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Taking Care of your Pet’s Teeth at Home

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by Dr. Daniel T. Carmichael

Taking Care of your Pet’s Teeth at Home

The consequences of poor dental health go way beyond bad breath.  Periodontal infection can lead to serious health concerns ranging from tooth loss to organ failure.  It’s also no secret that dental problems are common in animals – studies have shown dental problems to be the most common problem in both dogs and cats, with periodontal disease at or near the top of the list.  When our animal patients receive good dental care, they undoubtedly live longer and better lives.

The specific dental problem that we strive to prevent is periodontal disease, and the “cause” of periodontal disease is related to the presence of plaque bacteria on the tooth surface.  The goal of dental home care is to retard the accumulation of plaque and calculus on the tooth surface.  Plaque bacteria can colonize a clean tooth in a period of 24 – 36 hours.  This means that within just a few days following professional dental cleaning, the pet’s teeth are already starting to accumulate the bacteria that will again cause periodontal inflammation and disease.  The good news is that home care can prevent this.

Getting Started

Dental home care for the veterinary patient starts at the veterinary office.  Patients must be evaluated for the presence of dental disease, and treated, if necessary, prior to beginning a home care program.  The fact is that 80% of dogs over the age of three and at least 50% of cats have significant periodontal disease that requires immediate professional treatment.  Professional dental treatment, performed when needed and under general (inhalant) anesthesia, is the cornerstone of preventative dental health for our patients.  On average, dogs and cats benefit from an annual prophylaxis (cleaning) starting at the age of three, but each patient needs to have its dental program individualized.

Many dental problems in dogs and cats are painful.  For patients with painful dental problems, home care is contraindicated.  In fact, the discomfort caused by trying to brush a painful tooth may adversely condition the pet to future attempts at home care.  This is why home care should be instituted only after appropriate professional treatment has established a clean and healthy mouth (except in the youngest and healthiest of patients).  This concept especially applies to the institution of a textured dental diet.  Ideally, dental home care programs should be instituted with the puppy or kitten before any dental pathology has started.

What to Do

Look for the VOHC seal
The Veterinary Oral Health Council (VOHC) exists to provide an objective means of recognizing commercially-available products that meet pre-set standards of effectiveness in controlling the accumulation of dental plaque and calculus (tartar) in dogs and cats.  The VOHC does not test products itself.  Companies wishing to have a product reviewed submit a detailed report of the testing that has been performed using VOHC protocols and standards.  If, after detailed review of the submission, the VOHC agrees that the product meets its pre-set standards, the product is awarded the VOHC seal.  There may be commercial products available without the VOHC seal that are effective, but we can be sure that products that have earned the VOHC seal are truly effective and can be recommended without hesitation.  More information on the VOHC, and the products that have earned the VOHC seal, can be found at www.vohc.org.

Brush those teeth every day
Daily tooth brushing is the best thing you can do at home to promote good oral hygiene.  Brushing the teeth once a week, or every three days is not enough.  A daily tooth brushing is necessary because plaque bacteria can re-colonize the tooth surface in a period of 24 – 36 hours.

The basic tools of tooth brushing include a toothbrush and toothpaste.  The toothbrush should be soft bristled, and a battery-powered toothbrush (Hartz Mountain, Secaucus, NJ) for dogs has been found to be a good performer.  The vibrations of the battery-powered toothbrush seem to be well tolerated by most dogs.  Another appropriate choice is simply a soft-bristled, children’s toothbrush that is available at most drug stores and supermarkets.  The traditional pet toothbrush, long-handled and double ended, can be cumbersome for small breeds but is appropriate for large and dolichocephalic (long faced — like Greyhounds) breeds.

The toothpaste should be thought of as a flavoring to enhance acceptance of the toothbrush.  Studies in humans show the use of dentifrice does not contribute to the instant mechanical plaque removal during manual tooth brushing.  The mechanical action provided by the use of a toothbrush is the main factor in the plaque-removing process.

How to brush
To start, place a small amount of toothpaste on the finger and let the pet sniff and lick it.  If there is positive interest in the flavor of the toothpaste, use it.  If the pet is not interested in the toothpaste, brush the teeth without it.  Do not use human toothpaste because it contains fluoride that should not be swallowed.   Concentrate on the buccal (outside) surfaces of the teeth.  Go slowly, and be patient.  If things aren’t going well, wait a few hours before trying again.  The toothbrush should be held at a 45° angle to the tooth surface, with the bristles pointing toward the gingival (gum) margin.  This allows the cleaning of the gingival sulcus (under the gums) during the tooth brushing process.  Work the toothbrush in a circular motion concentrating around the canine tooth and upper fourth premolar tooth.  Try for 15 seconds on each side of the mouth.

Feed a dental diet
There are several commercial diets that have been shown to significantly impact periodontal health compared to “regular” dry food diets.  This isn’t just marketing hype — studies document significant reduction in the plaque, calculus and/or gingivitis index for the foods tested.  The mechanism of action for these dental foods is based on either enhanced textural characteristics of the kibble to provide for mechanical cleansing of the teeth (such as Hills T/D, Hills Oral Care, Purina Veterinary Diet DH, and Friskies Feline Dental Diet), or chemical coating of the food with polyphosphate (such as IAMS Dental Defense and Eukanuba Adult Maintenance Diet for Dogs).  The polyphosphate coating works by binding and chelating minerals in the saliva to make them unavailable for the development of calculus.  Therefore, the diets that utilize enhanced textural characteristics can reduce plaque as well as calculus, whereas the chemical coated diets are effective only against calculus.  Another dental diet, Royal Canin’s Dental DD, combines the mechanical and chemical properties of textural enhancement with pyrophosphate coating.  With the incidence of periodontal disease so high in dogs and cats, there are few reasons why anyone would choose to not provide a diet that promotes good oral health.

Offer appropriate chew treats
Rawhide treats and other consumable items are readily available to pet owners and are effective in the control and removal of plaque and tartar from dog’s teeth.  Rawhide is highly digestible, and has not been observed to cause the digestive problems that conventional wisdom ascribes to them in the numerous scientific studies documenting its effectiveness.  It has also been shown that coating rawhide treats with calcium sequestering substances such as sodium hexametaphosphate can further enhance plaque and tartar reduction.  Chew treats that have earned the VOHC seal of approval include: Del Monte Tartar Check Dog Biscuit: Small and Large Sizes, Friskies Cheweez Beefhide Treats, Greenie Edible Dog Treats – multiple sizes (Note: this is the “Old” greenie product that has had some controversy regarding gastrointestinal problems), Hartz Flavor Infused Oral Chews: Large Dog and Small Dog sizes, Vetradent Dog Chews, and Feline Greenies.

There are chew toy-type products on the market today that are not recommended due to their tendency to cause tooth fracture.  Products such as “nylon bones,” cow hooves, and “real bones” are too hard and often are associated with slab fracture of the carnassial teeth in dogs.  Tennis balls are notorious for causing attrition (mechanical wearing of the tooth surface) and are also not recommended.

Apply a barrier sealant
OraVet (Merial, Duluth, Georgia) is a biologically inert polymer that bonds to the surface of teeth and inhibits plaque and calculus adherence.  The product is very easy to apply on anesthetized patients after dental prophylaxis and must also be applied weekly at home to maintain the protective barrier.  A study by Gengler and co-workers has documented the effectiveness of OraVet in plaque and calculus removal.  OraVet should be thought of as another tool in the home care armamentarium that can be used in conjunction with tooth brushing and everything else mentioned to promote periodontal health.

Oral rinses and gels
Chlorhexadine gluconate, formulated as an oral rinse or a gel, is an excellent oral disinfectant.  The chlorhexadine will bind to gingival tissue, and can then exert its anti-bacterial effects over a 24 to 48-hour period.  Chlorhexadine kills the bacterial pathogens that contribute to periodontal disease and halitosis, and bacterial resistance does not develop.  Chlorhexadine can cause staining of the tooth surface that is reversible.  Chlorhexadine is recommended in chronic cases of periodontitis; instruct the owners use chlorhexadine twice a week, with “regular” tooth brushing on the other days.

