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.
According to “Bilateral iatrogenic maxillary fx after dental tx in 2 aged horses” by Widmer, Kummer, et al, in cases of a 21y and 17y horse, what were the type of fractures and what were they associated with? how were they both treated?
Case 1 (21y): epistaxis and difficulty chewing/mastication following dental float a few days before, suspect trauma during float by rDVM, on radiographs bilateral maxillary and incisive bone fx w 5cm vertical mucosal lesion found through nasal scope; Case 2 (17y): during routine dental ext for fx 110, crunching sound heard as horse chewed against speculum, radiographs revealed fx 110and 209, as well as a complete bilateral fx of rostral portion of maxilla, closed complete bilateral transverse fx of rostral portion of maxilla w minimal displacement; intramural cerclage wire applied under GA to both cases and by 3 and 6mo complete healing was noted and wire removed.
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, what are some listed ddx for jaw swellings in immature dogs? All 5 dogs in this case series were 3-5mo, male, and had mixed dentition. The puppies had no history of trauma, were non-painful and afebrile. Did blood tests reveal anything significant?
bone fx, callus formation, cellulitis, soft tissue abscess, tooth root abscess, dentigerous cyst, developmental abnormalities, fibrous osteodystrophy, odontoma, benign and malignant neoplasia, inflammatory periosteal bone formation (CMO); 1 dog mildly elevated WBC (16K) w lymphocytosis and eosinophilia and basophilia; unremarkable in other 4 puppies.
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, mixed dentition was noted on oral exam and radiographs were performed in all 5 dogs. What was the consistent finding between the cases radiographically? How were they treated?
Regardless of eruption status, from level of 3rd/4th premolar or 4th premolar/first molar all dogs had periosteal reaction and double cortex of the ventral mandible (all left!), 1 dog may have had slight changes to the right mandible; 2/5 dogs had a fluid filled bony pseudocyst (no lining) which was thoroughly derided and 4/5 had an incisional biopsy, curative resection was not attempted. In 4/5 NSAIDs +/- abx were prescribed, 1 dog had no meds and no biopsy.
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, In 4/5 dogs with a biopsy of the left mandibular bony proliferation, what did the histopathology reveal? What was the outcome?
severe, periosteal new bone formation with no inflammatory or neoplastic disease, fluid filled swelling bone had acute inflammation and pieces of necrotic bone (1 dog), marked hyperostosis with well differentiated lamellar bone (chronicity) was noted in 1 dog; 4/5 dogs had complete clinical resolution (1 was lost to follow up)
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, what was the consistent radiographic finding that let the authors to believe the diagnosis of periostitis ossificans was appropriate? what type of bone formation exists in the mandible? what is hyperostosis?
double cortex on the left ventral mandible (also noted on occlusal view in 3 dogs) with proliferative periosteum, where the proliferative periosteum in 2 dogs on the buccal surface formed pseudo cystic walls; intramembraneous bone formation around rod-like Meckel’s cartilage w 2 separate ossification centers (endochondral centers) at canine tooth region of Meckel’s cartilage and dorsocaudal border of mandible; excessive periosteal bone deposition which occurs circumferentially on the appendicular skeleton, mandible, and potentially any bone formed intramembraneously
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, what are CMO and ICH in dogs? How are they different from PO?
CMO (craniomandibular osteopathy) common in Westies, Scotties, Cairn Terries, bilateral PAINFUL mandibular swelling with fever, hyperostosis of mandibles, bull, and bones of cranium can restrict TMJ mvmt, rapid growth continues after 1y of age, often requires immunosuppression/NSAIDs; ICH (infantile cortical hyperostosis) in dogs is cortical thickening of calvarium in young male mastiffs due to bilateral periosteal new bone formation, self-resolving 80% of the time, no known causes, possibly genetic, DOES NOT AFFECT MANDIBLE; ICH in humans is very rare and can affect the mandibles 75-80% of the time
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, what is the functional matrix theory of jaw growth? How does this relate to a possible theory for young dogs developing PO?
The bones grow in response to the surrounding soft tissues such as masticatory muscles; insertion of digastrics m. on ventrocaudal mandibular cortex corresponds to the area where periosteal lifting occurred in all 5 puppies
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, in human’s what is another name for PO? what is PO often associated with in human medicine? what are criterion radiographically for human PO? what are some common features in dogs?
Garre’s dz; periapical infection of M1, although usually not painful; visible bone enlargement of the jaw, radiographic detectible periosteal duplication, evidence of infection as determined by erythema w or w/o induration, presence or history of abscess or sinus formation, and/or gross caries w periapical periodontitis, commonly unilateral (87%), 3:1 left to right ratio, ventral aspect of mandible most common location then buccal/lingual mandibular surface; dogs in this case series had unilateral condition, increased L:R ratio, predominantly ventral and buccal mandibular expansion, evidence of necrotic bone within core of fluid-filled lesion;
According to “Mandibular periostitis ossificans in immature large breed dogs: 5 cases (1999-2006)” by Blazejewski, Lewis, Reiter, et al, how does the onion layered appearance of periosteal proliferation form? in humans, what are potential causes of PO? hypothesized causes in dogs?
