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VETERINARY eMAGAZINE BEAT ISSUE 24 APRIL 2025 ANTICONVULSANT
MONITORING
DRUG
DENTAL ORAL PATHOLOGY: FIND IT AND FIX IT
highlights inside
TOP POISONS THAT KILL
UNLOCK THE MYSTERY: DECIDING WHEN TO USE NON-CORE VACCINES Learn about all these fascinating topics and more inside!
QUARTERLY BEAT / APRIL 2024 QUARTERLY BEAT / APRIL 2025
ANTICONVULSANT DRUG MONITORING 04
THAT KILL 06
DISORDERS 10
TOP POISONS
PEDIATRIC DENTAL
DENTAL ORAL PATHOLOGY: FIND IT AND FIX IT 14
UNLOCK THE MYSTERY: DECIDING WHEN TO USE NON-CORE VACCINES 18
MIND MASSAGE 20
TECH TIPS 24
UPCOMING WEBINARS 26
ISSUE 24 – APRIL 2025 beat TABLE OF CONTENTS
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ANTICONVULSANT
MONITORING
DRUG
Wondering when and how to monitor bloodwork for patients on anticonvulsant therapy? We’ve got you covered! In this VETgirl article, Dr. Missy Carpentier, DACVIM (Neurology) provides a comprehensive review of best practices for anticonvulsant therapy bloodwork monitoring. Read on to refresh your knowledge of what to test for and when for these common anticonvulsants!
Missy Carpentier, DVM, DACVIM (Neurology) Minnesota Veterinary Neurology, Columbus, MN Your epileptic patient just left the hospital, you have your anti-seizure medications prescribed, and you are feeling pretty good. Then you remember, you didn’t set up an appointment for the follow up blood work that is needed. But what blood work is needed, when is it needed, and is it necessary? Read along to find out! The ultimate goal for every epileptic patient is good seizure control with a good quality of life. We do our best to control the frequency, duration and severity of seizures with anticonvulsant medications. Currently, the most commonly prescribed anticonvulsant medications are phenobarbital, potassium bromide, levetiracetam (regular and extended release), zonisamide, and pregabalin. I have included a chart below that will help you determine when you should be collecting drug blood concentrations and if any other blood work is recommended. It should be noted that regardless of what medication a patient is receiving, I always recommend a yearly CBC and chemistry profile. Each and every patient needs to be looked at individually and it is important to recognize that despite what the number is that you receive on your drug
blood concentration, you need to correlate it to the patient. How are BOTH the patient and the owner handling the side effects of the medication, how is their seizure control, etc. Values for one patient may work great and for another the side effects may be significantly affecting their quality of life, and therefore adjustments need to be made. It is also important to recognize that the “therapeutic range” of a drug is just that, a range. A value in the therapeutic range doesn’t mean that you still cannot increase or decrease the dose of the medication, and it also doesn’t mean that you have maximized the potential of that drug. The chart to the right will help you with monitoring the drug blood levels of your patients and any other necessary blood work that is recommended. Remember, seizure management is an art and no two patients are alike!
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ANTICONVULSANT MEDICATION
DRUG BLOOD LEVEL
THERAPEUTIC LEVEL
· 2-3 weeks after initiating treatment, along with a CBC and liver profile · 2-3 weeks after any dose change · Long term q6 months with alternating q6m with a liver profile vs a full CBC and chemistry · Sampling time: ◦ Trough sample suggested, however, comparing samples from the same or very similar sample collection times is most important ◦ Peak and trough samples necessary only for animals in which a shorter half-life is expected and therefore a shorter dosing interval may be necessary to maintain appropriate drug concentrations throughout the dosing interval · “Steady-state” never truly occurs for dogs and may not in cats, because the drug DOES NOT accumulate with each dose. As such, testing can actually be quite complicated, because there is a large degree of fluctuation of the drug concentration during the dosing interval · Sampling time: ◦ Recommend a peak and trough when levetiracetam is started so you can determine your patient’s half-life · 2 weeks after starting or discontinuing phenobarbital as phenobarbital decreases the half-life of levetiracetam · I personally do not commonly evaluate these levels due to the large degree of fluctuation, cost, and safety margin of levetiracetam
· Canine: 20-40 mcg/ml · Recommend using a high end of 35 mcg/ml in most patients, though some refractory cases may need to go as high as 40 mcg/ml · Feline: 10-20 mcg/ml
Phenobarbital
· Canine and Feline: 5-45 mcg/ml
Levetiracetam
· 2.5-3 MONTHS after starting · 2-3 months after any dose change · 2-3 months after a diet change · Long term q6-12 months · Sampling time: ◦ Any time during the dosing interval
· Canine ONLY: · 1-3 mg/ml (monotherapy) · 1.5-2 mg/ml (in use with phenobarbital)
Potassium Bromide
· 2 weeks after treatment initiation, along with a liver profile · 2 weeks after any dose change · 2 weeks after starting or discontinuing phenobarbital as phenobarbital decreases the half-life of zonisamide · Long term q6-12 months · Sampling time: ◦ Trough sample suggested, however, comparing samples from the same or very similar sample collection times is most important ◦ Peak and trough samples necessary only for animals in which a shorter half-life is expected and therefore a shorter dosing interval may be necessary to maintain appropriate drug concentrations throughout the dosing interval
