IL1, TNFa) prostaglandins; PGE2 (remember orthodontic mvmt too); not necrosis but activity of living cells along bone, as soft tissue destruction occurs, exposes root and subsequent bone resorption occurs, tissue necrosis and purulent d/c is from the soft tissues, not bone, there is a normal turnover of periodontium by bacetierla proteinases and mediators and inhibition of host cells, in diseased state it is no longer in balance
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, what are the 2 types of pocket? what are some mentioned root surface applications mentioned? why not use them? what is the goal of this type of perio surgery with bone augmentation?
gingival/pseudopocket and periodontal pocket; root conditioners, etc to improve attachment/CT: citric acid (low pH causes damage to soft tissue), EDTA (not approved in vet texts), fibronectin and tetracycline (as well as citric acid) have no literature proving improved attachment over root planing alone; new attachment with periodontal regeneration
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, what happens if gingiva populates root surface first? bone? what is the difference btwn osteogenesis and osteoinductive? what are some examples of osteoconductive only grafts? what was used in this case report?
gingiva first leads to root resorption; bone first leads to root resorption or ankylosis; goal is to have periodontal tissues (PDL, cementum) repopulate first); osteogenesis has blasts within the graft, only autografts can do this, while osteoinductive means the product will aid in generation of new bone via BMPs converting neighboring cells into blasts to make new bone (DFBDA); FDBA (not decalcified), hydroxyapatite, tricalcium phosphate, bioactive glass; SBGP: synthetic bioactive graft particulate
According to “Open root planing for a PD pocket of a maxillary canine tooth” by Greenfield, how long does doxirobe last? what are its properties?
2-4 wks to aid in healing of perio tissues; antimicrobial, anti-collagenase, stimulates fibroblast activity
According to “A survey of equine oral pathology” by Anthony, Laycock, et al, 556 cadavers were examined. What were the most common findings? where did the majority of pathology occur? were there associations between the noted pathology?
sharp edges 48%, buccal abrasions, calculus 30%, lingual ulcers, gingival recession, periodontal pockets, ramps 15%, and waves 13% (in order); cheek teeth (only 28% did not had cheek tooth pathology); horses w sharp edges were 100x more likely to have buccal abrasions, 3.6x more likely to have lingual ulcers, and 2.3x more likely to have calculus than horses w/o sharp edges, lingual ulcers were 3.2x more likely to occur in horses w buccal abrasions, PP were 21x more likely to occur w gingival recession, etc.
According to “A survey of equine oral pathology” by Anthony, Laycock, et al, in regards to canine teeth and wolf teeth, were they typically present or absent? in all horses?
60% were missing all four canine teeth, more common in geldings and stallions; most horses did not have wolf teeth, those that did were maxillary (26%)
According to “A survey of equine oral pathology” by Anthony, Laycock, et al, were older or younger horses more likely to have normal cheek teeth? sharp enamel points were most associated with what 2 pathologies? what were PP associated with?
younger; buccal abrasions and lingual ulcers; most commonly seen in cheek teeth and closely associated w diastema, missing teeth and gingival recession
According to “Scanning electron microscopy of pulp cavity dentin in dogs” by Hernandez, Saccomanno et al, 36 teeth from 12 adult cadaver dogs 2.5-13y were taken from 104, third premolar, 409 and looked at radicular and coronal dentin to determine tubule density and diameter. They were split in 2 groups I (<7y), 2 (>7y). Was there significant difference between the 2 groups? what shape were most of the dentinal tubules?
no. round or oval.
According to “Scanning electron microscopy of pulp cavity dentin in dogs” by Hernandez, Saccomanno et al, what type of media was used to store teeth and clean teeth to limit shrinkage and dehydration? was there a decrease in # of tubules within the tooth, if so where? was tubule density influenced by age or occlusal function?
first bleach (2.5 -5%), then 100% acetone, best to maintain hardness and have least volume reduction; yes, decrease in # of tubules per mmsq moving from the pulp cavity towards enamel (90K at pulp, 24K at DEJ); also a decrease in diameter and area of tubules in a corona-ical direction and decreased as age increased; No.
Abstract: According to “Clinical periodontal and microbiologic parameters in patents with acute myocardial infarction (AMI)” by Stein, Conrads, et al, what were the find gins in this study?
104 patients (54AMI, 50 healthy control) sub gingival plaque analyzed for red pathogens and others, p w AMI had singiciantly higher frequency of probing depths than controls, all pathogens overrepresented by AMI p and positively correlated w increased PD AL; Porphyromonas gingivalis was an indicator for AMI. association btwn perio and AMI in PD correlated to presence of PD pathogens.