MaxiGuard (Addison Biological Laboratory, Fayette, Missouri) is an oral gel that contains zinc ascorbate.  Zinc is antibacterial and ascorbic acid (Vitamin C) is necessary for collagen production.  In a study in cats, there was a significant decrease in plaque, gingivitis, and anaerobic periodontal pathogens in the group treated with zinc ascorbate gel.

A vaccine to prevent periodontitis
Dental home care is traditionally thought of as what we can do at home to prevent the accumulation of plaque and calculus on the tooth surfaces.  Recently available is a novel approach to preventing periodontitis (periodontal bone loss) in dogs.  Recent studies have shown that the most commonly isolated periopathogens from the oral cavity of dogs with periodontitis are three species of the black-pigmented anaerobic bacteria:  Prophyromonas gluae, P. salivosa, and P. denticanis.  A bacterin (vaccine) has been created (Porphyromonas Denticanis-Gluae-Salivosa Bacterin, Pfizer Animal Health, New York) that has been shown to be safe in field studies, and effective in experimental models.  The experimental studies offer a “reasonable expectation of efficacy” for use in the real world.  This now available “periodontal disease vaccine” will provide veterinarians with an innovative tool to add to our arsenal in the fight to prevent this most common disease of dogs, and should be incorporated into a total home care program.

Feline Dental Problems

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by Dr. Daniel T. Carmichael

Feline Dental Problems

Introduction

Dental disease is common in domestic felines. In fact, dental problems are the most common disease that we see in cats, and many dental problems are painful. The most common sign of pain in cats, however, is no sign at all. By diagnosing and rendering appropriate treatment, we can eliminate pain and afford our feline patients a better quality of life.

The vast majority of feline dental problem can be grouped into one of five disease categories: Periodontal disease, feline odontoclastic resorptive lesions (FORL), fractured teeth, feline gingivitis/stomatitis syndrome, and oral neoplasia (cancer).

Basic Anatomy

Kittens are born adentuous (without teeth). By one to two weeks of age, the deciduous or temporary teeth begin to erupt. The six-week-old kitten should have a full complement of 26 deciduous teeth. Between four and five months-of-age the deciduous teeth will be shed, and the permanent teeth will erupt. By six months of age, a total of 30 permanent teeth will have erupted that comprise the complete feline adult dentition. These 30 teeth include 12 incisors, 4 canines, 10 premolars, and 4 molars. If the primary dentition fails to be shed by the time the permanent tooth erupts, a condition called “retained deciduous teeth” occurs.

The dental formula of the cat is as follows:

Cat:    Deciduous teeth: 2X (3/3 i, 1/1 c, 3/2 pm) = 26
Permanent teeth: 2X (3/3 I, 1/1 C, 3/2 PM, 1/1 M) = 30

Feline teeth are “hollow” and the hollow chamber inside the tooth– the pulp cavity (root canal)– contains the blood vessels, nerves and lymphatics that comprise the dental pulp. The pulp tissues communicate with the rest of the body through multiple small openings located at the root apex (tip of the root). The pulp chamber is surrounded with a tissue called dentin. Dentin is a hard tissue that is produced by odontoblasts, and forms the bulk of the tooth’s structure. As the tooth ages the odontoblasts continue to produce dentin, causing the dentin to thicken and the pulp chamber to narrow. On the crown of the tooth, which is the part of the tooth visible above the gum line, a protective layer of enamel covers the dentin. The root dentin is covered by cementum, which is where the periodontal ligament fibers insert.

The periodontium consists of the structures “around the tooth” that function to attach the tooth in the mouth. The periodontium consists of the gingiva, the alveolar bone, the cementum, and the periodontal ligament.

Pathology (Disease)

Pathologic conditions are common in the mouth of the cat. A broad classification of feline dental pathology includes disease conditions that affect the teeth, and disease conditions that affect the structures around the teeth. The common “tooth lesions” in cats are feline odontoclastic resorptive lesions and dental fractures. The common “around the tooth lesions” diseases include periodontal disease (gingivitis, periodontitis), and the severe inflammatory condition called feline gingivitis/stomatitis syndrome (lymphocytic-plasmacytic stomatitis). The lesions of feline gingivitis/stomatitis syndrome include inflammation of the periodontal structures as well as the oral mucosa (and sometimes the lips and tongue). Oral neoplasia (cancer) can affect soft tissue, bone, and tooth structure.

Equipment for Treating Dental Disease in Cats

A minimum amount of equipment that is necessary for performing routine dental care in feline patients includes a high-speed dental drill and a dental x-ray machine. Attempting to accurately diagnose and treat the most common dental problems in cats without intraoral radiography and high-speed drills puts both the practitioner and patient at a disadvantage. No small animal practice that performs dental procedures should be without this equipment.

Feline Periodontal Disease

Periodontal disease is very common in cats. Left untreated, periodontal disease can cause oral pain, oral abscess formation, osteomylitis, tooth loss, and vital body organ infections from bacteremia. Most cases of advanced periodontal disease in felines could have been preventedthrough a program of early disease detection and appropriate treatment.

Periodontal disease is caused by the presence of plaque bacteria on the teeth and the host’s response to that bacteria. The combined effects of bacterial toxins and the products of the host’s inflammatory response cause the periodontal tissues to become inflamed, and if the not checked by professional intervention, destroyed. An “over-response” by the host’s immune system may explain why some individual patients or certain breeds (Maine Coon, Ragdoll, Oriental Breeds, and others) exhibit rapidly progressing and/or more severe disease.

The early stage of periodontal disease is characterized by halitosis and gingivitis. Because the cat’s gingiva is very narrow, this gingivitis may not appear dramatic—but it is! This early stage of periodontal disease, gingivitis, is one of the few oral disease conditions where we can perform treatment and return things to a good state of health. Especially in cats, we need to look for this at an early age. It is not uncommon to see cats at 6 or 8 months of age with significant oral inflammation, the so-called juvenile-onset gingivitis. If left untreated, by the age of 12 -24 months this may quickly progress to irreversible periodontitis. Treatment recommendations for cats with early stage periodontal disease include frequent professional prophylaxis, and daily homecare.

Once periodontal disease has progressed into the more advanced stages, periodontitis, the treatment plan is geared more toward damage control than prevention. The loss of periodontal tissue (gingival, bone, periodontal ligament) that occurs with periodontitis is, in most cases, irreversible. In cats, advanced periodontal disease can quickly progress to a point where extraction is the only valid treatment option remaining. If the goal is to save teeth, aggressive treatment combined with daily homecare is required. If advanced periodontal treatment (flap surgery, etc.) is being considered, make sure you have good radiographic documentation to rule out feline odontoclastic resorptive lesions. The presence of FORLs will doom your periodontal treatment to failure. Clinically, there are very few cases where advanced periodontal surgery is warranted in felines. These select cases usually involve the canine teeth that have relatively longer roots. Because the roots of the incisors, premolars and molars rarely exceed 7-8 mm., periodontal pockets of similar depth that could reasonably be managed in a dog or in a human doom these short feline teeth for extraction. (Figure 3) There is a fine line between prophylaxis and exodontia in the cat.