· Canine: 10-40 mcg/ml · Feline: 10-40 mcg/ml
Zonisamide
Pregabalin
· Clinical testing not currently available
· Canine and Feline: 2-5 mcg/ml
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TOP POISONS THAT KILL Each year, the ASPCA Animal Poison Control Center manages hundreds of thousands of poisoning calls. The majority of toxicants affecting dogs and cats do not kill acutely 1 – it takes several days before end-stage effects from toxicosis occur (e.g., anuric renal failure, acute hepatic necrosis, etc.). Likewise, only a smaller percentage of toxicants result in acute death. 1 In this lecture, we will review the mechanism of toxicosis, clinical signs, and overall treatment of the deadly and most unusual drug overdoses seen in dogs and cats. The reader is advised to contact the ASPCA Animal Poison Control Center (888-426-4435) for lifesaving, 24/7 advice as needed. Justine Lee, DVM, DACVECC, DABT Director of Medicine, VETgirl ISONIAZID: Isoniazid (commonly known as INH) is a human medication used for tuberculosis. While it is used in veterinary medicine to treat Mycobacterium or Actinomyces, it has a narrow margin of safety in dogs and cats. 2,3 This drug works by blocking the synthesis of mycolic acid. INH depletes the CNS of pyridoxine and also decreases levels of GABA within the brain. Many assume that since this is an “antibiotic” that it is safe; however, when accidentally ingested in dogs (and rarely, cats), it can result in severe CNS signs (e.g., tremors, refractory seizures, coma, death). The LD50 in dogs is estimated to be as low as 50 mg/kg; 2,3 at this same dose, seizures can be seen. One 300 mg tablet can result in severe poisoning in a 10-pound dog. Other clinical signs include GI signs (e.g., hypersalivating, vomiting, diarrhea), acid-base disturbances (e.g., metabolic acidosis), hyperthermia (secondary to tremors or seizures), and organ injury (e.g., hepatic injury, acute kidney injury, etc.). Due to the rapid onset of clinical signs, it is often too late to decontaminate the patient. Gastric lavage under anesthesia may be necessary. Treatment also includes IV fluids, antiemetics, anticonvulsants, muscle relaxants, supportive care, and the antidote pyridoxine hydrochloride (typically available as 100 mg/ml) (Dose: suggested dose of 71 mg/kg IV, diluted to 5-10%, slow over 30-60 minutes). 2,3 Clinicopathologic monitoring should include a biochemistry panel and recheck hepatic panel 3-5 days later. 5-FLUOROURACIL (5-FU): The most life-threatening topical toxin to dogs and cats is 5-fluorouracil (5- FU). 5-FU, commonly known by the brand names Efudex®, Carac®, Adrucil®,
and Fluoroplex®, is a prescription anti-neoplastic medication that is often used for treatment of actinic keratosis or superficial basal cell carcinoma in humans. It is commonly sold in low concentration products (e.g., 0.5-5%), and works by inhibiting DNA and RNA synthesis and production, resulting in programmed cell death. 4-7 While IV administration of 5-FU is occasionally used as a chemotherapeutic agent in dogs (e.g., for mammary gland tumor, etc.), it is not recommended for use in cats. Decades ago, topical 5-FU was used in cats for the treatment of squamous cell carcinoma; however, it resulted in severe toxicosis and death due to its narrow margin of safety. Clinical signs of 5-FU toxicosis can often be seen within 30 minutes up to 6 hours; death has been reported as early as 7 hours. 4-7 Clinical signs include acute GI signs (e.g., hypersalivation, anorexia, vomiting, abdominal pain, diarrhea, bloody diarrhea, etc.), CNS signs (e.g., ataxia, tremors, seizures), and bone marrow suppression (e.g., anemia, leukopenia, thrombocytopenia). 4-7 The lowest reported toxic (oral) dose in dogs is 6 mg/ kg, while the minimal reported lethal dose is 20 mg/kg. One case report did have a dog survive ingestion of 46 mg/kg of 5-FU. 4-7 That said, the prognosis with 5-FU toxicosis is typically grave in cats and guarded in dogs (with a reported survival in dogs of approximately 25%). Death typically occurs due to secondary complications from the 5-FU such as sepsis (due to leukopenia), increased intracranial pressure (due to persistent seizures), intracranial hemorrhage (due to severe thrombocytopenia), or DIC (due to severe seizures). Unfortunately, most patients present with severe clinical signs, where it is too late to perform decontamination. Therefore, treatment should be aimed at symptomatic supportive care, anti-convulsant therapy, anti-emetics, anti-diarrheals, IV fluids (to help maintain perfusion), thermoregulation, broad-spectrum antibiotics, clinicopathologic monitoring, and symptomatic supportive care. If the patient is able to survive the acute In this VETgirl Webinar “Top Poisons That Kill” on December 18, 2024, Dr. Justine Lee, DACVECC, DABT reviews the top 5 poisons that have a high fatality rate, including isoniazid, 5-FU, ethylene glycol, organophosphates/carbamates, and bifenthrin. If you see any of these, you want to read on to make sure you’re aware of these top poisoning fatalities! In case you missed the webinar, watch it again HERE or read the cliff notes below!