According to “Effect of kibble size, shape, and additives on plaque in cats” by Clarke, Biouge et al, 40 mixed breed cats 1.5-7y were placed into 4 groups following 14d dry kibble only diet A for acclimation and dental charting and blood work. then a dental prophylaxis was performed following by 7d acclimation period on diet A. Then, cats were evaluated under GA, plaque scored and teeth were cleaned again, at that time, they were split into 4 groups. What were the 4 groups of kibble diet? Once diet was initiated 7d later plaque score was performed and again at 28d post diet change.
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According to “Effect of kibble size, shape, and additives on plaque in cats” by Clarke, Biouge et al, which diets contained STPP? PRN? Which were larger/rectangular?
Diet B and C had STPP (sodium triphosphate); Diet D had PRN; diet C/D were larger
According to “Effect of kibble size, shape, and additives on plaque in cats” by Clarke, Biouge et al, what was measured? was there any significant difference between cats fed diet A and B on day 7 or 28? what was the theory as to why cats fed diet with STPP did not change their plaque score?
individual coverage and thickness scores from gingival half of tooth (gingival half score) and a total mouth plaque score, mean gingival score, and coronal half plaque score; no; bc sodium triphosphate do not reduce plaque accumulation but are mineral chelators and mineralization inhibitors that bind salivary calcium helping to reduce the formation of calculus
According to “Effect of kibble size, shape, and additives on plaque in cats” by Clarke, Biouge et al, between diet C and D, which had better results? why was C better than A/B? Why was D better than A, B, and C at reducing plaque?
Diet D had a more significant reduction in plaque (43% less than A/B at day 28); C was a larger, harder kibble with greater SA and thickness providing more mechanical debridement; D contained not only STPP to prevent calculus formation, but was larger (like C) and contained PRN
According to “Effect of kibble size, shape, and additives on plaque in cats” by Clarke, Biouge et al, what is PRN? how does it work? Was Diet D larger or smaller than C? what is most important for reduction of plaque?
sodium ascorbic phosphate group (ascorbic acid- Vit C), water soluble vitamin promotes wound healing, helps maintain normal CT, and aids in promotion of healthy teeth and gums; ascorbic acid promotes collagen synthetic CT protein at the level of hydroxylation of propyl and lysol residues of pro collagen, has a direct effect on gingival inflammation, bleeding, risk of PD, and amount of visible plaque; D had slightly less SA and volume than C, but contained PRN which improved its efficacy (D had 12% less plaque than C at day 28); size and texture of kibble for mechanical debridement and addition of PRN may be useful
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, based on previous studies, what is the most common site for oropharyngeal neoplasia? 280 biopsies from 279 dogs were reviewed and categorized (retrospective) into 8 dx groups. What are they?
gingiva; benign, malignant neoplasm, reactive, dental, mucosal/inflammatory, bone, viral lesions, non-representative bx.
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, the majority of cases belonged to 3 groups, what are they? what were the most common oral lesions (sp. dx)?
Reactive 39%, benign neoplasia 27%, and malignant neoplasia 15%; fibrous hyperplasia 24%, POF 21%,
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, what percentage of biopsies were epulides? reactive lesions? benign? was there a significant age correlation found with malignant neoplasia and benign? pure-bred dogs had a higher prevalence of oral lesions than mixed breed, was this significant? which breeds were overrepresented?
69% were epulides, of these 49% were reactive and 36% were benign; median age for malignant was 10y, compared to reactive 8y (significant); yes!; boxers for benign tumors (significant), and dachshunds for malignant (significant)
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, were findings of this article consistent with previously reported studies in regards to most common oral neoplasm? the rate of malignant neoplasia was lower than previously reported. To what did the authors attribute this?
yes! POF!; referring biopsies to department primarily work with small animal dentistry and biopsy material is biased towards epulides and benign oral lesions at the expense of clinically obvious malignancies treated by other specialists
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, what was the overall median age? was the overrepresentation of males w malignant neoplasia significant? there was a higher number of POFs amongst females, is this consistent w previous studies? the most frequent breed represented per 1000 individuals was the Kerry Blue Terrier. Is this significant?