waxing/waning chronic active infection provides waves of periosteal new bone formation and patchy granularity on rads; extraction of M3 w periocoronitis; pericoronitis of M3, adjacent tooth follicle w changes of follicular cortex w infection, periapical infection; mandibular PO in large breed puppies results from inflamed or infected dental follicle developing unerupted tooth (most likely M1) and or secondary to pericoronitis (rapid onset due to fast eruption in dogs); PO is a type of osteomyelitis
According to “Care of metal crown restorations” by Crowder, what steps should be taken to care for a metal crown?
begins w good margins (appropriate contour, marginal fit, smooth surface for crown placement), home care for full metal crown restorations (plaque retentive); care of full metal crown restorations during professional scaling (U/S scaler will scratch metal crown); polishing full metal crown restorations
According to “Care of metal crown restorations” by Crowder, what is the ideal vertical taper of a full jacket metal crown? where should the crown be placed (margin made)? what is the first step to create good margins? why should U/S scalers be avoided on metal crowns?
6 deg; 1-2mm supragingivally to reduce subgingival inflammation; finishing: removal of marginal irregularities and defining anatomic contours w stone lubricated w silicon grease contra angle from metal crown to tooth at 45deg angle; they cause etching, scratches, pitting and deformation
According to “Care of metal crown restorations” by Crowder, how is the sub gingival scaling performed for a metal crown? what are some options for polishing a crown? what is the final step of polishing?
w u/s scaler or hand curettage; tin oxide prophylaxis powder mixed w water or glycerin or siliceous powder bound to wax in cake, and a final fine grit rubber point impregnated w silicon carbide in a 10:1 OR sintered aluminum oxide on contra angle on slow speed handpiece (high luster and polished appearance); use a rouge (iron oxide) on a cloth wheel (linen, muslin, cotton, felt) to a mandrel on slow speed handpiece for luster/smooth glossy surface
According to “Care of metal crown restorations” by Crowder, what are the noble metals? why are they important? what is meant by precious, non-precious or semi-precious metals? what are base metals? why are they used? what is corrosion?
Gold (Au), palladium (Pd), Platinum (Pt), Iridium (Ir), Rhodium (Rh), Ruthenium (Ru), Osmium (Os); least corrosive; relates to cost of noble metals; titanium (Ti), nickel (Ni), Copper (Cu), Silver (Ag), zinc (Zn); less resistant to corrosion, but offer strength flexibility and wear resistance; corrosion: dissolution, deterioration, or weakening of a solid
According to “Care of metal crown restorations” by Crowder, what is pitting corrosion? Stress corrosion? what is polish ability of a metal?
pitting corrosion: localized area where oxide layer of base metal like iron, nickel, chromium is degraded in acidic environment; stress corrosion: mechanical stress and corrosive environment exert a negative effect on metal resulting in a crack or hertzian fx; refers to the alloy’s hardness, alloy w high hardness scale (Knoop’s hardness number) is more difficult to polish and to indent
According to “Care of metal crown restorations” by Crowder, what is meant by two body abrasives? three body abrasive for polishing? what is tripoli?
2 body: abrading burs, bonded abrasives like rubber points w silicon carbide and coated abrasives; 3 body: small pieces of loose material circulating within contact zones of abrasive and substrate like polishing paste, tin oxide in glycerin, an aluminum oxide slurry, or diamond polishing paste; polish used in metal restorations from porous rocks in North Africa
According to “Multilobular tumor of bone in the mandible of a dog” by Eubanks, Anderson, et al, an 8y husky presented for a rostral mandibular oral mass noted 2 weeks prior. There was displacement of the teeth noted and missing mandibular incisors associated with bony destruction. What were the significant radiographic findings? An incisional biopsy was performed. What were the histologic findingS?
diffusely irregular bone w mottled appearance consistent w a “popcorn” lesion indicative of multi lobular tumor of the bone, teeth were displaced and no normal bony structures were present in the rostral mandible; lobules of central foci on bone marginated by plump mesenchymal cells w ovoid to slightly irregular nuclei w fine chromatin and mitotic figures, grade I multi lobular tumor of bone
According to “Multilobular tumor of bone in the mandible of a dog” by Eubanks, Anderson, et al, what was the recommended treatment of choice? Does this tumor now go by another name? Is there currently other treatments used for this tumor type (not mentioned specifically in the article)?
Surgical resection with clean 1cm margins; yes! MLO= multi lobular osteochondrosarcoma; YES! SRT or other types of palliative radiation, esp for calvarial MLO’s.
According to “Multilobular tumor of bone in the mandible of a dog” by Eubanks, Anderson, et al, what was the surgical outcome? what is the postulated derivation of this tumor type? when metastasis does occur, where is the most likely location? what are the most common clinical signs of mandibular MLO?
clean margins w dehiscence at 5d, healed by 8 weeks despite some saliva staining; derived from altered periosteal elements of the chondrocranium or viscerocranium (commonly in flat bones of skull), tumor is slow growing, potentially malignant and locally invasive; lungs; pain when opening mouth, halitosis and ptyalism
According to “Multilobular tumor of bone in the mandible of a dog” by Eubanks, Anderson, et al, what is the classic radiographic appearance of an MLO? describe the classic histo of this tumor
solitary nodular lesion with smoothly contoured, sharply demarcated border, lobulated pattern resulting in a stilled or coarsely granular appearance; distinct radiographic appearance “popcorn ball” appearance, limited lysis of adjacent bone with large areas of lysis or brush pattern along tumor borders may suggest malignant change; multiple lobules w centers of hyaline cartilage or immature bone, cartilage or bony center of each lobule is surrounded by a thin layer of spindle cells separated by fibrovascular septa, vessels may penetrate the centers of lobules if the cartilage is undergoing endochondral ossification
According to “Multilobular tumor of bone in the mandible of a dog” by Eubanks, Anderson, et al, what is the treatment of choice? What is a positive prognostic indicator? the authors mention Samarium-153-EDTMP, what is this?