Treatment Recommendations for Feline Periodontal Disease

  • Yearly or Semi-Annual Examination of the Oral Cavity Under General Anesthesia
    Dental prophylaxis, complete oral examination, and intraoral radiographs as indicated to evaluate for other pathology. Be prepared to perform extractions as needed. It is not uncommon to discover more pathology than you bargained for after the cat has been anesthetized, radiographed, and fully examined.
  • Daily Homecare
    Daily tooth brushing is the best thing you can recommend for pet owners to do at home to promote good oral hygiene. A daily tooth brushing is necessary because plaque bacteria can colonize on teeth in a period of 24-36 hours. This means that within a just a few days following your prophylaxis, the teeth are already starting to accumulate the plaque bacteria that cause periodontal disease. If nothing is done to prevent or retard the accumulation of plaque, the periodontal disease process will continue unchecked.
  • Dental Diets
    There are several commercial diets that have been shown to significantly reduce plaque and tartar when fed compared to “regular” dry food diets. This isn’t just marketing hype—studies document significant reduction in the plaque index for the foods tested. Specifically these foods are IAMS Daily Dental Care, Hills T/D (prescription diet) and Oral Care, and Friskies Dental Diet. With the incidence of periodontal disease so high, there are few reasons why anyone would not want to provide a diet that promotes good periodontal health.
  • Other Products
    Oral rinses, sprays, and other such products also have a role in homecare. These products are sometimes used after oral surgery when brushing is not appropriate. In pets that refuse brushing, these products may be the only kind of homecare possible.

Dental Fractures

Tooth fracture occurs most commonly in cats following trauma. When a tooth has been broken, the pulp chamber is often exposed to the oral environment. The pulp exposure can be visualized on oral examination as a pink (vital pulp) or black (necrosed pulp) spot at the site of exposure.

Any time a pulp cavity is exposed, it must be treated. Exposed pulp is painful to the animal and can lead to periapical osseous (bone) infection. There are two treatment options whenever an exposed pulp is encountered. The first is to extract the tooth; extraction fulfills the treatment goals of preventing pain and infection, as long as no broken roots are left behind. A second option is the save the tooth by performing endodontic therapy (root canal) if an intraoral radiograph shows the tooth to be treatable. Teeth with evidence of resorptive lesions are not candidates for endodontic therapy and should be extracted.

Feline Odontoclastic Resorptive Lesion (FORL)

Feline odontoclastic resorptive lesions (also known as neck lesions, cervical line erosions, and cat cavities) are the most common dental problem in cats. Studies worldwide have shown incidence rates in cats presented for dental problems of up to 75%! Feline odontoclastic resorptive lesions (FORL) are painful. Clinical signs associated with FORL include anorexia, drooling, refusal to eat the hard portions of the diet, and overall malaise. The most common sign of pain in cats, however, is no sign at all.

On oral examination, these lesions are often associated with a localized, cherry-red, sometimes-hyperplastic area of gingivitis. The most commonly affected teeth are the mandibular third premolars, the maxillary third and fourth premolars, and the canine teeth; however, all 30 teeth in the cat’s mouth are at risk. FORL lesions can be demonstrated on oral examination by gently brushing the suspected lesion with a thin wisp from a broken wooden “Q-tip”. Gentle stimulation of these lesions invokes a strong jaw-chattering response.

Restoration (fillings) of FORL is controversial. The controversy lies in the fact that the majority of restorations fail. With these poor results in mind, and the etiology of this disease unknown, it has been the opinion of the majority of the veterinary dental community that all teeth affected with FORL be extracted. A crown amputation procedure has been described for “extraction” of teeth exhibiting FORL. In this procedure, the crown of the tooth is removed while intentionally leaving the roots behind. Cats with associated periodontal disease or gingivitis/ stomatitis should never be considered candidates for crown amputation. Dental radiography is essential for accurate diagnosis and treatment planning.

Feline Gingivostomatitis

Probably the most frustrating oral disease we see in our clinical practice is feline gingivitis/stomatitis syndrome (FGS).  Cats will present with clinical signs of partial to complete anorexia, drooling, halitosis, and oral pain.  Physical exam will show various signs of gingivitis (inflammation of the gingiva), stomatitis (inflammation extending to the oral mucosa), palatitis, faucitis (inflammation of the caudal fauca), glossal ulceration, and pharyngitis.  There is often an associated submandibular lymphadenopathy (swollen glands).  When a cat presents with clinical signs compatible with this syndrome, a complete diagnostic workup is necessary.

To start with a complete physical exam, CBC/Chemistry, feline serology and other ancillary tests as indicated should be performed. The results of the blood tests are usually unremarkable, except for a hyperproteinemia resulting from a hypergammaglobulinemia. The feline retrovirus infections are certainly associated with oral inflammation, but most cats with FGS are retrovirus negative.

Next, a dental prophylaxis should be performed.  All teeth exhibiting feline odontoclastic resorptive lesions and all teeth with end-stage periodontal disease should be extracted.  Also, any root tips or fragments need to be removed.  Never leave root tips behind in these cases.  Dental radiographs are essential when evaluating for retained roots.  A biopsy should be performed, including samples from the gingiva and affected areas in the pharynx.

The results of the biopsy often show “lymphocytic-plasmacytic stomatitis”.  This is not a diagnosis.  This is the typical histological picture whenever cats have chronic inflammation.  The histopathological results that we may see to alter our treatment include eosinophilic granuloma, autoimmune diseases, or neoplasia.

Following dental prophylaxis, the owners need to be counseled to provide daily home care.  Most cases of feline gingivitis are thought to result from an over- exaggerated immune response to plaque bacteria.  In some cases, simply keeping the oral environment clean will keep this condition in check.

When the biopsy results show lymphocytic/plasmacytic inflammation and home care is not working, treatment options include medical or surgical management.  Surgical treatment, involving extraction of all teeth caudal to the canines, has been shown to be 85% effective in curing this disease.  This is a labor-intensive procedure, and will not be successful if any root fragments are left behind.  In some cases, areas of inflamed or infected bone surrounding the alveolus also need to be removed.  It is difficult, if not impossible, to perform this procedure without dental x-rays and high-speed drills.

Feline Oral Cancer

Unfortunately, the vast majority of tumors found in the mouths of cats are malignant and carry a poor prognosis.  Over 20 different types of cancer have been reported to occur in the oral cavity of felines, although only a few are observed commonly.  Among the more common feline oral neoplasms are squamous cell carcinoma (SCC), fibrosarcoma,  lymphoma, and malignant melanoma.  Squamous cell carcinoma is by far the most common, accounting for about 70% of feline oral neoplasms.  It is of extreme importance to identify the tumor type and commence treatment early in the course of disease if a favorable treatment outcome is to be achieved.  In the majority of cases, however, a clinical cure is not possible.

Any swelling (soft tissue or bony) or abnormal appearance of tissue in the oral cavity must be considered suspicious for neoplasia.  A common but very subtle presentation of oral neoplasia is when a tooth can be extracted too easily.  The results of the biopsy should be discussed with a veterinary oncologist to offer up-to-date treatment options and prognosis.

Cataract Referral

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by Dr. Noelle La Croix, DVM, Dip. ACVO

A cataract is any opacification of the lens.  Crystallins within lens fibers, or the lens fibers themselves, are disorganized within a cataract.  Ultimately, crystallin disorder decreases transparency or light transmittance.  Cortical cataracts are histologically associated with disordered, swollen, and ruptured lens fibers.  These ruptured fibers are not normally repaired.  In contrast, senile nuclear cataracts are characterized by disordered crystallins within dense but ordered fibers.  Cataracts have many etiologies including genetic, metabolic, environmental, and senility factors.

Stages and Referral

Cataracts can be classified by etiology, age of onset, location, appearance, and stage of progression. The stage of progression is the most widely used and useful classification. The most common progression stages are incipient, immature, mature, and hypermature. Incipient cataracts are the earliest to appreciate clinically and usually take up no more then 10 to 15% of lens volume (Figure 1).

Patients with incipient cataracts are ideal for referral to an ophthalmologist. Incipient cataract progression is dependent upon both position and appearance, as evaluated by slit lamp biomicroscopy. Incipient cataracts allow for a clear view of the fundus for diagnosis of retinal and vitreal disease without ultrasonography.