8y; no; Yes; while it was statistically significant, it may not be transferable to a larger population due to odd misrepresentation within the study population (geographically)
According to “Oral pathology in Swedish dogs: a retrospective study of 280 biopsies” by Svendenius, Warfvinge, define the structures at the arrows and asterisk. what is this gingival mass based on histo?
arrows: islets of odontogenic epithelium, asterisk/star: trabecular bone; POF
Abstract: According to “presence and quantification of mast cells in gingiva of cats w TR, PD, and FCGS” by Ari, Verstraete, et al, 32 cats affected by TR, FCGS and PD were compared to 7 healthy cat gingiva to determine mast cells and inflammatory infiltrate via H&E and toluidine blue stains. What were the significant findings regarding mast cells? Was there any difference between groups? was the inflammatory infiltrate the same amongst groups?
Mast cell densities were significantly increased in gingival tissues adjacent to teeth affected by TR, FCGS, and PD compared to healthy cats; no; no, significantly lower adjacent to teeth w TR than PD or FCGS;
Abstract: According to “presence and quantification of mast cells in gingiva of cats w TR, PD, and FCGS” by Ari, Verstraete, et al, why do the authors postulate that mast cells may play a role in TR?
bc of mild inflammatory infiltrate and high number of mast cells, pathogenesis of TR involves differentiation or activation of osteoclasts and RANKL, mast cells produce and maintain these mediators…
Abstract: According to “Mandibular Rim excision in 7 dogs” by Arzi, Verstraete, a case series of 7 dogs with mandibular rim excision were performed to 1cm margins. Why did they recommend a curvilinear rim mandibulectomy over right angled excision? what are some advantages to rim excision over segmental mandibulectomy? how often is the dog rechecked w rads, exam?
strong indications in ppl that curvilinear excision resists higher occlusal forces than R angled excisions, also tumors usually follow elliptiform pattern and thesis more bone sparing following tumor margins more appropriately; advantages include superior post op fxn, absence of mandibular drift, esthetics, well improved capacity for reconstruction and rehabilitation, spares mandibular canal and content; recheck 3-4 wks, rads at 6mo, and annual, or recommend q3-6mo following initial recheck
Abstract: According to “elastic training of the prevention of mandibular drift following mandibulectomy in dogs: 18 cases (2005-2008)” by Bar-Am, Verstraete, 18 dogs received placement of an elastic power chain to prevent mandibular drift following partial, segmental, or total mandibulectomy (caudal to 2nd premolar). Where were the orthodontic buttons placed? At what tension was the chain set? how often were chain changes recommended? Recheck appts?
lingual aspect of contralateral mandibular canine (not affected by mandibulectomy) and buccal aspect of maxillary fourth premolar; chain set at 75% of number of holes between brackets under no tension; change chain weekly; recheck at 2, 6, 10 weeks.
Abstract: According to “elastic training of the prevention of mandibular drift following mandibulectomy in dogs: 18 cases (2005-2008)” by Bar-Am, Verstraete, of the 18 dogs, 1 was lost to follow up and 1 was euthanized for metastatic disease. Of the 16 dogs, how many tolerated the appliance? How many had good owner compliance (change chain weekly and recheck)? of the remaining dogs with good owner and patient compliance, how many maintained successful occlusion while wearing the band? by 4-6mo, how many dogs were able to have the band removeD? what mechanical pull from a muscle is the chain counteracting? what percent of cases was mandibular drift prevented in dogs w elastic chain?
1/16 did not tolerate appliance, instead had CR/XP, VPT; 4/16 had poor owner compliance which left 11 dogs; by 4-6mo, 8 dogs had appliance removed with no mandibular drift; medial pterygoid m.; 100% of compliant owners/dogs (11) when wearing appliance, 50% of cases acquired some mandibular stability 4-6mo after elastic training (66% amongst compliant cases)
Abstract: According to “Histologic evaluation of use of membrane, bone graft, and MTA in apical surgery” what was the aim of the study? What were the 4 groups? Was there statistical difference between them?
compare periodical healing after use of membrane, BG, MTA in apical surgery of dogs. Induced apical lesions in 4 roots of 6 dogs after coronal access and pulp removal; 4 groups: 1 filled w blood, 2 filled w blood and covered w membrane, 3 filled with BG, 4: filled w BG and recovered w membrane; inflammatory infiltrate, healing process and behavior of MTA same in all groups; BG and membranes do not significantly alter periapical healing process after use of MTA
Abstract: According to “influence of apical foramen widening and sealer on the healing of chronic periapical lesions induced in dogs’ teeth” by Borlina, Neto et al, what was the goal of the study? What were the groups of teeth? what were the results?