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crisis, clinicopathologic monitoring is necessary every 3-4 days thereafter for 2-3 weeks, until bone marrow function returns to normal. 4-7
false positives for EG may be from other drugs such as propylene glycol, sorbitol, mannitol, alcohol, etc. Treatment for EG toxicosis includes antidote therapy, aggressive IV fluid therapy, monitoring urine output and clinicopathologic parameters, anti- emetic therapy, and symptomatic supportive care. The antidote, fomepizole (also known as 4-MP), is expensive but lifesaving when administered to dogs within the first 8-12 hours of ingestion. In cats, the antidote must be administered within 3 hours of ingestion to be effective. 8-9 Dosing for 4-MP is significantly different between dogs and cats. For dogs, the dose of 4-MP is: 20 mg/kg, IV, first dose; 15 mg/kg at 12 hours; 15 mg/kg at 24 hours; 5 mg/ kg at 36 hours. For cats, the dose of 4-MP is: 125 mg/kg, IV, first dose; 31.25 mg/kg IV at 12 hours; 31.25 mg/kg IV at 24 hours; 31.25 mg/kg at 36 hours. Ethanol can also be used as an antidote if fomepizole is not available, as it competes with alcohol dehydrogenase, thereby preventing metabolism of EG into its more toxic metabolites. A 7% of ethanol is made by removing 175 ml from a 1L bag of saline and adding 175 ml of an 80-proof vodka. If 190 proof grain alcohol is available, a 7% solution can be made by removing 74ml from a 1L bag of saline and adding 74 ml of the grain alcohol. Remember to use only “clear” alcohols on patients (e.g., grain alcohol, vodka, etc.). The dose of ethanol in dogs and cats is a loading dose of 8.6 ml/kg (600 mg/kg) 7% ethanol slow IV then continue with a CRI of 1.43 ml/kg/hr (100 mg/kg/hour) IV as a CRI for 24-36 hours. Regardless, antidote therapy must be started immediately to ensure good outcome. Once a patient has already developed azotemia, the prognosis is generally poor to grave without hemodialysis. EG toxicosis should be suspected in any patient with unexplained neurologic signs, metabolic acidosis or an elevated anion gap ((Na+ + K+) – (Bicarb + Cl-) >25). Any combination of these signs should prompt the administration of an EG blood test. The detection of calcium monohydrate oxalate crystalluria is virtually diagnostic for EG toxicosis. Be aware that ethylene glycol testing is only accurate within approximately the first 24 hours, as false negatives may be found thereafter due to complete metabolism of the EG to its more toxic metabolites. On veterinary specific EG tests, rare false positives for EG may be from other drugs such as propylene glycol, sorbitol, mannitol, alcohol, etc. ORGANOPHOSPHATES/CARBAMATES: Thankfully, carbamates and OPs are rarely seen now; the acutely seizing patient is rarely a result of this toxicosis nowadays. That’s likely a result of the Environmental Protection Agency (EPA) removing many of these dangerous insecticides off the market (replacing them with pyrethrins and pyrethroids instead). However, some products (particularly rose or plant fertilizer/insecticide combination products, cattle ear tags, etc.) still exist. 10-11 Add to the fact that gardeners often mix these dangerous chemicals with additional bone or blood meal (which is highly palatable to pets), thus resulting in increased ingestion of the toxin. Carbamates and OPs work by competitively inhibiting acetylcholinesterase and pseudocholinesterase (e.g., the enzymes that breaks down acetylcholine), which prevents
ETHYLENE GLYCOL (EG): Accidental or malicious poisoning with ethylene glycol (EG) is common, as the public is generally well aware of its toxic nature. Sources of EG include automotive antifreeze (radiator coolant, which typically contains 95% EG), windshield deicing agents, motor oils, hydraulic brake fluid, developer solutions, paints, solvents, etc. 8,9 As little as 4.4 ml/kg can result in severe acute kidney injury (AKI) in canine patients, while as little as 1.4 ml/kg can result in AKI in feline patients (based on high concentration EG products). 8,9 Ethylene glycol is metabolized by the body to highly poisonous metabolites (including glycoaldehyde, glycolic acid, and oxalic acid), which lead to severe AKI secondary to development of calcium oxalate crystalluria. 8,9
THREE STAGES OF ETHYLENE GLYCOL POISONING STAGE 1: This occurs within 30 minutes to 12 hours
and looks similar to alcohol poisoning. Signs of ataxia, hypersalivating, vomiting, seizuring, and polyuria/polydipsia are seen. 8,9
STAGE 2: This occurs within 12-24 hours post- exposure, 8 and clinical signs seem to
“resolve” to the pet owner; however, during this time frame, severe internal injury is still
occurring. Signs of ataxia may seem to improve during this stage, but signs of dehydration, tachycardia, and tachypnea may be seen. STAGE 3: In cats, this stage occurs 12-24 hours after
ethylene glycol exposure. 8,9 In dogs, this stage occurs 36-72 hours post-ingestion. 8 During this stage, severe AKI occurs secondary to calcium oxalate crystalluria. Severe anorexia, depression, hypersalivation, uremic halitosis, coma, vomiting, and seizures may be seen.