Not all incipient cataracts progress. Generally, congenital incipient cataracts within the lens nucleus will not progress. In most cases, non-progressive incipient canine cataracts do not require surgical removal as they do not limit functional vision. Incipient cataracts near the active proliferative lens equator will often progress. In these cases, anti-inflammatories can help prevent phacolytic uveitis. Cataract surgery is most successful on eyes without a clinical history of phacolytic uveitis.

The immature cataract is at the ideal stage for cataract surgery. Immature cataracts are characterized by low density areas, with clear lens fibers, that allow for tapetal reflection through the lens. Immature cataracts are often swollen with fluid, forming large separation clefts within the lens. These clefts can be used as areas for lens fracture during cataract surgery. However, extreme swelling can result in intumescence. Intumescent lenses are associated with glaucoma, and the loss of vision via pupillary blockage and ciliary cleft closure (Figure 2). Severe uveitis is also associated with intumescent lenses which leak large amounts of proteins into the aqueous humor.

Mature cataracts typically involve the entire lens, completely obscuring tapetal reflection. These advanced cataracts can be associated with uveitis, capsular plaques, and lens instability. Increased intra-operative and post-operative complications, and decreased visual outcome, are associated with mature cataract surgery. The lens fibers of mature cataracts continue to break down and release lens proteins. Over time, phacolytic uveitis progresses, and the lens capsule wrinkles from epithelial cell proliferation and shrinkage of the lens volume. A hypermature cataract has a wrinkled lens capsule with a swollen milky cortex. This is the result of autolysis of the lens fibers of a mature cataract. During cataract surgery distorted capsules predispose them to tearing and prevent the implantation of artificial lenses. In addition, some mature and hypermature cataracts are not candidates for surgery because advanced phacolytic uveitis has already caused glaucoma, retinal detachment, and/or retinal degeneration.

Veterinary Cataracts

Humans typically present earlier stages of cataracts then dogs. Human eyes contain an extremely dense area of cones (the macula and fovea) for sharp central vision. Any small opacity in the lens overlying this area is associated with a dramatic change in functional vision, quickly vocalized to an attending physician. In contrast, dogs contain a less dense area known as the “visual streak” and have an appreciably lower visual acuity then humans. If the typical human eye scores 20/20 on the Snellen eye chart, the typical canine eye would score 20/75. Anything below the 3rd line of the Snellen chart would be a blur to a dog. Therefore, typical domesticated dogs do not depend on fine visual acuity to survive, and will not usually show visual dysfunction with early stage cataracts.

In the veterinary world cataracts typically present in later stages, when first appreciated by owners. Ideally, incipient cataracts are managed medically to control phacolytic uveitis. Immature and mature cataracts can often be removed with phacoemulsification. Other ocular issues must be addressed including the control of phacolytic uveitis, intraocular pressure, and tear production. As with all anesthetic surgical procedures, pre-disposing conditions (diabetes; liver or kidney disease; elevated blood pressure, etc.) must be managed prior to cataract surgery. Infections (skin, oral, and bladder) should be resolved prior to cataract surgery to decrease the risk of post-operative endophthalmitis. Ocular and systemic issues can often be managed in tandem.

Post-operative care following cataract surgery is demanding. Owner and patient compliance with the large and precise regimen of medications should be considered prior to surgery. Cataract surgery is considered an elective procedure as most animals will adapt to visual losses. However, conditions associated with cataracts (uveitis, lens luxation, glaucoma, etc.) that affect an animal’s quality of life should always be addressed.

Captions:

Figure 1: A posterior subcapsular cortical cataract in the left eye of a 1.5-year old Golden Retriever. This incipient cataract has a genetic basis and is associated with phacolytic uveitis.

Canine Bacterial Keratitis – When Ulcers Go Bad

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by Dr. Noelle La Croix, DVM, Dip. ACVO

Canine Bacterial Keratitis – When Ulcers Go Bad

The cornea is a transparent tissue lacking pigments, blood vasculature, and keratinized epithelia. These properties are essential for vision, but also make the cornea susceptible to infection. The tear film acts as a physical barrier to microrganisms, prevents microbial growth with lysozyme and lactoferrin, and provides nutrition to the corneal epithelium. The tear film is replenished by the lacrimal glands, adheres to the corneal epithelium via mucin of goblet cells, and reforms during blinking. Lipids, excreted by the meibomian glands, prevent tear film evaporation from the corneal surface.

Minor injuries and abrasions to the corneal epithelium are well tolerated. These superficial (non-infected) ulcerations drive corneal nerves to release neuropeptides that restore epithelial integrity, promote cellular proliferation, and encourage wound healing. Mitotic cells slide into and fill these epithelial defects. An entire corneal epithelium can regenerate in most species within 48 to 72 hours.

When the corneal stroma is injured (deep ulceration), a more complex process of repair is instigated. In the damaged stroma, proteolytic enzymes are produced by inflammatory cells, corneal epithelia, fibroblasts, and introduced microorganisms. Excessive degradation (melting) is naturally prevented by proteolytic inhibitors found within the cornea and tear film. Clinically introduced inhibitors (0.2% EDTA, 0.1% doxycycline, 10% N-acetylcysteine, and/or 100% fresh serum) can further reduce this proteolytic degradation of the cornea. If proteolysis is not adequately inhibited, the melting cornea can perforate in less than 24 hours.

The clinical treatment for any corneal ulceration begins with a thorough examination, including Schirmer tear testing, fluorescein staining, and tonometry. Trauma and other medical history should be considered. The eyelids are examined for trichiasis, distichia, and ectopic cilia. Eyelid margins are inspected for meibomianitis. All conjunctival surfaces are examined for foreign bodies. Palpebral responses are tested. Finally the depth of the ulceration is accessed and classified as superficial or stromal.

Most simple superficial (often traumatic) ulcerations will heal within 7 days. To prevent infection, these uncomplicated ulcers are most effectively treated with a topical triple antibiotic (neomycin, polymyxin B, and bacitracin).

Corneal indentations and depressions are indicative of deeper stromal ulcerations. These ulcerations are often associated with bacterial infections (bacterial keratitis). Clinical signs of bacterial keratitis include corneal edema, corneal stromal cell infiltration, corneal melting, and the loss of corneal stroma (Figure 1). Scrapings of the infected area should be cytologically examined and submitted for culture and sensitivity testing. These serious infections usually require referral to an ophthalmologist, and/or hospitalization for hourly antibiotic and antiprotease treatment. Antibiotics and other drugs are delivered via the tear film since the cornea lacks a blood supply. Therapeutic drug concentrations are difficult to sustain in dogs with their high tear film turnover rate.

Most dogs with bacterial keratitis are brachycephalic, and about half will show decreased tear production (< 15 mm/min). Many brachycephalic dogs are lagophthalmic and so poorly replenish the tear film by blinking. In these breeds, medial canthal trichiasis and distichia can both cause ulceration and inoculate bacteria within the tear film. Dogs with decreased tear production do not effectively remove and lyse bacteria from the corneal surface. In these cases, bacterial access to the corneal epithelium is also increased.

Staphylococcus intermedius (29%), beta-hemolytic Streptococcus spp. (17%), and Pseudomonas aeruginosa (21%) are the most common organisms found in cases of canine bacterial keratitis. Many bacteria contain at least one antibiotic resistance gene, so a prophylactic combination of antibiotics (e.g.; tobramycin/ciprofloxacin) is often prescribed.

Both superficial and stromal ulcerations should be re-evaluated within 48 hours of initial examination. Superficial ulcers can quickly develop stromal involvement requiring more aggressive therapy. The close monitoring of the ulcerated patient will help prevent corneal melting and loss of vision.

Captions:

Figure 1: A melting corneal ulcer in the left eye of a Jack Russell Terrier. Photo credit: Laura Eppig.

