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80 Cards in this Set
- Front
- Back
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Enamel |
o Covers crown o Produced by ameloblasts before eruption o Hardest substance in body o 1-2 mm thick o all form/there before it erupts, not after |
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Dentin |
§ Found beneath enamel, extend to root tip § Makes up bulk of tooth § Produced by odontoblasts before and aftereruption o Odontoblast- contains calcium and fluoride.Active all the time § Bone-like substance § Fills pulp chamber |
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Types of Dentin |
§ Primary dentin- dentin produced before the toothhas erupted. § Secondary dentin- darker in color- changes withtime § Tertiary dentin- produced when teeth areinjured. To plug up hole- very dark brown § Adult- inside of tooth gets filled with secondary dentin § Lighter in color after eruption |
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Pulp cavity |
§ Found in center of tooth § very big in young animals § Divided into two areas: Pulp chamber, Pulp canal/root canal |
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Pulp canal |
§ Contains odontoblasts, connective tissue, bloodvessels, lymph vessels, nerves § Where it gets its nutrients § Vessels and nerves enter through apical delta(foramen) § Apical foramen- large hole at apex of root. Inyoung animals. Hole get smaller as the animal gets older § Diameter becomes reduced w/ dentin deposition |
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Periodontium |
Supporting tissue structures that surround thetooth |
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Gingiva |
o Protects tooth from trauma caused by chewing Protects the neck of the tooth- gingival connectsto dentin. Very sensitive |
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Gingival margin |
edge of free, nonattached gingiva |
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Gingival sulcus |
space between gingival marginand gingival attachment to tooth |
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Crevicular fluid |
contains antibodies to preventcolonization of bacteria. In the sulcus |
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Cementum |
· Bone-like substance that covers tooth root · Helps to anchor tooth in the bone socket |
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Periodontal ligaments |
o Fibrous structures that insert into attachedgingiva, cementum, and alveolar bone to hold the tooth in place o Fibers are elastic Hold the tooth in the socket. |
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Alveolar bone |
o Forms socket in which tooth sits o Softer than regular bone |
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Coronal |
towards the crown |
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Apical |
towardsthe root/apex of root |
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Buccal Labial |
towards the cheek towards the lips Outside surface or the tooth |
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Palatal/ Lingual |
towards the palate/ towards the tongue |
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Occlusal |
the grinding surface of the tooth. |
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Mesial |
towards the midline of the mouth |
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Distal |
farther from the midline of the mouth |
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Supragingival |
above the gum line |
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Subgingival |
below the gum line |
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Incisorteeth |
· Small, one root · Occlude w/ opposite incisors · Used for nibbling, tearing small pieces oftissue, grooming |
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Canine teeth |
· Large, one root · Override w/ opposite canine · Used to grasp and tear w/ great force |
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Premolars |
· Wide occlusal surface · # of roots vary (1-3) · Interdigitate w/ opposite premolars · Used for tearing food |
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Molars |
· Wide occlusal surfaces · # of roots vary (1-3) |
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Herbivore teeth |
·have broad occlusal surfaces forgrinding food · Herbivore teeth are continuously growing(open-rooted) Teethwear down as animal chews |
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Deciduous teeth Eruption time |
Eruptshortly after birth 2-8wks in puppies 2-6wks in kittens Smallerthan permanent teeth, thinner wall, longer root |
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Deciduousteeth Dental formula |
Dog 2(Di3/3Dc1/1Dp3/3)=28 Cat 2(Di3/3Dc1/1Dp3/2)=26 |
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Permanentteeth eruption |
Eruptat 2-7 months of age in dog Eruptat 3½-6 months of age in cat |
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Permanentteeth Dentalformula |
Dog 2(I3/3C1/1P4/4M2/3)=42 Cat 2(I3/3C1/1P3/2M1/1)=30 |
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Normaldental occlusion in dogs |
Scissorbite of the incisor teeth- upper occludes in front of bottom Interdigitationof canine teeth Interdigitationof premolar teeth Mesiobuccalsurface of lower 1st molar occludes with palatal surface ofmaxillary 4th premolar |