surgical resection w clean margins; tumor-negative surgical margins; radiopharmaceutical drug that can be used if surgical resection is not indicated or impossible…. OR SRT/other types of radiation therapy would be what we would recommend in 2018
According to “Oromaxillonasal fistula in a horse” by Pizzigatti, what happened in this case? what was interesting regarding the mandibular teeth? what percent of horse skulls have oral disease or dental disease? what teeth are most commonly affected by fracture and what causes it? what is the suspected cause of dental fracture in this region?
A 10y mixed breed mare had 1 yr hx of respiratory distress, bilateral nasal discharge, halitosis, she was anemic, dyspneic, and cachectic, oral exam revealed chronic fx 208 with SEVERE oroantral fistula with impaction and infection involving the left maxillary and conchal sinuses, the owner euthanized; the 308 was elongated 4cm into the ONF; 80%; maxillary molars (108/208, 109/209 at 68% mandibular molars 32%); idiopathic; infundibular caries esp involving maxillary molar teeth
According to “Tooth resorption and Vet D3 status in cats fed premium dry diets” by Girard, Biourge, et al, 64 cats (26 DSH, 38 pedigrees) ate a normal commercial diet and had routine dentals to evaluate them for TR (Type 1/2) and had serum measurements of 25-OH-D concentrations to determine if elevated Vit D3 was linked to TR. What did the authors find?
62.5% of cats had TR (1/2), and mean serum concentration in affected cats was 164 nmol/L which was lower than cats WO TR 226.8 nmol/L; The study revealed NO significant difference associated w TR lesions and elevated Vit D3 in cats, in fact serum concentration was higher in cats wo TR
According to “Wire-composite splint for luxation of the maxillary canine tooth” by Startup, in this step-by-step, a lateral luxation injury is diagnosed in a dog and replaced then splinted using wire. what is a critical predictor to a favorable outcome? Lunation injuries fall into 6 categories, what are they? What is the FIRST STEP in any trauma case?
time lapse between accident and tx can be critical to a favorable outcome; concussion, subluxation, lateral luxation, extrusive luxation, intrusive luxation, avulsion; first step is to stabilize the patient!
According to “Wire-composite splint for luxation of the maxillary canine tooth” by Startup, what are the properties of an ideal splint? following cleaning, a wire was placed across the palate to stabilize the canine (figure 8), then acid etch and dentinal bonding agent followed by composite. What is the optional step mentioned?
semi-rigidity allowing for some vertical movement of the tooth, esthetic and easy to clean, uncomplicated to make, stable w accurate repositioning, does not impede other necessary therapy such as endodontics; can place composite buccally and cover wire twist OR can also place palatal composite to completely cover wire while utilizing bite wax or another spacer (3mm) between palate and composite, the splint is then smoothed w diamond bur, white stone and other polishing discs
According to “Wire-composite splint for luxation of the maxillary canine tooth” by Startup, the author mentions tx of TDI in 2 stages, what are they? Luxation (lateral at least), usually requires endodontic therapy. When is this recommended? What are the guidelines from the International association of dental traumatology regarding tx of lateral luxation and avulsion?
short-term emergency tx and stabilization and long-term mgmt and review; endodontic therapy is usually recommended 7-10d after injury to prevent pulp infection and root resorption, this doesn’t usually work for our patients bc it requires anesthesia; according to guidelines, for lateral luxation or avulsion, splint should be placed for 4 weeks and RCT w calcium hydroxide should be performed 7-10d following injury but can be done sooner, remaining endodontic therapy w GP and final restoration should be done in ~1month, hence in vet med we typically do temporary RCT w CaOH, then place splint and remove splint and complete RCT at 1 mo.
Abstract: According to “MMP expression in teeth w apical periodontitis is differentially modulated by the modality of RCT” by Paula-Silva, Silva, Kapila, what was the point of this study? was it clinically significant?
apical periodontitis induced in dogs, RCT was performed in a single visit or by using an additional CaOH root canal dressing, 180d post tx inflammation was examined and bacterial status, tissues were stained for MMP1, 2, 8, 9, apical periodontitis that had RCT in a single visit had higher inflammatory cell infiltrate, disorganized tissue and presence of bacteria, higher MMP expression, teeth treated w CaOH had lower inflammatory cell infiltrate, more organized CT< and less bacteria, less MMP expression; teeth tx w CaOH may have lower percentage of bacteria, lower MMP expression, less inflammation and better organized CT matrix, may be useful to place CaOH
Abstract: According to “Post mortem survey of peripheral dental caries in 510 Swedish horses” by Dixon, 510 skulls were examined post mortem for prevalence, site and severity of peripheral caries (PC). PC affected which teeth? What prevalence? What location on tooth? infundibular caries were present in what percent of skulls w PC?
only affected cheek teeth in 6.1% of skulls; peripheral cementum 87% of PC occurred in 3 caudal cheek teeth (09-11); 32%; clinically look for peripheral caries when you see infundibular caries in cheek teeth!