Interventional Radiology Techniques

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by Dr. John Fondacaro, Diplomate ACVIM & Dr. Sean Hillock, Diplomate ACVIM

Interventional Radiology Techniques (Offered at the Veterinary Medical Center of Long Island Internal Medicine Department) 

Bronchoscopic intraluminal stents for tracheal collapse and other occlusive tracheal diseases.

Urethral stents for obstructive urethral diseases.

Transurethral submucosal collagen implantation.

Since there is not an abundance of information about these procedures in the literature, the following general information will help you decide which patients may be possible candidates and allow you to adequately prepare owners prior to referral.

Bronchoscopic intraluminal tracheal stents:
Self-expanding metallic tracheal stents are an effective alternative to surgical placement of extraluminal support rings. They are mainly indicated for patients with severe intra or extrathoracic dynamic tracheal collapse that continue to cough and remain uncomfortable despite aggressive medical management for their conditions. Other potential indications include tracheal stenosis, neoplasia, and strictures. The stents are placed with bronchoscopic guidance after full assessment of the lower and upper airways and careful measurement of the affected segement(s).

Medical management with weight control, corticosteroids, antitussives, bronchodilators, +/- antibiotics, and sedatives should be tried before the patient is referred for stent placement. Not all patients with tracheal collapse are candidates for this procedure. Pre-placement bronchoscopy to fully evaluate the lower airways for bronchomalacia and lower airway collapse will be required. If found to be a candidate, thoracic radiographs with positive end-expiratory pressure and negative pressure applied to the airways will be performed to size the stent for the individual patient.

Owners should be made aware that this is a salvage procedure, continued medical management will be required lifelong, and that complications are more likely to occur over time (especially if coughing is not controlled with medical management). Follow-up bronchoscopy will be strongly recommended, if not required, within the first three months after placement (or sooner if the patient is having difficulties) to check for complications such as granuloma formation, migration, infection, fracture, and adjacent segment collapse.

Urethral stents:
Urethral stenting is a novel treatment modality for obstructive diseases of the urethra, mainly urethral and prostatic neoplasia. This palliative procedure can allow normal urine flow despite some very aggressive obstructive urethral disease. This procedure will allow time for chemotherapeutic intervention (chemo, NSAIDS) to affect the tumor or to allow time until natural disease progression occurs, if the owners do not elect chemotherapeutic intervention. As with the tracheal stents, careful measurement of the urethra is required. This is done with the use of positive contrast to accurately measure normal urethral diameter and the affected length of the urethra prior to stent placement.

Owners should be made aware of the potential for urinary incontinence (approximately 25-35% of the time), urinary tract infection, re-stricture due to re-growth of tumor at the opposing ends of the stent, and stent migration.

Urethral collagen implantation:
This procedure is a novel treatment for urethral sphincter mechanism incontinence that is non or no longer responsive to medical management with estrogen, PPA, and/or imipramine, etc. This procedure can be performed on an outpatient basis. Bovine collagen is injected at the urethral orifice and acts as an anatomic sphincter to prevent urine leakage. There are few complications associated with this procedure, but mainly include continued urinary incontinence or relapse of incontinence over time. Most patients that relapse will require a repeat injection or concomitant therapy with PPA and/or estrogen.

I am very excited to offer these novel therapeutic interventions to our referring veterinarians and their patients. Over time, I hope to expand the scope of what we can do with similar techniques. Please do not hesitate to contact either Dr. Fondacaro or Dr. Hillock at the VMCLI if you have any questions regarding these new procedures.

Cranial Curuciate Ligament Instability: Introducing the Tibial Tuberosity Advancement

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by Dr. Margret Puccio, DVM, Diplomate ACVS

Cranial Curuciate Ligament Instability: Introducing the Tibial Tuberosity Advancement

Cranial cruciate ligament injuries are one of the most common causes of acute and chronic lameness in dogs and are also seen as a cause of lameness in cats. Unstabilized cranial cruciate ligament tears place the patient at risk of meniscal damage and osteoarthritis of the stifle joint. It has been reported that up to 80% of patients will have concurrent meniscal tears and 40% of patients will rupture the contralateral cranial cruciate ligament within one to two years. Reported success rates for surgical repair have been greater than 90%. Many surgical techniques for repair have been described to stabilize the cranial cruciate ligament deficient stifle. Currently, the most common surgical techniques performed include the Extracapsular Lateral Suture Technique, the Tibial Plateau Leveling Osteotomy, and the Tibial Tuberosity Advancement.

The Extracapsular Lateral Suture Technique is an effective and economical procedure and is technically the least challenging of the three fore-mentioned surgical techniques. This technique mimics the constraints and stability of the cranial cruciate ligament by placing a non-absorbable suture in an extracapsular, isometric position. The Extracapsular Lateral Suture technique can be performed in all sized dogs and cats.

More recently developed surgical techniques for reduced morbidity and greater stability in patients, particularly in active and larger sized dogs are the Tibial Plateau Leveling Osteotomyand the Tibial Tuberosity Advancement. Both techniques achieve stifle joint stability by neutralizing the tibiofemoral shear forces (cranial tibial thrust) dynamically in the cranial cruciate ligament deficient stifle. Both techniques involve an osteotomy of the proximal tibia for repositioning and are stabilized with specialized implants. Implants are rarely removed after bone healing is achieved.

The Tibial Plateau Leveling Osteotomy was developed by Dr. Barkley Slocum in the early 1990’s. With this technique cranial tibial thrust is stabilized by reduction of the tibial plateau angle. This is accomplished by a radial osteotomy of the proximal tibia and rotation of the segment in a caudal direction. The new position is maintained with a specialized left or right tibial plateau leveling osteotomy plate and screws until bone healing occurs. See Figure 1.

The Tibial Tuberosity Advancement was developed by Dr. Slobodan Tepic and Professor Pierre Montavon in the late 1990’s. The Tibial Tuberosity Advancement neutralizes tibial thrust by positioning the patella tendon perpendicular to the tibial plateau slope at the normal weight-bearing angle of 135 degrees. This is accomplished by an osteotomy of the tibial tuberosity and advancing the bone segment cranially in the frontal plane. The new position is maintained with specialized tibial tuberosity implants until bone healing occurs. See Figure 2.

Both the Tibial Plateau Leveling Osteotomy and the Tibial Tuberosity Advancement can be applied in small to large sized patients with the appropriately sized implants. Reports have demonstrated the techniques performed in dogs from 5 kg to 92 kg. Both techniques are comparable in cost. The Extracapsular Lateral Suture Technique is significantly less than both in cost. The advantages the Tibial Tuberosity Advancement offers over the Tibial Plateau Leveling Osteotomy are decreased morbidity immediately post-operatively; stability that is achieved without compromising joint congruity; and it is technically less invasive as the procedure does not alter the primary loading axis of the tibia.

Cranial cruciate ligament instability remains a commonly treated condition with many surgical technique options. Factors such as the patient’s health status, economics, activity, size, and age influence the decision making process for surgical repair. When deciding between the newer dynamic stabilization repair techniques, other considerations are bone confirmation and concurrent patella luxation.

Please feel free to contact me with any questions or concerns you may have in order that we may make the best recommendations and decisions for surgical treatment of your patients.

Genetic Testing in Veterinary Ophthalmology

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by Noelle La Croix, DVM, Dip. ACVO

Genetic Testing in Veterinary Ophthalmology

As discussed in an earlier article, the selective breeding of the canine has greatly diminished the genetic diversity within each specific breed.  In populations of low genetic diversity, recessive alleles are more likely to pair.  Paired non-lethal recessives often generate phenotypes with decreased biological fitness.  Recessive defective alleles are maintained in heterozygous (carrier) dogs within a population.  Genetic testing can screen for these “hidden” alleles, and reduce the likelihood of breeding animals with defective pairings.