Any patient suspected of EG toxicosis should have an EG blood test, venous blood gas, and urinalysis performed. Evidence of a positive EG test, metabolic acidosis, elevated anion gap, and presence of calcium oxalate crystalluria is consistent with EG toxicosis, and prompt therapy is indicated. Be aware that EG testing is only accurate within approximately the first 24 hours, as false negatives may be found thereafter due to complete metabolism of the EG to its more toxic metabolites. With EG testing, keep in mind that the toxic metabolites of EG are not typically detected on routine EG testing – only ethylene glycol itself. On veterinary specific EG tests, rare
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the breakdown of acetylcholine (AcH), resulting in too much AcH and stimulation of sympathetic, parasympathetic, and peripheral nervous systems. This results in AcH accumulation at nerve junctions, resulting in severe clinical “SLUDGE” signs (e.g., salivation, lacrimation, urination, defecation, gastrointestinal). Some carbamates and OPs have various levels of toxicosis (e.g., ranging from low to very high), depending on the active ingredient. Clinical signs can be seen as early as 30-60 minutes, and typically are seen within 6 hours (but rarely seen > 12 hours). By the time patients present to the veterinary clinic, it is typically too late to decontaminate safely. Clinical signs include severe GI signs (e.g., hypersalivation, vomiting, diarrhea), cardiovascular signs (e.g., tachycardia, bradycardia, pallor, shock), CNS signs (e.g., agitation, sedation, mydriasis or miosis, tremors, seizures, coma), and respiratory signs (e.g., tachypnea, dyspnea, hypoxemia). Death may occur due to fluid accumulation with the bronchi, or secondary to disseminated intravascular coagulation (DIC) secondary to hyperthermia from tremors and seizure activity. Very rarely, intermediate syndrome can be seen with OP toxicosis, where clinical signs are seen > 24-72 hours after onset of acute signs; these signs can last up to 7-14 days and include signs of neuromuscular weakness, ventroflexion of the neck, cranial nerve deficits, and even death from respiratory depression and hypoventilation. 10-11 Treatment includes aggressive decontamination (e.g., gastric lavage with an inflated endotracheal tube, administration of activated charcoal with a cathartic), fluid therapy, anti-emetics (e.g., maropitant), muscle relaxants (e.g., methocarbamol), anticonvulsants (e.g., phenobarbital, diazepam, levetiracetam, etc.), thermoregulation, electrocardiogram, blood pressure monitoring, and symptomatic supportive care. Most importantly, aggressive use of the antidote atropine or 2-PAM (which is rarely available from human medical facilities) is warranted. Atropine, an anticholinergic, blocks the neurotransmitter acetylcholine in the central and peripheral nervous systems. Atropine competes with AcH at the post-ganglionic parasympathetic sites (and hence is called an antiparasympathetic or parasympatholytic drug). 10-11 It is also called an antimuscarinic as it antagonizes the muscarine-like actions of AcH. 10-11 It is used for the treatment of SLUDGE signs from organophosphate or carbamate toxicity. With OP toxicosis, atropine should be given despite the tachycardiac; higher doses are often necessary. Doses for atropine are higher than anesthetic doses for bradycardia and range from 0.1-0.5 mg/kg IV or IM as needed. BIFENTHRIN: Bifenthrin is a synthetic derivative of pyrethroids and is commonly found in household insect sprays and insecticides (e.g., permethrin, cypermethrin, cyphenothrin, etc.). Bifenthrin in dogs causes the same clinical signs as permethrin in cats and can be quite profound as compared to other pyrethrins/pyrethroids; rarely, it can result in fatality. 12 Due to a cat’s altered liver glucuronidation metabolism, cats are significantly more sensitive to pyrethrins than dogs. While a precise toxic dose for cats is not well established, products containing greater than a 5-10% concentration of pyrethrins may lead to systemic toxicosis. The diluted amount found in household insect sprays and topical flea sprays and shampoos is typically < 1%. Toxicosis from exposure to these products is highly unlikely. The application of canine spot-on pyrethrin/pyrethroid based insecticides (typically ~40-50% concentration) to cats is the primary cause of feline pyrethrin toxicosis. Cats that groom dogs following recent spot-on applications are also at high risk for toxicosis; ideally, pets should be
separated until the spot-on product has completely dried on the dog to prevent cat exposure. Signs of systemic toxicosis of pyrethroid toxicosis in cats include GI signs (e.g., hypersalivation, vomiting, nausea), CNS signs (e.g., disorientation, weakness, hyperexcitability, tremors, seizures) and respiratory signs (e.g., tachypnea, dyspnea). Tremors are extremely responsive to methocarbamol (22-220 mg/kg IV PRN to effect), a centrally acting muscle relaxant, although oral absorption of methocarbamol is often slower in onset of action. In general, tremors are less responsive to benzodiazepines (e.g., diazepam). Seizures may be controlled with anticonvulsants (phenobarbital, 4-16 mg/ kg IV PRN to effect) or general gas anesthesia. Dermal decontamination is crucial but should be performed after stabilization. This should be performed with a liquid dish detergent (e.g., Dawn, Palmolive) or follicular flushing shampoo. Supportive care including the monitoring and maintenance of hydration, body temperature and blood glucose levels are necessary. Signs may persist for 1-4 days, depending on the animal. The prognosis is excellent with aggressive dermal decontamination and treatment. CONCLUSION: Pet owners should be appropriately educated on how to pet-proof the house and be trained on what common human medications can be toxic to pets. Pet owners should also be appropriately educated on crate training to help minimize toxin exposure. When in doubt, the ASPCA Animal Poison Control Center should be consulted for toxic ingestions that veterinarians are unaware of.
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REFERENCES
1. Swirski AL, Pearl DL, Berke O, O’Sullivan TL. Companion animal exposures to potentially poisonous substances reported to a national poison control center in the United States in 2015 through 2014. J Am Vet Med Assoc 2020;257(5):517-530. 2. Villar D, Knight MK, Holding J, et al. Treatment of acute isoniazid overdose in dogs. Vet Hum Toxicol 1995;37(5):473-7. 3. Schmid DR, Lee JA, Wismer TA, et al. Isoniazid toxicosis in dogs: 137 cases (2004-2014). J Am Vet Med Assoc 2017;251(6). 4. Powell LL. 5-Fluorouracil. The Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, IO: Wiley-Blackwell. pp. 164-169. 5. Dorman DC, Coddington KA, Richardson RC. 5-Fluorouracil toxicosis in the dog. J Vet Intern Med 1990;4:254-257. 6. Sayre RS, Barr JW, Bailey EM. Accidental and experimentally induced 5-fluorouracil toxicity in dogs. J Vet Emerg Crit Care 2012;22:545-549. 7. Friedenberg SC, Brooks AC, Monnig AA, Cooper ES. Successful treatment of a dog with massive 5-fluorouracil toxicosis. J Vet Emerg Crit Care 2013;23:643-647. 8. Khan SA, Schell MM, Trammel HL, et al. Ethylene glycol exposures managed by the ASPCA National Animal Poison Control Center from July 1995 to December 1997. Vet Hum Toxico l 1999;41:403-406. 9. Grauer GF, Thrall MA, Henre BA, Hjelle JJ. Comparison of the effects of ethanol and 4-methylpyrazole on the pharmacokinetics and toxicity of ethylene glycol in the dog. Toxicol Lett 1987;35(2-3):307-14. 10. Klainbart S, Grabernik M, Kelmer E, et al. Clinical manifestations, laboratory findings, treatment and outcome of acute organophosphate or carbamate in toxication in 102 dogs: A retrospective study. Vet J 2019;251: doi: 10.1016/j.tvjl.2019.105349. Epub 2019 Jul 31. 11. Askoan VR, Kerl ME, Evans T, Harmon M. Organophosphate intoxication in 2 dogs from ingestion of cattle ear tags. J Vet Emerg Crit Care 2019;4:424-430. 12. Buchweitz JP, Mader D, Lehner AF. Bifenthrin fatality in a canine: A case report with postmortem concentrations. J Anal Toxicol 2019; 43(1):72-78.