Abstract: According to “Nasolacrimal obstruction caused by root abscess of the upper canine in a cat” by Anthony, Laycock, et al, what happened in this case report?
10y MC DSH presented w chronic ocular d/c from OS, epiphora and mucopurulent d/c with normal ocular exam, nasolacrimal obstruction suspected, swelling of L side of face, severe PD dz, and CCF 204 noted; dacryocystorhinography revealed narrowing of nasolacrimal duct above root of 204 and periapical lucency associated w 204; 204 extracted, ocular d/c and facial swelling resolved. 2y later cat normal. Extraluminal compression of nasolacrimal duct, imp oral exam when normal ocular exam!
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, 224 dogs >1y presented for perio tx and had full mouth radiographs. Of those, evidence of TR was considered and classified according to human classification system (Andreasen, Andreasen). What are the 7 classifications of TR? Were all of them seen in the study population? despite being a clinical radiographic diagnosis, how are all of these types truly differentiated?
external surface resorption, external replacement resorption, external inflammatory resorption, external cervical root surface resorption, internal surface resorption, internal replacement resorption, internal inflammatory resorption; internal inflammatory resorption was NOT seen in the study pop; histology
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
external replacement resorption
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
external inflammatory TR
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
external surface resorption
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
external cervical root surface resorption
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
internal inflammatory TR
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what type of TR is this?
internal surface resorption
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what percentage of dogs had evidence of TR radiographically? of teeth? was there any significant correlation to age, breed, weight, or sex for external replacemenet resorption? were maxillary or mandibular teeth more prevalent? Which teeth?
53.6%; 11.1%; prevalence of TR increased significantly w age and weight; maxillary (12.3% vs 10.1%); maxillary PM1, mandibular second premolar
Abstract: According to “Radiographic evaluation of the types of tooth resorption in dogs” by Peralta, Verstraete, Kass, what were the most common types of TR?
external replacement resorption 34.4% of dogs, external inflammatory resorption 26% dogs, external cervical root surface resorption 5.8% dogs, then external surface resorption, internal inflammatory resorption, and internal surface resorption; NO internal replacement resorption noted
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, this article explored using the AVDC 5 stages of TR for TR in dogs. What are the 5 stages?
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Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, when comparing the Andreasen/Andreasen classification system for TR and the AVDC classification for TR, which classified a higher percentage of teeth? where did this classification system fall short? what are the limitations to the AVDC classification?
Andreasen/andreasen 96.3% of teeth; the AVDC extent of TR in this article only detected 90%; external inflammatory TR classifying only 46% (less than half!); does not consider location and radiographic pattern of lesions, no stage 1 lesions were detected (cementum not visible on rads), all external surface resorption was classified as stage 2 (bc they don’t typically involve pulp),
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what Stage and type of TR is this?
Stage 2; external surface root resorption
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
stage 3, external inflammatory root resorption
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
408: stage 4c (mostly roots affected), 409: stage 2; 408: external replacement resorption, 409: external root surface resorption
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
Stage 4b: crown more affected; external inflammatory tooth resorption
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
Stage 4a (crown more affected)
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
Stage 5; external replacement resorption
Abstract: According to “Radiographic evaluation of the classification of the extent of tooth resorption in dogs” by Peralta, Verstraete, Kass, what stage and type of TR is this?
did not state in article: stage 2? associated with perio-endo lesion? or external inflammatory root resorption
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, a 6mo old Bassett presented w R sided maxillary swelling and DT/P 504, initially, what were some early indicators this was more than just abscessed 504 with osteomyelitis? The possibility of coagulopathy and neoplasia was discussed with the owners. What modality did they decline? What did they agree to?
Excessive gingival inflammation with maxillary enlargement from 104-107, CBC revealed normochromic, normocytic anemia (22%) pre op with low TP (5.3) indicating possible blood loss, thrombocytopenia (8K, at risk for spontaneous bleeding, manual count revealed 124K), rare acanthocytes, rare Howell jolly bodies, polychromatic, reactive lymphocytes, lobulated lymphocytes, large platelets, mild hyponatremia, hyperkalemia, hyperalbuminemia, hyperbilirubinemia, lipemia, icterus, and hemolysis, PT/PTT normal, USG 1016; Declined CT; agreed to rads, ext 504 and biopsy of the area
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, what did the incisional biopsy reveal following extraction of 504? bone was submitted for biopsy. What were the top differentials? What did histo reveal?
There was excessive bleeding, diseased underlying bone was palpated, 104 partially erupted, radiographs revealed incisive and maxillary bones to have diffuse, mottled appearance w lytic “soap bubble” irregularities extending from 104-106; abscessation and osteomyelitis secondary to DT/P 504 or early onset neoplasia; reactive bone with no clear evidence of neoplasia
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, what happened on recovery? A recheck CBC was done 10d post op, what did this reveal? what happened 18d after initial presentation?