Eliminating all the carriers within a gene pool would unfortunately further reduce a breed’s genetic diversity.  The remaining gene pool might have reduced biological fitness for other unforeseen traits.  For example, a dog carrying genes asssociated with progressive retinal atrophy (PRA) might also carry associated genes promoting healthy hip conformations.  The general goal of selective breeding is therefore to reduce but not necessarily eliminate non-lethal alleles.

Human genetic testing became routine in the 1960’s with the karyotyping of fetal cells following amniocentesis.  Molecular biology techniques developed over the last 30 years have rapidly advanced and refined this genetic screening for numerous abnormalities.  In 1999, the chromosomal location of genes associated with Progressive Rod Cone Degeneration (PRCD) was determined in dogs.  The chromosomal location for PRCD is equivalent to that associated with human retinitis pigmentosa.  Although the actual protein product(s) responsible for the PRCD have yet to be determined, genetic screening for PRCD is now common.

Genes or markers for different forms of retinal dysplasia and retinal degeneration have been determined.  The Collie eye anomaly (CEA or choroidal hypoplasia) is a disorder associated with incomplete choroidal vasculature development.  Approximately 25% of dogs afflicted with CEA develop retinal detachments, optic nerve colobomas, and/or abnormal vascularization with secondary hemorrhage.  A recessive gene responsible for CEA can be screened for.  A gene associated with lens luxation has also been recently discovered.

There are two common types of genetic screenings.  The first are “marker-based” tests in which a disease is closely associated with a known, and sometimes seemingly unrelated, genetic sequence.  For example, Multiple Congenital Ocular Anomalies (MCOA) is most typically found in silver-colored horses of the Rocky Mountain breed.  The silver-color genes map to the same chromosomal location as those involved in MCOA.  The silver color can therefore be used as a marker for genetic predisposition to MCOA.  The specific genes responsible for MCOA are not known, but can thus be screened for indirectly.

The second common type of screening is “gene-specific.”  Mutations in genes known to cause disease are directly screened for.  The risk of error for true Mendelian disease traits (with complete penetrance) is extremely low when using these tests.  The specificity and sensitivity of gene-specific tests can reach 100%.  Very few “false positive” or “false negative” results are generated.  However, laboratory error, mis-sampling, and/or misinterpretation of results can still invalidate even a gene-specific test.

Many breeders request their family veterinarian to perform genetic screening for ocular and other disorders.  Generally, 2 or more mls of whole blood are collected in tubes with EDTA to prevent coagulation.  In New York, Cornell’s OptiGen® genetic screening laboratory accepts mailed samples on weekdays, but not on weekends and holidays.  Detailed packaging requirements, and the variety of available genetic screenings, can be found at www.optigen.com.

As with any clinical test, genetic screening results must be interpreted with regard to each individual patient for future breeding.  The tests can provide accurate and meaningful information to breeders and other owners.  If you have any questions about inheritable ocular disorders or their genetic screening, please feel free to consult with a veterinary ophthalmologist.

Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006

https://www.vmcli.com

Figure 1: Retinal Degeneration and CEA found in different breeds for 2008 by OptiGen®.

Ocular Herpes in Kittens

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by Noelle La Croix, DVM, Dip. ACVO

Ocular Herpes in Kittens

The feline herpesvirus (FHV-1) was first isolated in 1958. The virus can replicate within the conjunctival epithelia, upper respiratory tract epithelia, and sensory ganglia. Neuronal infection with FHV-1 establishes lifelong latency with intermittent re-activation and viral shedding. Virus transmission is commonly associated with exposure to acutely infected cats, or recrudescing latently infected cats. Environmental contamination with FHV-1 is not considered a significant route of transmission.

The feline herpesvirus can be transmitted via oral, nasal, and/or conjunctival routes. Kittens under 6 weeks of age do not typically show clinical signs of herpes as maternal antibodies confer passive immunity. The primary source of kitten infection is also their lactating mothers who shed the herpesvirus after queening. Clinical signs of FHV-1 infection typically last 2 weeks while virus is actively shed for 1 – 3 weeks. Cats that exhibit clinical signs of herpes will generally become lifelong carriers of this low mortality and mild morbidity virus. The herpesvirus is believed to be endemic within the cat population, so that any stressed or immunosuppressed cat has the potential for recrudescence. In one study, 70% of cats shed herpesvirus when administered glucocorticoids.

Immunity to FHV-1 is primarily cell-mediated. Vaccination is recommended for all cats between 9 and 12 weeks of age, followed by a booster 1 year later. Vaccinated indoor cats have a low risk of viral exposure and should be re-vaccinated every 3 years. Free-roaming cats should be re-vaccinated yearly. Importantly, vaccination decreases the likelihood of displaying the clinical signs of herpes, but it does not protect against initial or repeat infection with FHV-1.

Acutely FHV-1 infected kittens display fever, depression, anorexia, and serous oculonasal discharge. Secondary bacterial infection is associated with a purulent oculonasal discharge. Some infected kittens also develop viremia or pneumonia. The infection can be lethal. Less frequently oral, ocular, and/or skin ulcerations are associated with infection. Secondarily infected corneal ulcerations can lead to corneal rupture and subsequent globe loss.

A common secondary complication of corneal ulceration associated with herpes is symblepharon, in which the erosive surfaces of the conjunctiva and cornea adhere to each other (Figure 1). Adhesions lasting beyond a few days can permanently fibrose. Ideally, during an active herpes infection, any early conjunctival-corneal adhesions should be broken down every 2 – 3 days with a cotton applicator to prevent fibrosis. Fibrosis can also be inhibited by decreasing the factors (fibrinogen, thromboplastin, and other clotting factors) associated with fibrin production. Frequent lubrication, medication, and flushes of the eye can reduce these factors.

When a cat presents with fibrosed symblepharon and corneal scarring, veterinarians are often tempted to break down these adhesions to improve vision. However, mechanical breakdown of these fibrosed adhesions is highly inadvisable. Fibrosed symblepharon can mask corneal ruptures and removing conjunctival tissue may result in globe rupture. Conjunctival cells have also transferred to the cornea in symblepharon. The removal of conjunctival tissue will therefore not prevent re-scarification, since conjunctival cells will multiple to seal any newly created defects. Symblepharon resection will also not typically remove eyelid scar tissue that can interfere with eyelid function. All erosive epithelial surfaces tend to re-adhere, and so there is a high risk for symblepharon recurrence. Cats with symblepharon and limited vision may not be helped by attempting to break their adhesions by any means.

Scarification is often associated with symblepharon and herpes because of the phenomena known as corneal limbal stem cell exhaustion (Figure 2). Corneal epithelia are continuously lysed by herpesvirus, so that corneal stem cells become overburdened attempting to replace them. Conjunctival cells will then act as replacements, resulting in scarification.

The ocular manifestations of herpes are common in young cats, but few older cats show both ocular and respiratory signs at the time of presentation. Kittens presenting with bilateral oculonasal purulent discharge are commonly diagnosed with herpes. Primary treatment should include restoring fluid and pH balance (preferably via IV fluids). Food intake is extremely important in these kittens, and I recommend hand-feeding of a palatable diet. Nasogastric tube feeding can be initiated if an infected kitten does not eat for 3 consecutive days. Broad spectrum antibiotics, such as Clavamox (amoxicillin/clavulanic acid), will help prevent secondary bacterial infections. Topical ocular antibiotics, such as erythromycin or Terramycin, will also decrease the likelihood of Chlamydia, mycoplasma, and other secondary bacterial infections. Pain management should be initiated as the erosions associated with herpes are painful. The eyes and nostrils of kittens should be cleaned routinely, and nebulization of acetylcystine will increase comfort. As previously stated, any early conjunctival-corneal adhesions should be broken down every 2 – 3 days to prevent permanent fibrosis.

Antiviral therapy is also important in controlling the ocular manifestations of herpes. Herpesvirus replication is inhibited by 0.1% idoxuridine (Wedgewood Pharmacy) applied topically 6 times daily. Alternatively, Viroptic (trifluridine) can be used, but burning or stinging during ocular application is common. An ocular flush with a dilute (0.2%) iodine solution can also be effective.