IMPORTANT NOTE: WHEN IN DOUBT, ALL DRUG DOSAGES SHOULD BE CONFIRMED AND CROSS- REFERENCED WITH A REFERENCE VETERINARY DRUG GUIDE.
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PEDIATRIC DENTAL DISORDERS
Michael Balke, DVM, FAVD, DAVDC Arizona Veterinary Dental Specialists, Gilbert, AZ Understanding the nuances of canine and feline pediatric dentition is crucial for identifying and managing dental conditions during the first year of life. This article offers a concise overview of normal pediatric dental development and highlights common abnormalities that general practitioners may encounter. While not exhaustive, it aims to provide a solid foundation in veterinary pediatric dentistry, with a focus on diagnostic approaches and treatment options to support optimal oral health in young patients. EXAMINATION: Every patient, whether young or old, should have a complete oral examination performed at each visit. This can prove challenging in the young patient that resists oral manipulation. A systematic approach should be employed to look at the lips, dentition, palate and soft tissues. In order to recognize abnormalities, one must first know what is normal. The following are the normal dental formulas for the dog and cat, eruptions times and normal/abnormal occlusion classes:.
In this VETgirl Webinar “Pediatric Dental Disorders” presented live on February 5, 2025, Dr. Michael Balke reviews the normals and abnormals of pediatric dentistry! In case you missed the webinar, check it out HERE or take a look at the cliff notes below!
APPROXIMATE ERUPTION TIMES* (WIGGS AND LOBPRISE)
DOG
PRIMARY (WEEKS)
ADULT (MONTHS)
Incisors
3–5
3–5
Canines
3–6
3.5–6
Premolars
4–10
3.5–6
Molars
N/A
3.5–7
PRIMARY DOG DENTAL FORMULA
CAT
PRIMARY (WEEKS)
ADULT (MONTHS)
2 x (i 3/3, c 1/1, p 3/3) = 28
Incisors
3–5
3–5
SECONDARY (ADULT) DOG DENTAL FORMULA
Canines
2 x (I 3/3, C 1/1, P 4/4, M 2/3) = 42
3–6
3.5–6
Premolars
4–10
3.5–6
PRIMARY FELINE DENTAL FORMULA
Molars
N/A
3.5–7
2 x (i 3/3, c 1/1, p 3/2) = 26
* Eruption times can be quite varied based on size of the breed and characteristics within the breed (ex. Tibetan terriers are slow to lose primary teeth). OCCLUSION CLASSES: Occlusion is defined as the contact of the maxillary teeth with those in the mandible. Occlusion may be classified into three general categories: deciduous only, mixed (deciduous and permanent), and permanent only.
SECONDARY (ADULT) FELINE DENTAL FORMULA
2 x (I 3/3, C 1/1, P 3/2, M 1/1) = 30
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FRACTURED DECIDUOUS TEETH: Deciduous teeth can be more prone to fracture than the adult teeth because of their fragile structure. If pulp exposure occurs in a deciduous tooth, it is painful and will become infected. The adult tooth is forming at the apex of the deciduous tooth therefore infection/inflammation can lead to developmental defects such as enamel defects of the adult tooth. When a fractured deciduous tooth is noted, extraction should be performed as soon as possible. MALOCCLUSIONS: Discovering a discrepancy in jaw length in a puppy or kitten is not uncommon as the jaws grow independent of one another. If there is no abnormal tooth- on-tooth or tooth-on-soft tissue contact, then the occlusion can be monitored. If the occlusion is resulting in trauma to the dental tissues then treatment needs to be performed. A common malocclusion noted in puppies is a class II occlusion which results in the mandibular canine teeth traumatizing the palatal mucosa (Fig. 2). This can lead to pain, infection, inhibit mandibular growth and affect the developing adult dentition. Extraction of the teeth causing trauma is recommended as soon as the condition is noted. The owners should be educated that further orthodontic treatment of the adult dentition may be required if it also leads to a traumatic occlusion.
CLASS 0: Normal or orthoclusion CLASS I: A normal rostrocaudal relationship of the maxillary and mandibular dental arches with malposition of one or more individual teeth (e.g., base narrow mandibular canines with otherwise normal occlusion). CLASS II: An abnormal rostrocaudal relationship
between the dental arches in which the mandibular arch occludes caudal to its normal position relative to the maxillary arch.
CLASS III: An abnormal rostralcaudal relationship between the dental arches in which the mandibular arch occludes rostral to its
normal position relative to the maxillary arch.
CLASS IV: Asymmetry in a rostrocaudal, side-to-side, or dorsoventral direction. The expression "wry bite" is a layman term that has been used to describe a wide variety of unilateral occlusal abnormalities. Because "wry bite" is non-specific, its use is not recommended.