PCV 11%, recommended blood transfusion, owner declined, slow, poor recovery, recommended workup for coagulopathy and further imaging or at least recheck rads in 1 mo to confirm healing bone; normal Hct with microcytic, hypo chromic anemia with lymphocytosis; dog had acute severe oral hemorrhage and owner elected euthanasia, post op found extensive increased bone opacity, mottle lucency extending 50% width of maxilla, necropsy revealed poorly demarcated neoplastic spindle cell mass with no differentiation btwn new bone neoplastic bone, bone was forming large irregular channels of blood filled regions w loose fibrovascular stroma w thick trabeculae of woven bone lined by osteoblasts
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, there is little known about intraosseous hemangioma in vet med, in humans how do they typically present and what is the tx? what are risks of embolization?
benign, slow growing lesions in vertebra or skull, preference for females (2-3:1), endothelial differentiation and proliferation of mesenchymal rests into blood vessels, CSs anomalies in dentition or eruption, tooth mobility or loss, paraesthesia, tumescence of gingiva, hemorrhage at cervical region, diagnosis is made through biopsy, however, given the risks in surgery a presumptive diagnosis can be made if enough evidence supports it, radiographic appearance: soap bubble, honeycomb, sunburst osteolytic pattern, CT for extent or angiography (requires carotid access); Surgical resection after considering pre-op embolization (within 48h do sx to reduce tumor blood volume) which is curative, little response to radiation therapy, cryotherapy for small lesions; cerebral or pulmonary vessel embolization (accident), hemiplegia, blindness, facial paralysis;
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, what is the other big differential for this tumor type? why is this important for sx? what could have been done differently to determine a prognosis for this dog?
vascular malformation, need IHC to differentiate; bc hemangiomas have a potentially curative involution phase 80-90% of the time where vascular malformations do not; IHC to determine if hemangioma (could spontaneously regress/involute) vs vascular malformation
According to “Intraosseous maxillary hemangioma in an immature bassett hound” by Hansen, Speltz et al, what histologic tumor is shown here?
Not vascular beds–> intraosseous hemangioma; would have soap bubble appearance on rads
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what is the main goal of fracture repair? what are some internal and external surgical techniques for fixation of mandibular fx? what are the 3 biomechanics factors that must be considered for repair?
re-establish physiological occlusion and masticatory fx; IM pins, orthopedic wires, intraoral splints, external fixators, bone plates, combinations of these; masticatory muscles, direction of fx line, forces involved on the repair of the fx
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, how many screws historically need to be placed on either side of the plate for internal fixation? what is the tension surface of the mandible? why does this pose a problem for surgical repair?
2 screws on either side of plate; alveolar border; avoid damage to tooth roots associated w screw insertion, plates must be placed on lateral or aboral surface of mandible;
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, how is the biomechanical disadvantage of plate placement (cannot be on tension surface) overcome? what was the point of this study? A 35kg cadaver dog head was used for CT to make reconstructs and format into a computer software for FEM. Then 3D reconstructed models of the jaw were made as well as double-arch format fixation plate alloys (120Ti 6Al 4V) w self-tapping screws (3.5x0.5mm thread, 5.2mm diameter, 8.0mm length, 5.0mm body, 3.0mm head length). What were the mandibles made of?
by orienting the plate according to the bending forces or by supplementing the fixation w a second plate in large patients or interdental wires; develop a plate for treating oblique fx of the mandibular body in dogs and to validate the project by finite element modeling (FEM) and biomechanics evaluations; rapidly prototyped in nylon 6 or polycaprolactam ( polymer formed by ring-opening polymerization) using selective laser sintering, all prototypes included tooth roots and mandibular canals
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what fractures were created? How were they separated into groups? What is CAD? FEM? what type of plate system was used? Where were the screws placed? what was first tested?
ventrorostral (favorable) and ventrocaudal (unfavorable), 10 of each; CAD=computer aided design; FEM= finite element modeling where different stress/strain/tension properties are tested; Synthes; 2 locking mono cortical screws at each end of the fx, a second CT was performed to check placement; once plates were placed (G1=3 holes on either side, G2=3 caudal 2 rostral, G3=2 caudal 2 rostral), 1 mandible from each group set the machine standard (elasticity modulus and maximum tension) and the other 9 were used to test the actual material
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what is meant by “relative rigidity” of a mandible? maximum deflection? what is meant by plastic deformation? elastic deformation? what was the maximum load used in both fx types during bending tests?
relative rigidity=stiffness or resistance to being deformed; maximum deflection=stress or the amount of TENSION applied along an elastic body; irreversible process where load is sufficient to permanently deform the material; reversible process load is removed and material returns to its original confirmation; 40N
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, for FEM and CAD, what are splines and NURBS? what were the assumptions for FEM? which category had the highest deflection?
splines are a curve that is generated by computer-graphics program and non-uniform rational basis splines (NURBS) for surface representation; istoropic, linear, homogenous materials (pure titanium, titanium alloys, nylon 6); G3, 2 screws on either side
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, which fractures had a higher mechanical resistance? in which fx group was the overall average of deflection higher?
favorable fx over unfavorable in the deflection test; statistically higher in unfavorable fx group when compared w favorable fx group
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, which group of fx prototypes had a higher mechanical resistance in the deflection test? which had higher deflection? in the favorable fx group was there significant difference btwn types of screw plate configurations? what about the unfavorable group?
favorable fx had higher mechanical resistance; overall defection was higher in unfavorable group; No (see pic); yes! significant difference between G3 (2x2) and G1 (3x3) and between G3 and G2 (3x2)
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, when comparing 2 fracture types, was there a difference in overall structural rigidity? was there a difference in overall structural rigidity across the favorable group btwn screw-plate configurations? unfavorable?