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Anteriorcrossbite |
Commonin dogs Oneor more upper incisors occlude caudal to lower incisors |
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Posterior crossbite |
Mandiblewider than normal at level of carnassialteeth Lowercarnassials occlude buccal to upper ones |
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Malocclusion of canine teeth |
Typicallycaused by the presence of retained deciduous canine teeth when permanentcanines erupt |
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Mandibularprognathism |
Shortenedupper jaw (undershot jaw) Characteristicof brachycephalic dog breeds Overcrowdingof teeth w/ tooth rotation Prematurewearing of tooth surface possible Damageof soft tissues in lower jaw by incisors possible |
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Mandibularbrachygnathism |
Shortenedlower jaw (overshot jaw) Prematurewearing of tooth surfaces possible Damageof soft tissues in oral cavity possible |
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Oligodontia |
have less the normal amount of teeth |
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Polyodontia
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more than the normal number of teeth
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Retaineddeciduous teeth |
Geneticabnormality in small dog breeds Deciduoustooth remains alongside permanent tooth, buccal to it Mustbe extracted to allow permanent tooth to move into its normal position |
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Enamelhypoplasia |
Partialloss of normal enamel Enamelis irregular, pitted, thinner than normal Causedby systemic disturbances during tooth development Abnormalformation of enamel before eruption Malnutrition,fever, heavy parasitism, viral infections- can cause enamel defect at a few monthsold |
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Tetracyclinestaining |
Causedby administration of tetracycline antibiotics to pregnant dam or growinganimals Yellowish discoloration of dentin and enamelspace Yellowdiscoloration of bones too |
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Periodontal Disease |
Diseasecondition characterized by inflammation and destruction of the periodontaltissue that supports the tooth Majorcause of tooth loss in dogs effects85% of dogs and cats over 6 years of age Periodontal disease is caused by plaque build up!! |
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Plaque |
Plaqueis caused by bacterial attachment and reproduction on the tooth’s surface 1.Bacteria attaches to irregular tooth surface or contact points between teeth/gingiva 2. #of bacteria increase to form a visible, soft, creamy layer of semisolidmaterial over tooth 3.Plaque mineralizes to form hard, brown to yellow deposits called calculus (tartar) |
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Gingivitis |
Stage1
Inflammationof the gum tissue around the crowns Causedby bacterial toxins, the immune system’s reaction to the bacteria, and themechanical trauma cause by calculus Clinicalsigns: red gingival margin, edemaof gingival tissue, gingivalbleeding, exudatefrom sulcus, fetidbreath |
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Periodontits |
Stages2-4 Inflammationof subgingival periodontal structures Firstobserved in animals 4-6 yrs. of age Causedby extension of plaque buildup and inflammation begun at gingiva progressivedestruction of periodontal ligaments, cementum, and alveolar bone ensue Resultingdamage may be irreversible |
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Stage 2 |
Up to 25% loss of tooth attachment
Initialperiodontal ligament & bone loss Hyperplasiaand/or recession of gingival tissue Subgingival/Per-iodontal pocket formation span |
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Stage3 |
Upto 50% loss of tooth attachment Moderatebone loss Rootsand furcations may be exposed Periodontalpockets deepen; intrabony pockets may form Teethbecome mobile |
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Stage4
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>50%loss of tooth attachment
Severebone loss Heavytartar build; sometimes with necrotic tissue, blood, pus, fetid breath Teeth often lost or need to be extracted |
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Toothattrition |
wearing down of tooth from use |
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pulpitis |
inflammation of the pulp chamber inside the tooth. When the pulp tissue dies. Itchanged color to a purple grey-ish colored |
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Gingivalhyperplasia |
overgrowth of the gum tissue. Can be genetic or drug induced |
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Epulis |
localizedswelling/growth on the gum. Benign |
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Neoplasia |
malignant cancers: Malignantmelanoma Squamouscell carcinoma Fibrosarcoma |
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Malignantmelanoma |
most common dental cancer in dogs. pigmented |
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Squamous cell carcinoma |
lookslike periodontal disease. Eats away tissue and bone. Most common in cats |
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Fibrosarcoma |