Goal to evaluate influence of apical foramen widening on healing of chronic periapical lesions in dogs’ teeth after toot canal filling w Sealer 26 or endomethasone; 49 root canals of dogs’ teeth used, and instrumented up to 55k file at apical barrier, 20 canals cemental canal penetrated and widened up to size 25, other 20 roots had no widening, all received calcium hydroxide dressing for 21 d then filled w GP and 1 of 2 sealers, group 1: sealer 26 apical foramen widening, group 2 Sealer 26 no apical widening, group 3 endomethasone apical foramen widening, group 4 endomethasone no widening, animals euthanized after 180 days and histo performed on roots; repair of cementum and bone resorption presence of microbes, inflammatory cell infiltrate and PDL conditions were significantly better following foramen widening and Sealer 26 (epoxy resin sealer)
Abstract: “Comparison of periodontal pathogens btwn cats and their owners” by Booij-Vrieling, Hazewinkel, et al what was the aim of the study and what were the results? were they significant?
compare microflora of cats and owners mouths as animal to human and vice versa transmission may have public health concerns; P. gulae, P. gingivalis, T. forsythia isolates, in cats Porphyromonas were 64 cats was catalase positive and negative in owners (7), T forsythia in 63 cats and 31 owners higher in cats w PD, in one owner the T forsythia isolates were the same. Transmission from cats to owners had occurred in cats w T. forsythia positive isolates making cats a possible reservoir.
Abstract: “Pseudoangiomatous SCC in the oral cavity of a dog” Cushing, Peters et al, an 8y FS Lab mix w OM 208/209 first biopsied as poorly differentiated SCC. Following surgical excision, histo revealed what? Why is this important?
HSA-like mass composed of numerous vascular clefts and variable numbers of keratinizing epithelial cells. Histo and IHC were compatible w pseudoangiomatous SCC, well recognized variant of acanthomatous SCC; clinicians should be aware bc of its histomorphologic similarities w canine gingival HSA (vascular growths)
Abstract: “Revascularization and periapical repair after Endodontics tx using apical negative pressure irrigation vx conventional irrigation plus triantibiotic intracranial dressing in dogs’ teeth w apical periodontitis” by da Silva, Preto et al, what was the aim of the study? What were the groups? What were the results? were they significant?
evaluate in vivo revascularization and the apical and periapical repair after end tx w negative pressure vs positive pressure irrigation and triabx canal dressing in immature dogs’ teeth w apical periodontitis; induced apical periodontitis, Group1 apical neg pressure irrigation (endovac), 2 apical positive pressure irrigation plus triabx canal dressing, group3 positive control w no tx for periapical lesions, group4 negative control composed of sound teeth; animals killed 90d later for histo. group 1 presented more exuberant mineralized formations and structed apical and periapical CT and better repair than 2 (but only inflammatory infiltrate was statistically significant)
Abstract: “Dental abnormalities associated w X-linked hypohidrotic ectodermal dysplasia in dogs” by Lewis, Reiter, Casal et al, what is meant by XLHED? how is it different from ED in chinese crested dogs?
X-linked hypohidrotic ectodermal dysplasia (XLHED) manifests in structures of ectodermal origin (absent or malformed) including skin, lacrimal glands and teeth; In chinese crested dogs with ectodermal dysplasia this is an autosomal dominant trait.
Abstract: “Dental abnormalities associated w X-linked hypohidrotic ectodermal dysplasia in dogs” by Lewis, Reiter, Casal et al, 17 mixed breed dogs (16male, 1 female) and 9 controls were evaluated by awake, and sedated oral exam and rads to look for abnormalities. What was the most common abnormality? Other common abnormalities?
Missing teeth (mostly premolars) in 100% of dogs more common on left side of maxilla/mandible, mostly mandible; deciduous teeth persistent 55% (mixed dentition), malocclusion in 94%, mesioversion 88%, conformational crown and root abnormalities of premolar/molar teeth 100%,
Abstract: According to “Effect of periodontitis on susceptibility to atrial fibrillation in an animal model” by Yu, Shu et al, what is the aim of the study? How was it induced? Were the results significant?
Is periodontitis related to AF?; 22 mixed dogs induced periodontal in 12 dos, other 10 controls, had ligation at day 30, 60, 90 and then ECG evaluation to measure atrial refractoriness and AF indelibility by delivering a single atrial extra stimuli in the high R atrium, atrial septum and coronary sinus, measure C-reactive protein in blood and TNF alpha. Euthanized at 90d. Inflammatory cells were found in the atria of perio group. Periodontitis led to inflammatory responses in atrial myocardium which disturbed structural and electrophysiologic properties of the atrium and facilitated AF.