Yes, significantly lower for prototypes in unfavorable group than favorable; no; avg of structural rigidity was significantly lower for the G3 (2x2) compared to G1 (3x3) and G2 (3x2)
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what is meant by rotating displacement? was there a difference between G1, G2 G3 in regard to FEM analysis for favorable fx? unfavorable?
rotating displacement: drawing bone and plate closer together; using von Mises stress analysis, by removing both dorsal screws stress was increased in most ventral screw in rostral segment for favorable fx and G3 maximum stress was more uniform when compared to G1/G2 redwing stress in bone; for unfavorable, G3 configuration had higher von MIses stress concentration mainly around lower screw of caudal region of plate
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, is this a favorable or unfavorable fx? Where is maximum stress concentration via Von Mises stress concentration using FEM?
unfavorable fx; maximum stress concentration over ventral screws of caudal portion (lower screw)
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what are some benefits to the plate developed in this study? what is a benefit to the Synthesis system used? why were compression tests not performeD? why was titanium the material of choice for the plates?
has good mechanical resistance and can be placed adjacent to alveolar surface of mandible (site of maximum tension stress) since cannot go on true tension surface (alveolar crest); the SPS free-block system allows the screw to be locked due to presence of a long ring positioned inside the plate enabling angular placement of the screw; mandibles perform only flexion movement, no compression; mechanical characteristics (lowest elastic modulus of biocompatible metals but still high compared to elastic modulus of bone), biocompatibility, no artifacts on CT exam;
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, why were only bending tests performed on the prototypes of mandibles w fractureS? was the resistance force higher for favorable or unfavorable fx? by how much?
bc the canine mandible performs bending movements NOT tension or compression movements; favorable; by 4x higher compared to unfavorable
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what was the conclusion regarding number of screws and structural rigidity? with regard to fx type? was there a difference among favorable fx types in regard to screw-plate configurations? unfavorable?
more screws leads to higher structural rigidity and smaller amount of deflection; favorable fx type was 2x higher structural rigidity than unfavorable; no difference; G3 of unfavorable fx was statistically different than G1/G2 and had higher deflection and lower rigidity than favorable
According to “Finite Element modeling for development and optimization of a bone plate for mandibular fracture in dogs” by Freitas, Warrak et al, what conclusion was drawn regarding removing screws for favorable fx? unfavorable?
of screws and fx type have significant impact on plate fixation, when screws were removed better tension distribution in bone w decrease in maximum tension (tension distribution in bone) from 20MPa (G1) to 15.34MPa (G3, 2x2), most uniform tension using 2x2 (G3) for favorable fx is best choice!; removing screws for unfavorable increased maximum tension online the caudal segment, concentration of stress is associated w bone resorption, uniform stress is associated w bone regeneration;
According to “Lip avulsion and mandibular symphyseal separation repair in an immature cat” by White, a 12wk old cat had sustained unknown trauma 48h prior to presentation including symphyseal separation, comminuted rostral fx of mandibles, lip avulsion, and fx teeth. What were treatment options for the symphyseal separation? What was elected to be performed?
circumferential wiring, composite bridging of mandibular and maxillary canine teeth, Stout or Essig ID/WIR, any combo; surgical repair of symphyseal separation w cerclage wire, lip avulsion repair, XSS 504, 604, 704, 202
According to “Lip avulsion and mandibular symphyseal separation repair in an immature cat” by White, following significant necrotic bone removal, the symphyseal separation was reduced and stabilized w a circumferential wire. What size needle and wire were used? how many twists were left? how often was the cat rechecked and when was the wire removed? what was noted 6mo post injury on radS?
20g needle and 26g wire (bc kitten); 4 twists of wire; 1 week post op to monitor occlusion (304/404 starting to erupt), 2 weeks at which time symphyseal wire was removed (and radiographs), 8 weeks to monitor occlusion (normal), 9.5mo w radiographs to recheck occlusion and development of 304/404; enamel hypoplasia of 304/404, possible class II secondary to lack of mandible, non-traumatic occlusion, partial bony union of mandibular symphysis.
According to “Lip avulsion and mandibular symphyseal separation repair in an immature cat” by White, what was performed at 6 mo recheck to treat new pathology? what is the most common maxillofacial fx in the cat? what is the most common cause? what is the most common cause of maxillofacial fx repair? what are the most common complications of lip avulsion repair? how many dentinal tubules are there /mm squared? what are other tx options that could have been used to hopefully prevent EH from forming?
mandibular symphyseal bony union was non-painful and not affecting QOL or eating so left alone, 4th generation bonding agent (self etching) was used over 304/404 for areas of EH; symphyseal separation; HBC or high rise (regionally dependent), 82%; malocclusion; dehiscence (can use bone tunnels or rotating laps), and secondly infection (need thorough debridement); 30-40K tubules /mm squared; instead of cerclage wire (could have been caused by pressure, trauma from initial injury, iatrogenic while removing necrotic tissue) could use suture, tape muzzle, w no fixation of symphysis just lip repair
According to “Multifocal odontoblastic dysplasia in a dog” by Smithson, Smith, Gamble, a 2y Boerboel dog had an intrinsically stained 204. What were the findings radiographically? Why was an RCT not performed?