PERSISTENT DECIDUOUS TEETH: Persistent deciduous teeth occur when there are 2 teeth in the same spot at the same time (Fig. 1). The rule of dental succession is: “No two teeth should occupy the same space at the same time.” When deciduous teeth are persistent, it can lead to malocclusion and increased susceptibility to periodontal disease. Treatment should be performed as soon as the condition is diagnosed to avoid long-term issues. Removing deciduous teeth can be a tedious task that involves patience, surgical extraction, intraoral radiographs, an understanding of the developing oral anatomy, and pain control. The whole tooth needs to be removed; if root fragments are left, they could cause infection, pain, and misalignment of the adult dentition. Care must be taken to avoid damaging the adult tooth during extraction.
Figure 2. Class II Malocclusion in a young dog that is causing right mandibular deciduous canine to occlude into the palatal tissue adjacent to the right maxillary canine deciduous tooth. Image courtesy of Dr. Michael Balke, DAVDC.
CROWDED TEETH: All dogs, no matter what size, are supposed to have 42 teeth. In small, toy, and brachycephalic breeds, there is often not enough room for all the teeth, and crowding can occur. The tooth should have gingival tissue completely surrounding it. When teeth are crowded, the gingiva cannot attach effectively, resulting in pocket formation, trapping of debris, and a predilection for periodontal disease. It is often recommended to extract the smaller, less significant tooth in these situations to prevent advanced periodontal disease in the future.
HIGHLIGHTS
WEBINAR
Figure 1. Persistent deciduous maxillary canine behind an adult maxillary canine in a dog. Note the foreign material caught between the teeth that can lead to periodontal disease. Image courtesy of Dr. Michael Balke, DAVCD.
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MISSING TEETH: It is not uncommon in smaller breeds that certain teeth may be genetically missing, which can help prevent crowding and long-term periodontal issues. To truly know if a tooth is missing or is present and has not erupted, intraoral radiographs must be performed. The most common problem with unerupted teeth is the formation of a dentigerous cyst (Fig. 3). They are seen radiographically as a distinct radiolucent area surrounding the impacted tooth. They are caused by a dilation of the follicular space around the impacted crown and can become very invasive as they expand, resulting in bone destruction. Treatment requires complete removal of the cystic lining. In advanced cases, there is an increased risk of jaw fracture. The key to successful treatment is early diagnosis and treatment.
JUVENILE GINGIVITIS/PERIODONTITIS IN KITTENS: This condition is a pronounced inflammation of the gingiva in kittens typically first noticed between 7-10 months of age. It is thought to be due to over- exaggerated tooth eruption inflammation. Often, the condition can persist for up to two years. In some aggressive cases, periodontitis can occur in which alveolar bone is lost and extractions are required. These cats require professional periodontal therapy at least every 6 months and consistent daily home care. There is often hyperplastic gingival tissue that requires gingivectomy to bring the gingival margin to a normal height. I have seen some of these cases progress to stomatitis and require full mouth extractions. ENAMEL HYPOPLASIA: Enamel formation occurs in dogs between 2 weeks and 3 months of age. Trauma during enamel development is a common cause of enamel defects in dogs. However, in general, a history of oral trauma is nonexistent but, occasionally, can be traced to altercations with other pets or accidental drops, falls, etc. The result is generally seen in one or several teeth in a regional distribution. A febrile event that occurred during enamel development may be responsible for cases in which most or all of the dentition is affected. Systemic insults that may result in enamel defects include nutritional deficiencies, infection, fever, metabolic abnormalities, toxins, and parasites. Distemper viral infections and other morbillivirus species infections are classically recognized as causes of enamel hypoplasia or hypocalcification. Concurrent alterations in the dentin formation in teeth with enamel defects may result in root abnormalities. Treatment consists of smoothing the tooth surface and placing a bonding agent to prevent pain and infection of the tooth. Recognizing the differences between pediatric and adult dentition in canine and feline patients is vital for effective dental care. Early and thorough oral examinations, paired with a systematic approach to diagnosis, are critical to identify abnormalities and initiate timely interventions. Whether addressing malocclusions, persistent deciduous teeth, fractures, or congenital issues, such as cleft palates, proactive care during the first year of life can prevent long-term complications and ensure optimal oral health. By staying informed and employing best practices in pediatric dentistry, veterinarians can enhance the quality of life for their young patients while fostering strong, trusting relationships with pet owners.
Figure 3. Intraoral radiograph of right mandible in a dog with an unerupted first mandibular premolar (arrow) that has resulted in a dentigerous cyst (circle). Image courtesy of Dr. Michael Balke, DAVDC. CLEFT PALATES: The palate, both hard and soft, separates the oral cavity from the nasal cavity. Non-traumatic clefts are failures in development of the face and palate(Fig.4). Clefts can be unilateral or bilateral. Primary clefts are cleft lips and are formed along the incisive suture lines. Secondary clefts are a failure of the medially extending palatine shelves to meet on the midline with the ventrally projecting nasal septum. Most clefts will require surgical repair. Treatment should ideally be delayed until the animal is 4-6 months of age. This may require tube feeding by the owner to prevent aspiration pneumonia. These surgeries can be challenging, and dehiscence is not an uncommon complication that often requires multiple surgeries.
HIGHLIGHTS
WEBINAR
Figure 4. Secondary cleft palate in a six month old cat. Image courtesy of Dr. Michael Balke, DAVDC.