Abstract: According to A comparative study of dental pulp response to several pulpotomy agents” by Tabarsi, Asgary, et al, what was the aim. What were the groups? What were the results and were they significant?
in vivo response of dental pulp in dogs to 3 pulp captain agents; 36 second and third premolar teeth in 6 beagle dogs group1 calcium hydroxide, group2 MTA, group 3 endodontic calcium enriched mixture (CEM) cement; histo after 8 weeks @ of root canals w calcified bridge formation, pulp vitality and lack of inflammation statistically higher for MTA and CEM than CH; no sig difference between CEM and MTA. Either are good for pulp capping.
Abstract: According to “Tx of a caudal mandibular fx and TMJ-luxation using a bi-gnathic encircling and retaining device” by Nicholson, Langley-Hobbs et al, what was the aim of the study? What was the outcome?
describes BEARD (begnathic encircling and retaining device) for caudal mandibular and TMJ fx/luxations; 2 immature dogs w simple unilateral caudal fx, 6 cats w unilateral injury (2 TMJ lunation, 3 TMJ fracture-laxation, 1 caudal mandibular fx) 2 cats w bilateral (comminuted caudal mandibular fx w contralateral TMJ luxation); BEARD failed short term due to poor compliance in 1 cat, and concomitant injuries in another cat, 1 cat lost to follow up, rostral dental occlusion was normal in 6/7 cases. Complications: dorsal nasal skin swelling/discharge, e-tube dislodgment, BEARD loosening, regurge.
Abstract: According to “Use of Rim excision as a Tx for CAA” by Murray, Gottfired, et al, 13-14 dogs w CAA had rim excision. What was the outcome?
No recurrence. Canine was removed in 47% of cases, 33% were caudal. Rim excision great option for CAA resulting in improved dental occlusion, cosmoses, no evidence of epulis recurrence.
According to “Repair of palatal ONF using an auricular cartilage graft” by Watering, Reid, et al, the 2y lab w a former stick chewing injury to his palate had surgical repairs done twice prior to this attempt. The defect was ~4mm. How much larger than the defect does the graft need to be? Is it taken from the medial or lateral aspect of the pinnae?
1.5x bigger; medial;
According to “Repair of palatal ONF using an auricular cartilage graft” by Watering, Reid, et al, what additional technique is used to prevent the formation of aural hematoma at the donor site? what was the case outcome?
Through and through horizontal mattresses to decrease dead space; at 2 weeks, the graft was no longer visible, but a healthy bed of granulation tissue was forming. By 4 weeks, the previous defect had closed.
According to “Immunohistochemical localization of osteoclastogenic cell mediators in feline TR and healthy teeth” by Sennets, Stoffel et al, define odontoclasts. List the 3 cytokine-like proteins in the TNF superfamily involved in osteoclastogenesis.
tartrate resistant, acid phosphatase (TRAP)-positive, multinucleate giant cells what fulfill the same fx in dental tissues as osteoclasts in bone; Receptor activated NFkappa beta ligand (RANKL) a type II transmembrane polypeptide expressed in lymphoid tissues and on leukocytes, osteoblasts, lymphocytes, and stromal cells; receptor activator NFkappa B (RANK) type I membrane receptor expressed in dendritic cells, foreskin fibroblasts, some T cells, and osteoclasts and their precursor cells; binding of RANK to RANKL on osteoclast precursor cells induces differentiation into mature, activated osteoclasts which iniaites bone resorption; lastly, osteoprotegerin (OPG) secreted by osteoblasts and stroll cells in soluble form as both a monomer and dimer acts as a decoy receptor for RANKL; OPG inhibits osteoclastogenesis by preventing RANK-RANKL interaction
According to “Immunohistochemical localization of osteoclastogenic cell mediators in feline TR and healthy teeth” by Sennets, Stoffel et al, describe the relationship between RANK, RANKL, and OPG (chart).
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According to “Immunohistochemical localization of osteoclastogenic cell mediators in feline TR and healthy teeth” by Sennets, Stoffel et al, 38 mandibular teeth (25 premolar and 13 molars) from 8 animals age 3-19 were separated radiographically by TR (RG1,2,3,4) and histo (HG1,2,3,4) performed including immunostaining for RANK, RANKL, OPG. What significant findings were there? radiographically what was the prevalence of TR? were radiographic and histologic findings consistent?