Radiographically, there was mineralization within the pulp canal of 204, minor changes in 203, 103, and 104 and very very mild changes in 304, 404; an RCT could not be performed due to the mineralization within the canal that obstructed the Endodontic shaping/filing
According to “Multifocal odontoblastic dysplasia in a dog” by Smithson, Smith, Gamble, 204 was extracted for histopathology. What was the description? what was the clinical diagnosis? what happened to 103, 104, 203, 304, 404?
hist: mineralized dentin in pulp canal, dentinal tubules were observed, but many were randomly oriented, mixture of dysplastic dentin and cementum at tooth root apex, diagnosis from histo was dentinal dysplasia; based on clinical description and comparison in human literature a diagnosis of odontoblastic dysplasia was made; radiographic monitoring as there was mineralization in all pulp canals to some degree but not affecting the vitality of the teeth.
According to “Multifocal odontoblastic dysplasia in a dog” by Smithson, Smith, Gamble, what is osteogenesis imperfecta? dentinogenesis imperfecta?
hereditary dz of bone that can affect dentin causes opalescent teeth, similar to dentinogenesis imperfecta; in deciduous and permanent dentition blue to brown discolored translucent appearance, teeth have bulbous crowns, cervical constriction, thin roots and early obliteration of root canals and pulp chambers (some may have normal sized pulps or pulp enlargement-shell teeth), interlobular calcification;
According to “Multifocal odontoblastic dysplasia in a dog” by Smithson, Smith, Gamble, what is dentin dysplasia type I (a, b, c, d)? type II?
Both are rare inherited autosomal dominant traits, type I more common and have higher incidence of periodical periodontitis; type I: rootless teeth or shortened roots associated w earlier onset of dentin disorganization, DDIa: no root formation or pulp chamber, DDIb: small crescent-shaped pulp that is oriented perpendicular to long axis of tooth and roots only few mm in length, DDIc 2 horizontally oriented present shaped pulp chambers surrounding an island of dentin and shortened root length (longer then DDIb), DDId: visible pulp chambers, normal length root, enlarged pulp stones in central portion of canal create localized bulging of canal and root, constriction of pulp canal apical to stone; DDII: root length normal in both dentitions, deciduous dentition has crowns that are blue to amber to brown to translucent, permanent clinically normal crowns w abnormal large pulp chambers and thistle-tube shape, radiopaque pulp stones form in the large chambers, DO NOT usually develop periapical periodontitis, interlobular dentin adjacent to pulp, DDII PULP STONES anywhere in pulp chamber
According to “Multifocal odontoblastic dysplasia in a dog” by Smithson, Smith, Gamble, why did the authors call this case clinical odontoblastic dysplasia? are there other possible explanations besides this? what cells make tertiary dentin? what type of dentin is deposited slowly over time on the walls of the pulp canal?
human case report revealed histo of pulp chamber and canals filled with tubular dentin, steodentin, irregular, globular trabecular masses of dentin, much like histo fo the dog; trauma– formation of plural dystrophic calcification or reparative dentin; death of original odontoblasts secondary to trauma/other leads to odontoblast-like cells (mesenchymal stem cells) forming a new less tubular and more irregular type of dentin; secondary dentin
According to “The Basics of Saliva” by Eubanks, Woodruff, what are the two main functions of secretory glands (in this case salivary)? what is the function and makeup of mucous?
supply digestive enzymes, provide mucous (a protective lubricant); provides protective barrier, composed of water, electrolytes, and glycoproteins
According to “The Basics of Saliva” by Eubanks, Woodruff, what do serous salivary glands do? what role does the ANS play in salivary production?
less viscous, carry digestive enzymes, hormones, vitamins, and contribute to volume of saliva; regulates it, PNS leads to basal flow rate, and can be increased, SNS causes constriction of blood vessels that supply glands and may decrease secretion, but can also increase it
According to “The Basics of Saliva” by Eubanks, Woodruff, what makes up saliva? what purposes do saliva serve for the teeth and overall oral health?
organic and inorganic substances: minerals, electrolytes, proteins, enzymes, vitamins, low molecular weight compounds, lysosomes, IgG/A, fluoride, etc, concentration relates to plasma levels, hormonal influences, and ANS; reduces tooth solubility, aids in remineralization of tooth surfaces, buffers acids, provides antimicrobial factors, cleanses the mouth
According to “The Basics of Saliva” by Eubanks, Woodruff, what is the pH of human saliva? dog/cat saliva? ruminant saliva? what are the major salivary glands and what do they produce? what are the minor salivary glands?
humans 6.6 (or 6.5 depending on reference, more acidic more prone to caries), dog/cat 7.5, ruminants 8.23 (more alkaline bc of bicarbonate); major: parotid (SEROUS), mandibular (MIXED), sublingual (MUCOUS), zygomatic (SEROUS) (dog/cat), molar salivary (cat, MIXED); lingual, labial, buccal, palatine
According to “The Basics of Saliva” by Eubanks, Woodruff, what is special about ruminant saliva? rat, pig, human or omnivore saliva?
contains bicarb to buffer fore stomach for rumination, may also serve as antifoaming agent within rumen, contents nitrogen, phosphorous, sodium; amylase which converts starch to maltose (IMP)
According to “The Basics of Saliva” by Eubanks, Woodruff, what is the importance of GCF? what is the long junctional epithelium permeable to? what does it contain?