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REC
DENTAL ORAL PATHOLOGY: FIND IT AND FIX IT
Stefanie Perry, CVT, VTS (Dentistry) VetNerd Dentistry Training LLC, Scottsdale, Arizona Taking care of an animal’s oral health is about more than just keeping their teeth clean - it’s essential to their overall well-being. Dental oral pathology can impact everything from eating habits to comfort and quality of life, making it vital to identify and address issues early. This article outlines a systematic approach to canine and feline dental exams, including standardized nomenclature, charting practices, and common oral pathologies. By maintaining consistent documentation and a solid understanding of these conditions, veterinary teams can effectively diagnose and treat problems, ensuring pets remain healthy and happy.
In this VETgirl Webinar “Dental Oral Pathology: Find It and Fix It” presented live on February 26, 2025, Stefanie Perry, CVT, VTS (Dentistry) takes us through the systematic approach to canine and feline dental exams and reviews ‘normals’ and ‘abnormals’ of the canine and feline oral examination! In case you missed the webinar, check it out HERE or take a look at the cliff notes below! Performing the intraoral exam in dorsal recumbency is helpful to make all tissues visible at once, eliminating the need to rotate the patient and interrupt heat support and anesthesia monitoring. If it’s preferred to examine one side at a time, the head and shoulders can be rotated in dorsal recumbency after briefly removing the anesthesia circuit. Follow the modified Triadan system by beginning in the right maxillary quadrant (100) then counterclockwise (to the patient) onto the left maxillary (200), left mandibular (300), and right mandibular (400) quadrant CROWN TO APEX Each tooth can be considered an individual patient therefore each gets an individual exam. Examining each tooth should be uniform to avoid missing pathology and provide speed and accuracy. • Briefly check the number of teeth in each arch to account for missing or extra teeth. • Assess mobility first using the probe to manipulate the tooth. • Begin with the crown and the condition of the enamel, i.e., fractures/abrasion/attrition/defects. • Move to gingival margin/mucogingival line to assess gingivitis, gingival recession, periodontal pockets, etc. PROBING TECHNIQUE There are several types/styles of periodontal probes, which are graded to measure the depth of the sulcus in millimeters. They most often have an explorer/shepherd’s hook at the opposite end of the instrument handle. The explorer is very sharp and used to assess the hard tissues only. Probing is a gentle process to avoid traumatizing the gingiva and underlying tissue. Aggressive probing can inadvertently create a deeper pocket
Abbreviations used here are based on the American Veterinary Dental College (AVDC) nomenclature/ abbreviations, or common shorthand. Many are shortened to a simpler acronym from the AVDC- established abbreviations. Unique abbreviations are acceptable if they are defined within the medical record and are utilized consistently among all team members. Always include a key in the dental chart that defines any terms or abbreviations used in the document.
POSITION AND APPROACH The exam begins during anesthetic induction with an assessment of the occlusion before the endotracheal tube is placed. The occlusion cannot be fully examined once the tube prevents the mouth from closing. As the patient is intubated, this is also the ideal time to see the caudal area of the mouth, tonsils, epiglottis, etc.
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or penetrate the nasal cavity in a very small patient. Apply a stair-step technique when measuring periodontal pockets; advance gently every few millimeters 360 degrees around each tooth. Sweeping the probe along the gumline can miss a focally deep pocket. By probing on every side of each tooth, pockets are measured as well as assessing any furcation exposure. Keep in mind that teeth with three roots have more than one furcation to assess. The deepest pocket is recorded on the dental chart diagram representing its actual location for future exams. Pockets of normal anatomical depth do not need to be charted. NORMAL SULCUS DEPTH • Dogs: up to 3mm, with some normal variation in very large dog breeds (i.e., a 4mm pocket of the maxillary canine in a Great Dane may be considered normal in the absence of gingivitis) • Cats: 0.5 to 1mm DIRECTIONAL TERMS • Rostral: near the front of the face • Caudal: toward the back of the mouth
completely crowding each other at a full rotation. These pathologies often go hand in hand. For example, brachycephalic patients with significant skeletal deformity of the skull and shortened facial features are prone to periodontal disease in these areas due to additional surface area for plaque accumulation. A brasion /A ttrition (AB or AT) A crown is affected by both internal and external factors. Abrasion is caused by outside influences such as wear from chewing hard or abrasive objects (tennis balls, treats, toys, etc.). Attrition is a defect caused by two teeth in the mouth making repeated contact, causing wear of the enamel. Both types of pathology are gradual and are accompanied by tertiary dentin, which is the body’s process of protecting the tooth by forming a barrier to the dentin and pulp. Tertiary dentin is smooth and glassy, often showing dark circles around the pulp beneath. C rown F ractures Fractures are classified by their effect on the tooth. Complicated fractures expose the pulp causing pain and immediate vulnerability to infection. Uncomplicated fractures do not expose the pulp but still make the tooth vulnerable to infection through the dentin’s microscopic tubules. Although unlikely to cause pain directly, it should be documented in the dental chart as an “area to watch”. When the fracture advances below the gumline, it is further classified with the following terms: • Complicated crown fracture: CCF • Complicated crown/root fracture: CCRF • Uncomplicated fracture: UCF • Uncomplicated crown/root fracture: CCRF (often referred to as Slab Fracture) G ingival R ecession (GR) Recession is measured in millimeters from the cementoenamel junction (the normal location of the gingival margin) to the current level of the gingiva which is part of a total attachment loss. E xtrinsic S taining (ES) Extrinsic staining effects only the enamel and is characterized by a tan, rust, or brown color. It can be found with or without enamel defects and can be referred to as generalized if it is affected by many/most teeth in the mouth. D iscolored T ooth (I ntrinsic S taining ) (IS) or N on - vital (T/NV) Staining inside the tooth (intrinsic) is a sign that the tooth has somehow been traumatized and inflammation occurred (pulpitis), leaving blood from the pulp canal to enter the dentinal tubules. As time passes, the tooth may appear pink, purple, grey, or tan. It is rare that a tooth can recover from pulpitis; most of the time, these teeth will be diagnosed by the doctor as non-vital. Evidence shows that 92% of discolored teeth are dead and 42% of those studied had no radiographic changes. Discolored teeth should be treated and thus recorded and discussed with the owner.