A number of oral medications are also used to treat herpes in cats. Oral L-lysine (250 – 500 mg BID) alleviates the clinical signs of herpes, and decreases viral shedding when administered to indoor or hospitalized cats. However, recent studies indicate that oral L-lysine may not be effective in preventing herpes outbreaks within shelters. Oral famciclovir (¼ of 125 mg tablet BID or ½ of 125 mg tablet SID) inhibits herpesvirus replication. Other medications that have been used to treat herpes include acyclovir, ganciclovir, cidofovir, and feline or human interferon.

Kittens commonly present with ocular manifestations of FHV-1 infection. Simple treatments can often alleviate their clinical signs of herpes. If you have any questions about ocular herpes, please do not hesitate to contact a veterinary ophthalmologist.

Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006

https://www.vmcli.com

Figure 1:  The right eye of a kitten with symblepharon.

Figure 2:  The left eye of a kitten with corneal scarification.

A Review of Canine and Feline Oral Tumors

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by Dr. Daniel T. Carmichael
(thank you to Jill Costigan for editorial advice)

A Review of Canine and Feline Oral Tumors

Key Points:

  • There are a variety of neoplastic (cancerous) and non-neoplastic lesions that can be found in the oral cavities of dogs and cats. An accurate diagnosis is required to offer appropriate treatment recommendations
  • Oral biopsy is a procedure that must be performed correctly to obtain an accurate diagnosis
  • Regional lymph node evaluation is an important part of a complete diagnostic workup for oral malignancies

The oral cavity is a common site of malignant neoplasia in both the dog and the cat. Tumors of the oral cavity can be classified as odontogenic tumors (neoplasia arising from tooth-forming tissues), non-odontogenic tumors, or non-neoplastic lesions.

In dogs, the non-odontogenic tumors include the three most common malignant oral neoplasms: melanoma, squamous cell carcinoma, and fibrosarcoma. Odontogenic tumors, generally considered to be rare, are actually common if the odontogenic benign tumors are included. Non-neoplastic lesions, such as cysts, hyperplasia, and inflammatory or infections processes, present a varied set of pathologies and treatment recommendations.

Unfortunately, the vast majority of neoplasms found in the mouths of cats are malignant and carry a poor prognosis. Over 20 different types of cancer have been reported to occur in the oral cavity of felines, although only a few are observed commonly. Among the more common feline oral neoplasms are squamous cell carcinoma (SCC), fibrosarcoma, lymphoma, and malignant melanoma. In fact, SCC alone accounts for about 70% of all feline oral tumors. Neoplasia must be suspected in all lesions of the feline oral cavity where an obvious cause is not clear. Any swelling (soft tissue or bony) or abnormal appearance of tissue in the oral cavity must be considered suspicious for neoplasia. In one study, however, it was shown that one-half of the swellings in the lower jaw bone of cats were non-neoplastic. A common, but very subtle presentation of oral neoplasia is when a tooth can be extracted too easily. Common presenting signs for cats with oral neoplasia include: an obvious oral mass, excessive salivation, weight loss, halitosis, bloody oral discharge, and dysphagia.

Initial work-up for oral tumors in dogs and cats

The successful management of any oral tumor depends on an accurate histopathological diagnosis prior to definitive treatment. An accurate histopathological diagnosis requires a representative sample of the tumor and a pathologist well versed in oral pathology to evaluate it.

Prior to the biopsy procedure, the patient should receive a thorough physical and oral examination. The oral lesion should be carefully inspected and described in terms of its location, size, shape, presence of ulceration or necrosis, and additional associated findings such as loose teeth in the tumor area. The regional lymph nodes should be carefully palpated, and irregular enlargements or lack of mobility (suggesting tissue fixation) must be noted. Finally, a thorough physical examination of the entire patient should be performed to detect signs of distant metastasis or other problems Blood work (CBC and blood chemistry analysis), urinalysis, and chest x-rays are also indicated to complete a pre-biopsy workup.

Obtaining an oral biopsy

The recommended method for obtaining an oral biopsy sample is an incisional biopsy taken from the within the boundaries of the tumor so that no marginal tissue planes are violated by the biopsy procedure. The biopsy sample should be taken atraumatically to restrict exfoliation of neoplastic cells. In larger tumors, it is best to obtain multiple samples from different locations within the mass. Oral biopsy procedures should be performed under general anesthesia maintained with a cuffed endotracheal tube. At the time of biopsy, existing dental pathology should be addressed if possible. The area suspected of containing the neoplasm should be radiographed, ideally with intra-oral dental radiographs because of their superior detail.

At the time of oral biopsy, while the patient is under general anesthesia, radiographs and other diagnostic imaging (CT, MRI) can be performed.

Treatment: canine tumors

“Epulis”

The term epulis has been applied to a variety of oral tumors. The so-called fibromatous and ossifying versions of epulis are actually odontogenic fibromas (arising from periodontal ligament), and are curable with complete surgical removal. The so-called acanthomatous epulis, on the other hand, is actually a peripheral ameloblastoma and is very locally aggressive (but will not metastasize.) The “acanthonmatous epulis” can also be cured by surgical resection, but wide margins are necessary to obtain complete excision. This tumor is also radiosensitive as well as sensitive to localized chemotherapy, but surgical excision is generally considered the most appropriate course of treatment.

Oral malignancies

Non-odontogenic oral malignancies are best treated on a case-by-case basis based on the results of biopsy, lymph node analysis, and metastatic screening. Tumors that have already metastasized will obviously carry a poorer prognosis. Surgical excision remains the most frequently indicated and most practical method of treatment. In most cases, the ultimate goal is to cure the patient; this is achieved by adequate excision, tumor-free margins, and the absence of metastatic disease. If the extent of disease makes this impossible, palliative surgery can be performed to provide relief from symptoms for as long as possible.

The appropriate width of the surgical margins is paramount for success. The tumor type, size, and client expectations will determine if a marginal, en bloc, or radical excision is indicated. Client education is imperative. Clients must be informed of the possible complications, the esthetic consequences, and the long-term prognosis to avoid misunderstandings and surprises. Owners are often not aware of how good most dogs actually do following major resective surgery.

It is always beneficial to coordinate the efforts of the oral surgeon and an oncologist to offer the patient the most up-to-date treatment options for the best possible outcome. In some tumors, adjunctive therapy with radiation, chemotherapy, or immunotherapy can improve the odds of success following surgery.

Odontogenic tumors and cysts

Odontogenic tumors can present as soft tissue masses such as amelobastoma, or can also involve dental hard tissue, including enamel, dentin, cementum, and pulp. Some of the odontogenic tumors are known to invade bone, and for these tumors en bloc or radical excision is indicated.

Dentigerous cysts are often diagnosed in young adult dogs and commonly are associated with embedded or impacted teeth. Dentigerous cysts can occur in any breed, but are overrepresented in Brachycephalic breeds and are most commonly located just behind the mandibular canines involving with the first mandibular premolars. Any missing tooth, especially missing first mandibular premolar teeth in brachycephalic breed, should be radiographed and extracted if found impacted. The treatment for dentigerous cyst involves surgical debridement of the epithelial cyst-wall lining as well as removal of the offending tooth.

Non-neoplastic oral growths

Non-neoplastic oral growths are common in the dog and include such clinical entities as gingival hyperplasia, inflammatory lesions, and various types of cysts. It is imperative to accurately diagnose these with histopathological confirmation. Bottom line: all oral growths should be biopsied and definitive treatment should be rendered based on the results of that biopsy.