scant when normal periodontium, increased flow when PD, can be byproduct of bacteria or host derived, flushed out sulcus; permeable to albumin, endotoxin, histamine, phenytoin, horseradish peroxidase; normally contains proteins, antibodies, antigens, enzymes and cellular elements
According to “Tooth resorption in the Swedish Eurasian Lynx (Lynx lynx)”by Pettersson, what was the aim of the study and what did they find? what is the dental formula for heel lynx? how had these animals been aged previously?
determine prevalence of TR in Swedish lynx population via oral exam and radiographs post mortem; Found no true TR just ext inflammatory TR which they didn’t count, ~19.5% tooth fractures, 39.1% had supernumerary roots, and 13% had a peg tooth caudal to the mandibular molar (SN tooth); 28 teeth: 2(I3/3, C1/1, P2/2, M1/1); ext of 104 and cementum annuli analysis
According to “Surgery for cervical, sublingual, and pharyngeal mucocele” by Smith, what is a mucocele? What is the most common gland associated? cause? signalment?
accumulation of saliva in SQ tissue and consequent tissue rxn to saliva, non epithelial non secretory lining made up of fibroblasts and capillaries; sublingual is most commonly associated; Suspect trauma, but inability to induce mucocele in dogs indicates possible developmental predisposition; 2-4y GSD and mini poodles
According to “Surgery for cervical, sublingual, and pharyngeal mucocele” by Smith, what portion of the sublingual gland is most commonly the origin of the mucocele? where does it usually form? what are some clinical signs of a sublingual mucocele (ranula)? cervical mucocele? pharyngeal?
rostral portion; forms in the caudal intermandibular area (cervical mucocele most common); blood tinged saliva, poor prehension of food, reluctance to eat; acute, painful swelling from inflammatory response, then intermittently large fluid filled non painful swelling when chronic; respiratory distress and difficulty swallowing secondary to partial obstruction of pharynx
According to “Surgery for cervical, sublingual, and pharyngeal mucocele” by Smith, how are mucoceles diagnosed? What is seen on FNA? what are sialoliths made up of? how do you best determine the origin of a cervical mucocele? what should the surgeon do if no defect is found on the side the gland is being removed?
FNA (paracentesis) and/or sialography (requires GA and catheterization of duct), does not mention CT with contrast in this article; FNA has stringy, blood tinged fluid w low cell numbers; calcium phosphate or calcium carbonate concretions; dorsal recumbency to see which side the swelling locates to (side of origin); obligated to remove the other side;
According to “Surgery for cervical, sublingual, and pharyngeal mucocele” by Smith, what are treatment options for a mucocele? A skin incision is made from the caudal mandible to the jugular v. for removal of mandibular and sungligual salivary glands/ducts, what structures should be identified during blunt dissection? where is the vascular supply to the gland located (mandibular)? why is the mucocele not removed?
surgical removal of gland and duct and intimate association of mandibular and sublingual glands/ducts means removal of both; mandibular LN, maxillary v, linguofacial v, and salivary gland; medial aspect; bc it is much like a caterpillar nest and associated w too many structures, not safe
Abstract: According to “Analysis of immune cells within the healthy oral mucosa of specific pathogen-free cats” by Arzi, Murphy et al, what was the aim of the study? What did they find? What normal structure and where was it located in the oral cavity?
look for immune cell compartments in oral mucous membranes and anatomically related tissue in healthy cats; found T-lymphocyte subsets oral mucosal langerhan’s cells, mast cells and macrophages in different frequencies within the oral cavity, B lymphocytes were ONLY in the tonsils and mandibular lymph nodes; lymphoid aggregates (follicles) at palatoglossal arches and gingiva
Abstract: “Relevance of FCV, FIV, Felv, FHV, and Bartonella henselae in cats with chronic gingivostomatitis” by Berl, Munch et al, what was the point of the this study? What did they find?
look for underlying infectious agents associated w chronic gingivostomatits including FCV, FIV, Felv, FHV, Bartonela henslae in age matched control group and cats with gingivostomatitis, also looked at environmental conditions; FCV RNA significantly higher in cats w gingivostomatitis (54% vs 14%) and a significant difference in antibodies to FCV between FCGS and control cats, no other infectious agents were statistically significant, therefore, FCV is associated w FCGS
Abstract: “Association of Bartonella species, FCV, FHV1 infection w gingivostomatitis in cats” by Dowers, Lappin et al, what was the aim of the study? what were the findings?
look at prevalence of Bartonella, FCV, FHV1 in control and FCGS cats; only FCV RNA was singificantly higher (41%) vs control (0%) suggesting an association btwn FCV and FCGS
Abstract: “Biological behavior of oral and peri oral mast cell tumors in dogs: 44 cases (1996-2006)” by Hillman et al, what was the aim of the restrospective study? What were the findings?
MCT from oral mucosa, mucocutaneous junction or peri oral region of muzzle to look for chemokine receptor type 7 (CCR7) in relation to biologic behavior of tumors; MST for all dogs 52mo, those w LN mets was 14mo, 20/44 had CCR7 which was NOT associated w MST, LN mets, or severity of tumor, presence of LN mets was negative prognostic indicator,