• Mesial: toward the midline (nose) • Distal: toward the back of the mouth
• Palatal: inside surface of a tooth on the maxilla • Lingual: inside surface of a tooth on the mandible • Combinations of these terms to describe exact location: mesiobuccal, distopalatal, mesiolingual, etc.
STAGES AND INDICES S tages of P eriodontal D isease • PD0 Anatomically normal, no gingivitis • PD1 Mild gingivitis, no bone loss • PD2 Early perio, <25% attachment loss • PD3 25 - 50% attachment loss • PD3 25 - 50% attachment loss • PD4 >50% attachment loss F urcation I ndex • F1 Probe halfway into the furcation • F2 Greater than halfway • F3 Through and through C alculus I ndex - C rown is C overed • C1 <25% • C2 25-50% • C3 >50% M obility I ndex • M1 0.2 - 0.5mm in one direction • M2 0.5 – 1mm in one direction • M3 – 1mm in any direction: “the joystick” COMMON PATHOLOGY R otation and C rowding - ROT/CWD
HIGHLIGHTS
WEBINAR
Rotation is an abnormal angle of a tooth relative to other teeth in the arcade. Crowding is when teeth lack an interdental space, either overlapping or
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S uper - eruption (SE) Not to be confused with gingival recession, super-eruption is a pathology where the tooth is being pushed out in cats with inflammation from periodontal or endodontic disease. It may be bilateral, or a unilateral affected tooth can be compared to the contralateral tooth. S upernumerary (SN) An abnormal increase in the number of teeth or tooth structure is referred to as supernumerary, a tooth with an additional root, an additional tooth in a normal configuration in an arch, or an additional tooth in an abnormal location. They can be documented as duplicates of an anatomically normal tooth. For example, the presence of a right maxillary first premolar (105) and an additional tooth of similar conformation can be charted as 105 and SN 105. An illustration of the additional tooth in a diagram contributes to thorough recordkeeping. D raining T ract (DT) A draining tract can occur inside or outside the mouth. Inside the mouth, they can be very subtle near the location of the apex of a tooth, with or without bleeding or purulent discharge. F istula /F istulae Fistulation (an abnormal path into or through a structure) occurs in several common locations. On the palatal aspect of the maxillary canines, a fistula leading into the rostral nasal cavity is called an oronasal fistula (ONF). Similarly, a fistula in the maxilla's caudal aspect that communicates with the sinus cavity is called an oroantral fistula (OAF). An orofacial fistula (OFF) communicates from a tooth root to the outside of the mouth with a typical presentation of a draining tract below the eye. O ral M asses (OM) Abnormal tissue of any kind should be measured and documented. With or without pigmentation and attachment, any type of abnormal gingival or mucosal tissue may be considered a mass. C hewing L esions (CL) Chronic trauma to the mucosa is common in patients with malocclusion or excessive tissue in the cheeks or under the tongue. This tissue is not usually ulcerated but cannot be definitively diagnosed without a biopsy. Measure and document regardless of if a biopsy is collected. G ingival E nlargement (GE) Do not refer to a gingival mass as an “epulis” or excessive gum tissue as hyperplasia, as is common in general practice. Those are histopathological diagnoses and terms that cannot be used without a biopsy. Measure the abnormality in millimeters and document it on a diagram. T ooth R esorption (TR) There are 3 types and 5 stages of tooth resorption that can occur in both dogs and cats. During oral exams, it can be documented as TR if a lesion is found above or at the gumline level. The type is assessed via radiographic interpretation and can be further noted in the doctor’s assessment and treatment plan. Touching these lesions with an explorer instrument can elicit chattering even under anesthesia.
F eline C hronic G ingivostomatitis (FCGS) There are several facets to the diagnosis of FCGS, none of which are fully assessed by the oral exam alone. Documenting caudal inflammation (the back of the mouth) and proliferative (extra) tissue is the extent of what is documented outside of the SOAP. C aries (CA) Caries are the equivalent of “cavities” in humans. They affect the crown and often cause discomfort or pain if they advance deep into the dentin. Using the explorer tip helps detect cavities by identifying areas that lack enamel. This is common on the occlusal surface of the maxillary molars. A systematic approach to dental exams combined with accurate documentation makes a world of difference in managing oral health issues in animals. By following these steps, utilizing tools like the AVDC nomenclature and modified Triadan system, and recognizing key pathologies, veterinary teams can catch problems early and take action before they progress. With strong teamwork and attention to detail, the "find it and fix it" mindset ensures pets get the care they need to live healthier, more comfortable lives.
REFERENCES
1. AVDC® Nomenclature. American
Veterinary Dental College, 3 Apr. 2024, avdc.org/avdc-nomenclature/. 2. Hale FA. Localized intrinsic staining of teeth due to pulpitis and pulp necrosis in dogs. J Vet Dent. 2001;18(1):14-20. 3. Holmstrom, S. E. (2013). Veterinary dentistry: A team approach. Elsevier/ Mosby. 4. Niemiec, B. A. (2012). Veterinary Periodontology. John Wiley & Sons. 5. Niemiec, B. A. (2013). Small animal dental,
Oral & Maxillofacial Disease: A Color Handbook. Manson Publishing/The Veterinary Press; CRC Press.
HIGHLIGHTS
WEBINAR
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