Treatment: feline tumors

Squamous Cell Carcinoma

Feline oral SCC is an extremely invasive and malignant neoplasm. Unfortunately, to date, there are no therapies, or combinations of therapies, that are substantially beneficial for feline oral SCC. The recurrence rate for cats with oral SCC treated with surgery alone (and/or with radiation therapy) is felt to be extremely high with a median survival time less than 6 months, and these authors believe a median survival time of 30 – 60 days is more likely. The exception to this are cats with extremely small oral SCC involving the lower jaw that may be able to undergo major oral surgery, however, it must be stated that even these cases can have recurrence in the face of histopathologically-determined “clean” margins. In addition, the use of radiation therapy as a sole treatment modality is also felt to be correlated with a median survival time less than six months, with a recent report documenting a median survival time of only 60 days with 3 large doses of palliative radiotherapy. Though relatively few reports exist on the sole use of chemotherapy for feline oral SCC, it too is generally felt to be minimally beneficial when used in this way. In fact, these authors believe that the use of single modality therapy for feline oral SCC should be discouraged unless the tumor is a small lower jaw SCC, or if the tumor is being palliatively treated with 3 – 6 large doses of radiation therapy.

The aforementioned lack of efficacy with single modality therapy in feline oral SCC suggests that multimodality therapy and/or novel therapies are necessary to make advances in the treatment of this aggressive cancer. Unfortunately, relatively few reports exist in the literature in this regard.

Fibrosarcoma

Fibrosarcoma (FSA) is the second most common tumor of the feline oral cavity. Approximately 10 – 20% of feline oral tumors are FSA. FSA generally occurs in older cats (median age 10 – 12 years), however, cats as young as one year of age and as old as 22 years have been reported. There does not appear to be any gender predisposition or oral cavity site predilection, however, most cats with oral FSA have their tumors starting in the gingiva.

Other than the above descriptive data, there is extremely little clinical information on cats with oral FSA. Most cats with oral FSA will present for the same problems as cats with oral SCC; however, cats with oral FSA invariably will have a mass effect at the primary tumor site. Non-ulcerated oral FSA invariably has a significant amount of hyperplastic epithelium overlying the tumor, and therefore, procurement of a deep incisional biopsy is recommended to best ensure a correct histopathological diagnosis.

Feline oral FSA are extremely invasive malignancies necessitating wide surgical extirpation. Though few reports exist concerning recurrence rates with feline oral FSA, minimal surgical removal generally results in recurrence. Unfortunately, aggressive surgical extirpation of these tumors with histopathologically determined “clean” margins likely results in recurrence in 20 – 30% of cases due to their incredibly invasive nature. The routine use of radiation therapy in cats with large bulky oral FSA is generally discouraged. However, the use of radiation may be beneficial in cases with incomplete surgical resection for feline oral FSA, or if the radiation is being used palliatively (3 – 6 large doses). Similarly, the use of chemotherapy in this disease is generally discouraged due to the relative chemo resistance of soft-tissue sarcomas. However, chemotherapy is occasionally used in cats with large oral FSA in an attempt to shrink the tumor for later surgical resection, or in cats with high-grade (and therefore greater chance for metastasis) oral FSA.

Fortunately, feline oral FSA are not generally very metastatic. Less than 10% of feline oral FSA cases will have metastasis at the time of presentation. Therefore, this tumor is best treated with locally aggressive therapies. In summary, feline oral FSA are incredibly invasive, but minimally metastatic tumors that can potentially be cured via aggressive local therapies including surgery and/or radiation therapy.

Other Tumors

Though rare, a variety of other diagnoses are on the differential list for feline oral neoplasia. These include lymphoma, osteosarcoma, melanoma, chondrosarcoma, granular cell tumors, fibropapillomas, hemangiosarcoma, ameloblastomas and fibromatous or ossifying epulides. The prognosis for cats with oral lymphoma or hemangiosarcoma is presently unknown because it is such a rare site of involvement, however, the use of local therapy (surgery and/or radiation therapy) and adjuvant chemotherapy would be recommended due to its aggressive local and systemic nature. The other tumors listed above would be generally thought of as locally aggressive, but minimally to non-metastatic tumors, suggesting that aggressive local therapy would have a high chance of being curative.

Ophthalmoscopy

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by Noelle La Croix, DVM, Dip. ACVO

Ophthalmoscopy

To the casual observer a pupil appears black, even though there is a direct transparent pathway from a pupil to a colorful retina.  Ambient light enters an eye through its pupil at a multitude of different angles.  Some of this light is subsequently reflected by the retina, and exits the pupil in assortment of different angles.  The reflected light’s intensity (brightness) is usually below an observer’s threshold for perceiving a clear image of the retina, and this absence of light appears as blackness.  However, a condensed (bright and compact) light source can easily generate an observable reflection from a retina.  In photography this phenomenon is known as ‘red-eye’ and it occurs when a flash (condensed light) is reflected by a subject’s eyes.  Fortunately the reflection of condensed light has been put to practical clinical use in visualizing the retina.  It is the underlying principle of all ophthalmoscopy.

Direct ophthalmoscopy uses a condensed light source to reflect an erect (non-inverted) image of a subject’s retina to an observer.  It is a simple technique that typically produces highly magnified images of retinae.  However, a 15 to 17 fold magnification greatly reduces an observer’s field of view.  Only a fraction of a retina can be visualized at any particular moment.  A thorough retinal exam by direct ophthalmoscopy is therefore time consuming, and made more difficult by moving animal subjects.

Direct ophthalmoscopy is also limited by relatively dim light sources that cannot be reflected by a ‘cloudy’ media.  Retinae are poorly visualized in cases of nuclear sclerosis, or in any eyes with hazy vitreal or aqueous fluid.  A direct ophthalmoscope’s light source can also be advantageous.  Dimmer lights reflect truer color images of optic nerves than brighter lights.  This is particularly useful in diagnosing optic nerve atrophy or neuritis.  The bright light source of an indirect ophthalmoscope will generally blanch out the color of an optic nerve.

In indirect ophthalmoscopy, a convex lens is placed between the observer and subject generating an inverted image.  A binocular indirect ophthalmoscope emits a bright light that is reflected back to both eyes of an observer.  This results in a significant increase in the depth perception of an observer.

An indirect ophthalmoscope typically produces images with lower magnification than that of a direct ophthalmoscope.  The associated increase in an observer’s field of view significantly reduces the time it takes to thoroughly visualize an entire retina.  The difficulty of this technique involves maintaining a direct line of sight.  A light source, lens, and reflected image must be maintained in a straight path from an observer to subject at all times.  An observer can only visualize reflected retinal light within a limited field of view dictated by this line of sight.  Novices will typically move their head during indirect ophthalmoscopy in an attempt to ‘see around’ the retina.  This head bobbing will remove an observer from a line of sight and a retinal image will be quickly lost.  With indirect ophthalmoscopy the only way to scan an entire retina is by establishing multiple lines of sight.The bright light source of an indirect ophthalmoscope can also be used to visualize a retina through a cloudy media.  The high quality lenses of indirect ophthalmoscopes are designed to reduce both spherical and chromatic aberrations.  These instrument can even be used to visualize an undistorted retina behind lenticular, aqueous, or vitreal opacities.

A monocular indirect ophthalmoscope produces an erect magnified image.  It is therefore simple to use (like a direct ophthalmoscope) and also has an increased field of view (like an indirect ophthalmoscope).  However, it lacks the stereopsis and the larger image size of a binocular indirect ophthalmoscope (Figure 1).

All forms of ophthalmoscopy are best performed in a darkened room.  Pupillary dilation allows for more thorough retinal scanning during the procedure.  Ophthalmoscopy can be used to routinely monitor the visual and systemic health of both dogs and cats.  If you have any questions about ophthalmoscopy, please don’t hesitate to contact a veterinary ophthalmologist.

Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006

https://www.vmcli.com

Figure 1: The normal canine fundus as it appears through direct (A), monocular indirect (B), or indirect (C) ophthalmoscopy (photos courtesy of David Ramsey).