TR increased in frequency w age; 47% teeth had at least 1 lesion; yes in 84% of teeth (32/38)
According to “Immunohistochemical localization of osteoclastogenic cell mediators in feline TR and healthy teeth” by Sennets, Stoffel et al, what conclusions can be drawn about RANK, RANKL, and OPG in TR cats?
presence of fibroblasts and stromal cells in TR lesions, secretion of OPG by odontoblasts may contribute to the signal, but RANk, RANKL, and OPG were absent in some areas of active repair (others they we represent)…. no great conclusion.
According to “Regional Odontodysplasia in a juvenile dog” by Schamberger, Maretta, Dubielzig, a 7mo beagle dog had deformed minimally erupted 104 w brown staining and right maxillary swelling. There was no history of trauma, DT/P, or Endodontics disease of 504. A radiograph revealed mutiple folding and idlacerations from 104-106, radio dense areas in pulp chamber, with no enamel on visible intraoral crown. What are some differentials?
Complex odontoma (although, not typically what would be seen on rads), odontodysplasia, trauma/malformed tooth bud, dentinal dysplasia, dentinal amelogenesis, dentinogenesis imperfects, other
According to “Regional Odontodysplasia in a juvenile dog” by Schamberger, Maretta, Dubielzig, What were treatment options and why was extraction chosen?
Orthodontic extrusion, but not possible given dilacerations; endo therapy given shape of canal and presence of PP; minimal functionality given 2mm of eruption; extraction, can submit for histo and write a cool case report!
According to “Regional Odontodysplasia in a juvenile dog” by Schamberger, Maretta, Dubielzig, histologically what supported the diagnosis of odontodysplasia? what was the outcome?
complex folding and segmental disorganization at the midsection of tooth, disorganized cementum intermingled w dentin mostly well organized but occasionally poorly formed, enamel matrix present after deminerazliation indicated enamel was poorly mineralized (and only present in some areas), crown dentin disorganized forming small tubular whirls reminiscent of bone; great. Recheck at 4mo rads were normal; 10mo doing great on oral exam
According to “Regional Odontodysplasia in a juvenile dog” by Schamberger, Maretta, Dubielzig, what are some synonyms for regional odontodysplasia, a rare developmental abnormality in humans? where is it most common in humans? what are gross and radiographic features? histologically?
odontogenic dysplasia, odontogenesis imperfecta, ghost teeth; maxillary central, lateral incisors or canines typically permanent teeth, but if deciduous are affected adults will definitely be; grossly abnormal shaped rough surface w yellow/brown color, rads abnormal tooth morphology w marked reduction in radio density, reduced thickness of hard tissues and wide pulp chamber; marked reduction in art of dentin and irregular tubular pattern of dentin, areas of interglobular substance, hypo calcification of hypo plastic enamel
According to “Regional Odontodysplasia in a juvenile dog” by Schamberger, Maretta, Dubielzig, what is important to distinguish RO from dentinal dysplasia/other dentinal issues and odontomas? are there suggested etiologies for RO?
does not affect the entire dentin and does not affect bone quality; unknown, but may be mediations, trauma, viral infection, ischemic event, irradiation, mutation, metabolic/nutritional disturbances, failure of migration of neural crest cells
According to “Soft palate advancement flap for palatal ONF” by Rocha, Beckman, define what is indicated by the arrows.
green: major palatine foramina; yellow arrow: palatine sulcus (where palatine v/a/n run); red arrow: palatine fissure where palatine a enters nasal cavity
According to “Soft palate advancement flap for palatal ONF” by Rocha, Beckman, how much further past the bony defect is the defect debirded in the hard palate? A divergent flap is made caudally into the soft palate to cover the ONF. how many layers is it closed in?
2mm; 2 layers, nasal mucosa SI 5-0 monofilament absorbable suture and palatal aspect rostral to caudal with 4-0/5-0 SI pattern inverted w knots on nasal aspect
According to”Prosthodontic Tx of a wild jaguar” by Emily, why…. just WHY?
They took a 4y jaguar with a CCF 104 and instead of just RCT they placed a crown extension prosthesis with a post and 4 TMS pins (2 internal/exernal) and used composite to stabilize it; So now when the jaguar refractures its tooth, the entire post will come out exposing the poorly filled RCT OR it will be killed for the gold tip on its tooth. Nice work.