visiblenodule, Isolated to one area of the mouth |
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Gingivostomatitis |
Severeinflammation of the soft tissues in the oral cavity of cats Cat’smouth may be sore/painful Oftenassociated w/ plaque build up Seemsto be the result of a: u Hyperresponsiveimmune system, submucosal inflammatory cells present |
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FelineOdontoclastic Resorptive Lesions (FORL)/cervical line lesions/ neck lesions |
Resorptionof cementum, dentin and enamel byodontoclasts Lesionsoften hidden under gingival tissue or calculus Buccalsurfaces of premolar and molar teeth most often involved Treatedby extraction or crown amputation |
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Wound Healing |
Dynamic process designed to restore tissuecontinuity in an injured area of the body |
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Phases of Wound Healing |
1. Inflammatory/Debridementphase 2. Proliferative/Repairphase 3. Maturationphase |
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Inflammatory/Debridement phase |
Beginsimmediately after injury Initialhemorrhag = vasoconstriction After 5-10 minutes = vasodilation w/ leakage of clotting proteins After6 hours =WBC’s leak into the wound |
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Proliferative/Repair phase |
· Usually starts 3-5 days after the injury · Fibroblasts and new capillaries invade the wound · Granulation tissue formation proliferating pinkish,granular mass of fibroblasts and capillaries · New epithelial cells begin to reproduce at theedge of the wound · At 5-9 days, special fibroblasts in thegranulation tissue pull the wound edges together |
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Maturation phase |
· Begins approximately 4 weeks after the injury · There is remodeling of the fibrous tissue in thescar to increase wound strength |
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Clean wound |
Surgical wounds created under aseptic conditions |
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Clean-contaminated wound |
Minimal contamination; level of contaminationcan be reduced or removed |
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Contaminated wound |
Heavy contamination present- presence of foreignmaterial |
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Infected wound |
Contaminated wounds colonized by bacteriaexhibiting varying degrees of inflammation, pus formation and necrotic tissue |
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Debridement |
o Removal of adhered debris and dead tissue o Can be performed with scalpel/scissors or usinggauze sponge bandages (dry-to-dry or wet-to-dry) |
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Drains |
Surgical implant that provides a channel forfluid or gas to drain from the wound |
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Primary closure |
· The wound is suture closed · Performed on fresh wounds w/ minimal tissuedamage and contamination Clean or clean-contaminated wounds |
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Delayed primary closure |
· Wound remains open for 1-5 days before closure · Performed on moderately contaminated ortraumatized wounds · Closure performed before granulation tissueforms |
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Second-intention wound healing |
· The wound is left open to heal on its own · Old wounds w/ significant tissue damage/loss orvery dirty and contaminated |
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Third-intention wound healing/Secondaryclosure |
· The wound is sutured closed after a bed ofgranulation tissue has formed (5 or more days after initial wound occurred) Used in severely contaminated or traumatizedwounds |
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Factors that affect wound healing |
Host Factors Wound Characteristics Externalfactors |
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Immediate open wound care |
· Cover open wound w/ clean, dry bandage until itcan be treated · Desensitize wound by applying lidocaine-soakedgauze for 1-2 minutes · Clip hair around wound -Keep clipped hair from falling into open wound · Lavage wound with sterile fluid if necessary Scrub wound edges for surgical closure |
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Wound characteristics |
· Foreign material-- increasesthe extent of the inflammatory reaction and inhibits the animal’s immune system · Necrotic tissue-- must be removed from a woundbefore healing can occur Dead space and fluid accumulation-- impair woundhealing and increase risk of infection |
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Indications/reason to spay |
· Sterilization of the female dog or cat · Elimination of estrous cycle · Treatment/Prevention of infections of thereproductive tract · Treatment/Prevention of cancer · Traumatic injuries to uterus |
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Disadvantagesof performing OVH |
can’t reproduce urinary incontinence
Alopeica |
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Postoperativecare |
· Restrict exercise until external sutures areremoved (or 2 wks.) · Keep pet clean and dry · Inspect surgical site daily · Report any abnormalities to the veterinarian |
